Wayne Notes Surgery

Wayne Notes
Senior Surgery
2nd Edition
Now with Wayne's Notes on Urology,
ENT & Instruments
Notes Prepared and Created by:

Wayne Robinson (Class of 2015)
Compiled and Bookmarked by:

Anggelos
Wayne Robinson, MBBS Class of 2015
General Surgery
Trauma
Sources: TEAM Booklet (ATLS), Essential Surgery 5E
March 2015
ATLS ALGORITHM STARTS ON PAGE 3

Some general points
§ Major trauma is the most common cause of death in young people almost everywhere
TRIMODAL DEATH DISTRIBUTION

Death due to injury occurs in one of three time periods.
1. First peak of death = within seconds to minutes from injury =

§ Deaths generally result from lacerations of the (brain, brain stem, high spinal cord), (heart, aorta, and other large blood
vessels). Very few of these patients can be salvaged due to the severity of their injuries. Only prevention can significantly
reduce this peak of traumatic deaths
2. Second peak = within minutes to several hours following injury (ATLS focuses primarily on this peak)
§ Deaths usually due to: HEAD = (subdural and epidural haematomas), CHEST = (haemopneumothorax), ABDOMEN =
(ruptured spleen, liver lacerations, pelvic fractures), and/or other multiple injuries associated with significant blood loss.
Hard Signs vs Soft Signs of Vascular Injury
§ The "first hour" = “golden hour” (Famous MBBS question)
3. Third peak = several days to weeks after the initial injury. Hard Signs - Signs that require immediate
surgical exploration w/o imaging
§ Deaths most often due to sepsis and multiple organ system failure Pulsatile bleed, Expanding Hematoma,
Vascular Occlusion (Pulselessness, Pallor,
The most important concept of ATLS is to treat the greatest threat to life first! Parathesia)
Soft Signs - Needs imaging to determine next
“PHYSIOLOGIC APPROACH” step in treatment
Hematoma, Neurological deficit
§ The physiologic approach to the evaluation and treatment of the injured patient is based on the fact that the airway, breathing, and circulation are
an integrated system of organ function designed to carry oxygen to the body's cells.
§ Core organs (for example, brain) require a continuous supply of oxygen and nutrients for optimal function. Because of the sequential nature of
oxygen delivery, a patent airway and adequate breathing are necessary before the circulation can deliver oxygen.
§ Therefore, the loss of an airway or ability to breathe kills more quickly than does diminished circulating blood volume
Mnemonic "ABCDE" should be followed in all injured patients:
A. Airway maintenance with cervical-spine protection + adjuncts

B. Breathing and ventilation with life-threatening chest injury management + adjuncts
C. Circulation with control of haemorrhage +adjunts
D. Disability or neurologic status with intracranial mass lesion recognition

E. Exposure (undress) and Environment with maintenance of body temperature + adjuncts
(Don’t forget the parts that come after the “with”!!!! Especially for A. NEVER forget to say “with c-spine stabilization” for A in trauma)
Assessment and Management Sequence
1. The PRIMARY SURVEY, conducted simultaneously with resuscitation, consists of a rapid, systematic evaluation of the airway, breathing,
circulation, disability, and exposure/environment, treating life-threatening conditions as they are discovered. Adjuncts, such as urinary
and gastric catheters, vital signs, monitoring devices, and chest and pelvic x-rays included
2. SECONDARY SURVEY, AMPLE Hx + thorough head to toe examination. A - Allergies, M - Medication, P - Past medical history,
L - Last meal eaten (food and drink incl. EtOH), E - Events prior to accident
The primary and secondary surveys should be repeated frequently to identify any deterioration
In the actual clinical situation, many of these activities occur in parallel or simultaneously!!!
DON’T FORGET: All personnel who have contact with the patient must be protected from communicable diseases. Most prominent among these
diseases are hepatitis and human immunodeficiency virus (HIV) infection. The Centers for Disease Control and Prevention (CDC) and other health
agencies strongly recommend the use of standard precautions (for example, cap, face mask, eye protection, water-impervious gown/apron, leggings,
and gloves) when coming in contact with body fluids. The ACS Committee on Trauma considers these to be minimum precautions and protection of all
health care providers. This also is an Occupational Safety and Health Administration (OSHA) requirement in the United States.
PRIMARY SURVEY
Patients are assessed and their treatment priorities established based on their injuries, their vital signs, and the injury mechanism. These priorities are
the same for ALL injured patients, including the adult, pediatric, and pregnant patients!
The patient's vital functions must be assessed quickly and efficiently. Patient management must consist of a rapid primary evaluation, resuscitation
of vital functions, a more detailed secondary assessment, and finally, the initiation of definitive care
ABCDE frequently accomplished simultaneously
§ Re: Children: Vigorous initial response BUT limited compensatory reserves, so short lived. priorities for the care of the pediatric patient are the
same as for adults
§ Re: Elderly: Aging diminishes physiologic reserve.

o Chronic cardiac, respiratory, and metabolic disease may reduce the ability of the patient to respond to injury in the same manner that
younger patients are able to compensate for the physiologic stress imposed by injury.
o Comorbidities, such as diabetes, congestive heart failure, coronary artery disease, COPD, coagulopathy, liver disease and peripheral
vascular disease are more common and adversely affect outcome following injury to the older patient.
o ALSO, the chronic use of medications may alter the usual physiologic response to injury. The narrow therapeutic window frequently leads to
over or under resuscitation
§ Re: Pregnant: Priorities for the care of the pregnant woman are similar to those for the nonpregnant patient. First priority is maternal
resuscitation
REMEMBER THIS PRINCIPLE FOR THE ABCDEs OF THE PRIMARY SURVEY:
EACH STEP CONSISTS OF AN ASSESSMENT AND AN ACTION/INTERVENTION

SEE NEXT PAGE
A. AIRWAY AND C-SPINE PROTECTION

Goals: 1. Identify airway compromise/obstruction and 2. Secure a definitive airway
1. AIRWAY
ASSESSMENT ACTION/INTERVENTION
First determine patency. 1. Establish patency while protecting c-spine using chin-lift or modified jaw thrust as
Determine patency by asking pt to speak. If they speak initial maneuver
their airway is patent. Also feel for air on yourhands or
face to check for breathing. - Anggelos 2. Airway suctioning next – to clear excess secretions
Features suggesting airwayobstruction include:1. 3. Finger sweep or forceps to remove particulate matter if present
Gurgling
2. Stridor 4. Airway adjuncts as necessary (see BLS notes for the 7 adjuncts):
3. Hoarseness § NPA – If conscious
4. Rocking chest wall motions § OPA – If unconscious/no gag reflex
If definitive airway needed (E.g. GCS 8 or less, severe head injury):
(Must also recognize potential for progressive airway § ET tube
loss) § Surgical airway: Cricothyroidotomy if ET tube contraindicated or cannot be
established (swelling, jaw fractures)
2. C-SPINE PROTECTION
*Aim is to protect the spine and spinal cord
1. Always protect c-spine while managing airway (Don’t hyperflex, hyperextend or rotate)
2. “Manual inline immobilization” Done to prevent the conversion of a partial cervical injury into a complete cervical injury
3. Then apply appropriate immobilization devices: rigid cervical collar + sandbags or lateral head supports + strapping tape +
long spinal board
↓
B. BREATHING
Only assess after airway secure. (Ventilation requires good function of lungs + chest wall + diaphragm)
PHYSICAL EXAMINATION
Inspection, palpation, percussion, auscultation 1. ALL trauma patients get supplemental oxygen via 1. facemask with
nonrebreather bag or 2. bag valve mask if intubated (usually
1. Expose chest wall to assess for adequate high-flowoxygen (15 L/min))
excursions, accessory muscle use, respiratory rate
2. Visual inspection + palpation for injuries 2. TREAT LIFE-THREATENING CHEST INJURIES NOW!!! Immediately life-
3. Percuss for air/fluid e.g. blood threatening chest injuries must be recognized and managed during the primary
4. Auscultate for airflow in lungs survey!!!
5. Pulse oximeter
--
Observe specifically for injuries
1. Open chest wound: Seal with 3-way occlusive dressing to limit mediastinal ‘flap’
Open wound,flail segment of chest wall)
movement with each breath + tube thoracostomy
Bech's Triad = Muffled heart sounds + Distended 2. Flail segment: Oxygen, monitoring, analgesia + endotracheal (ET) intubation +
neck veins + Decrease Pulse (cardiac tamponade) assisted ventilation if deterioration
Tracheal deviation and asymmetrical expansion 3. Cardiac tamponade: Pericardiocentesis then thoracotomy
(pneumothorax/tensionpneumothorax)
Dull percussion note (haemothorax) 4. Pneumothorax: May need chest drain/tube thorocostomy if large pneumothorax
5. Tension pneumothorax: Needle chest aspiration + tube thoracostomy
6. Haemothorax: Tube thoracostomy
7. Diaphragmatic rupture: Repair surgically
8. Serious head injury: ET tube + assisted ventilation
↓
C. CIRCULATION
Assess circulation only when the patient’s airway is secure and the above life-threatening conditions have been excluded, or
identified and treatment under way.
(See haemorrhage classification table)
MOST CRITICAL STEP IS TO RECOGNIZE 1. MOST CRITICAL STEP IS TO STOP THE BLEEDING
SHOCK
§ External bleeding à Control by direct pressure on gauze pack
1. Central pulse (femoral or carotid) BILATERALLY o Tourniquets should NOT be used as they crush tissues and cause distal ischaemia,
2. Cold/clammy extremities except in unusual circumstances such as a traumatic amputation of an extremity
§ Internal bleeding à Operative intervention!!!!
3. Pallor
4. Blood pressure
2. AFTER controlling haemorrhage, next vital step is restoring blood volume by 2 large bore
5. Level of consciousness!! (may indicate IV cannulae into antecubital fossa or other large veins (BUT!!! SEE PERMISSIVE
impaired cerebral perfusion!) HYPOTENSION). LR preferred
6. Catheterize and urine output!! (Reflects
volume statis AND renal perfusion!)
§ If cannulation not possible, venous cut-down (Saphenous Vein used. Located 2cm
Note contraindications: Transurethral bladder above & anterior to medial malleolus or direct bone infusion (Interoseous Infusion
catheterization is contraindicated in patients in whom may be necessary
urethral transection is suspected. Urethral injury should § When venous access achieved, send blood for urgent cross-matching, and standard
be suspected if there is (1) blood at the penile meatus, biochemical and haematological analysis
(2) perineal ecchymosis, (3) scrotal hematoma, (4) a § In the shocked patient, rapidly infuse 2 liters of WARMED crystalloid solution
through both peripheral intravenous lines; monitor response of pulse palpability, rate
high-riding or nonpalpable prostate, or (5) a pelvic
and BP and titrate rate of infusion (note permissive hypotension may be
fracture. Accordingly, the urinary catheter should not be
appropriate)
inserted before an examination of the rectum and
§ If the patient fails to improve, consider transfusion of red cells (type-specific blood
genitalia. If urethral injury is suspected, urethral integrity
should be confirmed by a retrograde urethrogram before preferred). If the patient is rapidly deteriorating, O negative blood can be given
inserting catheter § Consider likely causes of significant blood loss in the light of the history and clinical
findings: e.g. thoracic trauma, abdominal injury, pelvic fracture, long bone fracture
Classification of Hemorrhage § Catheterize the bladder to monitor urine production and to provide a guide to renal
perfusion
Stage 1 - Loss of <= 750 mls (Give Crystalloids)
§ Fracture management — reduction of fractures may assist in haemostasis, especially
Stage 2 - Loss of 750 mls - 1500 mls (Give Colloids) femoral shaft fractures and sometimes pelvic fractures (also helps pain relief)
Stage 3 - Loss of 1500 mls - 2000 mls (Give Colloids + § Further management of circulation depends on likely source of blood loss, e.g. if
Bld) abdominal injury is likely FAST (Focused Assessment with Sonography in Trauma)
Stage 4 - Loss of > 2000 mls (Give Colloids + Bld) ultrasound confirms and laparotomy may be required tocontrol haemorrhage
NOTE: Hypovolemic shock should NOT be treated by vasopressors, steroids, or sodium

bicarbonate, or continued crystalloid/blood infusion. If blood loss continues this should be
controlled by operative intervention
↓
D. DISABILITY
of the central nervous system. Do not move on to assess ‘D’ until patient’s circulatory state is stable
Basic neurological assessment is made using the AVPU score:

A — Alert
V — responding to Verbal stimuli
P — responding to Painful stimuli
U — Unresponsive
Pupil size, inequality and reactivity to light is also assessed
Estimate Glasgow Coma Scale (GCS) if practicable and look for other neurological deficits
A unilaterally dilated pupil is an ominous sign that indicates the presence of a mass lesion, usually an expanding intracranial haematoma.
Immediate consultation with the neurosurgeon is necessary. Failure to recognize and manage an intracranial hemorrhage can lead to
transtentorial herniation and death.
Despite proper attention to all aspects of managing the patient with a closed head injury, neurologic deterioration can occur, often rapidly. The lucid
interval commonly associated with acute epidural hematoma is an example of a situation where the patient will "talk and die."
↓
E. EXPOSURE of the whole patient, ENVIRONMENT and ‘EXRAYS’ (imaging)
The patient is fully exposed, including removal of all clothing, to allow rapid ‘top to toe’ assessment for external injury and for signs of injury which have
not already been recognised and managed. The patient must be kept warm including warming intravenous fluids (Hypothermia is a potentially lethal
condition!!)!!! Completion of the trauma series X-rays, CT scans and FAST ultrasound is performed
Consider the following measures to monitor the patient and aid further assessment, if not already done
§ Urinary catheterization
§ Nasogastric or orogastric tube placement: A gastric tube is indicated to reduce stomach distention and decrease the risk of aspiration.
Decompression of the stomach reduces the risk of aspiration, but does not prevent it entirely
§ X-rays of cervical spine (lateral), chest and pelvis (trauma series)
§ Focused abdominal sonography for trauma (FAST)
X-rays and diagnostic studies:

“Trauma series x-rays” à
1. Cervical Spine
i. Cervical Spine - AP
ii. Cervical Spine - AP Open Mouth (Odontoid)
iii. Cervical Spine - Lateral - Horizontal Ray
iv. Cervical Spine - Swimmers if C7-T1 not visualized
2. Chest - AP
3. Pelvis - AP
Other investigations. Re: CT SCAN;

§ Patients should not be moved to the CT scanner until they are stable— the machine is known as the ‘donut of death’ in ATLS parlance.
SECONDARY SURVEY
The secondary survey is a head-to-toe evaluation of the trauma patient, that is, a complete history and physical examination, including a reassessment
of all vital signs. Each region of the body is completely examined
RE: “PERMISSIVE HYPOTENSION”
More recent studies indicate that permissive hypotension is often a better strategy than the previous recommendation of
rapid indiscriminate crystalloid infusion. If organ perfusion can be maintained, there are advantages in keeping the pressure low in trauma
patients.
Reason:
§ Physiological compensation is effective at systolic pressures between 70 and 85 mmHg, and cerebral perfusion and urinary output are well
maintained.
§ Above this pressure, fresh clot is often dislodged (‘pop a clot’) and then bleeding recurs.
§ A further disadvantage of unnecessary fluid resuscitation is that infusing just 750 ml of crystalloid activates cytokines and causes dilutional
coagulopathy.
Fluid & Electrolyte Management- 6/10/09- Dr. Fray
** In an average person water is 60% of total body weight
- 40% of body weight is intracellular fluid
- 20% is extracellular fluid
Note: ICF is 2/3 of total body fluid and ECF (interstitial + intravascular) is 1/3 of total body
water
- Fluid may cross from compartment to compartment by osmosis which depends on a
solute gradient
- Fluid can also cross based on filtration which is a result of the hydrostatic pressure
gradient
** Intracellular fluid has a low sodium and high potassium concentration

- Extracellular fluid has a high sodium and low potassium concentration
- In the extracellular compartment, interstitial fluid has a low protein concentration in
comparison to intravascular fluid which has a high protein concentration
** To calculate daily fluid and electrolyte requirements, the daily losses should be measured or
estimated
- 100 ml/kg for the first 10 kg
- 50ml/kg for the next 10 kg
- 20ml/kg for the remainder of the weight
** Therefore the maintenance requirement is defined by weight of the patient

** Normal urinary losses are around 1500-2000ml/day
** Normal fecal losses is about 300 ml/day
Electrolyte Requirements
1- Potassium- 0.5 – 1 mEq/kg/day
2- Sodium- 1-2 mEq/kg/day
** In 1L of normal saline there is 154 mEq of sodium

- In 500ml of Lactated ringers there is 139 mEq of sodium
- In the maintenance regime 1 L is given as normal saline and the rest is given as dextrose
water
** All NG losses are added to the maintenance as normal saline

- Therefore for every L of NG aspirate, add 1 L of normal saline to the maintenance
regime
- Also for every L of NG aspirate add 10-20 mEq of potassium
Effects of Surgery
** ADH is released in response to surgery; therefore water tends to be conserved
- Hypovolemia will cause aldosterone secretion and salt retention by the kidney
- Potassium is released by the damaged tissues and potassium levels can be further
increased by blood transfusions.
- Therefore if renal perfusion is poor and urine output is decreased, potassium can build up
in the body post-surgery
- Therefore supplementary potassium may not be necessary in the first 48 hrs following
surgery or trauma
Note: The metabolic response to the injury of surgery causes Na+, K+ and water retention
- Therefore potassium should not be added to the regime until the patient is passing
adequate urine
** Potassium is an irritant to peripheral veins. Therefore administration can cause thrombosis of
the veins
- As a result the drip site should be changed daily
- Potassium should NOT be given as a bolus because it will stop the heart
- Should be added to the fluid bag
- Never give more than 20eQ of potassium in 500 ml
EXAMPLE:
** In a 70-kg patient with normal U/Es and a daily urine output of 1500 ml who also has NG
losses of 2L what should the fluid replacement regime be?
ANS: Total volume to be replaced is 4.5 L (2.5L maintenance + 2L NG replacement)
- 3L = normal saline and 1.5 L = dextrose water
- 60 mEq of KCl should also be added
Note: For every ml of blood lost, 3 ml of crystalloids should be given as replacement
- This is because at least 2 ml of the crystalloid will move into the interstitial compartment
and 1 ml will stay in the intravascular compartment
General Surgery
IV Fluids and Fluid therapy (Can come in OSCE)
Sources: Lecture Notes in Clinical Anaesthesia, Harold Ellis, Dr. Scarlett Lecture
March 2015
BODY FLUID COMPARTMENTS

In the ‘average’ person, water contributes 60% to the total body weight: Therefore, 60% of 70 kg is 42 à 42 L for a 70 kg man.
UWI SAYS, OF THIS 42 L, 2/3 intracellular (ICF = 28 L) and 1/3 extracellular (ECF = 14 L) (ECF = 2/3 interstitial = 9, 1/3 intravascular = 5 L)
The electrolyte composition of each compartment differs.

§ Intracellular fluid has a low sodium and a high potassium concentration.
§ In contrast, extracellular fluid (intravascular and interstitial) has a high sodium and low potassium concentration. Only 2% of the total body
potassium is in the extracellular fluid
SOURCES: LECTURE NOTES IN CLINICAL ANAESTHESIA + TORONTO NOTES

Three types are used: crystalloids, colloids and blood and its components.
§ TOTAL FLUID REQUIREMENT = Deficit + Maintenance + Ongoing loss
§ In surgical settings this formula must take into account multiple factors including pre-operative fasting/decreased fluid intake, increased losses during
or before surgery, fluid shifting during surgery, fluids given with blood products and medications
WHAT ARE THE ONGOING LOSSES?

1. GI: nasogastric aspirates, vomiting, diarrhoea and stomas, fistulae,
2. Tubes/Drains
a. Foley catheter, NG, surgical drains
3. Third spacing (other than ECF, ICF)

a. Pleura, GI (e.g. ileus), retroperitoneal, peritoneal
b. Evaporation via exposed viscera, burns
4. Blood loss
CRYSTALLOIDS
These are solutions of crystalline solids in water.
The solutions can be considered in two groups;
1. Those that contain electrolytes in a similar composition to plasma, have an osmolality similar to plasma and are often referred to as being isotonic,
and
2. Those that contain less or no electrolytes (hypotonic) but contain glucose to ensure that they have an osmolality similar to plasma.
Once these fluids are given they are redistributed amongst the various body fluid compartments, the extent depending on their composition.
CRUCIAL POINTS
§ For example, 0.9% saline is distributed throughout the intravascular and interstitial volumes (extracellular fluid compartment, ECF) in
proportion to their size. After 30 min, only 30% of the volume administered remains intravascular!!! Therefore, if such a fluid
is used to restore the circulating volume, three to four times the deficit will need to be given.
o Traditionally, 0.9% saline solution has been widely used in the perioperative period and as the first line for emergency fluid resuscitation.
However large volumes cause hyperchloraemic metabolic acidosis, as although regarded as isotonic, it
contains a greater concentration of chloride than plasma!!!.
§ If a hypotonic solution is given, for example 5%

glucose , once the glucose is metabolized the remaining fluid is distributed
throughout the entire body water (extracellular and intracellular volumes) and less than 10% will remain intravascular.
Glucose-containing solutions are a way of treating dehydration as a result of water losses but may cause hyponatraemia. They are not routinely
used perioperatively.
RECENT CONSENSUS GUIDELINES RECOMMEND:

§ When crystalloid resuscitation or replacement is indicated, balanced salt solutions, for example Ringer’s lactate/acetate
or Hartmann’s solution, should replace 0.9% saline to reduce the risk of hyperchloraemic acidosis.
§ Excessive losses from gastric aspiration/vomiting should be treated with an appropriate crystalloid solution, which includes an appropriate
potassium supplement. Hypochloraemia is an indication for the use of 0.9% saline, with sufficient additions of potassium and care must be taken
not to produce sodium overload.
§ Losses from diarrhoea/ileostomy/small bowel fistula/ileus/obstruction should be replaced volume for volume with Hartmann’s or Ringer-
Lactate/ acetate type solutions. ‘Saline depletion’, for example due to excessive diuretic exposure, is best managed with a balanced electrolyte
solution such as Hartmann’s.
Saline is also available as a hypertonic solution consisting of between 1.8% and 7.5% sodium chloride solutions. When given, these raise the osmolality
of the ECF (mainly the intravascular component) and create a gradient such that water moves from the intracellular fluid (ICF) into the plasma. The
intravascular volume is expanded by a greater volume than the volume of hypertonic solution given, for example 250mL 7.5% saline results in plasma
expansion by up to 1.5 L. If given repeatedly they will result in intracellular dehydration, which must be corrected subsequently. There is no evidence for
their routine use during in the perioperative period, however, they may have a role in resuscitating patients with traumatic brain injury, where they appear
to reduce cerebral oedema, restore cerebral perfusion and help reduce neuronal injury
Toronto Notes: Crystalloid Infusion

§ Maintain euvolemia in patient with blood loss: 3 mL crystalloid infusion per 1 mL of blood loss for volume replacement (i.e. 3:1
replacement). Controversy surrounds this as an initial vs. maximal replacement target
§ If large volumes are to be given, use balanced fluids such as Ringer’s lactate, as too much normal saline (NS) may lead
to hyperchloremic metabolic acidosis!!!
MUST MEMORIZE THE FOLLOWING FOR LACTATED RINGERS AND NORMAL SALINE
Approach to Crystalloid Fluids -

CRYSTALLOIDS Anggelos
1. Define crystalloid
2. Define type of crystalloid (iso, hypo,
NORMAL SALINE (0.9%) (N/S) – MUST KNOW BY HEART FOR OSCE!! hyper)
+ -
3. State fluid content and assos.
§ Na and Cl content = 154 mmol/L each (THEREFORE THE 500 ML BAG HAS 77 MEQ/L) values (Na, Cl, K, Glucose)
§ Osmolality = 308 mOsm/L 4. State distribution
§ (ALMOST) Isotonic solution – will stay in the ECF (BUT only about 30% remains intravascular after 30 minutes) 5. State complications of use
§ VERY IMPORTANT: “ALMOST” because both the sodium and the chloride content exceed that of normal plasma!! 6. State main usage/Indication
§ So much so that in large volumes, normal saline causes a HYPERCHLORAEMIC METABOLIC ACIDOSIS (Due to the high chloride content AND
recall the pH is also 5.5 – far below the normal 7.4 of plasma!).
§ So it is actually a slightly hypertonic solution at an osmolality of 308 mmol/L, even though it is classified as an isotonic solution!
For hyponatremic patients must know how to correct Na [Na + 2.5 ((Glucose - 5.5) /5.5) and determine Na rate [TBW of male or female * kg * 0.5]
5% DEXTROSE SOLUTION (D/W)
§ 50 g dextrose per L (i.e. 5% = 5 g dextrose in 100 mL, therefore 50 in 1000 ml. So any % dextrose, just multiply it by 10 to get how
much is in 1 liter)
§ 50 g dextrose contains (50 x 4) calories = 200 calories per L & 100 calories per bag (500 ml)
§ Hypotonic solution at 252 mOsm/L
§ If administered in large quantities, will act as a hypotonic solution. Why?
o Once the glucose is metabolized the remaining fluid is distributed throughout the entire body water (extracellular
and intracellular volumes) and less than 10% will remain intravascular.
o Glucose-containing solutions are a way of treating dehydration as a result of water losses but may cause hyponatraemia. They are not
routinely used perioperatively
5% DEXTROSE SALINE
§ 50 g dextrose per L in normal saline

+ -
§ Na = 154 mmol/L and Cl = 154 mmol/L
§ Hypertonic solution – Because the normal saline was already ISOtonic, so the added 50g dextrose per liter even further increases the
osmolality!!
o It increases the osmolality of the ECF. Therefore water is drawn from the ICF compartment à intra-cellular dehydration
5% DEXTROSE 0.2% SALINE (& 7.5% DEXTROSE 0.2% SALINE)

th
§ 50 or 75 g dextrose per L in 1/5 N/S (i.e. 5% = 5 g dextrose in 100 mL, therefore 50 in 1000 ml)
+ th
§ Na = 1/5 = 31 mmol/L
§ Isotonic solution
th
§ Used esp. in children, hypernatraemia (the 1/5 saline allows Na dilution when infused), renal impairment
NaHCO3 8.5% SOLUTION (ALSO HAVE 4.2% SOLUTION) – CAN COME IN OSCE!!!
§ 1 ml of 8.5% NaHCO3 = 1 mmol of bicarb!!!!, or 1 ml of 4.2% = 0.5 mmol.

+
§ High Na content - 1000 mmol/L
§ Osmolality = 2008 mOsm/L
§ Used in CPR
§ Main indication = SEVERE metabolic acidosis
§ MUST KNOW: Formula used to determine necessary amount = 1/3 x body weight x base excess
§ ***VERY SMALL AMOUNT USUALLY REQUIRED (AVERAGE IS 2-4 MLS OVER 15 MINUTES!!!)
§ The goal of bicarbonate therapy is to raise the blood pH to 7.3 and the plasma bicarbonate to 12-15 mmol/l
MUST KNOW: PROF. MCFARLANE LIKES TO ASK THE EQUATION!!

§ Using sodium bicarbonate in severe metabolic acidosis NaHCO3 may be given undiluted as a 4.2% solution. However, some prefer diluting it in 5% dextrose in
water or hypotonic (0.45%) saline solution, depending on the clinical setting.
§
§ The amount necessary can be calculated using the formula: 1/3 x body weight (kg) x base excess, expressed in mmol bicarbonate. (One ml 8.5%
NaHCO3 = 1 mmol, or 1 ml of 4.2% = 0.5 mmol.)
§ It is wise to give only two-thirds of the calculated amount initially, and then reassess the situation. An average dose is 1-2 mmol/kg (2-4 ml) of a 4.2% solution over 15
minutes. (Several formulae exist to calculate the dose of NaHCO3.) About 30 minutes must elapse after the administration of NaHCO3 before its effect can be
judged.
MANNITOL – 10 & 20% SOLUTION – CAN COME IN OSCE – MUST KNOW
§ ? mg/ml OR per Litre

§ Used in pts with:
o raised ICP due to cerebral oedema (e.g. trauma, hyponatraemia)
o renal impairment
HYPERTONIC SALINE
§ Twice & thrice normal – (i.e. 1.8, 2.7% & 5% solution respectively)
§ Used in pts with dilutional hyponatraemia. E.g.:
o TURP/PUERP syndrome
o SIADH secretion
COLLOIDS
These are suspensions of high molecular weight particles
§ CLASSIFY: NATURAL vs. SYNTHETIC

§ ALSO CLASSIFY: PROTEIN COLLOIDS (albumin and gelatin solutions) vs. NON-PROTEIN COLLOIDS (starches, e.g. hydroxyethol starch
(HES) and dextrans)
§ Derived from gelatin (for example, Haemaccel, Gelofusine), protein (albumin) or hydroxyethyl starch, HES (for example, hetastarch).
§ Colloids primarily expand the intravascular volume and can initially be given in a volume similar to the estimated deficit to maintain the circulating
volume (i.e. 1:1 ratio).
§ However, they have a finite life in the plasma and will eventually either be metabolized or excreted, and therefore need
replacing.
§ There is no limit on the volume of gelatins that can be given (provided that haemoglobin concentration is maintained!), however, of the colloids,
they have the greatest tendency to release histamine and may rarely cause anaphylaxis (1–2 cases per 10 000 units given).
§ Hydroxyethyl starch products differ widely, particularly in terms of their molecular weight (70– 650 kDa) and resistance to breakdown (expressed as
their degree of substitution (DS) of glucose for hydroxyethyl units), which in turn affects their duration in the plasma.
o This has reduced the early problems of renal failure, coagulopathy and bleeding, but HES is still associated with reductions in factor VIII.
o Itching may also be a problem in some patients and may be prolonged. The volume of starches that can be given is limited to 30–50 mL/kg,
depending on the formulation used.
Approach to Colloids - Anggelos
Toronto Notes + UHWI: Colloid Infusion
1. Define colloids
2. Classify colloid
§ Referred to as IV volume expanders 3. Characteristics of colloids
§ Increase osmotic pressure 4. Adv of colloids (reduce risk of overload)
5. Disadv of colloids (allergic rxn, pull fluid out of vessel if bad membrane interrgrity, reduce factor 8)
§ Stay in the IV compartment for up to 24 hrs IF capillary membrane integrity is normal!!! – OTHERWISE THEY EXTRAVASATE AND
CAN ACTUALLY PULL FLUID OUT OF VESSES!!!
o Duration changes with sepsis & severe burn injury
§ Decrease risk of fluid overload cf. crystalloid
§ Must monitor the pt.
§ 1:1 ratio (infusion:blood loss) vs. 1:3 for crystalloid
§ HES colloids remain in intravascular space (metabolized by plasma serum amylase and renally excreted)
§ Beware of coagulopathy with large volume colloid infusions
There is no evidence that use of colloids improves survival in trauma patients, burn patients or post-operative patients when compared to crystalloid
solutions. Given the increased cost of colloids as compared to crystalloids, it is recommended that crystalloids be the fluid of choice in these patients.
COLLOIDS
Naturally occurring & synthetic
A. NATURAL
1. Plasma
o
2. Albumin (human) – made from pooled donor plasma and is pasteurized by heating to 60 C for one hr.
B. SYNTHETIC
1. Gelofusine
2. Hydroxyethyl starch/ hetastarch – hespan or pentastarch
3. Dextran - 40, 70, 110
Blood
1. Whole blood
2. Packed cells
3. Cryoprecipitate
4. Platelets concentrates
5. Various factors concentrates
--
PLASMA
§ Volume supporting capacity less than the synthetic colloids
§ Because of vasoactive substances which influences vascular tone and capillary permeability
§ May increase the risk of post-traumatic multi-organ system failure
§ It may enhance the activation of cascade systems
§ The risk of transferring infection and effects of immunocompetence
ALBUMIN
§ 5% & 20% solution
§ Average MW = 69,000 daltons
§ Increase COSP
§ 20% solution – the volume of water absorbed into the intra-vascular compartment is 3-5 Xs its volume
§ Free radical scavenger
§ Anticoagulation properties - inhibits platelet aggregation and enhance the inhibition of factor Xa by antithrombin Π
GELATIN
§ Gelofusine (Succinylated gelatin) available at UHWI
§ Derivative of collagen
§ T ½ = 6-8 hrs.
§ Average MW = 35,000 dalton
§ Available in three commercial forms
DEXTRAN – 40, 70, 110

§ Dextran 40 also use for thrombo-embolic prophylaxis
COMPLICATIONS OF FLUID THERAPY

1. Volume overload (esp. in renal failure?)
2. Electrolyte imbalance
3. Haemodilution and coagulopathy
4. Hyper/hypoglycaemia
5. Allergic/anaphylactic reaction. Esp synthetic colloids. Dextran > Gelofusine > hetastarch.
6. Complications of blood transfusion
GET STARLING FORCES INFO FROM MY PLEURAL EFFUSION NOTES
FLUID AND ELECTROLYTE LOSSES

§ Fluid is lost from 4 routes: the kidney, the gastrointestinal tract, the skin and the respiratory tract. Losses from the last two routes
are termed insensible losses.
MUST KNOW: INSENSIBLE LOSSES = SKIN + RESPIRATORY TRACT LOSSES

§ Inspired air is humidified in its passage to the alveoli, and much of this water is lost with expiration. Fluid is also lost from the skin, and the total
of these insensible losses is around 700 mL/day. This may be balanced by insensible production of fluid, with around 300 mL of ‘metabolic’
water being produced endogenously.
UHWI LECTURE
METHOD OF ASSESSING FLUID DEPLETION
1. History
2. Examination
3. Investigations
History – vomiting, diarrhoea, intake excessive sweating, burn injury, copious or reduced urine ??
Laboratory tests:
§ Haemoglobin § Specific gravity of urine
§ Sodium, Urea & creatinine § Urine sodium *
§ Protein § Acid-base status
§ Osmolality of plasma & urine § How would the above parameters change?
GRADING DEHYDRATION
§ Mild – 5-10% of BV
§ Moderate 10-15%
§ Severe > 20%
POTASSIUM – MUST KNOW – CAN COME IN OSCE!!!

Normal plasma K+ levels = 3.5 – 5.0 mEq/L
Effects of surgery
ADH is released in response to surgery, conserving water. Hypovolaemia will cause aldosterone secretion and salt retention by the kidney. Potassium is
released by damaged tissues, and the potassium level may be further increased by blood transfusion, each unit containing in excess of 20 mmol/L. If
renal perfusion is poor, and urine output sparse, this potassium will not be excreted and instead accumulates, the resultant hyperkalaemia causing life -
threatening arrhythmias. This is the basis of the recommendation that supplementary potassium may not be necessary in the first 48 hours following
surgery or trauma.
HYPERKALAEMIA
SEE NOTES IN MEDICINE FOLDER
HYPOKALAEMIA
CAUSES:
§ Metabolic alkalosis (e.g. excess vomiting)
§ Diuretic therapy
§ Hyperaldosteronism (e.g. Conn’s syndrome – aldosterone producing adenoma)
§ Inadequate intake
§ Iatrogenic
CVS
§ Cardiac dysrhythmias (PVC)
st
§ ECG changes – widened QRS, ST segment depression & 1 degree AV blockade
§ U-waves
§ Potentiates digitalis toxicity
§ Postural hypotension
CNS/Neuromuscular
§ Skeletal muscle weakness, hyporeflexia, confusion
Renal
§ Polyuria, concentrating defect
Metabolic
§ Glucose intolerance
§ Potentiation of hypercalcaemia and hypomagnesaemia.
TREATMENT
Correct precipitating factors
§ Alkalaemia
§ Drugs (diuretics),
§ Hypomagnesaemia
– Mild hypokalemia – oral (tablet or mist potassium citrate) OR IV KCL.

+
– Severe (< 2 mmol/L) – infuse KCL up to 80 mmol/L. Continuously monitor ECG. Monitor plasma K 2-4 hourly. High doses should be given via a
CVP. WHY?
Junior Surgery
Fluid Balance Tutorial
KPH
January 29, 2013
Type of fluids:
1. Isotonic
2. Hypotonic
3. Hypertonic
Groups of IV fluids:
• Crystalloids
• Colloids
Crystalloids are usually clear made up of water and electrolyte solution. Small molecules.
NOTE: 3 ml of isotonic crystalloid solution are needed to replace 1 ml of patient blood. Therefore need a lot of fluid.
Too much crystalloid cause fluid overload
Colloids: Large molecular weight solutions.

Too much colloid can cause coagulation problems and fibrinolysis problems. Can send patient into DIC. (Give max 1.5-2 L)
Normal fluid losses of an adult - look up
Calculating daily fluid requirement:
Normal requirements:
• Maintenance fluid
• Na
• K
(See lecture notes for some of calculations. Na+ an K+ daily requirements in lecture notes)
(The amount given varies within the allowed range based on U&Es)
NOTE: 1 L of normal saline has 154 meq Na+. So 500 ml has 77 meq Na+. Therefore after giving a 70 kg man 500 ml, the remaining fluid
has to be 5% dextrose which has no sodium. (Due to his daily Na+ requirement being 70-140)
(But up to 160 meq is safe for this patient and after surgery it is better to give sufficient within the range rather than below the lower
limit.)
Dextrose water gives very small amount of calories.
NOTE!!: Never give K+ without knowing urine output. Normal K urine output is (0.5 – 1). 0.5-1 ml/kg/hr/day
NOTE!!!: Cant put > 20 mEq K+ in 500 mls NaCl (Normal Saline)
NOTE!!: After surgery, K+ is usually high so K+ is not administered IV until day 2 post-op. K+ given as KCl
(Patient should be under constant cardiac monitoring if giving K+ constantly because of risk of arrhythmias)
At KPH K+ is split into portions due to lack of sufficient machines and patients changing the rate of flow.
Example 1:
Maintenance of 80 kg man, day 2 post-op:
Maintenance fluid requirement: 1000 + 500 + 20*60 = 2700 ml
Na+: 2 bags N/S to be safe (to not give too little) so 154 ml
K+: 80*0.5 = 40 mmol
For NG losses: RULE: For every 1 ml of NG losses, replace volume for volume with normal saline. (Eg 50 ml for 50ml)
ALSO For every litre NG loss give 20 milliequivalents of K+.
Example 2:
70 kg male, day 2 post-op and has 1 L of NG losses. Normal U&Es and normal urine output.
CALCULATE MAINTENANCE:
Maintenance fluids: 1500 + (50*20) = 2500 ml

Na+ 2 bags (154 meq)
K+: 35 mmol
CALCULATE NG LOSSES REPLACEMENT:
For NG losses:
N/S: 1 L
K+: 20
Total K+ = 35 + 20 = 55
Total fluid: 2.5 L + 1 L = 3.5 L
*** HOW TO GIVE THIS FLUID:
(Given as 1 (500 ml) bag saline + 2 (500 ml bags) of normal saline for NG losses + 4 (500 ml) bags of 5% dextrose water)
So 7 bags fluid to be given over 24 hrs. 24 divided by 7 is 3.xx hours. So each bag is given over approximately 3.5 hours.
*** Usually write on fluid balance chart starting from 8 am:
"8-11:30", "11:30-3" etc for the entire 24 hrs. Then on the normal saline side write the addition of K+ that is required.
So, put 500 ml NS + 20 meq K+, 500 ml NS + 20 K+ + 500 ml, NS + 15 K+
So how the chart would look:
8:00 am – 11:30 am 500 ml 0.9% N/S + 20 meq K+

11:30 am – 3:00 pm 500 ml 0.9% N/S + 20 meq K+
3:00 pm – 6:30 pm 500 ml 0.9% N/S + 15 meq K+
6:30 pm – 10:00 pm 500 ml 5% Dextrose
10:00 pm – 1:30 am 500 ml 5% Dextrose
1:30 am – 5:00 am 500 ml 5% Dextrose
5:00 am – 8:00 am 500 ml 5% Dextrose
Lactated ringers: LR composition is close to plasma. It is not considered a maintenance fluid. It is a resuscitative fluid. Has lactate added
which acts as a buffer against acid?. LR protects against acidosis. For patients in shock, burns patients etc.
Bolusing of patient: giving fluid quickly. Depends on the patient’s body weight. Range 20-30 per kg of body weight. Eg. Restoring
intravascular fluid in a patient in shock.
Eg. 3
80 kg pt day 1 post op. Normal urine ouput and u and es no ng losses.
Fluid: 2.7 l
Na+: 2 bags (154)
K+: none as day 1
General Surgery
Surgical Nutrition
Sources: Dr. D.I.G Mitchell lecture, Essential Surgery 5E
March 2015
Prerequisites
§ Physiology of intermediate metabolism
§ Anatomy of the GI tract and vascular systems
§ Basic Surgical Knowledge
Aims of Surgical Nutrition
Recognizing and treating pre-existing malnutrition and preventing postoperative starvation are important aspects of surgical
management that are often neglected. In practice, most surgical patients have no special nutritional requirements and easily withstand
the short period of starvation associated with their illness and operation
§ Maintain or attain Ideal Body Weight before elective surgery

§ Correct electrolyte/metabolic imbalance
§ Limit the post stress catabolism in emergency surgery and other stressors
Nutritional support is generally recommended in well-nourished patients who are unable to tolerate oral feeding for 7–10 days, or 5–7
days if already malnourished.
Objectives
1. Identify patients at risk for malnutrition
2. Assess Nutritional Status of patients
3. Describe the methods of altering the nutritional status of patients
4. Discuss the advantages and disadvantages of various feeding methods
5. Discuss the contraindications and complications of feeding methods
Patients at risk
Causes of malnutrition include:
1. Reduced food intake (anorexia, fasting, dysphagia, odynophagia, physical or mental impairment),
2. Malabsorption (impaired digestion or absorption, or excess loss from gut) and
3. Increased metabolism (trauma, burns, sepsis, surgery, cancer cachexia, hyperthyroidism).
§ In severe trauma or major surgery, and particularly in sepsis, energy requirements increase by 20–100% of normal.
§ **As in simple starvation, lipid becomes a major fuel source; this decreases glucose utilization, but fatty acids other than
glycerol cannot be used for glucose synthesis. Hepatic glucose production increases, but peripheral glucose utilization is
impaired, often leading to hyperglycaemia.
MUST KNOW: NUTRITIONAL ASSESSMENT
1. History – Suggestive of an underlying cause for malnutrition

2. Physical signs (Incl. BMI)
3. **Anthropometry
§ Triceps skin fold thickness—technically difficult to perform but provides a good proxy for body density and hence
overall fat content
§ Mid arm circumference—unreliable because of technical measurement artefact and lack of dependable data upon
which to base measurements
§ Waist circumference
4. **Investigations
§ Reduced plasma albumin, prealbumin or transferrin.
o ***In critically ill patients, plasma albumin of < 35 g/L is associated with a five-fold increase in complications and
a 10-fold increase in death rate!!! Note that low plasma albumin alone is not an accurate marker of malnutrition
but may be caused by other metabolic abnormalities
§ Dr. Leake: Also, caeruloplasmin. Look up – nitrogen balance, respiratory quotient, Harris-Benedict equation
(age, weight, height, stress factor) as measures of malnutrition/need for parenteral nutrition
§ Reduced lymphocyte count.

o If plasma albumin AND lymphocyte count are both low, there is a 20-fold increase in death rate in critically ill
patients
(Paediatric Surgery à (Marasmus vs. Kwashiorkor vs. M-K))
ADVERSE EFFECTS OF PROTEIN/CALORIE DEPLETION IN SURGICAL PATIENTS
1. Postoperative complication rates are higher—2-3 x the complication rate and mortality rate compared with well-nourished
patients
2. Impaired wound healing and higher rates of wound breakdown

3. Impaired immune function and the ability to combat infection
4. Skeletal muscle mass is lost à reducing muscular strength and general physical activity à increases the risk of
thromboembolism and pressure sores
5. Thoracic muscle mass depletion à depresses respiratory efficiency à increases risk of atelectasis & pneumonia
6. Small bowel mucosal atrophy reduces its ability to absorb nutrients and may lead to bacterial translocation into the bloodstream
because of loss of mucosal integrity
7. Albumin becomes depleted à generalised oedema
8. Impaired mental function leads to apathy, depression and low morale
Combinations of these factors lead to prolonged recovery times and longer hospital stays
METABOLISM (DOUBT WE NEED TO MEMORIZE THESE EQUATIONS)

§ Estimate energy expenditure
o 28 vs. 30 vs. 35 vs. 40 kcal/kg/day
§ Basal energy expenditure (BMR in kcal/day)

o F = 665 +(9.6 x wt) + (1.8 x ht) – (4.7 x age)
o M = 66 + (13.7 x wt) + (5.0 x ht) – (6.8 x age)
§ Actual energy expenditure

o BEE x (Activity Factor) x (Stress Factor)
o AF (normal 1.25, bed rest 1.15 & ventilator 1.10)
o SF (El 1.24, trauma 1.37-1.61, Sepsis 1.79 & burns 2.32
Nitrogen Balance
§ N intake – N excretion
§ < 0 à Loss of lean mass
§ > 0 à Gain in lean mass or refeeding
Respiratory Quotient
§ Ratio of CO2 production to O2 consumption
§ Fat 0.7, Protein 0.8, CHO 1.0
§ 0.7 in starvation, > 1 fat synthesis
***CALORIC VALUE OF FOOD

§ Fat = 9 kcal/g
§ Carbohydrates
o Enteral = 4 kcal/g
o IV = 3.4 kcal/g
§ Protein = 4-5 kcal/g
METHODS OF GIVING SUPPLEMENTARY NUTRITION
The gastrointestinal tract should be used whenever possible because any form of enteral feeding is intrinsically safer than
parenteral nutrition and is much cheaper.
In addition, the small intestinal mucosa tends to atrophy when not used. Results in 2 problems:
1. Enteral feeding supports the gut-associated immunological shield and prevents microorganisms translocating into the
circulation, reducing the chances of blood-borne infection. This support is lost with parenteral nutrition
2. Impairment of absorptive ability when enteral nutrition resumed after parenteral nutrition
Contraindications to enteral feeding include:

1. Intestinal obstruction, ileus,
2. High-output intestinal fistula,
3. Intractable vomiting or diarrhoea, and
4. Severe malabsorption
IMPORTANT TABLE
ENTERAL NUTRITION
Add some background info/introduction here
INDICATIONS
1. Malnutrition
2. Hypermetabolic state
o Major trauma, burns, sepsis, etc.
3. Dysphagia
4. Low output GI fistulae
CONTRAINDICATIONS
1. Intestinal obstruction, ileus,

2. High-output intestinal fistula,
3. Intractable vomiting or diarrhoea, and
4. Severe malabsorption
5. GI Bleeding
ADVANTAGES
1. Cheaper
a. Personnel
b. Equipment
2. Maintains trophic effects on bowel mucosa (discussed above)
a. ↓ translocation of bacteria
b. Gut absorptive function maintained
ROUTES
§ Even if the patient is unable to swallow (for example, because of bulbar palsy, unconsciousness or facial fractures), complete
enteral nutrition can be delivered by means of a fine-bore nasogastric or nasojejunal tube, the latter for those who require
“post-pyloric” enteral feeding, e.g. in acute pancreatitis).
§ Feeding tubes can also be placed percutaneously into stomach or jejunum, either at operation (if feeding problems are
anticipated) OR with endoscopic or laparoscopic help.
a) Gastrostomies are often employed in patients after stroke or in those with upper gastrointestinal anastomoses or obstructing
lesions
a. The usual technique nowadays is by percutaneous endoscopic gastrostomy (PEG), combining gastroscopy
and percutaneous placement.
b. PEG tubes are contraindicated in peritonitis, ascites and prolonged ileus.
b) For jejunostomy placement, the tube is tunnelled submucosally for a distance before entering the bowel lumen using a
wide-bore needle; this minimises the risk of leakage.
a. Jejunostomy tubes MUST BE PLACED UNDER DIRECT VISION AT OPERATION OR LAPAROSCOPICALLY!!!
STOMACH FEEDING SMALL BOWEL FEEDING

NG tube, OG tube, gastrostomy, PEG Naso-enteral (e.g. nasojejunal), jejunostomy
o *Simple, cheaper o *Less aspiration so better for comatose pts

o *Physiologic • BUT
o *Bolus & high osmolality tolerated o *Difficult to place properly
• BUT o *Dislodgement (ejection by “reverse peristalsis”) &
o *Risk of aspiration pneumonitis; intact gag required! obstruction
o *May erode nasal septum o *Continuous, low osmolality feeding required
Components (1-2 kcal/ml)

§ CHO
§ Fat (vegetable oils, medium chain TG)
§ Protein (intact vs. partial hydrolyzed)
§ Vitamins & Minerals
§ Fibre
§ Glutamine 6-8 g/day (main fuel for mucosa)
REMEMBER: CLOSE MONITORING IS A PART OF THE MANAGEMENT

§ Daily wts. including fluid shifts
§ Intake & output charting
+
§ Maintain K balance
§ Maintain normoglycaemia
§ Enteral Alimentation
COMPLICATIONS
1. Diarrhoea à Rx: Slow rate or reduce volume of feeds
2. Aspiration
3. Nasal erosion
PARENTERAL NUTRITION
FIRST POINT: Parenteral nutrition should be reserved for appropriate cases of intestinal failure (see below) and
should not be embarked upon lightly!!!
TPN formulations principally contain a mixture of glucose, amino acids, lipids, minerals and vitamins
The osmolality of the mixture is usually high so that administration needs to be via a dedicated central venous line to
minimise the risk of venous thrombosis; formulations for peripheral infusion are available but the technique is losing favour.
The usual aim of TPN is to provide sufficient nitrogen and energy to offset the catabolic demands of surgery and/or trauma and their
complications and, if possible, compensate for any pre-existing malnutrition.
In calculating requirements, protein intake should be matched to estimated nitrogen losses; this can be calculated by measuring urinary
nitrogen losses as urea or else a standard formula (which also estimates other requirements) can be employed.
INDICATIONS
Parenteral nutrition should be reserved for patients who are already malnourished (or are likely to become malnourished), in whom the
GI tract is not functional or is inaccessible AND is likely to remain so for a substantial period of days or weeks. Note that in major
sepsis, the metabolic changes described earlier mean that TPN brings little benefit.
GI tract unavailable, i.e. contraindications to enteral nutrition:

1. Severe malabsorption (e.g. coeliac sprue, etc.)
2. High output enterocutaneous fistula
3. Short bowel syndrome where there is insufficient residual absorptive capacity after massive small bowel resection (< 150 cm
of small bowel) – Indication for permanent parenteral nutrition
4. Intestinal obstruction, paralytic ileus
5. Inflamed bowel or intraabdominal infection (radiation, IBD etc)

6. Intractable vomiting or diarrhoea
7. Severe Pancreatitis (controversial)
CONTRAINDICATIONS
1. Functional GIT
2. < 10 days required
3. Little benefit expected cf. risk
METHODS OF GIVING TPN

Parenteral nutrition is usually delivered into the superior vena cava via the internal jugular or subclavian vein. This is so that high
venous flow rapidly dilutes the hyperosmolar solution, minimising thrombosis risk. If long periods of nutritional support are
anticipated, a designated tunnelled line is usually employed, with the skin access point remote from the venous entry point to minimise
risk of line infection.
Parenteral nutrition is costly in materials and staff time and is prone to complications; it should be discontinued as soon as nutrition can
be supplied by an enteral route. Patients on TPN need close and regular monitoring for a range of problems including line problems,
local and systemic infection, fluid balance and deficiencies of electrolytes
ADVANTAGES
§ High caloric density tolerated
§ Provides adequate nutrition
§ Facilitates fluid restriction
DISADVANTAGES
§ Expensive (Equipment and staff costs)
§ Mucosal atrophy of GIT
§ Non-physiological
§ All risks associated with cental and peripheral venous lines
§ Higher risk
COMPONENTS
1. Macronutrients
a. CHO (dextrose 3.4 kcal/g)
b. Fat including essential fatty acids
at 1.1 – 2.2 kcal/ml
c. Amino acids à Protein 1-2 g/kg/day
d. Cal:Prot = 135-200:1
2. Water 500-800 mls extra
3. Electrolytes
a. Na, K & Cl 1-2 mEq/kg/day
b. Ca 0.2-0.3 mEq/kg/day
c. Mg 0.25-0.35 mEq/kg/day
d. PO4 7-9 mmol/1000 kcal/day
4. Albumin: 25 g/day until Normal
5. Vitamins & Trace elements

a. Zn, Cu, Mn, Ch, Se
6. Heparin à 1000 U/L

7. Glutamine (labile)
MONITORING
1. Input-Output charting
2. Daily weights, ± oedema
3. U&E’s, glucose daily
4. Urine ketones, SG
5. Weekly Ca, P, Mg, LFT’s, CBC, Protein, TG, Nitrogen balance
6. Change central lines weekly
COMPLICATIONS
1. Catheter complications (emboli, sepsis, etc.)
2. Electrolyte abnormalities (Na, PO4)
3. Metabolic complications (Hypo/hyperglycemia, refeeding syndr, CCF)
4. Local and systemic sepsis (gut translocation)
Catheter problems (10% of central lines develop substantial complications)

1. Central venous line placement problems, e.g. failure to cannulate, trauma to great arteries or veins, pneumothorax,
haemothorax, brachial plexus injury, loss of Seldinger wire into vein
2. Line infection—a common cause of fever and tachycardia likely to progress to systemic sepsis. If suspected, blood cultures
should be taken from the line. If positive, line must be removed and tip cultured
3. Blockage, breakage or leakage of catheter
4. Air embolism
5. Central venous thrombosis
Metabolic problems (5% develop metabolic derangements)

1. Electrolyte abnormalities (Sodium, phosphate, etc)
2. Hypo/Hyperglycaemia
3. Overnutrition
4. Long-term—fatty degeneration of the liver
5. Trace element and folate deficiency
6. Deranged liver function tests
7. Linoleic acid deficiency
Summary
§ Assess patient before
§ Choose method
§ Count calories etc
§ Commence feeding
§ Monitor patient continuously
§ Stop, when not necessary
ITEM IN UHWI OSCE BOX USED TO START TPN DISCUSSION

REFEEDING SYNDROME
Refeeding syndrome was first described in prisoners in the Far East after the Second World War who developed cardiac failure when starting to eat after
prolonged starvation. With reduced carbohydrate intake, insulin secretion falls and fat and protein are catabolised in place of carbohydrate. This results
in loss of intracellular electrolytes, particularly phosphate, which becomes depleted. Phosphate is essential for generating adenosine triphosphate and
for other vital phosphorylation reactions.
When enteral or parenteral feeding is restarted after starvation, there is sudden reversion from fat to carbohydrate metabolism. Insulin secretion rises
and cellular uptake of glucose, phosphate, potassium and water increases. This can lead to profound hypophosphataemia, often with hypokalaemia and
hypomagnesaemia. Note that all extracellular fluid is affected by declining levels of these electrolytes. In the starved state, there is total body depletion of
electrolytes but plasma concentrations can be misleadingly normal because of renal compensation.
Refeeding syndrome occurs when plasma phosphate falls to less than 0.50 mmol/L. Clinical features include cardiac and respiratory failure, arrhythmias,
rhabdomyolysis, white cell dysfunction, seizures, coma and sudden death. Early signs may go unrecognised; the plasma phosphate may not be
measured or the significance of grossly abnormal results not appreciated.
Malnourished patients at risk of refeeding syndrome should start artificial feeding with a quarter to half of the expected calorie requirements. Plasma
phosphate, magnesium, calcium, potassium, urea and creatinine concentrations should be measured daily and deficiencies corrected. If required, 50
mmol of intravenous phosphate is given over 24 hours and may need repeating. Thiamine must also be replaced in these patients.
General Surgery
Burns
Sources: Toronto, Some Harold Ellis, CRH class
February 2015
CAUSAL CONDITIONS
1. Thermal – Most common – (flame contact, scald) (Surgical tutor: Thermal damage occurs above 48 ºC)
2. Chemical
3. Radiation (UV, medical/therapeutic)
4. Electrical
MOST COMMON ETIOLOGY

Children: scald burns
Adults: flame burns
Skin Function and Burn Injury
Skin Function Consequence of Burn Injury Intervention Required
1. Thermoregulation Prone to lose body heat Must keep patient covered and warm
2. Control of fluid loss Loss of large amounts of water and protein Adequate fluid resuscitation is imperative
from the skin and other body tissues
3. Mechanical barrier to bacterial High risk of infection Antibiotic ointments (systemic if signs of specific infection
invasion and is an immunological present) Tetanus prophylaxis if necessary
organ
CLASSIFICATION OF BURNS (ACCORDING TO DEPTH)

Burns may be classified into partial thickness and full thickness, depending on whether or not the germinal epithelial layer of the skin is intact or
destroyed
Nomenclature Traditional Depth Clinical Features

Nomenclature
1. Erythema/Superficial First degree Epidermis Painful, sensation intact, erythema, blanchable, no blisters
2. Superficial-Partial Second degree Into superficial dermis Painful, sensation intact, erythema, blisters with clear fluid,
Thickness skin blanchable, hair follicles present. Heals with no scarring in
10 days
3. Deep-Partial Thickness Second degree Into deep dermis (reticular Varying degrees of sensation, difficult to distinguish from full
dermis) thickness, NOT blanchable, some hair follicles still attached,
softer than full thickness burn. Healing occurs in 14 days with
scarring
4. Full Thickness Third degree Through epidermis and Insensate/painless (nerve endings destroyed), hard leathery
Fourth degree dermis eschar that is black, grey, white, or cherry red in colour, hairs do
(burn injury into not stay attached, may see thrombosed veins
bone or muscle) Injury to underlying tissue
structures (e.g. muscle, bone)
GENERAL CLINICAL FEATURES (Harold Ellis – Go back to page 42 for the details)
1. Pain
2. Plasma loss
3. Hypovolaemic shock
4. Anaemia
5. Airway
6. Stress reaction
7. Haemoglobinuria and renal damage
PATHOPHYSIOLOGY OF BURN WOUNDS
Amount of tissue destruction is based on temperature, time of exposure, and specific heat of the causative agent
§ Zone of hyperaemia: Vasodilation from inflammation;

o Entirely viable, cells recover within 7 d; contributes to systemic consequences seen with major burns
§ Zone of stasis (oedema): Decreased perfusion; microvascular thrombosis of vessels results in progressive tissue necrosis à cellular death in
24-48 h without proper treatment
o Factors favoring cell survival: moist, aseptic environment, rich blood supply
o Zone where appropriate early intervention has most profound effect in minimizing injury
§ Zone of coagulation (ischaemia): No blood flow to tissue à irreversible cell damage à cellular death/necrosis
DIAGNOSIS AND PROGNOSIS

§ Age: More complications if < 3 or > 60 yr old
§ Burn size
o % of TBSA (total body surface area) burned: Wallace rule of 9s for 2° and 3° burns only (**children <10 yr old use ***Lund-
Browder chart)
- NOTE WELL: TBSA does NOT include areas with 1° burns!!
o NOTE WELL: For patchy burns, surface area covered by patient’s palm (fingers closed) represents approximately 1% of TBSA
- Each upper limb = 9%
- Each lower limb = 18%
- Anterior and posterior trunk = 18% each Total is 100%
- Head and neck = 9%
- Perineum and genitalia = 1%
§ Depth: Difficult to assess initially. See table – history of aetiologic agent and time of exposure helpful
§ Location: Face and neck, hands, feet, perineum are critical areas requiring special care of a burn unit
§ Inhalation injury: Can severely compromise respiratory system
§ Associated injuries (e.g. fractures)

§ Co-morbid factors (e.g. concurrent disability, alcoholism, seizure disorders, chronic renal failure) can exacerbate extent of injury
Prognosis best determined by burn size (TBSA), age of patient, presence/absence of inhalation injury.
GET PIC OF RULE OF 9s
Indications for transfer to burn center

American Burn Association Criteria
- Total 2° and 3° burns >10% TBSA
- Burns involving the face, hands, feet, genitalia, perineum, or major joints
- 3° burns in any age group
- Electrical burns, including lightning (internal injury underestimated by TBSA)
- Chemical burns
- Inhalation injury (may lead to respiratory distress)
- Burns associated with major trauma/serious illness
MANAGEMENT
PRINCIPLES:
1. Acute management of patient
2. Subsequent treatment of:
a. Local condition (prevent infection + promote healing),
b. General condition (mitigate systemic effects),
c. Reconstruction and rehabilitation
GENERAL ACUTE CARE OF BURN PATIENTS

1. Manage the patient as per strict ATLS protocol (ABCs) – SEE BELOW
A+B:
2. Identify and treat immediate life-threatening conditions of the airway and breathing (e.g. A: inhalation injury, B: CO poisoning)
§ Signs of inhalation injury: Facial burns, soot in nostrils or sputum etc.
§ Carbon monoxide poisoning: Patient may appear 'pink' with a normal pulse oximeter reading
3. Relieve respiratory distress IF INHALATION INJURY EVEN SUSPECTED: INTUBATION AND/OR ESCHAROTOMY (see below)
C:
4. Fluid resuscitation using Parkland formula to restore plasma volume and cardiac output
§ NOTE VERY WELL: IV fluid replacement needed for burns >10% BSA in child or >15% BSA in adult Parklands Formula
does not work for
§ 2 large bore IV cannulae into antecubital fossa or other large veins
burn % > 50%. Fluid
§ Parkland’s formula: Uses time of injury, patient weight, %BSA involved Tx has to be
§ 4 ml RL x kg x % TBSA over first 24 h (1/2 within first 8 h OF SUSTAINING BURN, 1/2 in next 16 h) individualized -
§ Use Wallace rule of 9 for %TBSA Dr Marshall KPH
a. Take baseline laboratory studies at this time (Hb, U/A, BUN, CXR, electrolytes, ECG, cross-match, ABG, carboxyhemoglobin)
b. Extra fluid administration required if:
i. Burn >80% TBSA
ii. 4° burns
iii. Associated traumatic injury
iv. Electrical burn
v. Inhalation injury
vi. Delayed start of resuscitation
vii. Pediatric burns
5. Monitor fluid resuscitation
§ Urine output is best measure: maintain at >0.5 ml/kg/h (adults) and 1.0 ml/kg/h (children <12 yr). Foley cath is mandatory!!!
§ BP and CVP may be necessary Triple Tube Therapy (IV, U Cath, NG)
§ Maintain a clear sensorium/mental status, HR <120/min, MAP >70 mmHg
SPECIFIC:
6. Burn specific care
a. Prevent and/or treat burn shock: 2 large bore IVs
§ Burn shock describes the loss of fluid from the intravascular space as a result of burn injury, which causes “leaking capillaries” that
require crystalloid infusion
b. Determine TBSA affected first, since depth is difficult to determine initially (easier to determine after 24 h)
7. Analgesia/Pain management – EDIT CLASS NOTES HERE
8. Tetanus prophylaxis if needed

§ Stress (All patients with burns >10% TBSA, or deeper than superficial partial thickness, need 0.5 cc tetanus toxoid
§ Also give 250 U of tetanus Ig if prior immunization is absent/unclear, or the last booster >10 yr ago
9. Stress (Curling’s ulcer) ulcer prophylaxis – H2 blocker aka Ranitidine
10. Cleanse, debride, and treat the burn injury (antimicrobial dressings)
§ Early excision and grafting important for outcome
RE: RESPIRATORY PROBLEMS

3 major causes
1. Smoke inhalation leading to pulmonary injury
§ Chemical injury to alveolar basement membrane and pulmonary edema (insidious onset)
§ Risk of pulmonary insufficiency (up to 48 h) and pulmonary edema (48-72 h)
§ Watch for secondary bronchopneumonia (3-25 d) leading to progressive pulmonary insufficiency
§ Intubate patient with any signs of inhalation injuries
2. CO poisoning
§ May present immediately or later
§ Treat with 100% O2 by facemask (***decreases half-life of carboxyhemoglobin from 3.5 h to 1 h) until carboxyHb <10%
3. Burn eschar encircling chest (circumferential)

§ Distress may be apparent immediately
§ Perform escharotomy to relieve constriction
Inhalation Injuries 101

MUST KNOW!!!: Indicators of inhalation injury
§ Injury in a closed space
§ Facial burn
§ Soot around nose/oral cavity
§ Singed nasal hair/eyebrows
§ Conjunctivitis
§ Dyspnoea/Tachypnea
§ Hoarseness
§ Carbon particles in sputum
§ Elevated blood CO levels (i.e. brighter red)
§ Low O2 sat
§ Confusion, headache, coma
Ø SUSPECTED inhalation injury requires immediate intubation due to impending airway edema. Failure to diagnose
inhalation injury can result in airway swelling and obstruction, which, if untreated, can lead to death.
Ø Neither CXR or ABG can be used to rule out inhalation injury.
Ø Direct bronchoscopy is now used for diagnosis.
BURN SHOCK RESUSCITATION (PARKLAND FORMULA)
Hour 0-24 4 ml RL/kg/% TBSA with 1/2 of total in first 8 h from time of injury and 1/2 of total in next 16 h from time of injury
Hour 24-30 0.35-0.5 ml FFP/kg/%TBSA
>Hour 30 5% Dextrose water at rate to maintain normal serum sodium

BURN WOUND HEALING
Depth Healing
First degree (Erythema) No scarring. Complete healing
Superficial partial thickness Spontaneously re-epithelialize in 7 to 14 d from retained epidermal structures

(Superficial second degree)
± Residual skin discolouration
Hypertrophic scarring uncommon. Grafting rarely required
Deep partial thickness Re-epithelialize in 14-35 d from retained epidermal structures

(Deep second degree)
Hypertrophic scarring frequent
Grafting recommended to expedite healing
Full thickness Re-epithelialize from the wound edge

(Third degree)
Grafting/flap necessary to replace dermal integrity, limit hypertrophic scarring
Fourth degree Often results in amputations

If not requiring amputation, needs flap for coverage after debridement (do not reepithelialize – cannot graft!)
TREATMENT
3 stages:
1. Assessment: Depth determined
2. Management: Specific to depth of burn and associated injuries
3. Rehabilitation
A. Superficial/Erythema
§ Treatment aimed at comfort
§ Topical creams (pain control, keep skin moist) ± aloe
§ Oral NSAIDs (pain control)
B. Superficial partial thickness – (DON’T NEED GRAFTS)

§ Daily dressing changes with topical antibiotics (see table below), polysporin, pain medications
§ May use a temporary biological or synthetic covering to close the wound; leave blisters intact unless circulation impaired or unless over joint
inhibiting motion
§ Most do not require skin grafting
C. Deep partial thickness AND Full thickness – (NEED GRAFTS)

§ Prevent infection and sepsis (significant cause of death in burn patients)
§ Most common organisms: S. aureus, P. aeruginosa and C. albicans
- Day 1-3 (rare): Gram-positive
- Day 3-5: Gram-negative (Proteus, Klebsiella)
1. Topical antimicrobials: prevent bacterial infection (from skin flora, gut flora or caregiver) and secondary sepsis (see Table 19
below)
2. Surgically debride necrotic tissue, excise to viable (bleeding) tissue
3. Early grafting
Ø Early EXCISION AND GRAFTING is the mainstay of treatment

o Priority areas for skin grafting: Skin grafting is carried out immediately if the eyelids are involved in order to prevent ectropion with the
risk of corneal ulceration. The face, hands and the joint flexures are next in priority for skin grafting procedures, as scarring at these
sites will obviously produce considerable deformity and disability.
Ø Initial dressing should decrease bacterial proliferation

Ø Indication for skin graft: deep 2° or 3° burn that is > size of a quarter
Ø Prevention of wound contractures: pressure dressings, joint splints, early physiotherapy
OTHER CONSIDERATIONS IN BURN MANAGEMENT
1. Nutrition
§ Hypermetabolism: TBSA > 40% have BMR 2-2.5x predicted
§ Calories, vitamin C, vitamin A, Ca2+, Zn2+, Fe2+
2. Immunosuppression and sepsis

5
§ Must keep bacterial count <10 bacteria/g of tissue (blood culture may not be positive)
§ Signs of sepsis: sudden onset of hyper/hypothermia, unexpected CHF or pulmonary edema, development of ARDS, ileus >48 h post-
burn, mental status changes, azotemia, thrombocytopenia, hypofibrinogenemia, hyper/hypoglycemia (especially if burn >40% TBSA)
3. GI bleed may occur with burns > 40% TBSA (usually subclinical)
§ Treatment: tube feeding or NPO, antacids, H2 blockers (preventative)
4. Renal failure secondary to *under-resuscitation, *drugs, *myoglobin, etc.
5. Progressive pulmonary insufficiency

§ Can occur after: smoke inhalation, pneumonia, cardiac decompensation, sepsis
6. Wound contracture and hypertrophic scarring

§ Largely preventable with timely wound closure, splinting, pressure garments and physiotherapy
COMPLICATIONS OF BURNS B. General - Anggelos

1. CNS (Seizures, Depression)
A. LOCAL
2. Respiratory (Laryngeal edema)
1. Wound sepsis 3. GI (Curling Ulcer)
2. Scarring (full thickness) 4. Kidney (Renal Failure)
3. Wound contractures 5. Hematological (Sepsis)
B. GENERAL
1. Sepsis, esp chest infection in inhalational injury, UTI from cath and septicaemia directly from wound invasion
2. Acute peptic ulceration (Curling’s ulcer)
3. Seizures in children (due to electrolyte imbalance)
4. Renal failure (due to initial hypovolaemia, precipitation of haemoglobin or myoglobin, or nephrotoxic antimicrobial agents)
5. Psychological disturbance
Special considerations
CHEMICAL BURNS
• major categories: acid burns, alkaline burns, phosphorous burns, chemical injection injuries
• common agents: cement, hydrofluoric acid, phenol, tar
• mechanism of injury: chemical solutions coagulate tissue protein leading to necrosis
ƒ. acids g coagulation necrosis
ƒ. alkalines g saponification followed by liquefactive necrosis
• severity related to: type of chemical (alkali worse than acid), temperature, volume, concentration, contact time, site affected, mechanism of chemical
action, degree of tissue penetration
• burns are deeper than they initially appear and may progress with time
Treatment (general)
• ABCs, monitoring
• remove contaminated clothing and brush off any dry powders before irrigation
• irrigation with water for 1-2 h under low pressure (contraindicated in heavy metal burns, such as sodium, potassium, magnesium, and lithium; in these
cases soak in mineral oil instead)
• inspect eyes, if affected: wash with saline and refer to ophthalmology
• inspect nails, hair and webspaces
• correct metabolic abnormalities and tetanus prophylaxis if necessary
• local wound care 12 h after initial dilution (debridement)
• wound closure same as for thermal burn
• beware of underestimated fluid resuscitation, renal, liver, and pulmonary damage
Speed is essential in the management of chemical burns as chemicals can continue to cause damage until they are removed or neutralized.
ELECTRICAL BURNS
• depth of burn depends on voltage and resistance of the tissue (injury more severe in tissues with high resistance)
• often presents as small punctate burns on skin with extensive deep tissue damage which requires debridement
• electrical burns require ongoing monitoring as latent injuries can occur
• watch for system specific damages and abnormalities:
ƒ. abdominal: intraperitoneal damage
ƒ.bone: fractures and dislocations especially of the spine and shoulder
ƒ. cardiopulmonary: anoxia, ventricular fibrillation, arrhythmias
ƒ.muscle: myoglobinuria indicates significant muscle damage g compartment syndrome
ƒ.neurological: seizures and spinal cord damage
ƒ.ophthalmology: cataract formation (late complication)
ƒ. renal: ATN resulting from toxic levels of myoglobin and hemoglobin
ƒ.vascular: vessel thrombosis g tissue necrosis (increased Cr, K+ and acidity), decrease in RBC (beware of hemorrhages/delayed vessel rupture)
Tissue Resistance to Electrical Current: nerve < vessel/blood < muscle < skin < tendon < fat < bone
Treatment
• ABCs, primary and secondary survey, treat associated injuries
• monitor: hemochromogenuria, compartment syndrome, urine output
• wound management: topical agent with good penetrating ability (silver sulfadiazine or mafenide acetate)
• debride non-viable tissue early and repeat prn (every 48 h) to prevent sepsis
• amputations frequently required
How is myoglobinuria treated?

To avoid renal injury, think “HAM”:
Hydration with IV fluids
Alkalization of urine with IV
bicarbonate
Mannitol diuresis
SURGICAL RECALL QUESTIONS

What is the major clinical difference between second- and third-degree burns?
Third-degree burns are painless, and second-degree burns are painful
What is the “rule of the palm”?

Surface area of the patient’s palm is _1% of the TBSA used for estimating size of small burns
What is used to evaluate the eyes after a third-degree burn?

Fluorescein
Can you place an IV or central line through burned skin?

YES
What fluid is used after the first 24 hours postburn?

Colloid; use D5W and 5% albumin at 0.5 cc/kg/% burn surface area
Why should D5W IV be administered after 24 hours postburn?

Because of the massive sodium load in the first 24 hrs of LR infusion and because of the massive evaporation of H2O from the burn injury, the
patient will need free water; after 24 hours, the capillaries begin to work and then the patient can usually benefit from albumin and D5W
Why do most severely burned patients require nasogastric decompression?

Patients with greater than 20% TBSA burns usually develop a paralytic ileus → vomiting → aspiration risk → pneumonia
What are the common organisms found in burn wound infections?

Staphylococcus aureus, Pseudomonas, Streptococcus, Candida albicans
How is a burn wound infection diagnosed?

Send burned tissue in question to the laboratory for quantitative burn wound bacterial count; if the count is _105/gram, infection is present and IV
antibiotics should be administered
Why are systemic IV antibiotics contraindicated in fresh burns?

Bacteria live in the eschar, which is avascular (the systemic antibiotic will not be delivered to the eschar); thus, apply topical antimicrobial agents
NB. IV antibiotics are reserved for established wound infections, pneumonia, UTIs, etc. in burn patients. Not given as prophylaxis. Not given as
prophylaxis in inhalational burns either!
Circumferential, full-thickness burns to the extremities are at risk for what complication?
Distal neurovascular impairment
Treatment: Escharotomy: full-thickness longitudinal incision through the eschar with scalpel or electrocautery
What is the major infection complication (other than wound infection) in burn patients?
Pneumonia, central line infection (change central lines prophylactically every 3 to 4 days)
Can infection convert a partial-thickness injury into a full-thickness injury?

YES!
Which electrolyte must be closely followed acutely after a burn?

Sodium
Neurosurgery
Head Trauma
Sources: Toronto Notes, Dr. Charles lecture
April 2015
§ 60% of trauma admissions have head injuries

§ 60% of MVC-related deaths are due to head injury
§ Falls and MVCs are the leading cause of head trauma
HEAD TRAUMA – SPECIFIC INJURIES

I. FRACTURES
Dx: NON-CONTRAST HEAD CT and PHYSICAL EXAM
A. Skull fractures
§ Vault fractures
o Linear, non-depressed (Most common)
§ Typically occur over temporal bone, in area of middle meningeal artery (commonest cause of epidural hematoma)
o Depressed
§ Closed vs. Open (associated overlying scalp laceration and torn dura, skull fracture disrupting paranasal sinuses or middle ear)
§ Basal skull
o Typically occur through floor of anterior cranial fossa (longitudinal more common than transverse)
o CLINICAL DIAGNOSIS SUPERIOR as poorly visualized on CT (Battle’s sign, raccoon eyes, CSF rhinorrhea/otorrhea, hemotympanum)
Signs of Basal Skull Fracture

1. Battle’s sign (retroauricular ecchymosis/mastoid process ecchymosis)
2. Raccoon eyes (periorbital ecchymosis)
3. Haemotympanum
4. CSF Rhinorrhoea/Otorrhoea
B. Facial fractures
§ Neuronal injury
§ Beware of open fracture or sinus fractures (risk of infection)
§ Unstable or displaced fractures (need semi-urgent plastics referral)
§ Severe facial fractures may pose risk to airway from profuse bleeding
II. SCALP LACERATION

§ Can be a source of significant bleeding
§ Achieve hemostasis, inspect and palpate for skull bone defects +/- CT head (rule-out skull fracture)
III. NEURONAL INJURY

A. Diffuse
§ Mild traumatic brain injury = concussion
o Transient alteration in mental status that may involve loss of consciousness
o Hallmarks of concussion: confusion and amnesia, which may occur immediately after the trauma or minutes later
o Loss of consciousness (if present) must be less than 30 min, initial GCS must be between 13-15 and post-traumatic amnesia must be less than 24 h
§ Diffuse axonal injury
o Mild: coma 6-24 h, possibly lasting deficit
o Moderate: coma >24 h, little or no signs of brainstem dysfunction
o Severe: coma >24 h, frequent signs of brainstem dysfunction
B. Focal injuries
§ Contusions
§ Intracranial hemorrhage (epidural, subdural, intracerebral)
ASSESSMENT OF BRAIN INJURY

HISTORY
§ Pre-hospital status
§ Mechanism of injury
PHYSICAL EXAMINATION
§ Assume C-spine injury until ruled out
§ Vital signs
o Shock (NOT likely due to isolated brain injury, except in infants)
o Cushing’s response to increasing ICP à (TRIAD: bradycardia, hypertension, irregular respirations)
§ Severity of injury determined by:

1. LOC
o GCS ≤8 à intubate, any change in score of 3 or more = serious injury.
o Traumatic brain injury (TBI): Mild = 13-15, moderate = 9-12, severe = 3-8
2. Pupils: Size, anisocoria >1 mm (in patient with altered LOC), response to light
3. Lateralizing signs (motor/sensory) may become more subtle with increasing severity of injury
§ Reassess frequently
INVESTIGATIONS
§ Labs: CBC, electrolytes, PT/PTT or INR/PTT, glucose, toxicology screen
§ CT SCAN (NON-CONTRAST) TO EXCLUDE INTRACRANIAL MASS LESIONS
§ C-SPINE IMAGING, often with CT HEAD AND NECK to exclude intracranial mass lesions
EMERGENCY MANAGEMENT – MUST FULLY KNOW

POINT: GOAL IN ED: Reduce secondary injury by avoiding hypoxia, ischaemia, decreased CPP, seizure
A. General Management
1. Strict ATLS protocol, completing a thorough primary and secondary survey
§ Clear airway and secure c-spine, ensure breathing, intubate if GCS ≤8
2. Ensure oxygen delivery to brain through intubation and prevent hypercarbia
3. Maintain BP (sBP >90)
4. Treat other injuries
B. “Early neurosurgical consultation” (MUST SAY IN EXAM) for acute and subsequent patient management!!!!
à Medical management
A. Treat suspected raised ICP – SEE SEPARATE DOCUMENT ON MANAGING ICP FOR THE FULL DETAILS!!! (MUST
KNOW – COMMON QUESTION)à consider if head injury with signs of increased ICP:
o
1. Raise head of stretcher 30 if patient haemodynamically stable
2. Intubate and hyperventilate (100% O2) to a pCO2 of 30-35 mmHg
3. Mannitol 1g/kg infused as rapidly as possible (***contraindicated in shock and renal failure/anuria)
4. Consider paralyzing medications if agitated/high airway pressures
5. Maintenance of CPP is critical (CPP=MAP-ICP)
B. Seizure treatment/prophylaxis
1. Benzodiazepines, phenytoin, phenobarbital
2. STEROIDS are of NO PROVEN VALUE
Other points:
§ Neurosurgical ICU admission for severe head injuries (HI)
§ In hemodynamically unstable patient with other injuries, prioritize most life-threatening injuries and maintain cerebral perfusion
§ For minor head injury not requiring admission, provide 24 h HI protocol to competent caregiver, follow-up with neurology as even seemingly
minor HI may cause lasting deficits
Warning Signs of Severe Head Injury

1. GCS <8
2. Deteriorating GCS
3. Unequal pupils
4. Lateralizing signs
N.B. Altered LOC is a hallmark of brain Injury
Treatment of Increased ICP

§ Elevate head of bed
§ Mannitol
§ Hyperventilate
§ Paralyzing/sedating agents
Mild Traumatic Brain Injury

EPIDEMIOLOGY
§ Traumatic brain injury results in 1.7 million deaths, hospitalizations and ED visits each year (US)
§ 75% are estimated to be mild TBI; remainder are moderate or severe
§ Highest rates in children 0-4 yr, adolescents 15-19 yr and elderly >65 yr
CLINICAL FEATURES
§ Somatic: headache, sleep disturbance, nausea, vomiting, blurred vision
§ Cognitive dysfunction: attention impairment, reduced processing speed, drowsiness, amnesia
§ Emotion and behaviour: impulsivity, irritability, depression
§ Severe concussion: may precipitate seizure, bradycardia, hypotension, sluggish pupils
AETIOLOGY
§ Falls, motor vehicle and traffic accidents, struck by an object, assault, sports
INVESTIGATIONS
§ Neuro exam
§ Concussion recognition tool (see thinkfirst.ca)
§ Imaging – CT as per Canadian CT Head Rules, or MRI if worsening symptoms despite normal CT
TREATMENT
§ Close observation and follow-up; patients at risk of intracranial complications [give appropriate discharge instructions to patient and family] watch for changes to clinical
features above, and if change, return to ER
§ Hospitalization with normal CT (GCS <15, seizures, bleeding diathesis), or with abnormal CT
§ Early rehabilitation to maximize outcomes
§ Pharmacological management of pain, depression, headache
§ Follow Return to Play guidelines: Cantu, Colorado Medical Society, American Academy of Neurology, 2008 Consensus Statement on Concussion in Sports – no data
on superiority
PROGNOSIS
§ Most recover with minimal treatment athletes with previous concussion are at increased risk of cumulative brain injury
§ Repeat TBI can lead to life threatening cerebral edema or permanent impairment
Neurosurgery Section
Trauma Assessment
INITIAL MANAGEMENT
§ ABCs of Trauma Management
NEUROLOGICAL ASSESSMENT
MINI-HISTORY
§ Period of LOC, post-traumatic amnesia, loss of sensation/function, type of injury/accident
NEUROLOGICAL EXAM
§ Glasgow Coma Scale (GCS)
§ Head and neck (lacerations, bruises, basal skull fracture signs, facial fractures, foreign bodies)
§ Spine (palpable deformity, midline pain/tenderness)
§ Eyes (pupillary size and reactivity)
§ Brainstem (breathing pattern, CN palsies)
§ Cranial nerve exam
§ Motor exam, sensory exam (only if GCS is 15), reflexes
§ Sphincter tone
§ Record and repeat neurological exam at regular intervals
INVESTIGATIONS
§ Spinal injury precautions (cervical collar) are continued until C-spine is cleared
§ C, T, L-spine x-rays
o AP, lateral, odontoid views for C-spine (must see from C1 to T1; swimmer’s view if necessary) or CT
o Rarely done: oblique views looking for pars interarticularis fracture (“Scottie dog” sign)
§ CT head and upper C-spine (whole C-spine if patient unconscious) look for fractures, loss of mastoid or sinus air spaces, blood in cisterns,
pneumocephalus
§ Cross and type, ABG, CBC, drug screen (especially alcohol)
§ Chest and pelvic x-ray as indicated
TREATMENT
Treatment for Minor Head Injury
§ observation over 24-48 h
§ wake every hour
§ judicious use of sedatives or pain killers during monitoring period
Treatment for Severe Head Injury (GCS ≤8)

§ clear airway and ensure breathing (if GCS ≤8, intubate)
§ secure C-spine
§ maintain adequate BP
§ monitor for clinical deterioration
§ monitor and manage increased ICP if present (see Herniation Syndromes)
Admission required if:

§ skull fracture (see indirect signs of basal skull fracture)
§ confusion, impaired consciousness, concussion with >5 min amnesia
§ focal neurological signs, extreme headache, vomiting, seizures
§ unstable spine
§ use of alcohol
§ poor social support
HEAD INJURY
EPIDEMIOLOGY
§ Male to female: 2-3:1
PATHOGENESIS
§ Acceleration/deceleration: contusions, subdural hematoma, axon and vessel shearing/mesencephalic hematoma
§ Impact: skull fracture, concussion, epidural hematoma
§ Penetrating: worse with high velocity and/or high missile mass
o Low velocity: highest damage to structures on entry/exit path
o High velocity: highest damage away from missile tract
SCALP INJURY
§ Rich blood supply
§ Considerable blood loss (vessels contract poorly when ruptured)
§ Minimal risk of infection due to rich vascularity
SKULL FRACTURES
§ Depressed fractures: double density on skull x-ray (outer table of depressed segment below inner table of skull), CT with bone window is
gold standard
§ Simple fractures (closed injury): no need for antibiotics, no surgery
§ Compound fractures (open injury): increased risk of infection, surgical debridement within 24 h is necessary
o Internal fractures into sinus may lead to meningitis, pneumocephalus
o Risk of operative bleed may limit treatment to antibiotics
§ Basal skull fractures: not readily seen on x-ray, rely on clinical signs
o Retroauricular ecchymoses (battle’s sign)
o Periorbital ecchymoses (raccoon eyes)
o Hemotympanum
o CSF rhinorrhea, otorrhea (suspect CSF if halo or target sign present); suspect with
o Lefort II/III midface fracture
INTRACRANIAL BLEEDING
§ See separate notes
BRAIN INJURY
Primary Impact Injury
§ Mechanism of injury determines pathology: penetrating injuries, direct impact
o Low velocity: local damage
o High velocity: distant damage possible (due to wave of compression), concussion
A. Concussion: a trauma-induced alteration in mental status

§ American Academy of Neurology (AAN) Classification (see sidebar)
§ no parenchymal abnormalities on CT
B. Coup (damage at site of blow) and contrecoup (damage at opposite site of blow) (see an image)
§ acute decompression causes cavitation followed by a wave of acute compression
C. Contusion (hemorrhagic)
§ high density areas on CT +/- mass effect
§ commonly occurs with brain impact on bony prominences (inferior frontal lobe, pole of temporal lobe)
D. Diffuse axonal injury/shearing
§ wide variety of damage results
§ may tear blood vessels (hemorrhagic foci)
§ often the cause of decreased LOC if no space occupying lesion on CT
Secondary Pathologic Processes

§ Same subsequent biochemical pathways for each traumatic etiology
§ Delayed and progressive injury to the brain due to
Ø High glutamate release à NMDA à cytotoxic cascade
Ø Cerebral edema
Ø Intracranial hemorrhages
Ø Ischemia/infarction
Ø Raised ICP, intracranial HTN
Ø Hydrocephalus
Extracranial Conditions
1. Hypoxemia
§ due to trauma to the chest, upper airway, brainstem
§ extremely damaging to vulnerable brain cells
§ leads to ischemia, raised ICP
2. Hypercarbia
§ leads to raised ICP (secondary to vasodilation)
3. Systemic hypotension
§ caused by blood loss (e.g. ruptured spleen)
§ loss of cerebral autoregulation leads to decreased CPP, ischemia
4. Hyperpyrexia
§ leads to increased brain metabolic demands g ischemia
5. Fluid and electrolyte imbalance
§ iatrogenic (most common)
§ SIADH caused by head injury
§ diabetes insipidus (DI)
§ may lead to cerebral edema and raised ICP
6. Coagulopathy
Intracranial Conditions
§ Raised ICP due to traumatic cerebral edema OR traumatic intracranial hemorrhage
Late Complications of Head/Brain Injury

§ Seizures: 5% of head injury patients develop seizures
§ Meningitis: associated with CSF leak from nose or ear
§ Hydrocephalus: acute hydrocephalus or delayed normal pressure hydrocephalus (NPH)
Neurosurgery
Intracranial Haemorrhage/Haematoma
Sources: Harold Ellis, Toronto Notes
March 2015
Classification
Haemorrhage within the skull following injury may be classified as follows.
1. Extradural
2. Subdural
a. Acute
b. Chronic
3. Subarachnoid
4. Intracerebral
5. Intraventricular
Toronto Notes Table: Comparison of Epidemiology and Etiology of Intracranial Bleeds
Types of Aetiology Epidemiology Clinical Features CT Features Treatment Prognosis

Hematoma/Hae
morrhage
Epidural Skull fracture causing M>F (4:1) Lucid interval before LOC Hyperdense Craniotomy Good with prompt
Haematoma middle meningeal bleed lenticular/biconvex mass management
Associated with trauma with sharp margins, usually (Note: respiratory arrest
limited by suture lines can occur from uncal
herniation)
Acute SDH Ruptured subarachnoid Age >50 No lucid interval HYPERdense crescentic Craniotomy if bleed Poor
bridging veins/vessels Contralateral hemiparesis mass, crossing sutures >1 cm thick
Associated with trauma Pupillary changes lines
Chronic SDH Ruptured subarachnoid Age >50 Often asymptomatic HYPOdense crescentic Burr hole to drain; Good
bridging veins/vessels mass, crossing suture lines craniotomy if recurs
EtOH abusers, anti- Minor H/A, confusion, signs
coagulated of increased ICP
SAH Trauma (most common) Age 55-60 Sudden onset thunderclap HYPERdense blood in Conservative: Poor: 50% mortality
Vs. headache cisterns/fissures NPO, IV NS, ECG, 30% of survivors have
Spontaneous (berry 20% cases under age 45 (Sensitivity decreases over Foley, moderate to severe
aneurysms, idiopathic, Signs of increased ICP time) BP 120-150, vasospasm disability
AVM) prophylaxis (nimodipine);
Vs. open vs. endovascular
Other surgery to repair if
rebleed
ICH HTN, vascular abnormality, Age >55, TIA-like symptoms, signs of HYPERdense Medical: decrease BP, Poor: 44% mortality due
tumours, infections, increased ICP intraparenchymal collection control ICP to cerebral herniation
coagulopathy Male, drug use (cocaine, Surgical: craniotomy
EtOH, amphetamine)
VERY IMPORTANT POINT TO UNDERSTAND
ANY space-occupying lesion (including intracranial blood) manifests itself in 2 ways:

1. By the general features of raised intracranial pressure
2. And by localizing signs.
EXTRADURAL (“EPIDURAL”) HAEMATOMA

AETIOLOGY
§ Trauma à Temporal-parietal skull fracture
§ 85% are due to ruptured middle meningeal artery
§ Remainder of cases are due to bleeding from middle meningeal vein, dural sinus, or bone/diploic veins
EPIDEMIOLOGY
§ Young adult, M > F, 4:1; rare before age of 2 or after age 60
CLINICAL FEATURES
1. CLASSIC SEQUENCE (NOTE WELL: Only seen in < 30%): Post-traumatic reduced LOC à a “lucid interval” of several hours à
then symptoms develop: altered LOC, hemiparesis, ipsilateral pupillary dilatation, and coma
§ The classic story is of a relatively minor head injury producing temporary concussion, recovery (‘the lucid period’) then, some hours later,
the development of headache and progressively deeper coma due to cerebral compression by the extradural clot
§ (It is important to note that this classic picture is NOT as common as is thought!! Often, there is no lucid period; the patient
progressively passes into deeper coma from the time of the initial injury)
§ Deterioration can take hours to days
Other signs and symptoms due to LOCAL MASS EFFECT vs. GENERAL EFFECTS OF INCREASED ICP
2. Can include H/A, N/V, amnesia, altered LOC, HTN and respiratory distress
§ The physical signs are those of rapidly increasing intracranial pressure (MUST see ICP notes).
§ In addition, there are certain localizing signs that may help the surgeon decide on which side to explore the skull. These are as follows:
1. IPSILATERAL pupillary dilatation: -– a good neurosurgical aphorism is ‘explore the side of the dilated pupil’. In 10% of patients, the
dilated pupil will be a false localizing sign!!!
2. CONTRALATERAL hemiparesis or hemiplegia (common) or focal fits (uncommon) usually indicate contralateral compression.
3. A boggy scalp haematoma usually overlies the extradural clot.
INVESTIGATIONS
§ NON-CONTRAST HEAD CT SCAN: Diagnostic. “Lenticular-shaped" usually limited by suture lines
TREATMENT
An extradural haemorrhage is one of the surgical emergencies where minutes really can matter.
DR: CHARLES:
§ CAN MANAGE NON OPERATIVELY UNDER SOME CIRCUMSTANCES
§ MUST FIRST SAY REFER TO AND MANAGE IN A NEUROSURGERY CENTRE
A. Admission and observation with serial CT indicated IF ALL of the following are present: à
3
1. Small volume clot (< 30 mm ) [If > 30 à craniotomy regardless of GCS]
2. Minimal midline shift (Midline shift (MLS) <5 mm)
3. GCS > 8
4. No focal deficit
B. Otherwise, craniotomy to evacuate clot + follow up CT!!!!
Mannitol pre-op if elevated ICP/brain herniation
TIMING: It is strongly recommended that patients with an acute EDH in coma (GCS score < 9) with anisocoria undergo surgical evacuation as soon as
possible.
METHODS: There are insufficient data to support one surgical treatment method. However, craniotomy provides a more complete evacuation of the
hematoma.
PROGNOSIS
§ Good with prompt management, as the brain is often not damaged
§ Worse prognosis if bilateral Babinski or decerebration pre-op
§ Death is usually due to respiratory arrest from uncal herniation (injury to the midbrain)
SUBDURAL HAEMATOMA (SDH)

ACUTE SUBDURAL HAEMATOMA
AETIOLOGY
§ Rupture of vessels that bridge the subarachnoid space (e.g. cortical artery, large vein, venous sinus) or cerebral laceration
RISK FACTORS
§ Often associated with severe head injury
§ Trauma, acceleration-deceleration injury, anti-coagulants, alcohol, cerebral atrophy, infant head trauma
CLINICAL FEATURES
§ No lucid period
§ Signs and symptoms of a space-occupying lesion (can include altered LOC, pupillary irregularity, hemiparesis)
INVESTIGATIONS
§ NON-CONTRAST HEAD CT SCAN: HYPERdense concave “crescentic” mass, crossing suture lines
TREATMENT
A. Craniotomy to release the subdural clot IF:

a. If haematoma >1 cm thick, or
b. If MLS >5 mm (optimal if surgery <4 h from onset);
c. Clinically symptomatic,
d. GCS drop by 2 or more points from the time of injury to hospitalization
B. Otherwise observe with serial imaging
The outcome may still be poor because of the severity of the underlying brain trauma
PROGNOSIS
§ NOTE: Prognosis poor overall since the underlying brain parenchyma is often injured!!! (Mortality range is 50%-90%, due
largely to underlying brain injury)
§ Prognostic factors: initial GCS and neurologic status, post-op ICP
CHRONIC SUBDURAL HEMATOMA
AETIOLOGY
§ Many start out as acute SDH
§ Blood within the subdural space evokes an inflammatory response:
o Fibroblast invasion of clot and formation of neomembranes within days à growth of neocapillaries à fibrinolysis and
liquefaction of blood clot
§ Course is determined by the balance of rebleeding from neomembranes and resorption of fluid
RISK FACTORS
§ Older
§ Alcoholics
§ Patients with CSF shunts, anti-coagulants, coagulopathies
CLINICAL FEATURES
§ Often due to minor injuries or no history of injury
§ May present with minor H/A, mental deterioration, confusion, language difficulties, TIA-like symptoms, symptoms of raised ICP +/-
seizures, progressive dementia, gait problem
§ Moderate papilloedema in about 50%
§ Obtundation disproportionate to focal deficit; “the great imitator” of dementia, tumours
INVESTIGATIONS
§ CT: HYPOdense (liquefied clot), crescentic mass
TREATMENT
§ Seizure prophylaxis only if post-traumatic seizure
§ Reverse coagulopathies
§ Burr hole drainage of liquefied clot indicated if
o Symptomatic or thickness >1 cm;
o Craniotomy if recurs more than twice
PROGNOSIS
§ Good overall as brain usually undamaged, but may require repeat drainage
CEREBROVASCULAR DISEASE
Ischaemic Cerebral Infarction (80%)
§ Embolic, thrombosis of intracerebral arteries, vasculitis, hypercoagulability, etc.
Intracranial Hemorrhage (20%)

§ Subarachnoid hemorrhage (SAH), spontaneous intracerebral hemorrhage (ICH), intraventricular hemorrhage (IVH)
SUBARACHNOID HEMORRHAGE (SAH)

DEFINITION
§ Bleeding into subarachnoid space (intracranial vessel between arachnoid and pia)
AETIOLOGY
1. Trauma (most common)
2. Spontaneous
a.Ruptured (berry) aneurysms (75-80%)
b.Idiopathic (14-22%)
c.AVMs (4-5%)
3. Coagulopathies (iatrogenic or primary), vasculitides, tumours, cerebral artery dissections (<5%)
EPIDEMIOLOGY
§ Peak age 55-60, 20% of cases occur under age 45
RISK FACTORS
§ Hypertension
§ Pregnancy/parturition in patients with pre-existing AVMs, eclampsia
§ Oral contraceptive pill
§ Substance abuse (cigarette smoking, cocaine, alcohol)
§ Conditions associated with high incidence of aneurysms
CLINICAL FEATURES OF SPONTANEOUS SAH

§ Sudden onset (seconds) of severe “thunderclap” headache usually following exertion and described as the “worst headache of my
life” (up to 97% sensitive, 12-25% specific)
§ Nausea/vomiting, photophobia
§ Meningismus (neck pain/stiffness, positive Kernig’s and Brudzinski’s sign)
§ Decreased LOC (due to either raised ICP, ischemia, seizure)
§ Focal deficits: cranial nerve palsies (CN III, IV), hemiparesis
§ Ocular hemorrhage in 20-40% (due to sudden raised ICP compressing central retinal vein)
§ Reactive hypertension
§ Sentinel bleeds
o Represents undiagnosed SAH
o SAH-like symptoms lasting <1 d (“thunderclap H/A”)
o May have blood on CT or LP
o ~30-60% of patients with full blown SAH give history suggestive of sentinel bleed within past 3 wk
Differential diagnosis: sentinel bleed, dissection/thrombosis of aneurysm, venous sinus thrombosis, benign cerebral vasculitis, benign exertional H/A
INVESTIGATIONS
1. Non-contrast CT – for diagnosis of SAH
§ 98% sensitive within 12 h, 93% within 24 h; 100% specificity
§ May be negative if small bleed or presentation delayed several days
§ Acute hydrocephalus, IVH, ICH, infarct or large aneurysm may be visible
2. Lumbar puncture (highly sensitive) – for diagnosis of SAH if CT negative but high suspicion:
§ Elevated opening pressure (>18 cm H2O)
§ Bloody initially, xanthochromic supernatant with centrifugation (“yellow”) by ~12 h, lasts 2 wk
§ RBC count usually >100,000/mm3 without significant drop from first to last tube (in contrast to traumatic tap)
§ Elevated protein due to blood breakdown products
For Aneurysms
3. Four vessel cerebral angiography (“gold standard” for aneurysms)
§ Demonstrates source of SAH in 80-85% of cases
§ Angiogram negative SAH: repeat angiogram in 7-14 d, if negative g “perimesencephalic SAH”
4. MRA and CTA: sensitivity up to 95% for aneurysms, CTA>MRA for smaller aneurysms and delineating adjacent bony anatomy
TREATMENT
§ Admit to ICU or NICU
o Oxygen/ventilation prn
o NPO, bed rest, elevate head of bed 30., minimal external stimulation, neurological vitals q1h
o Aim to maintain sBP = 120-150 (balance of vasospasm prophylaxis, risk of re-bleed, risk of hypotension since CBF autoregulation
impaired by SAH)
o Cardiac rhythm monitor, Foley prn, strict monitoring of ins and outs
§ Medications:
o IV NS with 20 mmol KCl/L at 125-150 cc/h
o Nimodipine 60 mg PO/NG q4h x 21 d for vasospasm neuroprotection; may discontinue earlier if patient is clinically well
o Seizure prophylaxis: levetiracetam (Keppra.) 500 mg PO/IV q12h x 1 wk
o Mild sedation prn
COMPLICATIONS
1. Vasospasm: vasoconstriction and permanent pathological vascular changes in response to vessel irritation by blood
§ onset: 4-14 d post-SAH, peak at 6-8 d; most commonly due to SAH, rarely due to ICH/IVH
§ clinical features (delayed ischemic deficit): confusion, decreased LOC, focal deficit (speech or motor)
§ risk factors: large amount of blood on CT (high Fisher grade), smoking, increased age, HTN
§ “symptomatic” vasospasm in 20-30% of SAH patients
§ “radiographic” vasospasm in 30-70% of arteriograms performed 7 d following SAH
§ diagnosed clinically, and/or with transcranial Doppler (increased velocity of blood flow)
§ risk of cerebral infarct and death
§ treatment
§ hyperdynamic (“triple H” – see sidebar) therapy using fluids and pressors, usually after ruptured aneurysm has been clipped/coiled
§ direct vasodilation via angioplasty or intraarterial verapamil for refractory cases
2. Hydrocephalus (15-20%): due to blood obstructing CSF drainage

§ can be acute or chronic, requires extraventricular drain (EVD) or shunt, respectively
3. Neurogenic pulmonary edema
4. Hyponatremia: due to cerebral salt wasting (increased renal sodium loss and ECFV loss), not SIADH
5. Diabetes insipidus
6. Cardiac: arrhythmia (>50% have ECG changes), MI, CHF
PROGNOSIS
§ 10-15% mortality before reaching hospital, overall 50% mortality (majority within first 2-3 wk)
§ 30% of survivors have moderate to severe disability
§ A major cause of mortality is rebleeding, for aneurysms:
a. risk of rebleed: 4% on first day, 15-20% within 2 wk, 50% by 6 mo
b. if no rebleed by 6 mo, risk decreases to same incidence as unruptured aneurysm (2%)
c. only prevention is early clipping or coiling of "cold" aneurysm
d. rebleed risk for “perimesencephalic SAH” is approximately same as for general population
Neurosurgery
Intracranial Tumours
March 2015
RE: SPACE OCCUPYING LESIONS IN GENERAL
CLINICAL FEATURES
A space-occupying lesion manifests itself by:
1. The general features of raised intracranial pressure and
2. By focal/localizing signs.
1. RAISED INTRACRANIAL PRESSURE

A space-occupying lesion within the skull produces raised intracranial pressure by
1. Its actual volume within the closed box of the cranium
2. By provoking oedema, and sometimes by
3. Impeding the circulation or absorption of cerebrospinal fluid (CSF) causing hydrocephalus
(E.g., a tumour in the posterior fossa may present rapidly with severe symptoms of raised intracranial pressure secondary to hydrocephalus)
SEE SEPARATE NOTES ON RAISED ICP FOR DETAILS
2. LOCALIZING SIGNS
§ Having diagnosed the presence of raised intracranial pressure, an attempt must be made to localize the lesion on the basis of the clinical
findings, although in some cases this is not possible. (MAY CHECK MEDICINE NOTES ON LOCALIZING LESION)
NB: Pupillary dilatation is a late sign, and is caused by the uncus of the temporal lobe being displaced through the tentorial
hiatus where it compresses the oculomotor nerve.
INVESTIGATIONS FOR SPACE-OCCUPYING LESIONS

1. CT with intravenous contrast enhancement, is a non-invasive and extremely accurate investigation for all cerebral tumours and other
space - occupying lesions.
2. MRI gives superb anatomical localization of intracerebral space-occupying lesions.
3. Positron emission tomography (PET) further complements MR.
4. Chest X-ray should always be performed if tumour is suspected to exclude a symptomless primary bronchogenic carcinoma; in the case of a
cerebral abscess, it may reveal the source of infection.
5. Burr-hole biopsy may be appropriate to establish a tissue diagnosis.
6. Skull X-ray has been largely SUPERSEDED IN THE DIAGNOSIS OF SPACE-OCCUPYING LESIONS BY CROSS-SECTIONAL IMAGING (CT
AND MR). Ten percent of tumours show calcification
§ (The pineal gland may be calcified (30% of 30 year olds, 70% of 70 year olds). Close inspection of the skull X - ray may show a shift of the
pineal to one side, indicating a space - occupying lesion on the other)
INTRACRANIAL TUMOURS
The only identified predisposing factor is previous cranial irradiation.
CLASSIFICATION
Common tumours include the following.
Intracerebral or extracerebral and either may include primary or secondary/metastatic
A. Intracerebral (same as intra-axial?)

1. Gliomas (45%), including
a. Astrocytoma (80%)
b. Medulloblastoma (10%)
c. Oligodendroglioma (5%)
d. Ependymoma (5%)
2. Lymphoma.
3. Pineal gland tumour.
4. Metastases (15-30%).
B. Extracerebral (Extra-axial?)
1. Meningioma (15%).
2. Neuroma, e.g. acoustic neuroma (5%).
3. Pituitary tumours (5%), including pituitary adenomas and craniopharyngiomas
4. Metastatic
PRIMARY BRAIN TUMOURS

§ Rarely undergo metastasis
§ Adults = mostly supratentorial
§ Children = mostly infratentorial
BRAIN METASTASIS
§ ~1/3 of all adult brain tumours Well circumscribed, often at grey-white matter junction
Primary Sources of Metastatic Brain Tumours

1. Lung 44%
2. Breast 10%
3. Kidney (RCC) 7%
4. GI 6%
5. Melanoma 3%
OTHER WAYS TO CLASSIFY
§ Primary vs. Metastatic,

§ Intra-axial (parenchymal) vs. Extra-axial
§ Supratentorial vs. Infratentorial
§ Adult vs. Pediatric
§ Benign: non-invasive, devastating due to expansion of mass in fixed volume of skull (mass effect)
§ Malignant: implies rapid growth, invasiveness, but rarely extracranial metastasis
CLINICAL FEATURES
Intracranial tumours cause GENERALIZED and FOCAL symptoms.
A. FOCAL SYMPTOMS (Most common) depend on the tumour location within the brain.
§ Progressive neurological deficit (70%): usually motor weakness,+/- CN deficits, sensory, cognitive, personality, endocrine deficits
§ These may localize lesion
B. GENERALIZED SYMPTOMS reflect a progressive increase in intracranial pressure and include headache (particularly in the early morning),
nausea and vomiting. Mental state changes and hemiparesis may also occur. (SEE RAISED ICP NOTES)
§ H/A (50%) +/- symptoms of elevated ICP
§ N/V (40%)
§ seizures (25%)
§ papilledema, vision changes
§ Symptoms suggestive of TIA (ictal, post-ictal, or ischemic 2o to “steal phenomenon”)

§ Rarely presents with haemorrhage
Familial syndromes associated with CNS tumours

1. von Hippel-Lindau (hemangioma)
2. Tuberous sclerosis (astrocytoma)
3. Neurofibromatosis type 1 and 2 (astrocytoma, acoustic neuroma respectively)
a. Type 1 aka: von Recklinghausen’s disease
b. Type 2 aka: "MISME Syndrome", for "Multiple Inherited Schwannomas, Meningiomas, and Ependymomas"
4. Li-Fraumeni (astrocytoma)
5. Turcot syndrome (glioblastoma multiforme)
6. Multiple endocrine neoplasia type 1 (MEN-1) (pituitary adenoma)
INVESTIGATIONS
§ Cross-sectional imaging: CT, MRI
§ Stereotactic biopsy (tissue diagnosis)
§ Metastatic work-up
GENERAL TREATMENT OPTIONS
§ Conservative: Serial Hx, Px, imaging for slow growing/benign lesions

§ Medical: corticosteroids to reduce cytotoxic cerebral edema, pharmacological
§ Surgical:
o Total or partial excision (decompressive, palliative)
o Shunt if hydrocephalus
§ Radiotherapy:
o Conventional fractionated radiotherapy (XRT),
o Stereotactic radiosurgery (e.g. Gamma Knife.)
§ Chemotherapy: e.g. alkylating agents (temozolomide)
METASTATIC TUMOURS
§ Most common brain tumour SEEN CLINICALLY
§ 15-30% of cancer patients present with cerebral metastatic tumours
o Most common sources: lungs, breast
o Other sources: kidney, thyroid, stomach, prostate, testis, melanoma
§ Haematogenous spread most common
LOCATION
§ 80% are hemispheric, often at grey-white matter junction or junction of temporal-parietal-occipital lobes (likely emboli spreading to terminal
MCA branches)
INVESTIGATIONS
§ Identify primary tumour

o Metastatic work-up: (CT chest/abdo/pelvis, bone scan, mammogram)
§ CT with contrast à round, well-circumscribed, often ring enhancing, ++ edema, often multiple
§ MRI more sensitive, especially for posterior fossa
§ Consider biopsy in unusual cases, OR if no primary identified
TREATMENT
Medical
§ Phenytoin (or levetiracetam) for seizure prophylaxis if patient presents with seizure
§ Dexamethasone to reduce edema given with ranitidine
§ Chemotherapy (e.g. Small cell lung cancer)
Radiation
§ Stereotactic radiosurgery: for discrete, deep-seated/inoperable tumours
§ Multiple lesions: use whole brain radiation therapy (WBRT); consider stereotactic radiosurgery if <3 lesions
§ Post-op WBRT is commonly used
Surgical
§ Single/solitary lesions: use surgery + radiation
PROGNOSIS
§ Median survival without treatment once symptomatic is ~1 mo,
§ With optimal treatment 6-9 mo but varies depending on primary tumour type
PRIMARY BRAIN TUMOURS

GLIOMAS
§ Gliomas arise from the glial supporting cells
§ They are classified according to the principal cell component.
§ Usually supratentorial.
§ The four important subgroups are as follows.
1. ASTROCYTOMAS (80%)
§ Most common primary intra-axial brain tumour, common in 4-6th decades

§ These are graded according to their mitotic activity, nuclear pleomorphism, endothelial proliferation and necrosis.
§ Grade 1 (pilocytic astrocytoma) and grade 2 (diffuse astrocytoma) are less aggressive
o Often cystic and slow growing,
o Although they may change over the years into less differentiated and more invasive tumours.
§ Grade 3 (anaplastic astrocytoma) and grade 4 (glioblastoma multiforme) gliomas are more aggressive;
o About half of all astrocytomas are the highly anaplastic glioblastoma multiforme, the median survival with which is 3 months.
CLINICAL FEATURES
§ Sites: cerebral hemispheres >> cerebellum, brainstem, spinal cord

§ Symptoms: recent onset of new/worsening H/A, N/V, seizure, Å} focal deficits or symptoms of increased ICP
INVESTIGATIONS
§ CT/MRI with contrast: variable appearance depending on grade (see Table 8)

§ Tissue biopsy: WHO grade and histology correlates with prognosis, but 25% chance of sampling error due to tumour heterogeneity
TREATMENT
Low-grade diffuse astrocytoma

§ Close follow-up, radiation, chemotherapy, surgery are all valid options
o Surgery: not curative, trend towards better outcomes
o Radiotherapy alone or post-op prolongs survival (retrospective evidence)
o Chemotherapy: usually reserved for tumour progression
High-grade astrocytomas (anaplastic astrocytoma and GBM)
§ Surgery
o Gross total resection: maximal safe resection + fractionated radiation with 2 cm margin + concomitant and adjuvant temozolomide
§ Except: extensive dominant lobe GBM, significant bilateral involvement, end of life near, extensive brainstem involvement
o Stereotactic biopsy if resection not possible, followed by fractioned radiation with 2 cm margin
§ Expectant (based on functional impairment – Karnofsky score <70; patient’s/family’s wishes)

§ Aim to prolong “quality” survival
§ Chemotherapy: ~20% response rate, temozolomide (agent of choice); better response to temozolomide predicted by MGMT gene
hypermethylation
Multiple gliomas: WBRT +/- chemotherapy
2. MEDULLOBLASTOMAS (10%)
§ These are rapidly growing small-cell tumours generally affecting the cerebellum in children, usually boys
§ Cells appear to be embryonal in origin with elements of ependymomas and medulloblastoma in varying proportions, and are now more
commonly called primitive neuroectodermal tumours (PNETs).
§ May spread via the CSF to seed over the surface of the spinal cord.
3. EPENDYMOMAS (5%)
§ These arise from the lining cells of the ventricles, the central canal of the spinal cord or the choroid plexus.
§ They usually occur in children and young adults.
4. OLIGODENDROGLIOMAS (5%)
§ Most are relatively slow growing and are usually found in the cerebrum in adults.
CEREBRAL LYMPHOMA
Uncommon but is increasing in incidence.
It occurs in two settings:

1. Immunosuppressed patients, whether through disease (e.g. AIDS) or for organ transplantation
a. Primary CNS lymphoma reported in 6-20% of HIV infected patients
2. In non-immunosuppressed patients, the incidence peaks in the 50s-60s and is often multifocal.
§ Diagnosis is by stereotactic biopsy

§ Treatment is chemotherapy.
EXTRACEREBRAL/EXTRA-AXIAL TUMOURS
MENINGIOMA
§ Arise from arachnoid membrane (Arachnoid cells in the dura mater)
§ Mostly benign (5% atypical, 1-2% anaplastic/frankly malignant), slow-growing, extra-axial, circumscribed (non-infiltrative – most do not invade
brain tissue!),
§ BUT involve brain by expansion and pressure
§ Tumour may, however, invade the skull, producing a hyperostosis, which may occasionally be enormous
§ Classically see Psammoma bodies on histology
§ Common locations: parasagittal convexity or falx (70%), sphenoid wing, tuberculum sellae, foramen magnum, olfactory groove
CLINICAL FEATURES
§ Typically found in middle aged, slight female preponderance (M:F = 2:3),

§ High progesterone receptors (increase in size with pregnancy),
§ Symptoms of increased ICP, focal deficits, usually solitary (10% multiple, likely with loss of NF2 gene/22q12 deletion)
INVESTIGATIONS
1. CT with contrast: Densely enhancing, along dural border (“dural tail”), well circumscribed
2. Contrast-enhanced MRI provides better detail
3. Angiography
4. Octreotide scintigraphy: to establish if expression of somatostatin receptor
TREATMENT
§ Conservative management for non-progressive, asymptomatic lesions

§ Surgery is treatment of choice if symptomatic or progression on sequential imaging (curative if complete resection)
§ Stereotactic radiosurgery (SRS) may be an option for lesions <3 cm
§ SRS or XRT for recurrent atypical/malignant meningiomas
PROGNOSIS
>90% 5-yr survival, recurrence rate variable (often ~10-20%)
VESTIBULAR SCHWANNOMA (ACOUSTIC NEUROMA)

NEUROMAS IN GENERAL are benign tumours that arise from the Schwann 2 cells of a cranial nerve.
§ The great majority arise from the eighth cranial nerve at the internal auditory meatus (acoustic neuroma).
§ Usually found in adult patients between the ages of 30 and 60 years and are
§ Occasionally associated with neurofibromatosis type II, when they may be bilateral.
§ Slow-growing (average of 1 mm/yr), benign posterior fossa tumour

§ Arises from vestibular component of CN VIII in internal auditory canal
§ If bilateral, diagnostic of neurofibromatosis type II
§ Epidemiology: all age groups affected, peaks at 4th-6th decades
Progressive unilateral or asymmetrical sensorineural hearing loss = acoustic neuroma until proven otherwise.
As the acoustic tumour slowly enlarges, it stretches the adjacent cranial nerves, VII and V anteriorly and IX, X and XII over its lower surface.
It also presses on the cerebellum and the brain stem, producing the ‘ cerebellopontine angle syndrome’ with the following features:
§ unilateral nerve deafness often associated with tinnitus and giddiness (VIII) is the first symptom;
§ facial numbness and weakness of the masticatory muscles (V);
§ dysphagia, hoarseness and dysarthria (IX, X and XII);
§ cerebellar hemisphere signs and, later, pyramidal tract involvement;
§ eventually features of raised intracranial pressure (LATE);
§ facial weakness with unilateral taste loss (VII) is very uncommon ( < 5%).
INVESTIGATIONS
§ MRI with gadolinium (>98% sensitive/specific)
nd
§ CT with contrast 2 choice
§ Audiogram, brainstem auditory evoked potentials, caloric tests
TREATMENT
§ Conservative: serial imaging
§ Radiation: stereotactic radiosurgery or fractionated radiotherapy
§ Surgery if: lesion >3 cm, brainstem compression, edema, hydrocephalus
o Curable if complete resection (almost always possible)
o Operative complications: CN VII, VIII dysfunction (only significant disability if bilateral)
PITUITARY TUMOURS
Pituitary tumours have three special features:
1. Local mass effects:

a. Visual field disturbance (bitemporal hemianopia) due to compression of the optic chiasm.
b. Headache, due to expansion of the pituitary fossa with dural stretching, erosion into the paranasal air sinus, and/or haemorrhage within the
tumour (pituitary apoplexy).
2. Hormone deficiency (hypopituitarism):
a. as the tumour grows, it compresses the normal pituitary around the tumour, resulting in reduced production of anterior pituitary hormones.
ORDER!!!: Deficiency tends to first suppress luteinizing and growth hormone production, followed in sequence by loss of thyroid-
stimulating hormone (TSH), adrenocorticotrophic hormone (ACTH) and follicle - stimulating hormone (FSH). The posterior pituitary
hormones are rarely affected. (Toronto Notes: GH > LH > FSH > TSH > ACTH > Prolactin)
3. Hormone excess: hormone–secreting adenomas may present with symptoms from the hormone, for example Cushing’s disease from ACTH
excess.
§ Hyperprolactinemia (prolactinoma): infertility, amenorrhea, galactorrhea, decreased libido

§ ACTH production: Cushing’s disease, hyperpigmentation
§ GH production: acromegaly/gigantism
§ Panhypopituitarism (hypothyroidism, hypoadrenalism, hypogonadism)
§ Associated MEN-1 syndrome
§ Diabetes insipidus
Pituitary apoplexy (sudden expansion of mass due to hemorrhage or necrosis)

§ Abrupt onset H/A, visual disturbances, ophthalmoplegia, reduced mental status, and Panhypopituitarism
They are named according to their staining on light microscopy.
1. CHROMOPHOBE ADENOMA (80%)

§ Commonest pituitary tumour,
§ Which, as it enlarges, compresses the optic chiasm, producing a bitemporal hemianopia.
§ Half are non-secretory tumours, which gradually destroy the normally functioning pituitary, producing hypopituitarism with secondary
hypogonadism,
§ Hypothyroidism and hypoadrenalism. In childhood there is arrest of growth together with infantilism.
§ Half produce prolactin, which causes infertility, amenorrhoea and galactorrhoea (discharge of milk from the nipple) in females.
§ These tumours rarely extend to involve the hypothalamus, producing diabetes insipidus and obesity.
2. EOSINOPHIL (ACIDOPHIL) ADENOMA (15%)

§ Slow-growing tumours, which secrete growth hormone.
§ If they occur before puberty, which is unusual, they induce gigantism.
§ After puberty, acromegaly results.
3. BASOPHIL ADENOMA (5%)

§ These are small tumours that produce no pressure effects and may be associated with Cushing’s syndrome
§ (Adrenocorticotrophic hormone production)
SPECIAL INVESTIGATIONS
1. Magnetic resonance (MR) imaging demonstrates the pituitary fossa, encroachment on the optic chiasm superiorly and laterally into the cavernous
sinus.
2. Hormone assessment, with basal assays of each pituitary hormone and change in hormone concentrations after stress created by insulin-induced
hypoglycaemia. (prolactin level, TSH, 8 AM cortisol, fasting glucose, FSH/LH, IGF-1), electrolytes, urine electrolytes, and osmolarity
3. Visual field mapping looking for evidence of bitemporal hemianopia.
TREATMENT
A. MEDICAL
§ Prolactin - secreting tumours (prolactinomas) usually respond to treatment with a dopamine agonist (e.g. cabergoline, bromocriptine) to
suppress prolactin secretion and reduce tumour size.
§ For Cushing’s: serotonin antagonist (cyproheptadine), inhibition of cortisol production (ketoconazole)
§ For acromegaly: somatostatin analogue (octreotide) +/- bromocriptine
B. SURGICAL
§ Pituitary tumours which are producing pressure/mass-effect symptoms on the optic chiasm etc. are treated by intracapsular removal
through a trans–sphenoidal (or occasionally transcranial) route.
CRANIOPHARYNGIOMA
Craniopharyngioma (suprasellar cyst, or cyst of Rathke’s pouch) is a benign but locally invasive tumour, usually cystic, which arises in the remnant of the
craniopharyngeal duct (the precursor of the anterior pituitary). It presents in childhood or early adult life and lies above and/or within the sella turcica.
The tumour produces hypopituitarism, raised intracranial pressure and optic chiasmal involvement. Craniopharyngiomas may be very difficult to remove
completely because of their close relationship to the hypothalamus, so treatment often involves subtotal removal with postoperative radiotherapy.
Neurosurgery
Intracranial Abscess
March 2015
PUS
Four routes of microbial access to CNS
1. hematogenous spread (most common): arterial (in a septic embolus) and retrograde venous
a. adults: chest is #1 source (lung abscess, bronchiectasis, empyema)
b. children: congenital cyanotic heart disease with R to L shunt
c. immunosuppression (AIDS – toxoplasmosis)
d. These abscesses usually occur in MCA territory
2. direct implantation (dural disruption)
§ trauma (Penetrating injury – Staph aureus most common in these cases. Penetrating wounds usually cause extradural abscess)
§ iatrogenic (e.g. following LP, post-op)
§ congenital defect (e.g. dermal sinus)
3. Contiguous spread (adjacent infection):
§ from infected air/mastoid sinus, infected frontal or ethmoid sinus, naso/oropharynx, surgical site (e.g. otitis media, mastoiditis, sinusitis,
osteomyelitis, dental abscess)
4. Spread from PNS (e.g. viruses: rabies, herpes zoster)
Common examples
1. Epidural abscess: in cranial and spinal epidural space, associated with osteomyelitis
§ Treatment: immediate drainage and antibiotics, surgical emergency if cord compression
2. Subdural empyema: bacterial/fungal infection, due to contiguous spread from bone or air sinus, progresses rapidly
§ Treatment: surgical drainage and antibiotics, 20% mortality
3. Meningitis, encephalitis
4. Intracerebral abscess
Intracranial abscesses may be INTRACEREBRAL, SUBDURAL OR EXTRADURAL
CEREBRAL ABSCESS
DEFINITION
Pus in brain substance, surrounded by tissue reaction (capsule formation)
AETIOLOGY
Modes of spread (see above): 10-60% of patients have no cause identified
PATHOGENS
§ Streptococcus (most common), often anaerobic or microaerophilic

§ Staphylococcus (penetrating injury)
§ Gram-negatives, anaerobes (Bacteroides, Fusobacterium)
§ In neonates: Proteus and Citrobacter (exclusively)
§ Immunocompromised: fungi and protozoa (Toxoplasma, Nocardia, Candida albicans, Listeria monocytogenes, Mycobacterium and Aspergillus)
RISK FACTORS
§ Lung abnormalities [infection, AV fistulas; especially Osler-Weber-Rendu syndrome (aka hereditary hemorrhagic telengiectasia)]
§ Congenital coronary heart disease: R-to-L shunt bypasses pulmonary filtration of micro-organisms
§ Bacterial endocarditis
§ Penetrating head trauma
§ Immunosuppression (e.g. AIDS)
§ Dental abscess
CLINICAL FEATURES
1. Features of the underlying cause (e.g. chronic mastoiditis)
Mass effect:
2. Focal neurological signs and symptoms - H/A, decreased LOC; hemiparesis and seizures in 50%
3. General features of increased ICP and sequelae (cranial enlargement in children)
4. Hemiparesis and seizures in 50%
5. +/- signs and symptoms of systemic infection (low-grade fever, toxaemia, leukocytosis)
§ Often, the abscess is walled off by a relatively thick capsule so that the general manifestations of infection (fever and toxaemia) are not
evident.
COMPLICATIONS
1. With abscess rupture: ventriculitis, meningitis, venous sinus thrombosis

2. CSF obstruction
3. Transtentorial herniation
INVESTIGATIONS
1. CT scan often first test in emergency department

2. MRI
§ Imaging of choice
§ Apparent diffusion coefficient (ADC) used to differentiate abscess (black) from tumour (white)
3. WBC/ESR may be normal, blood cultures rarely helpful and LP contraindicated if large mass
4. CSF: non-specific (high ICP, high WBC, high protein, normal carbohydrate), rarely helpful, usually negative culture
TREATMENT
1. Aspiration +/- excision and send for Gram stain, acid-fast bacillus (AFB), C&S, fungal culture
2. Excision preferable if location suitable
3. Antibiotics
§ Empirically: vancomycin + ceftriaxone + metronidazole or chloramphenicol or rifampin (6-8 wk therapy)
§ Revise antibiotics when C&S known
4. Anti-convulsants (1-2 yr) (Epilepsy develops in one - third of patients and anticonvulsant therapy is therefore given prophylactically)
5. Follow up CT is critical (do weekly initially, more frequent if condition deteriorates)
Harold Ellis:
In the first instance, the abscess is aspirated through a burr hole by means of a brain needle. Antibiotics are instilled into the abscess cavity and
resolution is followed by serial CT scans
PROGNOSIS
Mortality with appropriate therapy ~10%, permanent deficits in ~50%
Neurosurgery
Hydrocephalus
March 2015
THE CIRCULATION OF CSF

CSF is produced by the choroid plexuses of the lateral, third and fourth ventricles. It escapes from the fourth ventricle through the median foramen of
Magendie and the lateral foramina of Luschka into the cerebral subarachnoid space. About 80% of the fluid is reabsorbed via the cranial arachnoid villi.
The remaining 20%of the CSF is absorbed by the spinal arachnoid villi or escapes along the nerve sheaths into the lymphatics
§ CSF production = CSF reabsorption = ~500 mL/d in normal adults

§ Normal CSF volume ~150 mL (50% spinal, 50% intracranial à 25 mL intraventricular, 50 mL subarachnoid)
HYDROCEPHALUS
DEFINITION
§ Increased CSF volume
AETIOLOGY
1. Obstruction to CSF flow

2. Decreased CSF absorption
3. Increased CSF production (rarely) – e.g. choroid plexus papilloma (0.4-1% of intracranial tumours)
EPIDEMIOLOGY
§ Estimated prevalence 1-1.5%; incidence of congenital hydrocephalus ~1-2/1000 live births
Classification
CLINICAL FEATURES
A. Acute hydrocephalus
§ Signs and symptoms of acute elevated ICP (see ICP notes)
§ Impaired upward gaze (“sunset eyes”) and/or CN VI palsy
B. Chronic/gradual onset hydrocephalus (i.e. NPH)

§ Gradual onset of classic triad developing over weeks or months
§ Pressure of ventricle on LE motor fibres à gait disturbance (ataxia and apraxia usually initial symptoms)
§ Pressure on cortical bowel/bladder centre à urinary incontinence
§ Pressure on frontal lobes à dementia
§ CSF pressure can be measured within clinically “normal” range
Classic Triad of NPH Progression AID

1. Ataxia/Apraxia of gait
2. Incontinence
3. Dementia
INVESTIGATIONS
1. CT/MRI (Confirms ventricular enlargement. Periventricular lucency suggests raised CSF pressure)
2. Cranial ultrasound (through anterior fontanelle in infants)
3. ICP monitoring (e.g. LP) may be used to investigate NPH, test response to shunting (lumbar tap test)
4. Radionuclide cisternography can test CSF flow and absorption rate (unreliable)
5. β-2 transferrin assay to test for the presence of CSF leak
TREATMENT
§ Ventricular drainage
§ Surgical removal of obstruction (if possible) or excision of choroid plexus papilloma
§ Shunts
o Ventriculoperitoneal (VP): most common
o Ventriculopleural
o Ventriculo-atrial (VA): relatively increased risk of infections, shunt emboli
o Lumboperitoneal: for communicating hydrocephalus and pseudotumour cerebri
§ Third ventriculostomy (for obstructive hydrocephalus) via ventriculoscopy

§ LPs for transient hydrocephalus (e.g. SAH), IVH in premature infants, etc.
Harold Ellis
The goal of treatment is to divert the CSF around the blockage by means of a shunt. For non-communicating (obstructive) hydrocephalus, direct removal
of the occluding mass lesion is desirable.
Decompression of the hydrocephalus can be achieved by diverting CSF into the peritoneum (ventriculoperitoneal shunt) or right atrium via the internal
jugular vein (ventriculoatrial shunt). The shunts comprise silicone catheters with a regulator valve mechanism in the middle to permit CSF flow at a
certain ventricular pressure without overdrainage of the CSF.
In non-communicating (obstructive) hydrocephalus, an artificial outlet may be created through the floor of the third ventricle into the basal cisterns
(endoscopic third ventriculostomy).
General Surgery/ENT
Thyroid Nodules and Thyroid Carcinoma (MUST USE TORONTO NOTES FOR THE MEDICINE PART AND PHYSIOLOGY)
Sources: Dr. Smith notes, Dr. Ashman notes, Toronto Notes
February 2015
THYROID ANATOMY AND BLOOD SUPPLY (MEDSCAPE)

The thyroid is a highly vascular, brownish-red gland located anteriorly in the lower neck, extending from the level of the C5-T1
nd th
Formed by 2 elongated lateral lobes (with superior and inferior poles) connected by a median isthmus (overlying the 2 –4 tracheal
rings)
§ Occasionally, the isthmus is absent, and the gland exists as 2 distinct lobes
§ An inconstant, conical pyramidal lobe often ascends from the isthmus or the adjacent part of either lobe
§ Thyroid averages 25-30 g in adults (it is slightly heavier in women). The gland enlarges during menstruation and pregnancy.
This causes hyperplasia of the gland and predisposes women to goitre - Dr Hanchard
Remnants of the thyroglossal duct may persist as accessory nodules or cysts of thyroid tissue between the isthmus and the foramen caecum of the
tongue base. Hence it moves up when the tongue is protruded
Usually, 2 pairs of parathyroid glands lie in proximity to the thyroid gland
The thyroid has an inner true capsule, which is thin and adheres closely to the gland. Extensions of this capsule within the substance of the gland form
numerous septae, which divide it into lobes and lobules. The lobules are composed of follicles, the structural units of the gland, which consist of a
layer of simple epithelium enclosing a colloid-filled cavity
Epithelial cells are of 2 types:

1. Principal cells (aka, follicular) – responsible for formation of the colloid (iodothyroglobulin)
2. Parafollicular cells (aka, C, clear, light cells) – produce the hormone calcitonin, a protein decreases the serum calcium levels.
FASCIA AND LIGAMENTS

The thyroid gland is ensheathed by the visceral fascia, a division of the deep cervical fascia, which attaches it firmly to the “laryngoskeleton”.
§ The anterior suspensory ligament extends from the superior-medial aspect of each thyroid lobe to the cricoid and thyroid cartilage
st
§ The posterior suspensory ligament of Berry attaches the posteromedial aspect of the gland to the side of the cricoid cartilage and 1 and
nd
2 tracheal ring
EXAM ANSWER: The firm attachment of the gland to the laryngoskeleton by the anterior and posterior suspensory ligament
of Berry is responsible for movement of the thyroid gland and related structures during swallowing.
NERVE SUPPLY
Principal innervation of the thyroid gland derives from the autonomic nervous system.
1. Parasympathetic fibers à from the vagus nerves, and
2. Sympathetic fibers à from the superior, middle, and inferior ganglia of the sympathetic trunk. Autonomic nervous regulation of the
glandular secretion is not clearly understood, but most of the effect is postulated to be on blood vessels, hence the perfusion rates of the glands.
ARTERIAL SUPPLY
The arterial supply to the thyroid gland comes from:
st
1. The superior thyroid arteries (1 branch of external carotid)
2. Inferior thyroid arteries (arises from the thyrocervical trunk, a branch of the subclavian artery)
3. Occasionally, from the thyroidea ima. The thyroidea ima is a single vessel that, when present, originates from the aortic arch or the
innominate artery and enters the thyroid gland at the inferior border of the isthmus.
VENOUS DRAINAGE
3 pairs of veins provide venous drainage for the thyroid gland.
1. The superior thyroid vein – a tributary of the internal jugular vein.
2. The middle thyroid vein follows a direct course laterally to the internal jugular vein.
3. The inferior thyroid veins follow different paths on each side. Inferior thyroid veins drain to the right and left brachiocephalic veins
LYMPHATIC DRAINAGE
Lymphatic drainage of the thyroid gland is extensive. Immediate lymphatic drainage courses to the periglandular nodes; to the prelaryngeal (Delphian),
pretracheal, and paratracheal nodes along the recurrent laryngeal nerve; and then to mediastinal lymph nodes. Regional metastases of thyroid
carcinoma can also be found laterally, higher in the neck along the internal jugular vein. This can be explained by tumor invasion of the pretracheal and
paratracheal nodes causing an obstruction of normal lymph flow.
THYROID NODULES
IMPORTANT POINTS TO KNOW – MUST KNOW THEM PRECISELY!!:
1. Females > Males
2. 80% OF NODULES OCCUR IN WOMEN, BUT NODULES IN MEN ARE 3X MORE LIKELY TO BE MALIGNANT
3. Palpable or visible thyroid nodules in ~10-12% of population generally. Nodular (solitary or multiple) thyroid CAN MIMIC a DIFFUSE thyroid - Dr Roberts KPH
The above point is not
4. However in routine U/S and autopsy studies, ~50% of females > age 30 have thyroid nodules (75% multinodular goiters and 25% solitary
nodules)
5. Overall ~95% benign. 5% malignant
History, physical exam and investigation to help determine malignant vs. benign
TYPES OF THYROID CANCERS

CLASSIFY: PRIMARY vs. SECONDARY
A. PRIMARY:
CLASSIFY: CARCINOMA (DIFFERENTIATED VS. UNDIFFERENTIATED) vs. LYMPHOMA vs. SARCOMA
(JUST LIKE BREAST!!)
I. Carcinomas (95%)
A. Differentiated carcinoma (*Look and behave like normal thyroid tissue. 80% of thyroid neoplasms)
1. Papillary (Have “classic papillary” (~90%) and follicular variant (~10%), both similar prognosis. Also have insular variant,
columnar variant, tall cell variant of papillary – all rare (<1%) & more aggressive!)
2. Follicular
3. Hurthle cell variant of follicular
B. Undifferentiated carcinoma
1. Medullary
2. Anaplastic
III. Primary thyroid lymphoma
IV. Sarcomas, carcinosarcomas
B. SECONDARY – GENERALLY UNCOMMON
1. Renal Cell Carcinoma (Clear cell Ca.); **Classically described as able to metastasize to thyroid!!
2. Rarely breast and prostate
3. Direct invasion of the thyroid from nearby structures (Eg. Laryngeal ca. especially if subglottic involvement and Oesophageal cancers
involving the cervical oesophagus)
DR. SMITH SUMMARY:
PAPILLARY (75-80%) (PTC):

§ Most common, best prognosis. F > M (2.5:1)
§ “Classic PTC”: Defined by nuclear features: 1. Orphan-Annie/optically clear nuclei, 2. Nuclear grooving, 3. Pseudoinclusions.
§ ALSO: Psammoma bodies! (calcified clumps) à But these are in the cytoplasm. [Can be seen in any type of papillary carcinoma anywhere]
§ ALSO: Have a “Follicular variant” that only minimally has the above features!! (~10% of papillary cancers).
§ ALSO: “Insular variant” (<1%) – more aggressive
§ *Seen in a slightly younger cohort (~30s-40s but can be seen in younger)
§ Typically lymphatic spread
§ Prognosis: (~95% 10 year survival)
§ NB: ‘Lateral aberrant thyroid' almost always metastatic papillary carcinoma. (***Note the difference between aberrant thyroid and ectopic
thyroid tissue which is normal thyroid tissue usually found along its path of descent in the thyroglossal duct)
May actually occur much more commonly than it is diagnosed, with autopsy series finding small (< 1 cm) papillary cancers in as many of 30% of people
who have died of other causes. This suggests that small papillary cancers may be of minimal clinical significance.
FOLLICULAR (10%):
§ CANNOT be diagnosed on FNAC. To differentiate between a follicular adenoma and carcinoma à:
o CHARACTERIZED BY: MUST SEE capsular invasion AND/OR vascular invasion on histology.
§ *Seen in slightly older cohort than papillary (50s – 60s). F > M (3:1)
§ Haematogenous spread (Remember vascular invasion)
§ Prognosis: (~70-85% 10 year survival)
HURTHLE CELL VARIANT OF FOLLICULAR:

§ Oncocytic appearance defines it. It appears hypereosinophilic on H&E stain. Has a lot of stacked mitochondria in the cells.
§ NOTE WELL: Can have Hurthle cell adenoma or carcinoma and cannot make distinction on FNAC!!! POINT: Hurthle cells may be present in
benign lesions!!!
§ Same spread as follicular.
MUST KNOW: SOME STUDIES SUGGEST (BUT STILL NOT CONCLUSIVE) Hurthle cell has a slightly worse prognosis for 2 reasons
1. More aggressive inherently (and much higher rate of recurrence)
2. Not as iodine-avid, so does not take up as much therapeutic radioactive iodine!!!!
RE: PAPILLARY AND FOLLICULAR
o Many tumours are TSH dependent (i.e. TSH stimulates their growth)
o TSH suppression with post-operative thyroxine appropriate (exogenous thyroxine suppresses pituitary TSH)
o Thyroxine reduces recurrence and improves survival
MEDULLARY CARCINOMA (~5%):

§ First point: Arises from the parafollicular C-cells. May actually present with elevated calcitonin (used as a tumour marker)
§ 80% sporadic
§ 20% familial – And of the familial, 10% MEN 2A & 2B AND 10% Non-MEN (e.g. of non-MEN – FMTC “Familial Medullary Thyroid Cancer”)
o See all the MEN types on last page
§ Spread by all 3 routes: Haematogenous route + lymphatics + direct invasion of adjacent structures contiguously
§ Much more aggressive than papillary and follicular.

§ ~55% 5 year survival
§ CALCITONIN can be used as a tumour marker. Levels plummet after surgery. [NOTE: Because calcitonin has short absorption
and elimination half-lives of 10–15 minutes and 50–80 minutes, respectively]
ANAPLASTIC (~5%):
§ “One of the worst cancers known in man” – Dr. Smith. Does NOT resemble any normal thyroid tissue.
§ Bizarre and haphazard arrangement of cells with high mitotic index.
§ Usually in older patients (60s, 70s and above). Can result from DE-DIFFERENTIATION of an existing differentiated thyroid carcinoma!!
§ Usually rapid growth and invasion of surrounding tissues incl. trachea, oesophagus, skin. SVC syndrome possible
§ Prognosis: Extremely grim. ~25% 1 year survival. Most die within 9 months of diagnosis.
§ NOTE WELL: All cases of anaplastic carcinoma are regarded as T4 or stage 4 disease even the smallest anaplastic carcinoma.
PRIMARY THYROID LYMPHOMAS (<1%): Typically arise on the BG of a Hashimoto’s. ALMOST ALL ARE NON-HODGKIN WITH B-CELL
ORIGIN
§ NOTE WELL: Patients with Hashimoto’s thyroiditis have a 70 x higher incidence of lymphoma that the general population
§ Diagnosis can often be made by FNA cytology. Workup with CT abdomen, MRI, PET scan for extrathyroidal disease
§ CHEMORADIOTHERAPY is treatment of choice – CHOP THERAPY!! – excellent survival Cyclophosphamide - Hydroxydauomycin - Oncovin (Vincrysine) - Prednisolone
§ Surgical resection may enhance these results but has little role in patients with extrathyroidal disease
§ Prognosis is good - often more than 85% 5 year survival
SURGICAL TUTOR ON ASSESSMENT OF THYROID NODULES
History
§ Rapid painless growth and/or hoarseness suggests MALIGNANCY
§ Sudden painful growth suggests HAEMORRHAGE into degenerating colloid nodule
§ Family history - 20% medullary carcinomas are familial associated with MEN 2 Syndrome
 Multiple pregnancies esp in quick succession increases the risk (due to constant hyperplasia of the gland - Dr Hanchard :
Pathologist
§ History of radiation exposure
o In 1940s to 60s large numbers of children exposed in USA to low dose irradiation
o Used in treatment of tonsillar hypertrophy, acne, thymic enlargement
o Increased incidence of thyroid malignancy - usually papillary
o Most occult (<1.5 cm diameter) and multifocal
o Usually good prognosis
Examination
§ 80% solitary thyroid nodules occur in women
§ The risk of malignancy is increased three fold in men
§ Malignancy more common in children and >60 years
§ Assess whether true solitary or dominant nodule within goiter
§ True solitary nodule have 10% risk of malignancy
§ Dominant nodule in multinodular goiter has 2-5% risk of malignancy
§ Painless, firm, evidence of fixation or nodal involvement suggests malignancy
§ Most patients will be clinically and biochemically euthyroid!!!
§ Obstructive signs - stridor, tracheal deviation, neck vein engorgement
§ Hoarseness and vocal cord paralysis suggests recurrent laryngeal nerve palsy
§ 50% solitary thyroid nodules in children are cancers
§ 70% will have cervical and 15% pulmonary metastases on presentation
§ Childhood tumours have good prognosis with greater than 80% 10 year survival
DR. SMITH CLASS: APPROACHING A PATIENT PRESENTING WITH A THYROID NODULE
MUST START WITH A CAREFUL HISTORY AND EXAMINATION BEFORE ANY INVESTIGATIONS IN ASSESSING THYROID!
Hx, Exam, Investigations
2 broad bits of information derived from each

1. Function
2. Morphology
HISTORY
4 COMPONENTS: NODULE ITSELF + FUNCTION + MORPHOLOGY + RISK FACTORS
A. NODULE ITSELF
§ Duration, rate of growth, Pain (Pain present in < 10% of malignant thyroid nodules – more suggests thyroiditis or haemorrhage into a thyroid
nodule)
§ Compressive symptoms (Trachea: Dyspnoea, Oesophagus: Dysphagia)
§ HOARSENESS: SUSPECT MALIGNANCY UNTIL PROVEN OTHERWISE BY HISTOLOGY
B. FUNCTION
Hyperthyroid:
System by system:
§ Most predominant system affected = Cardiovascular
§ Cardio: Palpitations (Most common), features of cardiac failure e.g. Pedal oedema, orthopnea. Chest pain/Angina due to increased cardiac
demand exceeding blood supply
o (Arrhythmia: Afib*)
§ CNS: Agitated, irritable, insomnia

§ GI: Weight loss despite an increased appetite, hyperdefeacation
§ GU: Affects menses in any way. Menorrhagia OR Amenorrhea
§ Skin: Sweating, hyperpigmentation. Hair changes: thinning. Pretibial myxedema in Graves
Hypothyroid: Not the exact opposite

§ Weight gain is significant
§ CNS/Psych impact eg. depression. Also “Myxoedema madness”; a frank psychosis. Can mimic presenile dementia. Or most severe form:
Myxoedema coma.
§ Other earlier symptoms;

§ Weight gain. Associated with starting to snore and show features of upper airway obstruction
§ Very important: Tongue becomes thick, larynx and supraglottic structures thickened à Vocal cord thickened so voice changes.
These changes occur due to deposition of mucopolysaccharides etc.
C. MORPHOLOGY
1. Age; Thyroid nodules presenting for the first time at extremes of age are usually neoplastic (So very young and very old <20, >80)
2. Gender
D. RISK FACTORS FOR MALIGNANCY

1. Previous exposure to ionizing radiation (Usu. suggests papillary)
a. Dr. Ashman “low-dose gamma radiation (0.06-20 Gy)”. Increases risk of both benign and malignant nodules. Esp. papillary
2. Family history of any thyroid ca. ALSO DON’T FORGET: MEN, FAP, Gardner syndrome, Cowden syndrome
3. Previous history of thyroidectomy. Could be a recurrence (May especially occur if the lesion as multifocal)
ALSO NOTE (SABISTON): The incidence of thyrotoxicosis in association with a thyroid malignancy, including follicular cancer, is ONLY
approximately 2%
VERY IMPORTANT TO KNOW: 4 Causes of sudden increase in size:
1. Physiological increased demand e.g. Pregnancy.

2. Haemorrhage within a cyst/nodule (commonest cause!!!)
3. Inflammatory thyroid conditions
4. Malignant transformation
**Note: The commonest presentation of a thyroid malignancy is an asymptomatic, solitary thyroid nodule.
**But anaplastic usually declares itself
**Hoarseness (“Persistent hoarseness) is a suspicious historical finding. Secondary to vocal cord palsy that occurs on the same side of the thyroid
nodule – highly suggestive of malignancy (BUT large benign thyroid nodule may also cause this)
**Most patients with compressive symptoms usually have a large goiter.
EXAMINATION
A. FUNCTION
ASSESS PATIENT FROM FIRST SIGHT (GENERAL INSPECTION):
§ Nervousness, agitation
LOOK AT THE EYES:

§ Lid retraction: Caused by potentiation of sympathetic innervation to levator palpebrae superioris (Muller’s muscle). (It has a dual nerve
supply CN 3 and sympathetics)
o How to quickly determine: Can see the upper corneoscleral junction
§ Lid lag: Same cause
§ Proptosis: Due to deposition of immune complexes. A smouldering inflammatory process à
o Release of GAGs e.g. Hyaluronic acid. Pull water in so some of it is oedema
o All this pushes eye forward. Can threaten the vision. May require “orbital decompression” surgically
Other ophthalmopathy is specific to Grave’s disease:

1. Proptosis/Exophthalmos
2. Diplopia
3. Periorbital oedema
4. Conjunctival irritation
PALPATION
§ Warm, clammy hands. Palmar erythema

§ Increased pulse rate
§ Arrhythmias à usually Atrial fibrillation à Irregularly irregular pulse
§ Exaggerated fine tremor
B. MORPHOLOGY (NECK):
INSPECTION
(Note: Normal thyroid is NOT visible and NOT palpable)
1. Look for a visible mass

2. Skin changes on neck; hyperpigmentation, ulceration, scars from previous surgery!!!
3. Distended superficial neck veins; Likely the patient has a retrosternal thyroid compressing the veins in the root of the neck
4. Obvious pulsations
5. Ask patient to swallow

6. If the mass is in the midline, ask to protrude tongue
o A mass moving on swallowing ONLY is thyroid (The thyroid is attached to the laryngoskeleton)
o A mass moving on swallowing as well as on tongue protrusion is a thyroglossal duct cyst (due to the attachment of a persistent
thyroglossal duct to the foramen caecum)
PALPATION
§ PALPATE FROM BEHIND FOR ANY NECK MASS!

§ ONE SIDE AT A TIME – Don’t want to compress both the carotid sinuses at once (at the bifurcation). Reason: Carotid sinus massage can
cause severe bradycardia
§ Lumps: 5STCML important.

§ Size: In 2 dimensions
§ Shape
§ Site: Right, left or midline
§ Surface: Smooth? Irregular (raises suspicion)? MUST COMMENT: DIFFUSELY ENLARGED, SOLITARY NODULE OR MULTINODULAR
§ Sensitivity: Tenderness
§ Temperature
§ Consistency: Soft, firm, hard – If the mass has areas that are soft and areas that are hard, say that. Don’t say “soft to firm”, “firm to hard”
§ Mobility: Need to know if fixed to muscles or other structures (Expected that it will move on swallowing as it is attached to the trachea)
§ LYMPH NODES – SEE BELOW. ALL 7 LEVELS!!!
§ Thrills felt?
§ THEN COME BACK IN FRONT!!! à Tracheal centrality
§ *MUST ALSO: Can detect retrosternal extension on palpation. HOW: If you can define the inferior extent of the mass, no retrosternal
extension. Demonstrate and state in exam
POINTS:
- A hard craggy irregular mass, fixed to surrounding structures is highly likely to be malignant
- Malignancy is more common on solitary nodules than in multinodular lesions
- KNOW THIS: Incidence of malignancy in multinodular goiters is actually ~1%!!!
- KNOW THIS: 50-75% of clinically solitary thyroid nodules are found to be multinodular on ultrasound examination
- ***A dominant nodule in a multinodular goiter should be managed as if it was solitary as it may be malignant degeneration
- Presence of non-tender cervical lymphadenopathy is a strong indicator of the probability of thyroid malignancy
PERCUSSION: If there is evidence of retrosternal extension, percuss down sternum!
AUSCULTATION: Listen for a BRUIT, especially in the patient who is hyperthyroid
LYMPH NODE STATIONS IN THE NECK:
Occipital
Post-auricular/mastoid
Pre-auricular/parotid
Facial
Level 1A - Submental
Level 1B - Submandibular
Now at the neck ensure only palpating one side at a time. Want the neck to be flexed anteriorly and flexed to the side that
you’re examining (This relaxes the sternocleidomastoid). Feel for lymph nodes using a walking motion. These nodes are deep to
the sternocleidomastoid.
Level 2 – between the base of the skull and the lower margin of hyoid bone – the largest of this group is the jugulo-digastric
Level 3 – between lower border of hyoid and lower border of cricoid – largest group is jugulo-omohyoid
Level 4 – between the lower border of cricoid and sternal notch
Level 5 – Posterior triangle nodes
Level 6 – Paratracheal nodes
Level 7 – Mediastinal
Can also have pretracheal nodes (Delphian Nodes).
INVESTIGATIONS
NOTE VERY WELL: When the history and physical examination findings are very suggestive of a malignancy, then diagnostic
studies such as ultrasound, thyroid scan and fine needle aspirate are generally NOT indicated. HISTOLOGIC diagnosis is
mandatory and the most cost-effective method is to proceed with thyroidectomy direct after radiologic assessment of the
extent of the lesion (i.e. without FNAC or thyroid scan). However, 95% of all patients with malignant thyroid nodules will be
euthyroid AND asymptomatic. Diagnostic screening methods are therefore usually required to select the nodules that are likely to be malignant
Function:
1. Thyroid function tests (TFTs)

NB: Patients with nodular goiters are almost always euthyroid!!!
i. TSH – Most useful due to the high sensitivity of the pituitary to small changes in T3 and T4
ii. Free T4
iii. Free T3
2. Radioisotope thyroid scan (Test of structure)

§ Most common isotopes used are: iodine 131, iodine 123, Tc99m pertechnetate
§ NOTE WELL: The latter 2 have replaced radioactive iodine 131 because the high radiation dose with 131. ALSO à
§ Tc99m offers the lowest radiation dose and can be given IV and performed on the same day!!
§ I131 is now mainly used therapeutically and in screening for metastases
§ THYROID SCAN CANNOT DISTINGUISH BETWEEN BENIGN AND MALIGNANT THYROID NODULES BUT RATHER GIVE AN
INDICATION OF THE PROBABILITY OF MALIGNANCY IN A NODULE)
§ Nodules can be classified according to their ability to take up the radioisotope
1. Cold – non-functional (Highest probability of malignancy – 16% malignant)
2. Warm – Normally functional (9%)
3. Hot – Hyperfunctional (~4%)
§ Recommended ONLY in hyperthyroidism to see whether - toxic diffuse, - toxic multinodular or – solitary.
§ A cold nodule within a Graves gland is suspicious. Usually turns out to be a papillary carcinoma
§ Also used as follow-up after surgery for a differentiated thyroid cancer
Morphology:
1. Ultrasound of the neck: Provides much information:

1. Size/dimensions of the nodule
2. Solid vs. cystic
3. Solitary or multinodular (esp. to determine if it is actually a dominant nodule in a multinodular goiter)
4. Irregularity
5. Calcifications – suspicious – could be Psammoma bodies
6. Blood flow – Increased blood flow within the nodule (Centrinodular) increased blood flow is suspicious. Vs Perinodular
7. Presence of lymphadenopathy
8. Guide FNAC
§ Advantages: Non-invasive, repeatable, no radiation
2. FNAC
- Important to have an experienced cytopathologist
- Can be combined with ultrasound (U/S guided increases the accuracy of FNAC)
- Indications for U/S guided: 1. Large lesions that have > 50% cystic component 2. Small nodules that are detected incidentally 3. Deep nodules
that are hard to palpate.
- Procedure:
1. Aseptic NOT sterile. The difference between the 2 is the environment. To have a sterile operation, need to be in a sterile environment e.g.
Theatre where ventilation worked out to provide sterility.
2. Use a ~22 gauge needle. ~ 10 cc syringe. Put some air in the syringe as a buffer
3. Find the mass and steady it. Don’t usually use local.
4. Insert the needle into the center of the mass w/o applying suction when inserting
5. Once in the mass, apply suction and make 4-8 passes depending, through the mass in different directions all while staying within the
mass.
6. Before removing needle from mass, completely release the suction. Then remove the needle from mass.
o Once blood is seen in the hub of the needle, supposed to stop the suction.
o Can make additional passes to get some cells in the needle but stop the suction.
7. Remove the syringe from the needle, pull air in the syringe then put it back on. Then squirt out contents of needle onto a glass slide,
smear it, fix it, send it off. Only want the specimen that was in the needle (Fine NEEDLE aspiration) NOT the syringe.
MUST KNOW: Possible responses (VERY IMPORTANT): [SEE BETHESDA CLASSIFICATION BELOW FOR NEWER]
1. Malignant: Can pick up Papillary, medullary and anaplastic
2. Benign: Colloid goiter and hyperplastic nodule
3. Suspicious/Indeterminate: This category is mainly because FNAC cannot differentiate between FOLLICULAR CARCINOMA VS ADENOMA
4. Inadequate for diagnosis (Need to see 6 groups of 10-20 follicular cells each to make a comment. Anything less is inadequate.)
§ THE MAIN LIMITATION OF FNAC IS ITS INABILITY TO DISTINGUISH FOLLICULAR ADENOMA FROM THE WELL-DIFFERENTIATED
FOLLICULAR CARCINOMA – Instead, a diagnosis of “follicular neoplasm” is offered and a lobectomy with histologic diagnosis is required.
§ ***Vascular OR capsular invasion is necessary for the histologic diagnosis of follicular carcinoma to be made!
** Lesions diagnosed as “malignant” and those labeled “suspicious” should undergo at least a lobectomy unless the diagnosis is anaplastic carcinoma or
the patient is unfit for the procedure. Alternatively, suspicious lesions can be followed up with U/S and thyroid scan. Nodules labeled benign require
follow-up with observation for clinical features suggesting malignancy and the FNAC can be repeated because of the incidence of false-negative
aspirates.
FNAC is also useful in diagnosing and treating thyroid cysts.
Large thyroid cysts (> 4cm) and cysts that recur 3 times after repeated aspiration require lobectomy and histology because they can represent cystic
degeneration in a malignant nodule
OTHER INVESTIGATIONS:
Typically utilized after diagnosis:
1. X-rays: Can demonstrate tracheal deviation or evidence of retrosternal extension. Also pulmonary mets
2. CT Scan: Better. Even in benign e.g. In retrosternal goiter to know exactly how far down. BUT they
§ MAIN PROBLEM WITH CT: Often involve the use of significant amounts of iodine in contrast agents. Therefore can interfere with
subsequent radioactive iodine scans. SO MRI preferred
3. MRI: Determine extent
Toronto Notes: Approach to Thyroid Nodule

§ All patients with thyroid nodules require evaluation of serum TSH and ultrasound
§ Any nodule >5 mm with suspicious sonographic features (particularly microcalcifications) should undergo FNA
§ Any nodule >1 cm should undergo FNA
§ When performing repeat FNA on initially non-diagnostic nodules, U/S-guided FNA should be employed
§ Nuclear scanning has minimal value in the investigation of the thyroid nodule
§ Indications for post-op radioactive iodine ablation – I131
o Adjuvant therapy: decrease recurrent disease
o RAI therapy: treat persistent cancer
MANAGEMENT – MUST KNOW THOROUGHLY

DR. SMITH: GENERAL INDICATIONS FOR THYROIDECTOMY
1. Suspicion or confirmation of carcinoma

2. Compressive symptoms
a. Incl. Pemberton’s sign; Raise hands above head. Can see distended neck veins. Face may become flush. Increased sensation of
compression. Happens with a retrosternal goiter.
Wiki: Pemberton's sign is the development of facial flushing distended neck and head superficial veins, inspiratory stridor and elevation of the jugular
venous pressure (JVP) upon raising both of the patient's arms above his/her head simultaneously, as high as possible (Pemberton's maneuver).
3. Cosmetic concerns
4. Retrosternal goiter
5. Failed medical management for hyperthyroidism
QUICK SUMMARY: Ideal treatment for thyroid carcinoma: Depends on the type
[OVERALL AVAILABLE MODALITIES: THYROIDECTOMY, NECK DISSECTION, RADIOIODINE THERAPY, EXTERNAL BEAM RADIOTHERAPY,
CHEMOTHERAPY, PALLIATION]
Most commonly a TOTAL thyroidectomy +/- neck dissection (resection of LNs) for those that spread via lymphatics (Papillary and Medullary)
For DIFFERENTIATED ONLY, after this usually do a whole body iodine scan ~ 6 weeks after surgery. Purpose is to see:
1. Whether residual thyroid tissue
2. Whether metastatic thyroid tissue
THEN use this to calculate the dose of radioactive iodine for therapy. Remember this is for differentiated thyroid cancers as the other types don’t
take up iodine!!!
For anaplastic: Surgery recommended only for the T4A (where the tumour is confined to gland). For T4B where tumour extends outside the gland,
usually do surgery just to get access to the trachea to put in a tracheostomy. Then give radiotherapy etc.
For lymphoma: Treat with chemo +/- radiotherapy
DR. ASHMAN NOTES: TOTAL VERSUS PARTIAL THYROIDECTOMY

Considerable debate exists on the surgical aspects of the treatment of thyroid cancer. There is no large prospective, randomised clinical trial comparing
the efficacy of lobectomy and total thyroidectomy in the management of thyroid carcinoma.
With the exception of tumours localised to the isthmus, the minimum surgery that should be performed in a case of a thyroid nodule is an
ipsilateral lobectomy and isthmusectomy. (Nodules confined to the isthmus can be excised with a 1 cm resection margin of normal tissue from the
medial aspect of each lobe).
Partial lobectomy should generally not be done because:
a) Increases the risk of entering and disseminating tumour

b) Is associated with a higher recurrence rate and lower survival rate in the case of malignant nodules.
c) Risks a recurrence on the ipsilateral side and the recurrent laryngeal nerve and the parathyroids would then be in considerable danger of injury at revision surgery
There is general agreement that total thyroidectomy should be performed when there is:
1) Extrathyroidal or metastatic disease
2) Gross bilateral lobar involvement
3) Residual tumour after previous resection
4) History of significant radiation to the head and neck
There is considerable controversy on the extent of surgical resection necessary for the unilateral and grossly intrathyroidal, differentiated carcinoma of
the thyroid.
MUST KNOW:
ARGUMENTS FOR TOTAL THYROIDECTOMY:
1. Histologic sections have demonstrated microscopic foci of carcinoma in the contralateral lobe in up to 85% of cases of papillary
carcinoma. Total thyroidectomy would eliminate these foci, which are potential sources of “recurrence”. The lowest recurrence rate has
been found in patients who have had a combination of total thyroidectomy, radioactive iodine and TSH suppression using exogenous thyroxine.
2. It facilitates the use of radioactive iodine in the DIAGNOSTIC and THERAPUTIC mgmt of any local or metastatic lesions. Normal thyroid
tissue has a 100-fold greater affinity for iodine than papillary or follicular carcinoma of the thyroid. The presence of residual thyroid tissue
can therefore significantly impair the uptake of radioactive iodine by metastatic lesions.
3. The use of thyroglobulin levels as a tumour marker for recurrent thyroid carcinoma is also greatly facilitated by total thyroidectomy.
4. A true total thyroidectomy eliminates the 1% risk of anaplastic change that occurs in differentiated thyroid carcinomas.
ARGUMENTS FOR THYROID LOBECTOMY + ISTHMUSECTOMY

1. Incidence of recurrent laryngeal nerve palsy and that of permanent hypoparathyroidism is increased in total thyroidectomy compared to
lobectomy.
2. Significance of micro-foci in contralateral lobe is uncertain
3. Many patients do not require radioiodine
4. Progression to undifferentiated carcinoma is rare
5. No evidence that more extensive procedure is associated with better prognosis
SEE PROGNOSTIC FACTORS (AGES, AMES, MACIS) FROM SABISTON NOTES - INFLUENCES DECISION
OVERALL RECOMMENDATIONS
Total thyroidectomy is a relatively safe operation in the hands of experts with a 2% incidence of recurrent laryngeal nerve palsy and 3% permanent
hypoparathyroidism (Lore,1988). Total thyroidectomy facilitates radioactive iodine therapy and also facilitates the use of thyroglobulin as a tumour
marker for metastases, eliminates multifocal disease, reduces local recurrence and prevents anaplastic change in any tumour which would have
remained in the thyroid had a lobectomy been performed. It is difficult to argue against total thyroidectomy when this operation is performed with minimal
morbidity.
§ Papillary carcinoma that is associated with any of the factors (based on AMES, AGES of MACIS score) as indicators for a poor
prognosis, should be managed by total thyroidectomy.
o All other cases of papillary carcinoma can be treated by a lobectomy because this reduces the surgical risks to the patient and gives
equivalent recurrence and survival rates to total thyroidectomy in these patients.
o When nodal metastases are present, a modified radical neck dissection should be performed and any paratrachael or
superior mediastinal metastatic nodes resected. This approach will reduce the local recurrence rate but will not significantly alter the
survival rate in papillary carcinoma.
§ Follicular OR Hürthle cell carcinoma ALL patients should have a total thyroidectomy unless the patient is unfit for surgery or the
primary is not resectable. Follicular carcinoma and the Hürthle cell carcinoma tend to have worse prognoses than papillary
carcinoma.
§ Medullary carcinoma is best managed by total thyroidectomy AND unilateral or bilateral neck dissections.
§ Anaplastic carcinoma is usually not resectable at presentation and surgical management is often limited to incisional wedge biopsy
of the isthmus and tracheostomy. Radiotherapy and chemotherapy can be added but survival beyond the first year is very unlikely.
Radioactive iodine (I-131) is a useful adjunct to total thyroidectomy for the management of microscopic metastases in differentiated carcinoma of
the thyroid.
§ VERY IMPORTANT: High TSH levels and the absence of normal thyroid tissue enhance uptake of radioactive iodine by metastases. Thyroid
suppressive therapy should NOT be given in the first six weeks postoperatively but rather, the patient should be made hypothyroid allowing
the TSH level to rise to 30-60 mIU/L. This will facilitate the uptake of radioactive iodine by functional metastases in the whole body
diagnostic scan (5 mCi I-131) as well as therapeutic I-131 (50-150 mCi).
External beam radiotherapy should be added whenever there is gross focal metastatic disease or incomplete resection. Focal metastatic
lesions that do not take up radioactive iodine require excision along with external beam radiotherapy.
Chemotherapy utilizing doxorubicin and cisplatin has produced a response in only a SMALL MINORITY OF CASES of differentiated carcinoma of
the thyroid.
FOLLOW-UP
The patient is seen every 2 months in the first year, every 3 months for the next 2 years, every 6 months over the following 2 years; and then
123
annually. Chest X-rays and thyroglobulin levels should be obtained annually and when indicated clinically. Diagnostic whole body scans (I ) are
performed annually for the first 2 years and then every 3-5 years.
COMPLICATIONS OF THYROIDECTOMY
1. Haemorrhage
2. Wound Complications
a. Sepsis
b. Hypertrophic scarring
3. Respiratory Obstruction
a. Laryngeal mucosal oedema
b. Clot deep to strap muscles
c. Bilateral incomplete recurrent laryngeal nerve palsies
d. Tracheomalacia
4. Nerve Damage
§ Recurrent laryngeal nerve palsy
i. Incomplete - cord moves to midline
ii. Complete - cord in cadaveric position
§ Preoperative cord inspection is essential
§ 3% population have asymptomatic recurrent laryngeal nerve palsy
5. Hypocalcaemia (Permanent hypoparathyroidism)
6. Recurrent hyperthyroidism
7. Hypothyroidism
8. Thyroid Crisis
a. Fulminating hyperthyroidism
b. Hyperpyrexia
c. Arrhythmia
d. Cardiac Failure
-----
9. Pneumothorax
10. Air Embolism
THYROID CANCER DETAILED WORKUP AND MANAGEMENT
SABISTON
WORKUP OF SOLITARY THYROID NODULE
All patients with a thyroid nodule undergo thyroid function tests (at least for serum TSH). If the patient is hyperthyroid, a radiouptake scan is used to
confirm a hot nodule. If this is the case, the patient is carefully monitored with thyroid suppression and seen again after 6 months for confirmation of
successful suppression and reevaluation. If suppressive therapy fails, surgery (usually lobectomy) is highly effective, but not generally required
In a patient with a thyroid nodule and normal thyroid function test results, ultrasound is performed. Cystic lesions on ultrasound are usually benign;
however, cystic papillary carcinomas, although rare, do occur. Cystic lesions are aspirated; bloody or suspicious aspirates can be sent for cytologic
examination. After aspiration, these patients are seen again in 6 months. Patients with recurrent cysts are considered surgical candidates.
For patients whose nodules on ultrasound are solid or have mixed solid-cystic components, decision-making depends on additional information.
Depending on the history, examination, and imaging risk factors for malignancy, some patients will choose excision, regardless of further workup. In
most patients, FNA is indicated IF a decision for surgery has not already been made. FNA can be used to diagnose papillary cancer and is strongly
suggestive of medullary cancer or anaplastic cancer. It cannot confirm follicular cancer, nor can it confirm a completely benign diagnosis. Therefore, risk
assessment is crucial when advising patients with a solid nodule for whom the diagnosis is not secure with FNA. Colloid nodules are usually suggested
by a mixed solid-cystic appearance on ultrasound, and FNA shows colloid and macrophages. If not otherwise suspicious, these lesions can be
monitored closely with serial ultrasonography every 6 months to establish stability. Alterations in the appearance of the suspicious lesion indicate a need
for surgery
The increased availability of ultrasound appears to have affected the incidence of small thyroid cancers in the United States. Most seem to be
asymptomatic papillary carcinomas smaller than 1 cm. The fact that these lesions are highly curable and associated with almost nonexistent mortality
needs to be taken into account when deciding whether to perform FNA and proceed to surgery.
The finding of a thyroid nodule in a child or pregnant patient can be of particular concern to the patient, family, and referring clinicians. Although the
frequency of malignancy may be higher in children than in adults, the evaluation should generally proceed in the same fashion as for an adult. In
pregnant patients, it is not clear whether the incidence of malignancy for a given nodule is different than that in nonpregnant patients. The evaluation of
a thyroid nodule discovered in pregnancy is the same as in the nonpregnant patient EXCEPT that radionuclide scans are contraindicated. If a
nodule is found to represent papillary cancer during pregnancy and remains stable by midgestation or is diagnosed in the second half of pregnancy,
surgery may be deferred until the patient is postpartum. This practice is believed not to affect the oncologic outcome
THYROID MALIGNANCIES
§ Thyroid cancer represents approximately 3% of all malignancies in the United States
§ Almost 75% of cases occur in women
Thyroid Oncogenesis
Genetic Alterations
Genetic processes that lead to thyroid neoplasia include two important categories, mutated proto-oncogenes, which result in altered protein production
and in accelerated growth, and loss of function in tumour suppressor genes, allowing unregulated cell growth.
The PTC-RET proto-oncogene has received perhaps the most attention in thyroid tumorigenesis studies and has been well characterized. The
PTC-RET proto-oncogene encodes for a membrane receptor tyrosine kinase and is the most frequent genetic alteration in papillary thyroid cancer
(PTC), despite the absence of the RET protein product in normal thyroid follicular cells
As many as 40% of thyroid tumors may have one of three ras gene point mutations (H-ras, K-ras, or N-ras) and ras mutations may occur in
benign and malignant thyroid neoplasms, including follicular adenomas, follicular cancers, and follicular variant papillary cancers
K-ras mutations appear more frequently in radiation-induced papillary cancers. Follicular cancers with ras mutations are more aggressive than
those without ras mutations, and ras mutations may also be found in undifferentiated and anaplastic thyroid cancers
Tumor suppressor genes also play a role in thyroid malignancy. Loss of function of the p53 tumor suppressor gene is one of the most common
genetic alterations seen across all human cancers and is associated with radiation exposure.
IONIZING RADIATION
Ionizing radiation can cause genetic mutations leading to malignant transformation. This association is much stronger for thyroid cancer
than for other malignancies, and radiation is the only well-established environmental risk factor for thyroid malignancy!!!. The
risk of developing thyroid cancer after exposure to radiation is greater in those exposed during childhood. The association with radiation is much
stronger for papillary than for follicular cancer
Patients who receive external radiation for a soft tissue malignancy, such as Hodgkin’s lymphoma, have an increased incidence of thyroid
nodules and cancer (as many as 30% to 35% of those exposed). Acute environmental exposures, such as those seen following the Chernobyl (in
Ukraine) nuclear event, also have significant impact. The incidence of thyroid cancer in children in some areas affected by Chernobyl peaked at 100
times that seen prior to the accident
PAPILLARY THYROID CARCINOMA (PTC)

The most important risk factor for papillary cancer is childhood radiation exposure from medical or environmental sources .
Other important risk factors for papillary thyroid cancer include a history of thyroid cancer in a first-degree relative and the presence of a familial
syndrome that includes thyroid cancer, such as Werner syndrome, Carney complex, and familial polyposis
Papillary cancers may be partially cystic on ultrasound. Occasionally, a metastatic papillary cancer will present as a painless lateral neck mass that
is confirmed to be nodal metastatic thyroid cancer, even with a normal thyroid examination.
Most patients with papillary carcinoma can expect an excellent prognosis, with the 10-year survival rate above 95% for the most favorable stages.
Various factors in the clinical findings and pathologic staging, however, may alter the excellent prognosis
MUST KNOW:
Age at diagnosis is the most important prognostic factor in well-differentiated thyroid cancer. Diagnosis at an age younger than
40 years is associated with excellent survival. In women, this age benefit is extended to 50 years
----
Multicentricity can be anticipated in as many as 70% of patients with papillary cancer and may represent
intraglandular metastasis or multiple primary tumors
Also, cervical lymph node metastases are common, particularly in children, who have up to a 50% incidence of clinically detectable nodal
disease and up to a 90% rate of microscopically detectable nodal disease at the time of initial presentation; however, this does not appreciably affect
mortality. The presence of lymph node metastasis in patients with contained intrathyroidal primary papillary carcinoma also does NOT affect
long-term survival. If there is gross or microscopic extension of a primary papillary carcinoma through the thyroid capsule, a poor prognosis and
possibly a higher rate of lymph node metastasis may be anticipated
Because multicentricity and lymph node metastases are common, COMPLETE ULTRASOUND OF THE THYROID AND
CENTRAL AND LATERAL NECK NODAL BASINS should be performed PRIOR to thyroidectomy for known or suspected
malignancy. Although papillary cancer typically disseminates via lymphatic spread, distant metastases do occur and are present in 3% to 5% of
patients at the time of diagnosis. The two most common sites of spread are to the lungs and bones.
TREATMENT – PAY CLOSE ATTENTION HERE!
The primary treatment of differentiated thyroid cancer, including papillary and follicular thyroid cancer, is surgical ablation. Several factors enter into
surgical decision-making. As noted, although well-differentiated cancers generally have a good prognosis, there are high rates of
multicentricity within the thyroid and high rates of lymph node metastases, and recurrence is not infrequent. Furthermore,
although more aggressive resections of the thyroid and lymphatic beds expose the patient to more potential morbidity, they facilitate radioiodine therapy,
thyroxine suppression, and surveillance. With these considerations in mind, the objectives of initial therapy include the following: (1) remove the primary
tumor and involved cervical lymph nodes; (2) minimize treatment related morbidity; (3) stage the disease accurately; (4) facilitate postoperative
radioiodine therapy, if appropriate; (5) permit accurate long term surveillance; and (6) minimize risk of recurrence or metastasis.
Appropriate surgical options and terminology for known or suspected thyroid malignancy include the following:
1. Hemithyroidectomy (i.e. thyroid lobectomy, with or without isthmusectomy)
2. Near-total thyroidectomy, (defined by leaving less than 1 g of tissue adjacent to the recurrent laryngeal nerve at the ligament of Berry
on one side);
3. total thyroidectomy, defined by removal of all visible thyroid tissue.
Nodulectomy OR leaving more than 1 g of thyroid tissue in a subtotal thyroidectomy is NOT considered an appropriate
surgical option for thyroid malignancy!!
The advantages of total or near-total thyroidectomy include the efficient use of radioiodine postoperative treatment. Radioablation is much less
effective and requires a larger dosage if residual thyroid exists. Advantages of a procedure less than total or near-total thyroidectomy are
decreased rates of bilateral recurrent laryngeal nerve damage and hypoparathyroidism.
NOTE WELL: For patients who DO NOT have a biopsy-proven thyroid malignancy, the surgical option selected should balance the likelihood of
cancer with potential morbidity. Because of the higher likelihood of malignancy, the following patients with undiagnosed nodules should
undergo a total or near-total thyroidectomy as their initial resection: *patients with larger than 4 cm tumors, those with *marked atypia on biopsy,
those with *FNA results suspicious for papillary cancer, those with a *family history of thyroid cancer, patients with a *history of radiation exposure, and
men older than 50 years. In patients without these high-risk findings and without a diagnosis of malignancy, thyroid lobectomy is an appropriate initial
resection and serves as a diagnostic biopsy
NOTE WELL: Papillary cancers smaller than 1 cm in diameter are defined as microcarcinoma.
In patients who DO have cytologic and imaging diagnosis of a solitary intrathyroidal papillary MICROCARCINOMA (i.e. < 1cm), no clinically involved
cervical lymph nodes, and no history of head and neck radiation, a unilateral thyroid lobectomy and isthmusectomy is an appropriate resection.
Patients with a diagnosed thyroid cancer *larger than 1 cm OR a *smaller than 1 cm papillary cancer with clinical nodal disease,
*multicentricity, or *a history of head and neck radiation, the initial thyroid resection should be a total or near-total thyroidectomy, which will
most likely be followed with radioablation
The management of central and lateral neck lymph nodal basins has been a topic of active debate in the multidisciplinary
literature.
It is currently recommended that all patients with known or suspected papillary cancer undergo a thorough physical examination and complete
ultrasound of the central and lateral neck prior to resection of the thyroid lesion.
CENTRAL NECK NODES: If clinically positive adenopathy is detected in the central neck, a therapeutic LEVEL 6 (paratracheal)
or central neck lymph node dissection should be performed at the time of total or near-total thyroidectomy. There is an
emerging hypothesis that prophylactic level 6 dissection should be routinely performed, even in those patients with clinically
uninvolved nodes, but this remains a topic of debate.
LATERAL NECK NODES: The management of lateral neck lymph node basins has similarly been a topic of debate . Currently,
consensus supports a practice of ipsilateral therapeutic lateral neck dissection for patients who have biopsy-proven metastatic lateral
cervical disease. This should be undertaken as a formal clearance of a defined lymph node level, rather than isolated resection of the involved node, or
berry picking. Studies have shown that despite an almost 30% rate of micrometastases in lateral lymph nodes, there is little benefit of prophylactic
lateral neck dissection for clinically negative nodes
RE: COMPLETION THYROIDECTOMY

It is not infrequent to diagnose well-differentiated thyroid cancer or multicentricity after completing a diagnostic thyroid lobectomy or total
thyroidectomy performed for what was believed to be benign disease, such as symptomatic multinodular goiter. This presents the clinical
question of whether completion thyroidectomy and/or lymphadenectomy should be carried out. Completion thyroidectomy offers the benefit of complete
clearance of multifocal disease, facilitating radioiodine therapy, and enabling surveillance with determination of a serum Tg level. The downside involves
a reoperative intervention, which carries a risk of technical complications. Current recommendations are that completion thyroidectomy
should be performed if the original recommendation would have been total or near-total thyroidectomy if the pathology were
known preoperatively. In other words, completion thyroidectomy should be performed, except in those patients with small (< 1 cm), unifocal,
intrathyroidal, node-negative and otherwise low-risk papillary cancers. In patients that meet these low-risk criteria, thyroid lobectomy may be considered
an adequate resection and no further surgical intervention is required
Postoperative 131 I therapy has been advocated for those with known metastases, extrathyroidal extension, and tumors larger than 4 cm.
Recurrence in local or regional lymph nodes after initial surgery is treated by completion thyroidectomy, if residual tissue
exists, plus regional lymph node dissection
Patients who have undergone thyroidectomy will require exogenous thyroid hormone replacement, which also provides the benefit of suppressing TSH
and therefore suppressing a stimulus to further growth of differentiated thyroid cancers.
The presence of distant metastatic disease may be evaluated with chest radiography, radionuclide scanning, CT, and other modalities, as
guided by clinical suspicion. In patients after total thyroidectomy, postoperative Tg levels may be followed to monitor for recurrence, although
preoperative Tg levels are not needed
FOLLICULAR CARCINOMA
TREATMENT
Treatment of follicular carcinoma is primarily surgical. The diagnosis of the carcinoma CANNOT be determined by preoperative FNA or
intraoperative frozen section!!! The surgeon is left to select the most efficacious treatment of a follicular lesion, which, lacking the obvious gross
characteristics of malignancy and widely invasive follicular cancer, is most likely a benign lesion. If the lesion is 2 cm or smaller and well contained within
one thyroid lobe, an argument may be made for thyroid lobectomy and isthmusectomy. If the lesion is larger than 2 cm, the surgeon may well proceed
with total thyroidectomy. If the follicular lesion is larger than 4 cm, the risk for cancer is higher than 50%, and total thyroidectomy is an obvious choice. In
general, the recommendations for surgical management of follicular cancer mirror those of papillary cancer (see
earlier). Also, as noted, follicular neoplasms excised by thyroid lobectomy may turn out to be follicular cancers on final pathology. Current
recommendations support performing completion thyroidectomy if total thyroidectomy would have been offered if the diagnosis had been secured
preoperatively
Postoperative Treatment
Accepted postsurgical management of well-differentiated papillary and follicular thyroid cancers involves the use of radioiodine ablation and long-
term monitoring of Tg. 131I contains high-energy (gamma rays) and medium-energy (beta particles), which enhances the therapeutic effect.
Patients are usually withheld from thyroid replacement therapy so that TSH levels may become elevated, rendering the thyroid iodine avid and thus
maximizing the effect of 131I.
If a patient has undergone complete thyroid ablation, Tg levels should be UNDETECTABLE. The recent development of
human recombinant TSH has redefined the efficacy of monitoring stimulated Tg levels as evidence of recurrence. It is
possible that the use of human recombinant TSH can detect tumor recurrence earlier and allow earlier treatment.
Despite these advances, the use of Tg to monitor tumor recurrence remains imperfect à CHALLENGE WITH TG: As many as 15% to 30% of
patients with thyroid carcinoma have anti-Tg antibodies, which seriously compromises the use of Tg as a tumor marker!!!
MEDULLARY THYROID CARCINOMA (MTC)
Most patients with MTC or a syndromic predisposition to MTC without advanced disease should undergo at least a total thyroidectomy. Total
thyroidectomy allows complete removal of the gland and a search for multicentricity. Also level 6 neck dissection (central and lateral neck
dissection)
If MTC is diagnosed postoperatively in a patient undergoing less than total thyroidectomy, further operative intervention is indicated to complete therapy
as though the diagnosis were known preoperatively, including completion thyroidectomy and nodal dissection, as indicated. Patients with the
MEN2B RET mutation are recommended to undergo PROPHYLACTIC TOTAL THYROIDECTOMY WITHIN THE
FIRST YEAR OF LIFE. Other patients with germline RET mutations should undergo prophylactic total
thyroidectomy before age 5 years
A successful operation with a good prognosis à calcitonin levels are undetectable after surgery.
Recent reports have suggested that radioactive iodine scanning and therapy have little role in MTC, unless there is a concomitant PTC or FTC
ANAPLASTIC THYROID CANCER

Most aggressive form of thyroid cancer, with a disease-specific mortality approaching 100%. A typical manifestation is an older patient with
dysphagia, cervical tenderness, and a painful, rapidly enlarging neck mass
Treatment
The results of any surgical treatment of anaplastic thyroid carcinoma are tempered by its rapidly progressive clinical course. Distant spread is present in
90% of patients at the time of diagnosis, usually to the lungs, and most reports of resection are not optimistic. FNA is accurate in 90% of cases, thus
making open biopsy an uncommon surgical indication. Three types of cell populations have been classified—small spindle cell, giant cell, and
squamous. All have a poor prognosis
Postoperative external beam radiation or adjunctive chemotherapy adds little to the overall prognosis, but should be considered.
The finding of distant metastasis or invasion into locally unresectable structures, such as the trachea or vasculature of the anterior mediastinum, leads to
a more conservative surgical approach, such as tracheostomy. Because the prognosis is so grim in this disease, end-of-life planning and consideration
of palliation must be part of the very early management and counseling of these patients
SURGICAL APPROACH TO THYROIDECTOMY

STANDARD APPROACH IS A CERVICAL APPROACH WITH..
New Directions in Thyroid Surgery

Although the techniques described here remain the standard of care in the surgical management of thyroid pathology, a number of new avenues of
surgical intervention are being investigated. Many surgeons, including ourselves, have found that traditional surgical technique may be
accomplished through more limited skin incisions.
Other techniques allow even more limited cervical incisions or relocation of the incision away from the neck and, in one case, the skin incision
was entirely eliminated!!!
Minimally invasive video-assisted thyroidectomy (MIVAT) involves the use of a 1.5- to 2-cm anterior cervical incision, an endoscopic camera
placed into the wound for visualization, self-retaining retractors, and dedicated surgical instruments. This technique is generally applied to lobectomy for
benign disease, but has been used for small, well-differentiated thyroid cancers and even to total thyroidectomy for malignancy, although total
thyroidectomy requires a bilateral approach. This approach does result in longer operative times, which improve after a learning curve, and is believed to
have the same rate of technical complication as traditional thyroidectomy.
Robotically assisted approach to thyroidectomy: Kang and colleagues, in South Korea, have championed the use of a transaxillary, gasless,
robotically assisted approach to thyroidectomy. A 5- to 6-cm incision is made in the axilla and a subcutaneous plane is created anterior to the pectoralis,
between the heads of the sternocleidomastoid muscle, and deep to the strap muscles. A second incision (< 1 cm) is also required on the anterior chest.
Using these incisions, a self-retaining retractor, and robotic surgical system, total thyroidectomy may be performed. This approach has been applied to
benign disease and small malignancies. The authors include an ipsilateral level VI nodal dissection in all cases.
No skin incision: There is a single reported case of thyroid lobectomy performed with no skin incision. This technique involved several incisions in
the floor of the mouth, through which instruments were tunneled to a subplatysmal plane, the neck insufflated, and endoscopic thyroidectomy
undertaken. With the exception of a small hematoma, the patient reported to have undergone this procedure had a good recovery, but no series is yet
available to establish efficacy and safety
COMPLICATIONS OF SURGERY
The most significant complications are postprocedure hypocalcemia secondary to devascularization of the parathyroid (AND NOT
USUALLY DUE TO REMOVAL OF THE ACTUAL PARATHYROID!!!) and significant hoarseness caused by recurrent laryngeal nerve injury, induced by
traction or division
HYPOCALCEMIA
Rates of postprocedure hypocalcemia are approximately 5%; it resolves in 80% of cases in approximately 12 months. Therefore, every effort is made to
evaluate the parathyroid tissue intraoperatively. For glands that appear to be devascularized, the use of immediate parathyroid autotransplantation of
1-mm fragments of saline-chilled tissue into pockets made in the sternocleidomastoid or brachioradialis muscle is extremely effective for avoiding
hypocalcemia.
NERVE INJURY
Superior Laryngeal Nerve

The superior laryngeal nerve has two branches, an internal branch that supplies sensory fibers to the larynx and an external branch that supplies motor
fibers to the cricothyroid muscles and tenses the vocal cords. The external branch can run closely adherent to the superior thyroid artery, and care must
be exercised during dissection in this area. Injury to the branch causes voice changes, huskiness, poor volume voice fatigue, and an inability to sing at
higher ranges.
Recurrent Laryngeal Nerve

As noted, the recurrent laryngeal nerve arises from the vagus and is a mixed motor, sensory, and autonomous nerve that innervates the adductor and
abductor muscles. Unilateral injury is classically described as a paralyzed vocal cord, with loss of movement from the midline. A wide spectrum of
injuries to the voice, swallowing mechanisms, or both can occur because of the mixed fibers contained within the nerve. A temporary or permanent voice
change can result, which is extremely distressing to the patient.
BLEEDING
Other complications such as bleeding and wound hematomas may require immediate reexploration, which is done in the operating room unless airway
compromise dictates otherwise. These complications can be avoided by meticulous hemostasis at closing, which results in less than a 1% rate of
occurrence. Complication rates appear to be affected by surgeon experience. A study in Maryland of 5860 patients reported the lowest complication
rates in patients of surgeons who performed more than 100 neck explorations annually.
TORONTO NOTES SUMMARY TABLE
PAPILLARY FOLLICULAR MEDULLARY ANAPLASTIC LYMPHOMA
Incidence 75-80% 10% 3-5% 5% 1%

(% of all
thyroid (10% MEN 2A & 2B, 10% non-MEN
cancers) familial, 80% sporadic)
Route of Lymphatic Haematogenous Lymphatic and haematogenous
Spread
Histology Orphan-Annie nuclei Capsular/vascular invasion Amyloid Giant cells
Nuclear grooving Invasion influences prognosis May secrete calcitonin, Spindle cells
Pseudoinclusions prostaglandins, ACTH, serotonin,
Psammoma bodies kallikrein or bradykinin
Papillary architecture
Other Ps – Fs – Ms – Medullary cancer More common in elderly Usually non-Hodgkin’s lymphoma
Papillary cancer Follicular cancer Multiple endocrine neoplasia (MEN IIa 70% in women Rapidly enlarging thyroid mass
Popular (most common) Far away mets or IIb)
Palpable lymph nodes Female (3:1) aMyloid 20 to 30% have Hx of Hx of Hashimoto’s
Positive I131 uptake NOT FNA (can’t be diagnosed by Median node dissection differentiated thyroid Ca thyroiditis increases risk
Positive prognosis FNA) (mostly papillary) or nodular 60x
Post-op I131 scan to guide Favourable prognosis goiter mass 4:1 female predominance
treatments KRAS!!!
**Most common sites for metastatic Rapidly enlarging neck Dysphagia, dyspnea, stridor,
** The two most common sites deposits are lytic bone lesions and Rule out lymphoma hoarseness, neck pain, facial
of DISTANT spread are to the lung! edema, accompanied by “B”
lungs and bones. (Overall is symptoms*
lymph nodes)
Prognosis 99% at 10 yr 85% at 10 yr 50% at 10 yr 25% at 1 yr 5 yr survival

20% at 10 yr if detected when clinically 13% at 10 yr Stage IE 55%-80%
palpable Stage IIE 20%-50%
Stage IIE/IV 15%-35%
Treatment Small tumours: Small tumours: Total thyroidectomy Radiation and chemotherapy Non-surgical
(Not a good Near total thyroidectomy or Near total Median lymph node dissection if Small tumours: Combined radiation
summary) lobectomy thyroidectomy/lobectomy/isthmectomy lateral cervical nodes +ve Total thyroidectomy ± external Chemotherapy (CHOP**)
Modified neck dissection beam
Diffuse/bilateral: Large/diffuse tumours: Post-op thyroxine
Total thyroidectomy Total thyroidectomy Tracheostomy
± Post-op I131 tx Screen asymptomatic relatives
*B symptoms = fever, night sweats, weight loss >10% in 6 mo ** CHOP = cyclophosphamide, adriamycin, vincristine, prednisone
General Surgery
Chest Trauma
Sources: Toronto Notes, Sabiston
February 2015
MUST SEE MY SEPARATE ATLS NOTES!!!!
Toronto Notes: Summary of Chest Injuries

• Trauma to the chest accounts for 50% of trauma deaths.
• 80% of all chest injuries can be managed non-surgically with simple measures such as intubation, chest tubes, and pain
control.
• Two types: those found and managed in primary survey and those found and managed in secondary survey
Life-Threatening Chest Injuries Found in 1º Survey

ALWAYS SAY ABCDEs FIRST
PHYSICAL EXAM INVESTIGATIONS MANAGEMENT
Airway Obstruction Anxiety, stridor, hoarseness, Do not wait for ABG to intubate Definitive airway management
altered mental status
Intubate early
Apnea, cyanosis
Remove foreign body if visible with
laryngoscope prior to intubation
Tension Pneumothorax General: Respiratory distress, CLINICAL (Non-radiographic) Needle thoracostomy – large
nd
tachycardia, distended neck diagnosis bore (18 G) needle, 2 intercostal
Clinical diagnosis veins, shock, cyanosis, space (ICS) just lateral to mid-
asymmetry of chest wall motion clavicular line ON THE
One-way valve causing accumulation AFFECTED SIDE (to avoid
of air in pleural space Tracheal deviation away from internal carotid artery injury)
pneumothorax
Followed by chest tube in 5th ICS,
Hyperresonant percussion between the anterior and
midaxillary line (triangle of safety)
Unilateral ABSENT breath sounds
Open Pneumothorax Gunshot or other penetrating ABG: decreased pO2 Air-tight/occlusive dressing
wound (hole >2/3 tracheal sealed on 3 sides* (See below)
(“Sucking chest wound”) diameter) ± exit wound
Chest tube
Air entering chest from wound rather Unequal breath sounds
than trachea Surgery
Massive Haemothorax Pallor, flat neck veins, shock, Usually only able to do supine Restore blood volume
tachycardia, hypotension CXR – entire lung appears
>1500 cc blood loss in chest cavity radioopaque as blood spreads out Chest tube
Unilateral dullness to percussion over posterior thoracic cavity
Thoracotomy if:
Absent breath sounds >1500 cc total blood loss
≥200 cc/h continued drainage
Flail Chest General features of respiratory ABG: decreased pO2, increased 1. O2 + fluid therapy + pain control
distress pCO2 o Epidural analgesia preferred!
Free-floating segment of chest wall
due to ≥ 2 adjacent rib fractures, each Paradoxical movement of flail CXR: 2. Judicious fluid therapy in
at 2 sites segment 1. rib fractures, absence of systemic
2. lung contusion, hypotension
NOTE WELL!! Underlying lung Palpable crepitus of ribs 3. subcutaneous emphysema 3. Positive pressure ventilation
contusion = the actual cause of the 4. ± intubation and ventilation
morbidity and mortality Decreased air entry on affected 5. Chest physiotherapy!
side 6. ± Operative fixation of ribs
Cardiac Tamponade Penetrating wound (usually) Ultrasound (Echo) is a valuable IV fluids
tool for quickly assessing the
Clinical diagnosis Beck’s triad (presence highly pericardium for fluid and should Pericardiocentesis - which is only
variable): Systemic hypotension, be performed in all patients with a temporizing measure to à
Pericardial fluid accumulation distended neck veins, muffled haemodynamic instability.
impairing ventricular function heart sounds Open thoracotomy & repair
A subxiphoid pericardial
Tachycardia, tachypnea window remains the most ***Cardiac injuries resulting in
valuable means of evaluating cardiovascular collapse are
Pulsus paradoxus for cardiac injury and should be approached with a left
used in cases for which ultrasound anterolateral thoracotomy in the
Kussmaul’s sign (increased JVP is not available or the results are emergency department.
with inspiration) inconclusive. BUT injuries that are identified and
allow transport to the operating
A pericardial window allows direct room are best exposed through a
visualization of the pericardial space median sternotomy
and can be quickly extended to
perform a median sternotomy in the
setting of an identified injury.
Potentially Life-Threatening Chest Injuries Found in 2º Survey
PHYSICAL EXAM INVESTIGATIONS MANAGEMENT
Pulmonary contusion Blunt trauma to chest CXR: areas of opacification of lung Maintain adequate ventilation
within 6 h of trauma
Interstitial oedema impairs Monitor with ABG, pulse oximeter
compliance and gas exchange and ECG
Chest physiotherapy
Positive pressure ventilation if

severe
Oesophageal Injury Usually penetrating trauma (pain CXR: mediastinal air (not always) Early repair (within 24 h) improves
out of proportion to degree of injury) outcome but all require repair
Oesophagram (Gastrografin®)
Flexible esophagoscopy
Aortic Tear Sudden high speed deceleration CXR Thoracotomy (may treat other
(e.g. MVA, fall, airplane crash) CT scan severe injuries first)
Transesophageal echo (TEE),
90% tear at subclavian (near Complaints of chest pain, dyspnea, Spiral thoracic CT
ligamentum arteriosum), most die hoarseness (frequently absent) angiography (gold standard)
at scene
Decreased femoral pulses, See below table for CXR features
Salvageable if diagnosis made differential arm BP (arch tear)
rapidly
Ruptured Diaphragm Blunt trauma to chest or abdomen CXR: abnormality of Laparotomy for diaphragm repair
(e.g. high lap belt in MVC) diaphragm/lower lung fields/ and because of associated intra-
NG tube placement abdominal injuries!!!
CT scan and endoscopy –

sometimes helpful for diagnosis
Blunt Myocardial Injury Blunt trauma to chest (usually in ECG: dysrhythmias, ST changes O2
setting of multi-system trauma and Antidysrhythmic agents
(rare) therefore difficult to diagnose) Patients with a normal ECG and Analgesia
normal hemodynamics never get
Physical examination: overlying dysrhythmias
injury, e.g. fractures, chest wall
contusion
The presence of a pulmonary contusion or flail chest does NOT require mandatory chest tube placement in the absence of a pneumothorax
or haemothorax
RE: Pulmonary contusion: Intubation should be guided by the patient’s observed respiratory function and should NOT be performed
prophylactically simply on recognition of pulmonary contusion
3-WAY SEAL FOR OPEN PNEUMOTHORAX (I.E. SUCKING CHEST WOUND)
§ Allows air to escape during the expiratory phase (so that you don’t get a tension pneumothorax) but seals itself to allow adequate breaths during
the inspiratory phase.
MUST KNOW: AORTIC TEAR X-RAY FEATURES:

1. Wide mediastinum (most consistent)
2. Indistinct aortic knuckle
3. Pleural cap
4. Depressed left mainstem bronchus
5. Tracheal deviation to right side
6. Esophagus (NG tube) deviated to right
7. Haemothorax
(Note: present in 85% of cases, but cannot rule out)
Pulsus Paradoxus: a drop in BP of >10 mmHg with inspiration. Recall that BP normally drops with inspiration, but what’s “paradoxical” about this is that it
drops more than it should.
DDX OF LIFE THREATENING CHEST INJURIES

HOT and FAT CHEST
§ Haemothorax*
§ Open pneumothorax
§ Tension pneumothorax*
§ Flail chest
§ Airway obstruction
§ Tamponade*
§ Contusion: Pulmonary, myocardial
§ Hernia: Traumatic, diaphragmatic

§ Esophageal perforation
§ Tracheobronchial disruption
§ Traumatic injury/Thoracic Aorta Rupture*
*Rapidly Life Threatening
SABISTON NOTES
Algorithm for chest trauma
INJURIES TO THE CHEST INTRODUCTION (SABISTON)

Despite the seriousness of these injuries, most can be treated effectively by basic maneuvers that can be provided in the emergency department. MVAs
are the most common cause of blunt thoracic injuries, followed by falls, with injury resulting from the transmission of energy to the chest wall and underlying
structures. Direct compression, as well as deceleration and rotational physical mechanisms, contribute to the incidence of thoracic injury.
IMMEDIATE MANAGEMENT (SEE MY ATLS NOTES)

Many injuries to the thorax require immediate intervention during the primary survey to support cardiopulmonary function.
Establishment of a secure airway and ventilator assistance should occur immediately in patients with respiratory compromise. Poor compliance on
ventilation with decreased breath sounds may indicate a tension pneumothorax, which requires urgent placement of a tube thoracostomy.
External bleeding should be controlled with direct pressure while resuscitation with crystalloid solution and blood products is initiated. Hemodynamic
instability may indicate a tension pneumothorax requiring decompression, hypovolaemia requiring hemorrhage control and resuscitation, or cardiac
dysfunction secondary to pericardial tamponade, cardiac contusion or myocardial infarction, or coronary air embolism.
Evaluation for sources of bleeding should commence and an assessment for pericardial fluid with ultrasound or pericardial window be completed,
especially in the setting of penetrating trauma. Based on these initial interventions, decisions regarding subsequent management such as immediate
operation can be determined. Cardiac arrest, especially in the setting of penetrating mechanisms, requires resuscitative thoracotomy
EVALUATION
Most thoracic injuries can be identified with a physical examination and plain chest radiography.
Overall respiratory effort and chest wall movement can be visualized to reflect injuries to the ribs and sternum. Deviation of the trachea at the
sternal notch may reveal “intrathoracic tension” on the side opposite the trachea. Distended neck veins indicate cardiac failure, which requires
further evaluation.
1. Chest radiography is performed on all significantly injured patients at risk for thoracic injuries. This
study can be obtained rapidly in the trauma bay, with the results quickly revealed.
2. An ultrasound of the pericardium is a component of the FAST examination, which may reveal pericardial blood.
3. In recent years, spiral thoracic CT angiography has emerged as a valuable tool in the evaluation of blunt thoracic trauma.
a. CT provides visualization of the chest wall and hemithoraces, allowing determination of rib fractures, pneumothoraces and
haemothoraces, and pulmonary contusion.
b. Of great value has been the ability to evaluate the thoracic aorta for injury that historically required standard angiography when
suggested by a chest radiograph.
c. Chest CT angiography is able to identify transection of the aortic wall, as well as lower grade injuries that involve only the aortic
intima.
d. Many thoracic surgeons have even evolved their technique and proceed with operative intervention based on the chest CT alone,
without formal angiography.
e. Some injuries continue to require standard thoracic angiography to characterize anatomy better that is indeterminate on CT imaging.
MANAGEMENT
Up to 85% of all thoracic injuries can be managed with nothing more than a tube thoracostomy. In most cases, the
placement of a chest tube is urgent but may still be performed in a controlled manner that includes strict sterile preparation and excellent surgical
technique
***The skin incision should be at the level of the nipple to stay superior enough to avoid the highest reach of the diaphragm
MUST KNOW: Tube thoracostomies that drain large amounts of blood on initial placement or demonstrate ongoing output may indicate active
intrathoracic bleeding that requires thoracotomy:
• Typically, immediate thoracotomy is indicated for more than 1500 mL of blood drained on chest tube
insertion or more than 100-300 mL/hr for 3 hours.
Although these values clearly may be associated with intrathoracic bleeding, the decision to operate should be carefully considered, especially with
regard to the immediate output. Occasionally, chest tubes that initially drain 1500 mL but then have little ongoing output in the setting of
hemodynamic stability indicate bleeding from a lung laceration, which ceases with lung reexpansion and may not require or benefit from
thoracotomy. Other indications for immediate thoracotomy include a massive air leak with associated pneumothorax or drainage of esophageal or
gastric contents from the chest tube.
1. CHEST WALL AND PLEURAL SPACE INJURIES
RIB FRACTURES & FLAIL CHEST

Fractures of the ribs are the most common thoracic injury following BLUNT trauma, with almost 80% of patients with chest injuries sustaining
one or more fractures.
In its most severe form, large amounts of energy transferred to the chest wall can result in the creation of a FLAIL
SEGMENT, defined as two or
more adjacent ribs that are each fractured in two or more locations. This results in a separation of a segment of the chest wall.
• NOTE: Although pulmonary mechanics can be disrupted in the setting of a flail segment, the greatest physiologic insult is caused
by the underlying pulmonary contusion that almost invariably occurs
During the primary or secondary survey, chest wall injuries are commonly recognized. Chest wall tenderness and changes in chest wall
motion are suggestive. Some patients require immediate intervention for chest injuries, but most will subsequently undergo further evaluation.
Pneumothorax or a large haemothorax on a chest radiograph requires placement of a tube thoracostomy. Chest tube drainage should continue until any
pulmonary air leak has resolved and drainage is not excessive. Haemothoraces should be drained if it is thought that the quantity of blood in the
pleural space could result in lung entrapment as the haematoma matures.
• NOTE: Occasionally, haemothoraces that do not resolve after insertion of a tube thoracostomy benefit from thoracoscopic
drainage and tube placement.
• Patients who demonstrate an occult pneumothorax by chest CT and have no respiratory compromise can be managed with observation and a
repeat chest radiograph. Enlargement of the pneumothorax on follow-up imaging necessitates a chest tube
Rib fractures can vary greatly in severity, depending on the number present and patient characteristics.
Associated pain can be severe and a great concern is the development of respiratory infections!!!
2. Aggressive analgesia should be provided to allow adequate pulmonary toilet and promote comfort.
• MUST NOTE WELL: Adequate analgesia can be achieved with IV narcotics in mild cases BUT, in more
severe cases, patients benefit greatly from the provision of EPIDURAL ANALGESIA!!!
o Epidural analgesia after chest wall injuries has been associated with fewer ventilator days, shorter
ICU stay, and fewer hospital days.
o Fewer pulmonary infections and decreased duration of mechanical ventilation with the use of
epidural analgesia in patients with three or more rib fractures.
• NSAIDs are also beneficial in conjunction with narcotics.
3. Aggressive pulmonary toilet, including deep breathing, frequent coughing, and incentive spirometry, should
be highly encouraged. Chest physiotherapy and positive expiratory pressure exercises may also be beneficial.
Severe chest wall injuries with pulmonary failure may require mechanical ventilation.
4. There has been renewed interest in the operative fixation of rib fractures, although the optimal indications to
perform these procedures and their associated benefit remain incompletely defined. Sternal fractures are managed
similar to rib fractures requiring analgesia and pulmonary toilet.
2. PULMONARY INJURIES
The lungs are susceptible to injury during blunt and penetrating mechanisms. Among patients with blunt chest trauma, pulmonary contusion is
common, being identified in 40% of cases.
PULMONARY CONTUSION
Pulmonary contusion results from energy transfer through the chest wall to the pulmonary parenchyma, resulting in tissue damage, as well as
haemorrhage into the alveolar and interstitial spaces. The result is the development of physiologic shunt with hypoxemia. These injuries are also
associated with a profound inflammatory response that can lead to further respiratory dysfunction and systemic inflammation. Frequently, pulmonary
contusion is identified in the presence of a flail segment and is the major cause of associated morbidity and mortality.
Pulmonary injuries might first be identified on examination or through the drainage of large amounts of blood or air from a tube thoracostomy.
• Chest radiographs obtained shortly after patient arrival may not directly show lung contusion. BUT may demonstrate pneumothorax or
haemothorax indicative of an underlying pulmonary injury.
o Lung contusions may be present on the initial chest radiograph but typically require time to become evident on plain film
• A pulmonary contusion is easily identified by thoracic CT
In most cases, tube thoracostomy alone with lung expansion adequately manages low-pressure lung bleeding and small air leaks. Ongoing blood loss
indicates a more central, high-pressure source, which should prompt thoracotomy. Bleeding vessels within the parenchyma of the lung should be
identified and controlled with suture ligatures
Chest tube drainage of large quantities of blood or air may require thoracotomy. The classic guidelines have been described earlier, and the surgeon
must make a determination regarding the likelihood of ongoing bleeding that would benefit from operative management.
Occasionally, pulmonary resection is required in anatomic or nonanatomic patterns to manage larger segments of injured lung tissue
The management of pulmonary contusion is largely supportive. Patients should be monitored for indications of respiratory decompensation such as
hypoxemia, increased work of breathing, and agitation, which mandate intubation and mechanical ventilation. Pulmonary function is supported until the
physiologic insult related to the contusion resolves. Efforts to prevent ventilator-associated pneumonia are valuable because of a significantly increased
risk. Intubation should be guided by the patient’s observed respiratory function and should NOT be performed prophylactically simply on
recognition of pulmonary contusion. Similarly, the presence of a pulmonary contusion or flail chest does NOT require mandatory chest tube
placement in the absence of a pneumothorax or haemothorax. Patients with pulmonary contusion should not be managed with fluid restriction,
which is a common misconception.
5. CARDIAC INJURIES
RE: PENETRATING INJURY TO THE HEART:
In those that do survive to emergency department arrival, the mortality rate is 62%.
Penetrating cardiac injuries will frequently be evident on initial examination. A

significant number of patients will present in extremis
with pericardial tamponade or bleeding into one of the hemithoraces.
Diagnosis may then be made during resuscitative thoracotomy in agonal patients.
In others, indicators of pericardial tamponade may be present, including hypotension with distended neck veins and muffled heart sounds (Beck’s
triad), although their presence can be highly variable.
• Ultrasound is a valuable tool for quickly assessing the pericardium for fluid and should be performed in all patients with
haemodynamic instability.
• A subxiphoid pericardial window remains the most valuable means of evaluating for cardiac injury and should be used in
cases for which ultrasound is not available or the results are inconclusive.
o A pericardial window allows direct visualization of the pericardial space and can be quickly extended to perform a median
sternotomy in the setting of an identified injury.
***Cardiac injuries resulting in cardiovascular collapse are approached with a left anterolateral thoracotomy in the emergency department.
BUT injuries that are identified and allow transport to the operating room are best exposed through a median sternotomy***
Blunt cardiac injury resulting in cardiac contusion or more severe structural abnormalities such as septal defects or valvular failure result less frequently,
identified in only 3.8% of cases of blunt chest trauma. Most of these represent a contusion of the myocardium that results in arrhythmias and that are
frequently self-limiting. In rare cases, blunt cardiac injury results in heart failure, with cardiogenic shock.
4. THORACIC AORTIC INJURIES

Injuries to the thoracic aorta are also highly severe but fortunately not common. Only 0.3% of patients sustaining blunt trauma in the NTDB
sustained an aortic injury, although the associated mortality rate exceeded 47%.
As with cardiac injuries, this likely underestimates the true incidence because aortic transection is a common cause of immediate death in blunt trauma
patients who never present to the emergency department. In 3.8% of cases, the aorta is involved in penetrating thoracic trauma; almost all these injuries
are fatal (mortality = 86.1%).
The cause of blunt aortic injuries had traditionally been believed to be a result of rapid deceleration, which tears
the aortic wall in the vicinity of the ligamentum arteriosum, where it is fixed to the thorax.
The result of these mechanisms can range from a tear in the aortic intima to full-thickness transection of the wall.
Only patients who experience containment of the rupture by the surrounding mediastinal tissue present to the hospital.
Penetrating aortic injury may be discovered at the time of thoracotomy or sternotomy, often in the setting of patient extremis.
***Blunt aortic injury may be suggested by a chest radiograph that demonstrates findings such as a widened mediastinum, apical capping, loss of
the aortic knob, or deviation of the left mainstem bronchus.
• NOTE WELL: Because of a high rate of missed injuries by plain radiograph, most patients involved in high-energy injury mechanisms undergo
helical CT angiography of the chest to evaluate for aortic injury.
o Usually, this study alone is sufficient to plan operative repair, although standard angiography is necessary in some cases, usually at
the discretion of the thoracic surgeon
Patients who present with a blunt thoracic aortic rupture that is contained will require operative repair. The natural history of these injuries is
slow expansion, which ultimately culminates with free aortic rupture.
In the interim, medical therapy with beta antagonists aimed at controlling aortic wall stress is absolutely essential and should be instituted early. Open
surgical therapy to repair the aorta is accomplished through a left thoracotomy.
• Small penetrating injuries to the aorta can be closed primarily if exposed prior to exsanguination. Larger
penetrating injuries and blunt transection require replacement of a segment of the aorta with a prosthetic
graft
• More recently, there has been a great deal of interest in the use of endovascular stent grafts to repair the injured thoracic aorta.
o This is particularly appealing for those patients at high operative risk and with favorable vascular anatomy, but further study is
required to establish the role of this modality confidently. In many centers, this approach is becoming a mainstay of treatment for
managing these injuries.
o Described advantages associated with the endovascular repair of aortic injury include a reduction in the incidence of paraplegia and
a potential improvement in mortality.
Although rare, patients with an intimal tear only may be candidates for nonoperative management because many of these injuries will heal without
intervention. Patients should be treated with beta blocker therapy and undergo follow-up imaging to ensure the absence of expansion and ultimately the
resolution of the injury.
5. OESOPHAGEAL INJURY
Injuries to the thoracic esophagus occur predominantly after penetrating trauma but remain uncommon by any cause. Only 2% of all patients in the
NTDB with penetrating chest trauma sustained an injury to the esophagus. Most of these are caused by gunshot wounds, followed by stab wounds in
fewer than 20% of cases. The mortality associated with these injuries is significant (39%) because of the severe nature of esophageal perforation and
because the adjacent vital structures can also be injured along with the esophagus. Blunt esophageal injury is exceedingly rare
Penetrating esophageal injuries may be suggested by the trajectory of a missile or weapon. Injuries in the vicinity of the mediastinum require
consideration of possible esophageal injury.
• The esophagus is best evaluated through a combination of contrast esophagography and esophagoscopy.
o The combination of these two modalities results in a sensitivity of almost 100% for esophageal injury.
o Findings include extravasation of contrast from the esophageal lumen or a disruption of the mucosa visualized on endoscopy.
These studies should also be used to determine the location of the injury along the esophagus to assist in operative planning
• Chest CT may reveal air adjacent to the esophagus but outside the lumen, as well as surrounding soft tissue inflammation. At times,
the defect itself can be visualized on CT.
Esophageal injuries at the gastroesophageal junction may result in abdominal pain and tenderness.
The rapid identification and management of esophageal injuries are paramount because delays are associated with worse outcomes.
• Clinical evaluation and studies that reveal an esophageal injury should prompt immediate operative repair. The upper and
midthoracic esophagus are best approached through a right posterolateral thoracotomy through the fourth or fifth interspace, whereas the lower
esophagus is exposed from the left through the sixth or seventh interspace. Contrast studies that demonstrate the injury within the abdomen benefit
from a laparotomy to repair the esophagus from an abdominal approach.
• Chest and mediastinal drains should be placed in the vicinity of the repair to control any leak that may develop.
• A gastrostomy and feeding jejunostomy are frequently advisable to allow gastric decompression and early nutritional
support. Esophageal injuries that are identified late may not allow primary repair because of the massive amounts of inflammation that can
develop.
• In some situations, oesophagectomy is the only option to allow recovery from the associated inflammatory insult, followed by planned
elective reconstruction, when feasible.
--
Tension Pneumothorax
Sucking chest wound/open pneumothorax
Haemo/Haemopneumothorax
Flail Chest
Cardiac tamponade
Mediastinal Large Vessel Injury (Traumatic aortic tear)
Oesophageal Injury
General Surgery
Breast Cancer
Sources: Harold Ellis, Toronto Notes, Dr. P. Roberts sessions, etc. SEE MY SEPARATE NOTES FOR BREAST RECONSTRUCTION
February 2015
DDX FOR BREAST MASS
Benign: § Abscess
§ Fibrocystic changes § Silicone implant
§ Fibroepithelial lesions (fibroadenoma most common; benign
phyllodes also) Malignant:
§ Fat necrosis Primary
§ Papilloma/papillomatosis § Breast ca (likely invasive, DCIS rarely forms a breast mass)
§ Galactocele § Malignant phyllodes
§ Duct ectasia § Angiosarcoma (rare)
§ Ductal/lobular hyperplasia
§ Sclerosing adenosis Secondary
§ Lipoma § Direct invasion from tumours of the chest wall
§ Neurofibroma § Metastatic deposits e.g. from melanoma
§ Granulomatous mastitis (e.g. TB, granulomatosis with polyangiitis,
sarcoidosis)
CARCINOMA
EPIDEMIOLOGY
nd
§ 2 leading cause of cancer mortality in women (1st is lung cancer)
§ 1/9 of women (in Canada) will be diagnosed with breast cancer in their lifetime
§ 1/27 of women (in Canada) will die from breast cancer
RISK FACTORS
A. Demographic factors
1. Gender (99% female)
2. Age (80% > 40 yr old. 97% > 30)
B. Genetic factors
st
1. Family history: 1 degree relative with breast cancer (greater risk if relative was premenopausal)
§ Premenopausal relative: Risk = 25%
§ Postmenopausal = ~15%
§ Both mother and sister = 33%
2. Gene carriage (BRCA1 and 2 – Both autosomal dominant)

§ Lifetime risk of cancer = 80-90%
§ BRCA1 = 17q21, BRCA2 = 13q41
§ BRCA1 also increases ovarian cancer risk!
C. Hormonal factors
1. Early menarche < 12
2. Late menopause > 55
3. Nulliparity or first full-term pregnancy > 30 (Decreased risk with breastfeeding, early menopause, early childbirth)
4. HRT use > 5 years
5. Obesity – Peripheral conversion of androgen to oestrogen in adipose tissue
NOTE WELL: OCP use IS NO LONGER RECOGNIZED TO INCREASE THE RISK OF BREAST CANCER!!
D. Benign breast disease

1. Atypical lobular or ductal hyperplasia (4-5x increase)
2. Important risk factors are prior history of breast cancer and/or prior breast biopsy (regardless of pathology)
i. Surgical Recall (3% have a synchronous contralateral cancer à double-check this)
E. Radiation exposure (e.g. mantle radiation for Hodgkin’s disease)
PATHOLOGY
All breast cancers arise in the terminal duct lobular unit. Carcinomas that have not breached the basement membrane are carcinoma in situ
MOST COMMON SITE IS UPPER OUTER QUADRANT (~50%)
1. CARCINOMA
A. NON-INVASIVE (cannot penetrate basement membrane):
1. Ductal carcinoma in situ (DCIS):

§ Proliferation of malignant ductal epithelial cells completely contained within breast ducts. DO NOT PENETRATE BASEMENT MEMBRANE
§ Often multifocal!!!!
§ 80% non-palpable, detected by screening mammogram
o
§ NOTE WELL: < 2% risk of lymph node mets!!! (usually 2 to microinvasion)
§ Precursor to malignancy!! - ***Risk of invasive ductal carcinoma in same breast up to 35% in 10 years
§ Treatment Summary:
a. Must remove because of the risk of invasive cancer
b. BCS (lumpectomy with wide excision margins) + radiation (5-10% risk invasive cancer)
c. Mastectomy if large area of disease, high grade or multifocal (risk of invasive cancer reduced to 1%)
d. Possibly tamoxifen as an adjuvant treatment
e. 99% 5-yr survival
2. Lobular carcinoma in situ (LCIS):

§ Neoplastic cells completely contained within breast lobule
§ NO palpable mass, NO mammographic findings!!!!, usually incidental finding on breast biopsy!!! for another indication
§ NOT a precursor lesion, BUT considered a risk factor for invasive breast cancer development IN BOTH BREASTS (~20% in 10 yr)
§ NOTE: Type of invasive cancer that develops: Most commonly, infiltrating ductal carcinoma, with equal distribution in both breasts
§ 3 Treatment Options (MUST KNOW!!!!!)

1. Frequent clinical follow-up
2. Chemoprophylaxis (Tamoxifen) – **Evidence: Breast Cancer Prevention Trial of 13,000 women who were at increased
risk for breast cancer (not just LCIS patients) determined tamoxifen use FOR 5 YEARS reduced risk by ~50% across all ages
3. Surgery (Bilateral mastectomy) (uncommon)
B. INVASIVE:
1. Invasive ductal carcinoma (Most common breast cancer = 80-85%):
§ Originates from ductal epithelium and infiltrates supporting stroma
§ Characteristics: hard, scirrhous, infiltrating tentacles, gritty on cross-section
2. Invasive lobular carcinoma (10-15%):

§ Originates from lobular epithelium
§ 20% bilateral (i.e. more often than infiltrating ductal carcinoma)
§ Does NOT form microcalcifications!!! harder to detect mammographically (may benefit from MRI)
3. Paget’s disease (1-3%):

§ DUCTAL carcinoma (DCIS in 50%) that invades nipple with scaling, eczematoid lesion
§ Presents as unilateral, red, bleeding, eczematous lesion of the nipple and areolar epithelium
§ Histologically, multiple clear malignant Paget cells with small, dark-staining nuclei
§ Treatment is determined by the underlying breast carcinoma. Surgery is usually mastectomy +/- ALND
4. Inflammatory carcinoma (2%):

§ DUCTAL carcinoma that invades dermal lymphatics
§ Most aggressive form of breast cancer!! (5 yr = 50%, 10 yr = 30%). Most ER negative
§ Clinical features: Breast: (All features of inflammation: rubor, etc) erythema, skin edema, warm, swollen and tender breast ± lump
§ Peau d’orange indicates advanced disease (IIIb-IV)
5. Other types: *papillary, *medullary, *mucinous, tubular cancers
6. Male breast cancer (<1%):

§ Most commonly invasive ductal carcinoma (Nearly 100%!! – men do not usually have breast lobules)
§ Often diagnosed at later stages
§ Stage-for-stage similar prognosis to breast cancer in females
§ Consider genetic testing
ALSO:
2. **SARCOMAS: RARE
1. Most commonly Phyllodes tumour (cystosarcoma phyllodes), a variant of fibroadenoma with potential for malignancy
2. Can also be angiosarcomas – after previous radiation
3. **LYMPHOMA: RARE
§ Generally better prognosis
MUST KNOW: 5 PATHOLOGICAL TYPES OF DCIS: (SEE DR. P. ROBERTS NOTES)

1. Solid
2. Comedo (MOST COMMON. MOST AGGRESSIVE. ONLY ONE WITH MICROCALCIFICATIONS SO ONLY ONE THAT CAN BE SEEN ON
MAMMOGRAM)
3. Cribriform (sieve-like)
4. Papillary
5. Micropapillary
PATHOLOGICAL TYPES OF INVASIVE DUCTAL – (DOUBLECHECK WITH THE PATHOLOGY HANDOUT)

1. Scirrhous (80%)
2. Medullary
3. Mucinous
4. Papillary
5. Tubular
SPREAD
1. Direct extension
a. Superficially à Skin and SC tissues à retraction and dimpling (skin retraction is due to tumour involvement of Cooper’s ligaments
and subsequent traction on ligaments pull skin inward)
b. Deep à pec major, serratus anterior, eventually chest wall
2. Lymphatic
a. Blockage of dermal lymphatics results in cutaneous oedema that is pitted at the orifices of sweat ducts giving the appearance of an
orange peel (Peau d’orange)
b. Main lymph channels pass to ipsilateral axillary and internal thoracic lymph nodes. Later, supraclavicular, mediastinal,
abdominal, groin, contralateral axilla
3. Haematogenous
a. Bone > [lungs > pleura] > liver > brain (also ovaries, suprarenals)
CLINICAL FEATURES
LOCAL FEATURES: 5 common features of breast disease that require urgent attention
1. Majority of patients with INVASIVE carcinoma present with a lump in the breast. (most insitu = nonpalpable!) Other features:
2. Altered breast contour
3. Recent nipple inversion (nipple retraction)
4. Blood-stained nipple discharge
5. Unilateral eczema (Paget’s disease)
LOCALLY ADVANCED BREAST CANCER (Must use this term)

§ Regarded as a tumour that is not surgically resectable
§ Includes ANY evidence of local spread
§ Clinical features include:
1. Fixation to skin
2. Skin ulceration/erythema over the tumour
3. Dermal infiltration, including Peau d'orange
4. Fixation to chest wall, serratus anterior or intercostal muscles
5. Satellite nodules
SPREAD/METASTASIS: Features of spread:

§ Bone pain, cough, hepatomegaly, jaundice
NOTE: Breast cancer rarely causes constitutional symptoms!!!!!
Examination
§ Examine BOTH breasts
§ Examine BOTH axillae AND supraclavicular fossae!!!
§ Examine LIVER and LUNG for mets!!!! (DON’T FORGET TO SAY YOU WOULD LIKE TO EXAMINE THIS!!!!)
§ Palpate vertebral column for tenderness
RISK ASSESSMENT MODELS

1. Gail Model
2. Claus model
**Problem with Gail model is that it does not take into consideration the non-estrogen risk factors. Claus model addresses these**
INVESTIGATIONS
KEY PRINCIPLE: ALWAYS PERFORM TRIPLE ASSESSMENT TO DIAGNOSE BREAST LUMPS. INCLUDES:
1. Complete clinical examination of BOTH breasts and axillae
2. Radiological Imaging (MUST SAY BILATERAL!!!) – PURPOSE: To detect and assess the lesion size, multifocality
a. “DIAGNOSTIC” Mammography, usually if > 35 (must say the diagnostic!)
b. Ultrasound if < 35
c. MRI: Useful for.. and to detect recurrence
3. Biopsy – PURPOSE: To confirm/exclude cancer AND determine both histological and molecular classification
a. CORE biopsy (Don’t say FNAC – Cannot tell invasion or hormone receptor status!!!)
b. Rarely excisional biopsy
I. DIAGNOSTIC INVESTIGATIONS
A. RADIOLOGICAL
1. BILATERAL “DIAGNOSTIC” mammography (MUST SEE END OF DOC FOR BIRADS, AND ROBERTS NOTES FOR DETAILS)
§ Sensitivity for breast cancer = only 88%!!!
§ Have both “screening” mammography and “diagnostic” mammography
§ MUST KNOW (Dr. P. Roberts): Findings indicative of malignancy: 1. Linear microcalcifications, 2. Branched microcalcifications, 3.
Spiculated lesions (95% due to invasive ca), 4. Outline of a mass/circumscribed mass, 5. Distorted architecture
§ NOTE WELL: Normal mammogram does NOT rule out suspicion of cancer based on clinical findings
Other radiographic studies:

2. U/S: differentiate between cystic and solid, can guide core biopsies
3. MRI: high sensitivity, low specificity
4. Galactogram/ductogram (for nipple discharge): Identifies lesions in ducts
B. BIOPSY
1. U/S or mammography guided core needle biopsy (most common). Other types:
o Hookwire localization biopsy: GO TO DR. ROBERTS NOTES FOR DETAILS. REMEMBER: Removed breast tissue must be
checked by mammogram to ensure all of the suspicious lesion has been excised
o Stereotactic (mammotome) core biopsy: A stereotactic core needle biopsy uses x-ray equipment and a computer to analyze
pictures of the breast. The computer then pinpoints exactly where in the abnormal area the needle tip needs to go. This is often done to
biopsy suspicious microcalcifications (tiny calcium deposits) when a tumor cannot be felt or seen on ultrasound.
o Vacuum-assisted core biopsy: Done with systems like the Mammotome® or ATEC® (Automated Tissue Excision and Collection).
For these procedures, the skin is numbed and a small cut (less than ¼ inch) is made. A hollow probe is put in through the cut and
guided into the abnormal area of breast tissue using x-rays, ultrasound, or MRI. A cylinder of tissue is then pulled into the probe through
a hole in its side, and a rotating knife inside the probe cuts the tissue sample from the rest of the breast.
2. Excisional biopsy: only performed as second choice to core needle biopsy; should not be done for diagnosis if possible
C. TUMOUR MARKERS
1. CA 15-3
2. CA 27-29
3. CEA
4. Urokinase plasminogen activator (uPA)
II. METASTATIC WORKUP FOR STAGING
***FIRST POINT TO MAKE: MOST SURGEONS CONSIDER THE MINIMUM REQUIREMENT FOR ADEQUATE METASTATIC WORKUP IN BREAST
CANCER TO BE A CT CHEST/ABDOMEN/PELVIS AND A BONE SCAN!!!!!!
§ Lung: CT CHEST/ABDOMEN/PELVIS – MUST PERFORM

§ Liver: Abdominal U/S or CT (chest/abdomen/pelvis), (LFTs)
§ Bone: Bone scan, (serum calcium, ALP)
§ Brain: head CT (only if specific neurological symptoms)
§ Adrenals: CT pelvis
(Routine at UHWI: CT chest/abdomen/pelvis AND bone scan)
III. ALSO: PATHOLOGICAL INVESTIGATIONS FROM BIOPSY SPECIMEN
1. Receptor status
§
IMPORTANT FOR 2 REASONS: 1. To guide adjuvant therapy, 2. PROGNOSTICATION via molecular classification!!! (see below)
a. Oestrogen receptor (ER) + progesterone receptor (PR) testing
b. HER-2-Neu receptor testing – The HER2 gene is over amplified in 20% of breast cancers
2. Grade: modified Bloom and Richardson score (I to III) – histologic, nuclear and mitotic grade
3. Lymphovascular invasion (LVI)
ALSO GENETIC SCREENING

Consider testing for BRCA1/2 if:
§ Patient diagnosed with breast AND ovarian cancer
§ Strong family history of breast/ovarian cancer
§ Family history of male breast cancer
§ Young patient (<35 yr old)
§ Bilateral breast cancer in patients <50 yr old
STAGING
1. Manchester system
2. AJCC TNM
MOLECULAR CLASSIFICATION OF BREAST CANCER

Molecular subtypes of breast cancer:
1. Luminal A ER/PR strongly positive, HER-2 negative - Most common.. Best prognosis
2. Luminal B ER/PR weakly positive, HER-2 positive
3. HER-2 enriched ER neg/PR neg, HER-2 pos - Poor prognosis – May be treated with Herceptin
4. Basal-like (aka triple-negative) ER/PR negative, HER-2 negative – Aggressive - Poor prognosis - More common in black women
TREATMENT
PRINCIPLES: BASED ON STAGE, involves a multidisciplinary approach
AND MAY BE: CURATIVE or PALLIATIVE (IF METS)
OPTIONS. A COMBINATION OF:

1. ± Neoadjuvant chemotherapy (a.k.a. Primary systemic therapy)
2. Surgery
a. Tumour itself
b. Surgery to the axilla
c. Breast reconstruction
3. Adjuvant systemic therapy
a. Hormonal therapy
b. Monoclonal antibody
c. Chemotherapy
4. Adjuvant radiotherapy
GENERAL PRINCIPLES BASED ON BOTH MANCHESTER SYSTEM AND TNM

§ FOR STAGE I AND II – Surgery + adjuvant therapy
o Surgery may be BCS or mastectomy (i.e. only stage I and II are candidates for BCS but they can also get MRM)
§ FOR STAGE III – Neoadjuvant therapy + surgery + adjuvant therapy
o Only surgical option is mastectomy (NB!!: Neoadjuvant therapy is to downstage and may actually allow BCS)
§ STAGE IV – Palliative. (Systemic therapy only or with surgery for local control)
KNOW THIS TABLE WELL!!!!
STAGE PRIMARY TREATMENT OPTIONS ADJUVANT SYSTEMIC THERAPY
0 (in situ) 1. BCS (with 1 cm margins) + radiotherapy None

2. BCS alone if margins >1 cm and low nuclear grade
3. Mastectomy* ± SLNB
[**Point is that no axillary surgery is necessary]

I 1. BCS + axillary node dissection + radiotherapy May not be needed; discuss risks/benefits of chemotherapy
2. Mastectomy* + axillary node dissection/SLNB and tamoxifen
II SAME AS ABOVE Chemotherapy for premenopausal women or postmenopausal

and estrogen receptor (ER) negative, follow by tamoxifen if ER
positive
III § Neoadjuvant chemotherapy + mastectomy + axillary node Neoadjuvant therapy may be considered i.e. Preoperative
dissection + radiotherapy chemotherapy and/or hormone therapy. Adjuvant radiation and
chemotherapy may also be appropriate (i.e. post-op)
IV § Surgery as appropriate for “local control” ***Primary treatment is systemic therapy i.e. chemotherapy
and/or hormone therapy
Inflammatory Likely mastectomy + axillary node dissection + radiotherapy MUST GIVE NEOADJUVANT THERAPY
MAJOR POINT: WHENEVER BREAST CONSERVING SURGERY IS CHOSEN, MUST FOLLOW WITH ADJUVANT
RADIOTHERAPY IN ALL CASES!!
*If no reason to select mastectomy, the choice between BCS + radiotherapy and mastectomy can be made according to patient’s preference since
choice of local treatment does not significantly affect survival if local control is achieved
IMPORTANT DETAILS ON EACH OPTION
A. PRIMARY SURGICAL TREATMENT (NB: Breast and Axilla are always considered separately)
I. ADDRESSING THE BREAST

1. Breast-conserving surgery (BCS): lumpectomy with wide local excision
§ For treatment of stage I and II disease only
§ MUST BE COMBINED WITH RADIATION to achieve both local control and survival equivalent to mastectomy
§ NB: If the pathologic margins are positive following BCS à Patient sent back for “completion mastectomy”
§ NOTE WELL: MUST KNOW contraindications to BCS:

1. Large tumour to breast ratio (I.e. small breast, so even if tumour is small, wouldn’t make sense)
2. Central lesion (near the nipple i.e. ~2 cm)
3. Multifocal primary tumours
4. High risk of local recurrence: Extensive malignant-type calcifications on mammogram
5. AND Contraindications to radiation therapy!!! (Pregnancy!!!!, previous radiation to chest!, collagen vascular disease!)
2. Mastectomy
§ Simple/Total mastectomy: removes all breast tissue with nipple and skin (No nodes)
§ Modified radical mastectomy (MRM): removes all breast tissue, skin, and axillary nodes up to level 2
a. DRAINS ARE PLACED!!! TO DRAIN LYMPH FLUID (PLACED IN THE AXILLA AND CHEST WALL!!!)
§ Radical mastectomy (rarely done anymore): Removes all breast tissue, skin, pectoralis major and minor muscle, axillary nodes up to
level 3
§ Look up other types:
§ Skin-sparing mastectomy: Facilitates immediate, 1-stage breast reconstruction using implants
§ Subcutaneous (“Nipple-sparing”) mastectomy: all of the breast tissue is removed, but the nipple is left alone. Subcutaneous
mastectomy is performed less often than simple or total mastectomy because more breast tissue is left behind afterwards that could later
develop cancer.
3. Breast reconstruction (SEE SEPARATE NOTES)
MUST KNOW RE: “LOCALLY ADVANCED BREAST CANCER”: Usually defined as tumours > 5 cm with or without axillary lymph nodes OR
skin/deep tissue involvement
§ Treat the majority of these patients with neoadjuvant chemo
RE: Metastasis
§ Bone > lungs > pleura > liver > brain
§ Treatment is palliative: hormone therapy, chemotherapy, radiation
II. ADDRESSING THE AXILLA
1. Sentinel lymph node biopsy (SLNB)

1. Technetium-99 ± blue dye (methylene blue alone used in Jamaica) injected intradermal and periareolar prior to surgery to identify
sentinel node(s) [The first axillary node OR NODES draining the breast]
2. Excise the node
3. Intraoperative frozen section
4. Proceed with ALND if positive
§ **5% false negative rate
§ **NOTE VERY WELL: Only indicated for patients with clinically normal axilla and primary tumour < 5 cm. Not done
for advanced disease as it has a higher false-negative rate
§ Significance of micrometastatic deposits identified in sentinel nodes is unclear
2. Axillary sampling
a. Take 4 nodes for biopsy and histology (without SLNB)
3. Axillary lymph node dissection (ALND)

§ Performed if SLNB is positive OR nodes are clinically suspicious OR palliative
§ Surgical “clearance” of the axilla requires removing all nodes up to level II (lateral and deep to pectoralis minor)
§ Must remove at least 12 nodes
§ REMEMBER TO PLACE DRAINS! (Closed active usually. E.g. Hemovac or J-Vac)
§ WHEN TO REMOVE DRAINS: When there is < 30 cc of drainage per day, or on POD #14 (whichever comes first)
Lymph node levels in axilla:

1. Inferolateral to pectoralis minor
2. Deep/posterior to pectoralis minor
3. Superomedial to pectoralis minor
***Note that the SURGICAL landmark is the axillary vein – look up details
***In reality, these nodes are in continuity with each other but the concept of axillary node levels is useful when discussing the extent of axillary node
surgery.
Complications of ALND:
1. Arm lymphedema (10-15%) à Rare increased risk of lymphangiosarcoma!!
2. Decreased arm sensation (paraesthesias)
3. Shoulder pain
4. Axillary vein injury

5. Nerve injury (*Intercostobrachial nerve)
Look up more
NOTE VERY WELL: Level 3 not usually taken in axillary dissection. Not done because level 3 spread is considered distant
spread/metastasis. Would serve no therapeutic purpose and is not indicated ***
*** KNOW THIS: Best method for confirming presence of lymphoedema post level 3 dissection is displacement of water. Put both hands in water and if
the affected hand displaces more water. This is actually gold standard - Archimedes principle
B. ADJUVANT SYSTEMIC THERAPY

Involves the use of cytotoxic and/or endocrine agents
Adjuvant/Neoadjuvant (Neoadjuvant is also referred to as “primary systemic therapy”)

1. Hormonal/Endocrine therapy
§ Indications:
§ ER positive plus node-positive or high-risk node-negative (ER positive tumours more common in postmenopausal?)
§ Palliation for metastases
§ SERMs: Tamoxifen (usu if ER positive, both pre- and postmenopausal!!) (20 mg per day is as effective as higher doses)
a. NB: Tamoxifen is also effective in ~10% of ER negative breast cancers but greater benefit seen in oestrogen receptor rich
tumours
b. Value of treatment beyond 5 years is unknown
c. ***Side effects (think menopause): Endometrial cancer (2.5 x relative risk), DVT, PE, cataracts, hot flashes, mood swings
d. Others: Raloxifene, toremifene
§ Aromatase inhibitors: (e.g. Anastrozole). Used in ER positive ONLY IN POST-MENOPAUSAL PATIENTS!!

a. Reduces the peripheral conversion of androgens to oestrogens
b. HAS NO EFFECT ON PREMENOPAUSAL WOMEN
§ Ovarian ablation [only for premenopausal] (via. Radiotherapy, pharmacotherapy or surgery): (e.g. GnRH agonist, oophorectomy),
§ Progestins (e.g. megestrol acetate), androgens (e.g. fluoxymesterone) are other options
2. Chemotherapy
§ “Taxane-based” combination chemotherapy is the most modern
§ Example regimen: Docetaxel + Cyclophosphamide + Doxorubicin
§ CMF therapy was previously most commonly used: Cyclophosphamide, Methotrexate, 5-Flurouracil
§ CAF therapy was Cyclophosphamide, Adriamycin, 5-Flurouracil
§ Indications:
1. ER negative plus node-positive OR high-risk node-negative
2. ER positive
3. Stage I disease at high risk of recurrence (high grade, lymphovascular invasion)
4. Palliation for metastatic disease
§ RE: MUST KNOW!!! 2 MAIN ADVANTAGES OF NEOADJUVANT CHEMOTHERAPY

1. May downstage a locally advanced cancer (IIIA) to permit resection or even breast conservation surgery
2. IT ALLOWS FOR DETERMINING IF THE TUMOUR WILL RESPOND TO PARTICULAR CHEMOTHERAPEUTIC AGENTS
AFTER SURGERY. *(As the clinical response can be observed by a shrinking tumour that is still in situ!!)
§ RE: Clinical response in neoadjuvant chemotherapy:

o 70% tumours show a clinical response
o In 20–30% this is response is complete
o Surgery required even in those with complete clinical response
o 80% of these patients still have histological evidence of tumour
3. Monoclonal antibody
§ Trastuzumab (Herceptin) – If HER2 neu positive
o HER receptors are proteins embedded in cell membrane
o Regulate cell growth, adhesion and migration
o The HER2 gene is over amplified in 20% of breast cancers
o HER2 positivity is an independent poor prognostic factor
o Trastuzumab (Herceptin) is a monoclonal antibody that binds selectively to the HER2 receptor
o Has been shown to improve survival in both the adjuvant and metastatic setting
o Only works in HER2 positive cancers
o Major side effects are cardiac: Associated with cardiac dysfunction in 5% cases
C. RADIOTHERAPY
st rd
1. Radiation (started between 1 and 3 month post surgery)
§ Indications:
1. Decrease risk of local recurrence; almost always used after BCS, sometimes after mastectomy (if >4 nodes positive or tumour >5 cm)
2. Inoperable locally advanced cancer
3. Axillary nodal radiation may be added if nodal involvement
RE: Post-Treatment Follow-up

1. Clinical follow-up q3-6mo x 2 yr and annually thereafter!!! (frequency is controversial)
2. Annual mammography; no other imaging unless clinically indicated!!!
3. Psychosocial support and counseling
RE: Local/Regional Recurrence

1. Recurrence in treated breast or ipsilateral axilla
2. 1% per year up to maximum of 15% risk of developing contralateral malignancy
3. 5x increased risk of developing metastases
Surgical Recall: What is the treatment for local recurrence in breast after lumpectomy and radiation?
§ “Salvage” mastectomy
PROGNOSTIC FACTORS
CLASSIFY: CHRONOLOGICAL vs. BIOLOGICAL
Prognostic factors can be:
A. Chronological
§ Indication of how long disease has been present
§ Relate to stage of the disease at presentation
B. Biological
§ Relate to intrinsic behaviour of tumour
§ Basically everything the pathologist looks for on biopsy
A. CHRONOLOGICAL
1. Axillary node spread – single best determinant of prognosis
2. Age – Younger women have poorer prognosis, stage for stage
3. Tumour size – Increased size, increased metastatic potential
4. Metastasis – Distant mets worsen survival
B. BIOLOGICAL
1. Receptor status/Molecular class: Luminal A = best. Basal like & HER-2 enriched = worst
a. ER/PR expression = Less aggressive
b. HER2 neu overexpression (15-20%) = Worse prognosis
2. Tumour grade (Modified Bloom-Richardson) – I best, III worst (Based on mitotic rate, nuclear pleomorphism & tubule formation)
3. Histological type
§ Some histological types associated with improved prognosis:
a. Tubular
b. Cribriform
c. Mucinous
d. Papillary
e. Micro-invasive
4. Vascular invasion – increased risk of recurrence
5. Oncogenes: Tumours that express C-erb-B2 oncogene likely to be: Resistant to CMF chemotherapy, resistant to hormonal therapy.
Respond to anthracyclines, respond to taxols
6. Proteases: Urokinase and cathepsin D found in breast cancer. Presence confers a poorer prognosis
LOOK UP SCREENING RECOMMENDATIONS

General Surgery
Breast Reconstruction
Sources: Toronto Notes, Wikipedia, http://www.cancer.org/acs/groups/cid/documents/webcontent/002992-pdf.pdf
February 2015
EXTERNAL PROSTHESIS vs. BREAST RECONSTRUCTION
1. EXTERNAL PROSTHESIS (FORM)

1. External silicone breast prosthesis: The prosthesis is designed to weigh the same as the natural breast to help prevent
shoulder drop and poor balance.
2. Nonsilicone breast prosthesis: This prosthesis is a lightweight breast form made of foam or fiberfill and can be worn
right after a mastectomy. It can also be worn during exercise, swimming, and in hot weather.
3. Attachable breast: An attachable breast is fastened to the chest wall using adhesive strips.
4. Adhesive nipples
2. BREAST RECONSTRUCTION
Two basic methods:
1. Prosthetic implants
a. (1-stage or 2-stage) (with or without tissue expanders)
b. Types: Saline filled vs. silicone gel-filled vs. form-stable implants
2. Autologous tissue (Flap reconstruction)

a. Types: TRAM flap, latissimus dorsi flap, DIEP flap, GAP, TUG
Breast reconstruction is the rebuilding of a breast post BCS or mastectomy, usually in women. It involves using autologous tissue or
prosthetic material to construct a natural-looking breast. Often this includes the reformation of a natural-looking areola and nipple.
This procedure involves the use of implants or relocated flaps of the patient's own tissue. Breast reconstruction is a large undertaking
that usually takes multiple operations. Sometimes these follow-up surgeries are spread out over weeks or months.
One of the challenges in breast reconstruction is to match the reconstructed breast to the mature breast on the other side (often fairly
'ptotic' - droopy.) This often requires a lift (mastopexy), reduction, or augmentation of the other breast
Integral part of breast cancer treatment
TIMING: May be IMMEDIATE or DELAYED

1. Immediate: Done, or at least started, at the same time as the mastectomy. An advantage to this is that the chest tissues are not
damaged by radiation therapy or scarring. This often means that the final result looks better. Also, immediate reconstruction
means less surgery.
2. Delayed: Means that the rebuilding is started later. This may be a better choice for some women who need radiation to the chest
area after the mastectomy. Radiation therapy given after breast reconstruction surgery can cause problems like delayed healing
and scarring.
The infection rate may be higher with primary reconstruction (done at the same time as mastectomy), but there are psychologic and financial benefits to having a single
primary reconstruction. Patients expected to receive radiation therapy as part of their adjuvant treatment are also commonly considered for delayed autologous reconstruction
due to significantly higher complication rates with tissue expander-implant techniques in those patients. Waiting for six months to a year following may decrease the risk of
complications, but this risk will always be higher in patients who have received radiation therapy.
TYPES – SEE BOX ABOVE

Several types of operations can be used to reconstruct your breast. You can have a newly shaped breast with the use of a breast
implant, your own tissue flap, or a combination of both.
BREAST IMPLANTS
This is the most common technique used worldwide.
*With tissue expanders: The surgeon inserts a tissue expander, a temporary silastic implant, beneath a pocket under the pectoralis
major muscle of the chest wall. In a process that can take weeks to months, saline solution is injected to progressively expand the
overlaying tissue. Once the expander has reached an acceptable size, it may be removed and replaced with a more permanent implant.
Reconstruction of the areola and nipple are usually performed in a separate operation after the skin has stretched to its final size.
Types of implants
1. Saline-filled implant – Most common
2. Silicone gel-filled implants are also an option for breast reconstruction. Not used as often as they were in the past because of
concerns that silicone leakage might cause immune system diseases. But most of the recent studies show that silicone
implants do not increase the risk of immune system problems, and the FDA approved silicone implants again in 2006.
3. Some newer types use thicker silicone gel, called cohesive gel. They are more accurately called form-stable implants,
meaning that they keep their shape even if the cover is cut or broken
Types of implant surgery

§ One-stage: Immediate breast reconstruction may be done at the same time as mastectomy. After the general surgeon
removes the breast tissue, a plastic surgeon places a breast implant. The implant may be put in the space created when the
breast tissue was removed
§ Two-stage reconstruction or two-stage delayed reconstruction is the type most often done if implants are used. It’s easier
than the immediate operation if your skin and chest wall tissues are tight and flat. An implanted tissue expander, which is like a
balloon, is put under the skin and chest muscle. Through a tiny valve under the skin, the surgeon injects a salt-water solution at
regular intervals to fill the expander over a period of about 4 to 6 months. After the skin over the breast area has stretched
enough, a second surgery will remove the expander and put in the permanent implant. Some expanders are left in place as the
final implant.
Considerations about implants

1. Implants often do not last a lifetime. May need more surgery to remove and/or replace your implant later. In fact, up to half of
implants used for breast reconstruction have to be removed, modified, or replaced in the first 10 years.
2. They can break (rupture) or cause infection or pain. Scar tissue may form around the implant (capsular contracture), which can
make the breast harden or change shape, so that it no longer looks or feels like it did just after surgery.
3. MRIs may be needed every few years or so to make sure silicone gel implants have not broken.
4. Routine mammograms to screen on the remaining breast for breast cancer will be more difficult if you have a breast implant there
— you’ll need more x-rays of the breast, and the compression may be more uncomfortable.
5. Breast implants in the remaining breast may affect your ability to breastfeed, either by reducing the amount of milk or stopping
your body from making milk.
FLAP RECONSTRUCTION/TISSUE FLAP PROCEDURES

The second most common procedure uses tissue from other parts of the patient's body, such as the back, buttocks, thigh or abdomen.
This procedure may be performed by leaving the donor tissue connected to the original site to retain its blood supply (the vessels are
tunnelled beneath the skin surface to the new site) or it may be cut off and new blood supply may be connected.
The 2 most common types of tissue flap procedures are the TRAM flap (or transverse rectus abdominis muscle flap), which uses tissue
from the lower tummy area, and the latissimus dorsi flap, which uses tissue from the upper back.
Because healthy blood vessels are needed for the tissue’s blood supply, flap procedures are not usually offered to women with
diabetes, connective tissue or vascular disease, or to smokers.
TRAM (transverse rectus abdominis muscle) flap

The TRAM flap procedure uses tissue and muscle from the tummy (the lower abdominal wall). The tissue from this area alone is often
enough to shape the breast, so that an implant may not be needed. The skin, fat, blood vessels, and at least one abdominal muscle are
moved from the belly. (abdomen) to the chest. The procedure also results in a tightening of the lower belly, or a “tummy tuck” which
some women consider a benefit
There are 2 types of TRAM flaps:

§ A pedicle flap leaves the flap attached to its original blood supply and tunnels it under the skin to the breast area. This can leave
an area of fullness under the skin where the tissue is tunneled.
§ In a free flap, the surgeon cuts the flap of skin, fat, blood vessels, and muscle for the implant free from its original location and
then attaches it to blood vessels in the chest. This requires the use of a microscope (microsurgery) to connect the tiny vessels and
takes longer than a pedicle flap. The free flap is not done as often as the pedicle flap, but some doctors think that it can result in a
more natural shape.
Latissimus dorsi flap

The latissimus dorsi flap moves muscle and skin from your upper back when extra tissue is needed. The flap is made up of skin, fat,
muscle, and blood vessels. It’s tunneled under the skin to the front of the chest.
DIEP (deep inferior epigastric artery perforator) flap

The DIEP flap uses fat and skin from the same area as in the TRAM flap but does not use the muscle to form the breast mound. This
results in less skin and fat in the lower belly (abdomen), or a “tummy tuck. The procedure takes longer than the TRAM pedicle flap
discussed above, but leaves less muscle weakness and causes fewer hernias. It isn’t available in all areas.
GAP (Gluteal free flap)

The gluteal free flap or GAP (gluteal artery perforator) flap is newer type of surgery that uses tissue from the buttocks, including the
gluteal muscle, to create the breast shape. It might be an option for women who cannot or do not wish to use the tummy sites due to
thinness, incisions, failed tummy flap, or other reasons, but it’s not offered in many areas. Very similar to TRAM flap
Inner thigh or TUG (Transverse upper gracilis) flap

A newer option for those who can’t or don’t want to use TRAM or DIEP flaps is a surgery that uses muscle and fatty tissue from along
the bottom fold of the buttock extending to the inner thigh. This is called the transverse upper gracilis flap or TUG flap
NIPPLE AND AREOLA RECONSTRUCTION

To restore the appearance of the breast with surgical reconstruction, there are a few options regarding the nipple and areola.
A nipple prosthesis can be used to restore the appearance of the reconstructed breast
There are several methods of reconstructing the nipple-areolar complex, including:

• Nipple-Areolar Composite Graft (Sharing) - if the contralateral breast has not been reconstructed and the nipple and areolar
are sufficiently large, tissue may be harvested and used to recreate the nipple-areolar complex on the reconstructed side.
• Local Tissue Flaps
Pre-Reconstruction Considerations
§ Radiation: treatment before and after mastectomy is a relative contraindication to alloplastic reconstruction
§ Recipient tissue: Skin-sparing mastectomy allows for the use of implants without tissue expanders (1-stage process)
§ Donor tissue: limited availability of suitable donor tissue (lack of tissue, scar, previous surgery that interferes with blood supply)
may prevent the use of autologous tissue reconstruction
§ Contralateral breast: may not be possible to reconstruct a breast of the same size or shape as the contralateral breast. Breast
reduction or mastopexy may be considered in opposite breast (see Table 28)
§ Other considerations: patient’s age and co-morbidities, prognosis, body weight, characteristics of chest wall and patient’s attitude
General Surgery
Gall Bladder Disease
February 2015
OUTLINE OF NOTES
1. Cholelithiasis
2. Biliary colic
3. Acute cholecystitis
4. Choledocholithiasis
5. Ascending cholangitis
6. Gallstone ileus
7. Gallbladder carcinoma
8. Cholangiocarcinoma
9. Laparoscopic vs. Open surgery
10. Acalculous cholecystitis
11. Same-admission vs. Interval cholecystectomy
12. Routine vs. Selective intraoperative cholangiogram
CHOLELITHIASIS
North America: Mixed stones (80%) > Cholesterol stones (15%) > Pigment stones (5%)
KNOW WELL: 4 major factors explain most gallstone formation—

1. Supersaturation of secreted bile
2. Concentration of bile in the gallbladder
3. Crystal nucleation
4. Gallbladder dysmotility (à stasis)
RISK FACTORS
DEPEND ON TYPE
A. CHOLESTEROL STONES (Common adage: Fair, fat, fertile, females over forty):
§ Female – Probably most important!!
§ Age < 50
§ Obesity (fat)
§ Oestrogens: Multiparity, OCPs (fertile)
§ Ethnicity (fair): First Nations heritage (especially Pima Indians) > Caucasian > Black
DON’T FORGET!!:
§ ***Impaired gallbladder emptying:
o Starvation
o TPN
o Diabetes Mellitus (autonomic (vagal) paresis!!)
§ ***Terminal ileal resection or disease (interruption of the enterohepatic circulation) (e.g. Crohn’s disease)
§ Rapid weight loss: rapid cholesterol mobilization and biliary stasis
B. PIGMENT STONES (contain calcium bilirubinate): (2 types: Brown [associated with infection] vs. Black [haemolysis and cirrhosis])
§ Chronic haemolysis
§ Cirrhosis (Impaired conjugation of bilirubin. SO increased unconjugated bilirubin in bile)
§ Biliary stasis (strictures, dilation, biliary infection)
Protective factors: Statins, vitamin C, coffee
CLINICAL FEATURES
Possible outcomes of gallstones (follow the path of the gallstone from GB):
1. Asymptomatic (80%):
• Most do NOT require treatment
• ***Consider prophylactic cholecystectomy in 2 major scenarios:
1. Increased risk of malignancy (choledochal cysts, Caroli’s disease, porcelain or calcified gallbladder)
a. NB: ~50% of porcelain gallbladder have cancer!
2. Chronic haemolysis, e.g. sickle cell disease,
Others: Also, paediatric patient (high risk of becoming symptomatic at some point since so long), bariatric surgery, diabetes,
immunosuppression
• Otherwise, see other notes for argument against general prophylactic cholecystectomy (Basically, only ~20% of people with asymptomatic
stones will ever become symptomatic, and even more, only 1% of those will complicate before symptoms arise so prophylaxis is greater risk
than good)
2. Biliary colic (10-25%)

3. Cholecystitis
§ Mucocele
§ Empyema
4. Choledocholithiasis (8-15%)
5. Cholangitis
6. Secondary biliary cirrhosis (if prolonged, unrelieved obstruction of bile duct)
7. Gallstone pancreatitis
8. Gallstone ileus
9. Bouveret syndrome: gastric outlet obstruction secondary to impaction of a gallstone in the pylorus or proximal duodenum. It is therefore a very
proximal form of gallstone ileus.
Biliary Disease Investigations

1. U/S – DIAGNOSTIC PROCEDURE OF CHOICE!!! – See below for possible findings
2. ERCP (Endoscopic retrograde cholangiopancreatography):

• Visualization of upper GI tract, ampullary region, biliary and pancreatic ducts
• Method for treatment of CBD stones in periampullary region (by sphincterotomy aka. papillotomy, or by stone retrieval)
• Complications (8-10%): traumatic pancreatitis (1-2%), pancreatic or biliary sepsis
3. MRCP (Magnetic resonance cholangiopancreatography):

• Same information gained as ERCP but non-invasive!!!; cannot be used for therapeutic purposes
4. PTC (Percutaneous transhepatic cholangiography):

• Injection of contrast via needle passed through hepatic parenchyma
• Performed with 22G Chiba Needle
• Useful for intrahepatic or proximal bile duct lesions OR when ERCP fails, not possible or not available
• Requires prophylactic antibiotics
• Contraindications: coagulopathy, ascites, peri/intrahepatic sepsis, disease of right lower lung or pleura
• Complications: bile peritonitis, chylothorax, pneumothorax, sepsis, haemobilia
5. HIDA scan (Hepatobiliary imino-diacetic acid scan):

• Used less commonly. A FUNCTIONAL TEST
• Radioisotope technetium-99 injected into a vein is excreted in high concentrations into bile, allowing visualization of the biliary
tree 2 hours after injection
• NOTE WELL: Does NOT actually visualize stones; diagnosis made by seeing occluded cystic duct or CBD
6. CT scan
7. Plain abdominal radiograph – Only 10% of gallstones are radiopaque. Useful for exclusion of other differentials
8. Endoscopic ultrasound
9. Intraoperative cholangiography
Non-surgical treatment of gallstones (NOT used. But be aware of)

1. Gallstone dissolution:
§ Oral bile salts in the form of chenodeoxycholic acid or ursodeoxycholic acid
§ Treatment must be continued for many months, interrupted by attacks of biliary colic as small fragments of stones pass through the bile
ducts
§ ALSO, recurrences are very common after discontinuation as an abnormal gallbladder remains
2. Lithotripsy:
§ NOT used in routine practice
§ Ultrasonic destruction of small stones as used in the renal tract
§ BUT the small fragments of stone may cause biliary obstruction and pancreatitis
§ Also, residual fragments in gallbladder may provide a nidus for further stone formation
BILIARY COLIC
PATHOGENESIS
***Gallstone transiently impacted in cystic duct à NOTE WELL: NO INFECTION OR INFLAMMATION!!!!
CLINICAL FEATURES
§ Constant, severe dull pain in epigastrium OR RUQ for minutes to hours, crescendo-decrescendo pattern
o Can radiate to right shoulder or scapula
o Frequently occurs at night or after fatty meal, not after fasting
§ May present with chest pain
§ Patients often restless
IMPORTANT NEGATIVES:
§ NO PERITONEAL FINDINGS (E.G. TENDERNESS, etc.)
§ NO SYSTEMIC SIGNS!! (E.G. FEVER)
INVESTIGATIONS
§ Blood work will be normal: CBC, electrolytes, LFTs, bilirubin, amylase
§ U/S shows cholelithiasis, may show stone in cystic duct
TREATMENT
1. Analgesia
2. Rehydration during colic episode
3. Elective cholecystectomy (Laparoscopic vs. open) (95% success):
§ Laparoscopic cholecystectomy is the standard of care , no benefit to delaying surgery
§ Complications: CBD injury (0.3-0.5%), hollow viscus injury, bile peritonitis, vessel injury
§ Risk of open cholecystectomy higher in emergency situations
ACUTE CALCULOUS CHOLECYSTITIS

May be calculous of acalculous (5-10%)
PATHOGENESIS
§ Inflammation of gallbladder resulting from sustained gallstone impaction in cystic duct or Hartmann’s pouch and à
subsequent concentration of bile à chemical cholecystitis first!!!! àThen secondary infection (Surgical tutor says 20%
of cases)
§ No cholelithiasis in 5-10% (Acalculous Cholecystitis)
CLINICAL FEATURES
§ Often have history of biliary colic
§ Stone is not in the CBD so patient is NOT JAUNDICED (Unless Mirizzi’s syndrome)
§ Severe constant (hours to days) epigastric or RUQ pain +
§ SYSTEMIC FEATURES!!!: Anorexia, nausea, vomiting, low grade fever (<38.5ºC)

§ FOCAL PERITONEAL FINDINGS: Murphy’s sign, palpable, tender gallbladder (in 33%)
§ Boas’ sign: Right subscapular pain
INVESTIGATION
A. Bloodwork:
1. CBC: Elevated WBC and left shift
2. LFTs: Mildly elevated bilirubin, ALP, GGT, AST, ALT
B. Imaging
1. U/S: 98% sensitive
2. Consider HIDA scan if U/S negative!! – Failure of gallbladder to fill is basically diagnostic of cholecystitis
3. NB: CT scan is LESS sensitive for cholecystitis than both the above
MUST KNOW BY HEART: POSSIBLE ULTRASOUND FINDINGS IN ACUTE CHOLECYSTITIS:

1. Thickening of gall bladder wall (> 4 mm)
2. Distension of gall bladder
3. Pericholecystic fluid
4. Stones in the gall bladder (echogenic focus with posterior acoustic shadowing)
5. Dilated CBD (> 8-10 mm)
6. Sonographic Murphy’s sign
*** On U/S, gall bladder be shrunken/contracted with calcified walls in chronic cholecystitis à “Porcelain gall bladder” ***
COMPLICATIONS
1. Gallbladder mucocele (hydrops): Long term cystic duct obstruction results in mucous accumulation in gallbladder (clear fluid)
2. Empyema of gallbladder: Suppurative cholecystitis, pus in gallbladder + sick patient
3. Gangrene (20%) (Acute gangrenous cholecystitis) à
4. Perforation (2%) à : result in abscess formation or peritonitis
5. Cholecystoenteric fistula, from repeated attacks of cholecystitis, à can lead to gallstone ileus & Bouveret syndrome
6. Acute emphysematous cholecystitis: Infection with gas forming organism à bacterial gas present in gallbladder lumen, wall or
pericholecystic space (risk in diabetic patient)
7. Mirizzi syndrome: Extra-luminal compression of CBD/CHD due to large stone in cystic duct or inflammatory process
o Can result in cholecystohepatic or cholecystocholedochal fistulae
TREATMENT
MANAGEMENT IS RESUSCITATIVE + SURGICAL
AND THEN MENTION THAT TIMING OF SURGERY CAN BY “EARLY (<72 hr)” OR “DELAYED (~6 wk)”
1. Admit
2. NPO
3. IVF resuscitation
4. NG tube (If persistent vomiting from associated ileus)
5. Analgesics once diagnosis is made

6. Antibiotics – Cefazolin if uncomplicated cholecystitis
7. Cholecystectomy (IMPORTANT: EARLY vs. DELAYED AND LAPAROSCOPIC vs. OPEN):

§ Early “same-admission” (within 72 h) vs. Delayed “interval” (after 6 week) [COMMON DISCUSSION – See last page]
o Equal morbidity and mortality
o EARLY CHOLECYSTECTOMY PREFERRED: *shorter hospitalization and recovery time, *less economic loss, *no benefit to
delaying surgery
o Emergent OR indicated if high risk, e.g. emphysematous
§ LAPAROSCOPIC IS STANDARD OF CARE (convert to open for complications or difficult case)

o Laparoscopic: reduced risk of wound infections, shorter hospital stay, reduced post-op pain, but increased risk of bile duct injury
§ Intra-operative cholangiography (IOC): [See argument for routine vs. selective IOC]
§ Indications: Clarify bile duct anatomy, obstructive jaundice, history of biliary pancreatitis, small stones in gallbladder with a wide
cystic duct (>15 mm), single faceted stone in gallbladder, bilirubin >137 μmol/L
8. NB: Percutaneous cholecystostomy tube (instead of surgery): If critically ill or if general anaesthetic contraindicated!!!,
esp. in acalculous cholecystitis
Toronto notes boxes:

§ Biliary colic is treated with analgesia and elective cholecystectomy
§ Acute cholecystitis is treated with antibiotics and early cholecystectomy
Critical View of Safety: Space between the gallbladder and liver clear of any structures other than the cystic artery.
Rouviere’s Sulcus: Fissure between right lobe and caudate process of liver. Keeping dissection anterior to this landmark prevents bile duct injury.
CHOLEDOCHOLITHIASIS
DEFINITION
§ Stones in common bile duct (CBD)
**Primary vs. Secondary stones:

1. Primary (15%): Formed de novo in bile duct, indicates bile duct pathology (e.g. benign *biliary stricture, *sclerosing cholangitis,
*choledochal cyst, *cystic fibrosis)
2. Secondary (85%): formed in gallbladder
CLINICAL FEATURES
§ 50% asymptomatic
§ Often have history of biliary colic
§ *4 FEATURES OF OBSTUCTIVE JAUNDICE* Pale (acholic stools), dark urine, intermittent jaundice, pruritus
EXAMINATION
§ Afebrile. (Fever suggests ascending cholangitis! – [i.e. fever would make it Charcot’s triad])
§ *Tenderness in RUQ or epigastrium (foregut structure)
§ *Scratch marks/excoriations (from pruritus)
§ ***DON’T FORGET!!!: Petechiae/ecchymosis due to coagulopathy (bile required for absorption of vit K – needed for clotting factors 2, 7, 9, 10)
INVESTIGATIONS
A. GENERAL
1. CBC: Usually normal; leukocytosis suggests cholangitis!!!
2. LFTs: “obstructive picture” (elevated ALP, GGT and conjugated bilirubin, mild increase in AST, ALT)
3. Urinalysis will show present bilirubin BUT ABSENT urobilinogen!
4. Amylase/lipase: to rule out gallstone pancreatitis
B. SPECIFIC IMAGING
5. U/S: intra/extra-hepatic duct dilatation; differential diagnosis is choledochal cyst
6. ERCP, PTC
7. MRCP (90% sensitive, almost 100% specific, not therapeutic)
COMPLICATIONS
1. Ascending cholangitis
2. Gallstone pancreatitis
3. Biliary stricture
4. Secondary biliary cirrhosis!!!
TREATMENT
If no evidence of cholangitis:
1. ERCP with papillotomy and basket/balloon retrieval of stones (preoperatively) followed by elective cholecystectomy
a. Most stones will pass spontaneously after operation, but for large stones that were not amenable to ERCP à
i. Laparoscopic transcystic duct or trans common bile duct retrieval
ii. Open common bile duct exploration
ASCENDING CHOLANGITIS
PATHOGENESIS
§ MUST KNOW: 2 ABSOLUTE REQUIREMENTS FOR ASCENDING CHOLANGITIS
1. Obstruction in CBD &
2. Presence of bacteria in CBD
§ Obstruction of CBD leading to biliary stasis, bacterial overgrowth, suppuration and biliary sepsis
– MAY BE LIFE-THREATENING, especially in elderly
AETIOLOGY
1. Obstruction may be due to:
§ Stone: Choledocholithiasis (60%)
§ Stricture
§ Neoplasm (pancreatic or biliary)
§ Extrinsic compression (pancreatic pseudocyst or pancreatitis)
§ Instrumentation of bile ducts (PTC, ERCP), biliary stent
2. Organisms: E. coli, Klebsiella, Pseudomonas, Enterococcus, B. fragilis, Proteus
§ Gram-negative organisms (E. coli, Klebsiella, Pseudomonas, Enterobacter, Proteus, Serratia) are the most common
§ Enterococci are the most common gram-positive bacteria
§ Anaerobes are less common (B. fragilis most frequent)
§ Fungi are even less common (Candida)
CLINICAL FEATURES
Classically:
§ Charcot’s triad: Fever, RUQ pain, jaundice
§ Reynolds’ pentad: Fever, RUQ pain, jaundice + hypotension, altered mental status
§ ALSO may have nausea, vomiting, abdominal distention, ileus, acholic stools, tea-coloured urine (elevated direct bilirubin)
INVESTIGATIONS
A. GENERAL
1. CBC: elevated WBC + left shift
2. LFTs: “obstructive picture” (elevated ALP, GGT and conjugated bilirubin, mild increase in AST, ALT)
3. May have positive blood cultures
4. Amylase/lipase: rule out pancreatitis
B. IMAGING
5. U/S: intra/extra-hepatic duct dilatation
TREATMENT
MANAGEMENT IS 1. RESUSCITATION + 2. IV ABX & DECOMPRESSION + 3. CHOLECYSTECTOMY
Main principle: NEED TO GIVE ANTIBIOTICS AND DECOMPRESS THE BILE DUCT!!! à THIS TREATS THE 2 UNDERLYING CAUSES
A. Initial:
1. Admit
2. NPO
3. IV fluid and electrolyte resuscitation
4. ± NG tube
5. IV ANTIBIOTICS (Successfully treats 80%!!!)
B. Decompression procedure:
1. ERCP + sphincterotomy: diagnostic and therapeutic
IF ERCP not available or unsuccessful:

2. PTC with catheter drainage:
IF above fails:
3. Laparotomy with CBD exploration and T-tube placement
C. ALL patients should also have a cholecystectomy unless contraindicated
PROGNOSIS: Suppurative cholangitis mortality rate: 50%
GALLSTONE ILEUS
PATHOGENESIS
§ Repeated inflammation causing a cholecystoenteric fistula (usually duodenal) à large gallstone enters the gut and impacts FEW
CENTIMETRES PROXIMAL TO THE ileocecal valve, causing a mechanical bowel obstruction (note: ileus is a misnomer in this context)
CLINICAL FEATURES
1. Cardinal features of intestinal obstruction
NOTE WELL: Bouveret’s Syndrome: Gastric outlet/duodenal obstruction caused by a large gallstone passing through a cholecystogastric or
cholecystoduodenal fistula.
INVESTIGATIONS
RIGLER’S TRIAD of Gallstone ileus (SEEN ON EITHER X-RAY OR CT): 1. Pneumobilia (air in biliary tree), 2. SBO (partial or complete), 3.
Gallstone (usually in right iliac fossa)
1. AXR:
a. Dilated small intestine, air fluid levels (SBO)
b. Air in biliary tree (pneumobilia) (40%)
c. May reveal radiopaque gallstone
2. CT: More sensitive for pneumobilia, obstruction, gallstone in intestine
TREATMENT
MANAGE AS ANY MECHANICAL INTESTINAL OBSTRUCTION à RESUSCITATE THEN EMERGENCY LAPAROTOMY (Then cholecystectomy
later)
1. Fluid resuscitation
2. NG decompression
3. Surgery:
a. INSPECT BOWEL. If all viable:
i. Enterostomy and removal of stone
ii. REMEMBER: MUST inspect small AND large bowel for additional proximal stones!!!
iii. May close fistula surgically or manage expectantly (can resolve spontaneously)
b. If nonviable à RESECTION and primary anastomosis (as small bowel has good blood supply)
c. Cholecystectomy either during enterolithotomy or after recovery if patient experiences gallbladder symptoms
GALLBLADDER CARCINOMA
RISK FACTORS
1. Age (50-70),
2. Female sex (F:M, 2-3:1)
3. Chronic symptomatic gallstones (70% of cases), esp > 2.5-3 cm

4. Gallbladder polyps > 1 cm
5. Porcelain gallbladder
6. Chronic infection (Salmonella, Helicobacter)

7. Abnormal pancreaticobiliary duct junction
CLINICAL FEATURES
§ Majority are adenocarcinoma
§ May be incidental finding on elective cholecystectomy (~1% of elective cholecystectomies)
§ Many patients are asymptomatic until late (due to ~90% being in the body or fundus so asymptomatic when early)
§ Local: Vague RUQ pain, ± palpable RUQ mass

§ Courvoisier’s gallbladder
§ Systemic: Jaundice (50%) due to invasion of CBD OR compression of CBD by pericholedochal nodes,
§ Weight loss, malaise, anorexia
§ Early local extension to liver, may extend to stomach, duodenum
§ Early metastasis common to liver, lung, bone
INVESTIGATIONS
1. U/S: Mural thickening, calcification, loss of interface between gallbladder and liver, fixed mass
2. Endoscopic U/S (EUS): Good for distinguishing carcinomas from other diagnoses such as polyps, good for staging, allows sampling of bile for
cytology
3. Abdominal CT: polypoid mass, mural thickening, STAGING – CHEST/ABD/PELVIS: liver invasion, nodal involvement, distant metastases
4. MRI/MRCP: good for distinguishing benign and malignant polyps
TREATMENT
If carcinoma of the gallbladder is suspected preoperatively, an open cholecystectomy should be considered to avoid tumour seeding of the
peritoneal cavity
§ Confined to mucosa (rare): Open cholecystectomy
§ Beyond mucosa: Cholecystectomy, en bloc wedge resection of 3-5 cm underlying liver, dissection of hepatoduodenal lymph nodes
CHOLANGIOCARCINOMA
Definition: Malignancy of extra- or intrahepatic bile ducts
RISK FACTORS
§ Age 50-70
§ Any cause of chronic inflammation of bile ducts: Gallstones, ulcerative colitis, primary sclerosing cholangitis, choledochal
cyst, Clonorchis sinensis infection (liver fluke), chronic intrahepatic stones (hepatolithiasis)
CLINICAL FEATURES
§ Majority are adenocarcinomas
§ Gradual signs of biliary obstruction: jaundice, pruritus, dark urine, pale stools (Most common presentation is obstructive jaundice)
§ Vague RUQ pain, Courvoisier’s sign (if CBD obstructed), hepatomegaly
§ Anorexia, weight loss
§ Early metastases are uncommon, but commonly tumour grows into portal vein or hepatic artery
§ Klatskin tumour (2/3 of cases): cholangiocarcinoma located at confluence of the right and left hepatic duct
INVESTIGATIONS
1. CBC: Anaemia
2. LFTs show obstructive picture
3. U/S: bile ducts usually dilated, but not necessarily
4. CT: bile ducts usually dilated, but not necessarily
a. Triphasic CT to assess spread, mets and resectability
5. ERCP or PTC: to determine resectability, for biopsies
6. CXR, bone scan: for metastatic workup
7. CEA and CA-19-9 mainly for monitoring
TREATMENT
§ Generally palliative
§ If resectable: biliary drainage and wide excision margin
o Upper third lesions: duct resection + Roux-en-Y hepaticojejunostomy, ± liver resection
o Middle third lesions (uncommon): duct resection + Roux-en-Y hepaticojejunostomy
o Lower third lesions: Whipple procedure
§ Unresectable lesions: stent or choledochojejunostomy (surgical bypass)
PROGNOSIS
§ Radiotherapy useful for additional palliation, chemotherapy may be helpful
§ The more proximal to the liver, the worse the prognosis
§ Overall 5-yr survival: 15%
MUST KNOW: LAPAROSCOPIC VS. OPEN CHOLECYSTECTOMY

Laparoscopic Cholecystectomy
1. Shorter operating time (in developed countries)
2. Shorter length of hospital stay
3. Shorter sick leave and shorter time to return to daily activities
4. Less postoperative pain

5. Decreased use of postoperative analgesia
6. Less impairment in intestinal motility* (Handling bowel is partially what causes postop ileus. Lap has less handling of bowel)
7. Decreased reduction in pulmonary function*
8. Fewer pulmonary complications
9. Decreased acute phase response
10. Less wound infection

11. Cosmetic benefits
12. Less handling of bowel so less adhesions
13. Less incisional hernia
Disadvantages
May be “region-specific”:
1. More expensive in developING countries
a. Reason is laparoscopy trained surgeons are more scarce (In developed countries open surgery is actually more expensive)
b. Also because we use disposable equipment
c. Open is usually used for more difficult cases in developed countries so it total cost turns out to be more expensive than laparoscopy
2. Actually have a longer operating time in developing countries
3. May be more difficult if previous abdominal surgery with significant adhesions
Open Cholecystectomy
1. Lower conversion rates to open surgery (for mini-laparotomies)
*NOTE:
Pulmonary function = O2 consumption, spirometric parameters, arterial blood gases, and acid-base balance
Intestinal motility = auscultating intestinal peristalsis, abdominal circumference measurement, and time interval to restitution of defecation
MUST KNOW: POSTCHOLECYSTECTOMY SYNDROMES (MUST!!!! SEE MY LONG NOTES FOR DETAILS AND
MANAGEMENT)
1. Bile duct injury
2. Lost stones
3. Post-cholecystectomy pain
4. Retained biliary stones
5. Biliary leak
Calot’s triangle
Calot's Triangle - Calot's original description of the triangle in 1891 included the
1. Cystic artery superiorly (not the inferior border of the liver as is commonly believed).
2. Cystic duct laterally
3. Common hepatic duct medially
The cystic lymph node of Lund (also known as the Calot node) is within this triangle
This triangular space is dissected in order to identify, divide, and ligate the cystic duct and artery. The Calot node is the main route of lymphatic drainage
of the gallbladder.
Early versus Delayed Laparoscopic Cholecystectomy for Biliary Colic

Cochrane DB Syst Rev 2008;4:CD007196
Study: To assess the benefits and harms of early versus delayed laparoscopic cholecystectomy for patients with biliary colic due to gallstones.
Selection criteria: Only RCTs. 1 study including 75 patients found.
Results: During the waiting period in the delayed group (mean 4.2 mo), the complications that the patients suffered included severe acute pancreatitis
resulting in mortality (1), empyema of gallbladder (1), gallbladder perforation (1), acute cholecystitis (2), cholangitis (2), obstructive jaundice (2), and
recurrent biliary colic requiring hospital visits (5). The rate of conversion to open cholecystectomy was lower in the early group (0%) than the delayed
group (20%). There was a statistically significant shorter operating time and hospital stay in the early group than the delayed group (WMD -14.80 min,
95% CI -18.02 to -11.58 and -1.25 d, 95% CI -2.05 to -0.45 respectively). Fourteen patients (35%) required 18 hospital admissions for symptoms related
to gallstones during the mean waiting period of 4.2 mo in the delayed group.
Conclusion: Early laparoscopic cholecystectomy (<24 h of diagnosis of biliary colic) decreases the morbidity during the waiting period for elective
laparoscopic cholecystectomy, decreases the rate of conversion to open cholecystectomy, decreases operating time, and decreases hospital stay
Dr. Powell:
Same-admission approach has a substantially higher conversion rate in the acute setting
• 11% conversion rate vs. 3% in interval cholecystectomy
BUT!!! The benefits offered are generally agreed to outweigh this increased conversion rate. Considering the
1. Lowered interruption of life with less hospital stay
2. Cost benefit to patient
3. Avoidance of recurrence/subsequent stone complications in the interval
4. It is also suggested that the oedema/pericholecystic fluid aids operation
5. Avoids having to deal with inflammatory adhesions
• *** It is generally accepted that same admission cholecystectomy is the best option
**Remember if there is suspicion of stone, must perform ERCP BEFORE proceeding to surgery
Use of routine vs. selective intraoperative cholangiogram

The US data says there is benefit in performing it routinely. This is fairly dated research (2007). Concluded that routinely is the way to go.
*** This is contradictory to findings in local literature
*** Local opinion: Paper by McFarlane and McCartney looked at 225 pts. They approached it by doing selective, targeted intraop cholangiogram.
Demonstrated that routine intra-op cholangiogram offers NO significant decrease in the incidence of CBD injury.
• Therefore locally this is NOT performed routinely. Nobody here does it routinely.
Acalculous Cholecystitis
Acute or chronic cholecystitis in the absence of stones, typically due to gallbladder ischemia, stasis
Risk factors: DM, immunosuppression, ICU admission, trauma patient, TPN, sepsis
Clinical features same as Acute cholecystitis, occurs in 20% of cases of acute cholecystitis
Investigations: U/S shows sludge in gallbladder, other U/S features of cholecystitis (see above), CT or HIDA scan
Treatment: broad-spectrum antibiotics, cholecystectomy, if patient unstable à cholecystostomy
--
Preoperative ERCP is NOT routine prior to cholecystectomy. There are indications.
LFTs MUST be done in preoperative workup

*** Pre-operative ERCP not routine. Indicated if:
• Recent jaundice
• Abnormal liver function tests
• Significantly dilated common bile duct
• Ultrasonic suspicion of bile duct stones
*** Therapeutic indications of ERCP:

1. Endoscopic sphincterotomy (both of the biliary and the pancreatic sphincters)
2. Removal of stones (with a balloon or Dormia basket)
3. Insertion of stent(s)
4. Dilation of strictures (e.g. primary sclerosing cholangitis, anastomotic strictures after liver transplantation)
Surgical Recall:
How is an IOC performed?

1. Place a clip on the cystic duct–gallbladder junction
2. Cut a small hole in the distal cystic duct to cannulate
3. Inject half-strength contrast and take an x-ray or fluoro
What are the steps in lap chole (6)?

1. Dissection of peritoneum overlying the cystic duct and artery
2. Clipping of cystic artery and transect
3. Division of cystic duct between clips
4. Dissection of gallbladder from the liver bed
5. Cauterization; irrigation; suction, to obtain hemostasis of the liver bed
6. Removal of the gallbladder through the umbilical trocar site
Wayne Robinson, MBBS Class of 2015 - 1
Surgery Elective
Gall Stones – END OF THE DOCUMENT HAS ESSENTIAL SURGERY INFO ON “OPERATIONS ON THE COMMON BILE DUCT”
Dr. L. Powell
2014
Only took down the key information. Other information was textbook
Small’s triangle tries to explain supersaturation. Doesn't fully explain it:

1. It doesn't account for other substances in bile E.g. Bacteria
2. Doesn't account for the cholesterol in vesicles. Only in the micellar form
Which stones cause problems:

Extremes of size:
§ Very large
§ Very small < 1 cm
o “Sub-centimeter” stones – A new word in the literature
Laparoscopic surgery vs. Open surgery (SEE MY GALLBLADDER NOTES FOR FULL DETAILS)
Laparoscopic originated because surgeons thought it was a cool sexy way to approach. Not out of clinical need.
The advantages were developed after the fact
Advantages
1. Less scarring à Better cosmesis post-op

2. Less bleeding à Controversial
3. Hands not inside harassing bowel à less adhesions
4. Less post-op pain
5. Decreased post-op analgesia
6. Less hospitalization time
a. More rapid return to normal function
b. Quicker return to work.. Can spin off to benefit the economy as well
7. Less risk of wound infection
8. Less risk of hernia formation
Disadvantages
May be region-specific:
1. More expensive in developing countries
a. Reason is laparoscopy trained surgeons are more scarce (In developed countries open surgery is actually more
expensive)
b. Also because we use disposable equipment
c. Also because open is usually for more difficult issues
2. Actually have a longer operating time in developing countries

3. May be more difficult if previous abdominal surgery with significant adhesion
---
Concept of surgery called “mini-open cholecystectomy” à Instead of a big cut, do a small subcostal incision (3.7 cm)
§ Take out gall bladder with “fundus-first” approach

§ But need special retractors
§ Only used in patients whose body habitus permit
§ Outcome however is the same as laparoscopy. No advantage
§ Disadvantages: Sometimes pathology is not what you think it is, but preop investigations modern have minimized this
---
NOTE WELL: The fundus is the part of the gall bladder that perforates!!!
Sometimes ulcerates in the region of Hartmann’s pouch
----
Acalculous cholecystitis always perforates!!!
Patients predisposed to this:
§ Severe major surgery

§ Patients with vasculopathies get this.. Just have bad blood vessels
§ Theory of atherosclerotic obstruction of vessels
§ Or decreased splanchnic circulation in patients with these severe illnesses (Physiology of stress.. Abdominal organs are not
essential)
Gallbladder especially sensitive to ischaemia as it has 1 end artery à Cystic artery. No collateral
supply
(Branch of proper right hepatic artery)
***The decreased supply is felt worst at the furthest point from the supply à End of fundus
As sick as a patient is, once this is diagnosed, must go to surgery!!!
5% Interesting specific subset of people getting a calculous... Normal people
---
In general for surgery: PT/PTT only done when indicated
§ If history strongly suggests possible derangement

§ If vascular surgery where risk of bleeding is great
§ Surgeries where complications associated with bleeding are very significant
---
Opt for “same-admission cholecystectomy” à What determines this is if patient presents within 72 hours of onset!!
---
ERCP: Indicated when you demonstrate evidence of stone clinically (jaundice) or on both biochemistry and imaging U/S
ERCP performed BEFORE operation. Reasons:

Helps to decide laparoscopic vs. open:
§ I.e. Must determine if there are stones not amenable to ERCP, which would indicate intraop exploration is necessary. (If you
didn’t realize this beforehand and try to operate first and ERCP after à may fail and have to reoperate)
If exploration is indicated, then open procedure done majority of times, THOUGH laparoscopic exploration possible
MUST KNOW: STONE RETRIEVAL SYSTEMS AT OPEN CHOLECYSTECTOMY:
1. Desjardines forceps: Stone retrieval forceps – Hardly used anymore as were used form large ducts.. Patients nowadays..?
2. We now use biliary Fogarty catheters or Dormia baskets to remove at open exploration!
*** Ideally after finished exploring duct, should use a choledochoscope to confirm presence or absence of more stones. If not
available, at UHWI we are resourceful and often us the ureteroscope
If unsure and no scope available, how to check à Put T tube in system:

§ What do you do with t-tube now that you’ve closed the duct? Leave in for 10 days.
§ Doing the check cholangiogram before 10 days would result in high risk of leakage!! (No tract formed to permit a useful
cholangiogram)
§ T-tube is actually placed in where the incision in the common duct is made. I.e. Usually not through the cystic duct. Would be
very hard to put in through cystic duct.
§ One end comes out percutaneously
THEN perform a “check cholangiogram” at 10 days, looking for “RETAINED STONES” à

§ If clear: Just pull it out
§ If retained stones present: then DO NOT REMOVE T TUBE NOW because the biliary system at this point is not yet able to
tolerate instrumentation and manipulation. Leave the t-tube in for 6 weeks to allow a fibrous tract formed from duct right out to
skin. Once formed, pull out t-tube. Then put dilators, then scope down tract. THEN pass THEN pass a choledochoscope and
pass a dormia basket THROUGH THE CHOLEDOCHOSCOPE and retrieve stones (or Burhenne Basket à Harold Ellis). NB:
Stone retrieval systems DO NOT FIFT through the t-tube
Cholecystostomy cholangiogram – Another form of cholangiogram. This is performed through the fibrous tract that remains
after pulling out the t-tube
Intraoperative cholangiogram is very uncommonly performed nowadays as the information it provides is now acquired by ERCP or
preop investigation
KNOW: HOW TO CLOSE THE DUCT AFTER EXPLORATION:
1. Option 1: Suture
2. Option 2: T-tube (Actually has a higher stricture rate than a suture only closure)
3. Option 3: Biliary-enteric bypass: Anastomose site of incision for exploration to first part of duodenum. (So there will be 2
drainage orifices)
§ Said to be an increased risk of cancer with choledochoduodenostomy!!
§ Not with jejunostomy
---
SICKLERS
Unique in that they have high incidence of CBD stones
Must routinely investigate these patients with ERCP or MRCP
Complication rate very high. Was almost 40%

Try NOT to do ERCP: Do MRCP.. If stones found à ERCP
Problem with intraop investigation/exploration à Lengthens operating time. Know the issue with this in sicklers
MRCP is offered anywhere a modern MRI machine is!! So NOT at UHWI. Don't give sharp enough images
Best practice à MRCP then lap cholecystectomy
KNOW THIS:
§ By convention: If a stone is found in CBD after 6 months à Primary duct stone
§ But if found prior to this à “Retained stone”
SCENARIO: Post-op patient returns with jaundice
2 WEEKS
Think: Could be related to surgery, anaesthesia or totally unrelated. Treat patient as a jaundice patient considering everything. Don't
restrict yourself
Consider:
1. Retained stones
2. Injury with stricture
3. Injury with bile leak (If you put bile in peritoneum will be reabsorbed and will get jaundice)
Intra abdominal bleeding and bilirubin reabsorption

Sepsis with haemolysis
Hepatitis
Or incidental viral hepatitis

6 WEEKS
§ Hepatitis: Due to halothane or anaesthetic drugs. Subsequent exposure will cause much quicker jaundice
OPERATIONS ON THE COMMON BILE DUCT

Exploration of the common bile duct
If stones are known to be present in the bile ducts, the common duct may be explored laparoscopically or at open surgery. The duct is opened through a
longitudinal or transverse incision and stones retrieved by a combination of manipulation, irrigation, grasping with stone forceps or a Dormia basket or
use of a balloon catheter. Operative choledochoscopy is often used to check for residual stones and to remove difficult stones. A flexible fibreoptic
choledochoscope gives good visibility and manoeuvrability and can also be used in laparoscopic surgery. After exploration, a latex T-tube is usually
inserted to drain bile to the exterior, with the transverse limb placed within the common bile duct. The main purpose of a T-tube is to provide access to
the biliary tree for a further cholangiogram about 1week after operation (T-tube cholangiography, see Fig. 20.10).This is to ensure that no stones remain
and to allow any oedema at the ampulla to settle.
Endoscopic management of bile duct stones

With the widespread availability of ERCP and endoscopic sphincterotomy, stones in the common duct can often be retrieved without an operation. This
technique represents areal advance in the management of duct stones over the earlier need for open surgery but does carry its own risks. Endoscopic
sphincterotomy may be employed in the following circumstances:
• Urgent drainage of the bile duct in obstructive jaundice complicated by cholangitis. Definitive surgery can then be deferred until the risks of
infection have been minimized
• Retrieval of stones missed at operation. This avoids a difficult and hazardous operation to explore or re-explore the duct
• Removal of duct stones in patients unfit for operation (gall bladder left in situ)
• Some cases of acute pancreatitis due to gallstones
• Preparation of a jaundiced patient for elective gall bladder surgery
LAPAROSCOPIC VS OPEN CHOLECYSTECTOMY (SURGICAL TUTOR)
EDIT UP THIS DOCUMENT WITH INFORMATION FROM MY GALL BLADDER SUMMARY NOTES
§ First open cholecystectomy performed by Langenbuch in Berlin in 1882

§ Throughout this century open cholecystectomy has been associated with significant complications
§ Today mortality is approximately 0.5%
§ Morbidity includes:
o Specific complications - bile duct damage, retained stones, bile leak
o General complications - wound dehiscence, pulmonary atelectasis
§ Lead to the development of 'mini' cholecystectomy through a 5 cm transverse incision
§ Laparoscopic cholecystectomy introduced in 1988
§ Dissolution therapies
o High complication rate
o Poor long-term results
§ Extra-corporeal shock wave lithotripsy

o Poor stone clearance
Laparoscopic cholecystectomy
§ Shown to be equally as effective as open cholecystectomy in controlled trials
§ Pre-operative ERCP is indicated if:
o Recent jaundice
o Abnormal liver function tests
o Significantly dilated common bile duct
o Ultrasonic suspicion of bile duct stones
Technique
1. Routine use of nasogastric tubes and catheter controversial
2. CO2 pneumoperitoneum induced using either Veress needle or open (Hasson) technique
§ Open (Hasson) technique is believed to be safer
§ Over half of bowel injuries are caused by Veress needles or trocars
3. Abdominal pressure set to 12-15 mm Hg
High intra-abdominal pressure can:
a. Reduce pulmonary compliance
b. Decrease venous return
c. Higher end-tidal CO2 levels
4. Surgery usually performed using 4 standard ports (2 x10 mm & 2 x 5 mm)
5. Patient positioned with head up tilt and rolled to the left
6. Calot's triangle dissected using a retrograde technique
7. Cystic duct and artery identified
8. Ligated with clips or endo-loops
9. About 50% surgeons routinely use intra-operative cholangiography
10. Cholangiography allows:
a. Definition of biliary anatomy
b. Identification of unsuspected CBD stones (~10% patients)
Outcome
§ Conversion rates typically about 5%
§ Laparoscopic cholecystectomy associated with
o Reduced analgesic requirements
o Reduced postoperative stay
o Faster return to normal activity
Laparoscopic surgery in acute cholecystitis

§ In those with acute cholecystitis operation has usually been deferred 6-8 weeks
§ Recently shown that early laparoscopic cholecystectomy is safe
§ Associated with reduced conversion rate
§ Trend towards early surgery during first admission
Potential future improvements

§ Gasless pneumoperitoneum using mechanical abdominal wall retractors
§ Narrower ports and instruments
Surgical Recall
Reverse Trendelenburg
Patient supine with head elevated (usual position for laparoscopic cholecystectomy to make the intestines fall away from the operative field)
Ports used in laparoscopic Cholecystectomy

1. A 10 mm port at umbilicus that goes through fascia. It is the port used to insulflate C02, house the camera initially and to remove the gallbladder. It is the largest port and the
only on that a fascial incision has been made.
2. A 5 mm port at the epigastrium. This is the second port. When the C02 of about 10-12 mmHg (not more than 15 mmHg) has insuflated the abdomen through the first port the
camera is placed and the trocar used to go through the abdominal layers with good intra-abdominal vision.This is the operating port. Towards the end of the surgery when the
gallbladder is being removed it will house the camera.
3. A 5 mm port in the lower portion of the RUQ. This port grasps the fundus of the gall bladder and brings it up to the inferior liver edge pushing the liver cephalad.
4. A 5 mm port above the 3rdport inferior to the costal margin. This port grasps hartman’s pouch and pulls it down to expose Calot’s triangle
General Surgery
Acute Pancreatitis
Sources: Toronto Notes, Harold Ellis, Dr. Roberts Class, Surgical Recall
February 2015
Can use Harold Ellis book along with these notes. Especially for pathophysiology etc.
AETIOLOGY: Must know (Classic mnemonic): I GET SMASHED
When thinking about the causes of acute pancreatitis remember: I GET SMASHED, but vast majority due to gallstones (45%) or ethanol (35%)
• Idiopathic: thought to be hypertensive sphincter or microlithiasis
• Gallstones (45%)
• Ethanol (35%)
• Tumours: Pancreas, periampullary, choledochocele
• Scorpion stings
• Microbiological
o Bacterial: Mycoplasma, Campylobacter, TB, M. avium intracellulare, Legionella, leptospirosis
o Viral: Mumps, rubella, varicella, hepatitis viruses, CMV, EBV, HIV, Coxsackie virus, echovirus, adenovirus
o Parasites: Ascariasis, clonorchiasis, echinococcosis
• Autoimmune: SLE, polyarteritis nodosa (PAN), Crohn’s
• Surgery/trauma
o Manipulation of sphincter of Oddi (e.g. ERCP), post-cardiac surgery, blunt trauma to abdomen, penetrating peptic ulcer
• Hyperlipidemia (TG >11.3 mmol/L; >1000 mg/dL), Hypercalcaemia, Hypothermia
• Emboli or ischaemia
• Drugs/toxins
o Azathioprine, mercaptopurine, furosemide, estrogens, methyldopa, H2-blockers, valproic acid, antibiotics, acetaminophen,
salicylates, methanol, organophosphates, steroids (controversial)
PATHOGENESIS (See Harold Ellis text for more)

Some keywords to use in discussion:
1. Duodenopancreatic reflux (due to damage to ampulla of Vater, whether due to a gallstone or iatrogenic or trauma)
2. Enterokinase (from intestines enters the pancreas due to the reflux and activates the enzymes, that would normally be activated when they
reach the duodenum)
3. Trypsinogen and trypsin (this is first activated, which activates the other pancreatic enzymes)
4. Phospholipase A and lipase (cause cell membrane breakdown as well as fat necrosis)
5. Local autodigestion (due to inappropriate activation of proteolytic enzymes)
6. Systemic autodigestion (Significant amounts of inflammatory oedema, which may contribute to the significant shock that occurs in acute
pancreatitis
8. Multiorgan failure (due to the enzymes and toxic factors released into the systemic circulation)
Severe Acute Pancreatitis (SAP)

• Severe pancreatitis is associated with haemorrhagic necrosis of the pancreas and systemic release of many vasoactive peptides and enzymes,
as well as sequestration of large volumes of fluid within the abdomen.
• Acute lung failure occurs, characterized by increased capillary permeability and reduced oxygen transfer, and the combination of toxins and loss
of circulating fluid results in acute renal failure.
• Several criteria predictive of the development of severe pancreatitis have been identified
• Identification of such high-risk cases enables aggressive intensive management to be instituted at an early stage.
• Nevertheless, severe acute pancreatitis has a mortality of ~25%!
MACROSCOPIC/GROSS PATHOLOGY
Re: Pancreas itself: May have, depending on severity:
§ *Swollen pancreas
§ *Haemorrhagic pancreas
§ *Necrotic pancreas (may become infected (60%))
Also:
§ **Blood-stained peritoneal effusion
§ **White spots of fat necrosis throughout peritoneal cavity – Caused by pancreatic lipase being released and liberating fatty acids and
glycerol from fat. These fatty acids combine with calcium to produce insoluble white calcium soaps (saponification)
CLINICAL FEATURES
History
§ Epigastric pain: Sudden onset, severe epigastric, constant (Remember all foregut structures give epigastric pain!!)
o Can radiate to back - Reason – The pancreas sits on the coeliac plexus. These patients tend to lean forward as they essentially
move pancreas off the plexus
o Pain may improve when leaning forward (Inglefinger’s sign) OR improve on standing
§ Nausea and retching/vomiting
Examination
General
§ Fever: Chemical, NOT due to infection
§ Signs of shock: Tachycardia, cyanosis, altered level of consciousness
rd
o Hypotension/Hypovolemic shock: can lead to renal failure – Due to SIRS AND significant 3 spacing of fluids
§ Signs of respiratory compromise: Respiratory distress/ARDS
§ All above due to an overwhelming systemic inflammatory response - SIRS
o Some mediators: IL-2, 6, 8, TNF
Abdomen
§ Tender rigid abdomen; usually with guarding
§ Abdominal distention from paralytic ileus (due to the surrounding inflammation) (SO ALSO POSSIBLE DECREASED BOWEL SOUNDS)
§ **Jaundice (30% of cases): compression/obstruction of bile duct from oedema of the pancreatic head OR concomitant choledocholithiasis
§ **Cullen’s + Grey-Turner’s + Fox’s sign: In Severe Acute Pancreatitis (SAP) and haemorrhagic pancreatitis, large quantity of blood and
peritoneal fluid secreted. The blood is in the retroperitoneum. Therefore Scarpa’s fascia holds the blood preventing spread to thighs!!
Retroperitoneal haemorrhage results in:
o Grey-Turner’s sign: Right flank ecchymosis - This sign takes 24–48 hours
o Cullen's sign: Peri-umbilical ecchymosis.
o Fox’s sign: Ecchymosis of the inguinal ligament from blood tracking from the retroperitoneum and collecting at the inguinal ligament
*** ALSO, ALL organs can be affected due to SIRS: ***

Lungs
• Pleural effusion features
• Pulmonary oedema à impairment of carbon dioxide and oxygen exchange à paO2 falls
• May see changes of ARDS in x-ray à “Ground-glass appearance”
Kidney
Severe cases
• Tetany: transient hypocalcemia
• Acute respiratory distress syndrome
• Coma
Dr. Roberts: MUST KNOW: SEVERE ACUTE PANCREATITIS (SAP) DEFINITION

• 20% of cases
• Mortality of SAP ranges from 10%-20%
*** MUST KNOW: Defining SAP: Associated with 1 or more of the following:
1. Necrosis of > 1/3 of the pancreas
2. Local complications – Eg. Pseudocysts, abscesses
3. Distant organ failure
INVESTIGATIONS
A. BLOOD/LAB INVESTIGATIONS
1. CBC: Moderate leucocytosis (predominantly neutrophils) à Also helps to assess severity (Ranson’s criteria)
2. U&Es: Elevated urea and creatinine reflecting pre-renal renal failure
3. LFTs: Bilirubin, ALP, GGT may be elevated due to obstruction for reasons mentioned above (can say it shows an obstructive picture)
4. Calcium: Hypocalcemia due to fat saponification
5. Serum pancreatic enzymes

a. Increased Amylase (Usually significantly elevated [5-fold or more] in the ACUTE phase. **Normalizes after 2-3 days!!!
(Urinary amylase elevated for longer period (~2 weeks) and useful for later presentations!!)
i. When serum amylase > 3-5x normal, the cause is almost always pancreatitis OR renal disease!
ii. Dr. Roberts: This is NON-SPECIFIC. Looking for a significant elevation - Usually over 1000 (Some say 400)
iii. Sensitive, not specific
b. Increased Lipase
i. Higher sensitivity and specificity!! AND
ii. Stays elevated longer!!
6. Urinary amylase
7. Blood glucose often elevated
B. IMAGING à CT SCAN WITH IV CONTRAST = Most useful for diagnosis and prognosis
1. Abdominal x-ray: Cannot definitively diagnose acute pancreatitis Chest x-ray

a. “Sentinel loop” (dilated proximal jejunum – most common AXR sign!!!), a. Acalectasis
o
b. “Colon cut-off sign” (Dilated transverse colon 2 to colonic spasm) b. Pleural effusion
c. Elevated hemidiaphragm
c. Calcification
d. BUT, AXR is important to RULE OUT OTHER DIFFERENTIALS where CT UNAVAILABLE
2. CT scan with IV contrast: useful for DIAGNOSIS and PROGNOSIS because contrast is seen only in viable pancreatic tissue. Non-
viable areas can be biopsied percutaneously to differentiate sterile from infected necrosis. Indicated if diagnosis is unclear based on clinical
presentation and amylase levels
Dr. Roberts: This is investigation of choice in AP. 4 reasons:
a. *Diagnostic: Can see the oedematous pancreas AND to exclude other differentials
b. *Assess severity and prognostication (CTSI)
c. *Detect complications (e.g. pseudocyst, abscess, phlegmon)
d. *Guide interventional procedures e.g. Drainage of abscess, biopsy (**to differentiate sterile from infected necrosis)
§ Can't just request normal CT scan. Need a contrast enhanced CT scan
3. U/S: Useful for evaluating biliary tree (67% sensitivity, 100% specificity) [identify gallstones and CBD dilatation]
4. ERCP or MRCP If cause uncertain, assess for duct stone, pancreatic or ampullary tumour, pancreas divisum.
MUST KNOW!!!: Causes of Increased Amylase and Lipase

Causes of Increased Serum Amylase
A. Pancreatic disease
§ Pancreatitis, pancreatic duct obstruction (e.g. ampullary cancer), pseudocyst, abscess, ascites, trauma, cancer
B. Non-pancreatic abdominal disease (almost any surgical abdominal condition!)

§ Biliary tract disease, bowel obstruction/ischemia, perforated or penetrating ulcer, ruptured ectopic pregnancy, aneurysm, chronic liver
disease, peritonitis
C. Non-abdominal disease
§ Cancer (lung, ovary, esophagus, etc.), salivary gland lesions, renal transplant/insufficiency, burns, ketoacidosis
Causes of Increased Serum Lipase

A. Pancreatic disease: same as above
B. Non-pancreatic abdominal disease (mild elevations only): same as above
C. Non-abdominal disease
§ Renal failure
PROGNOSIS
PROGNOSTIC INDICATORS
§ *** Mainly to determine SAP – MANY systems developed. Most commonly used:
§ *** Once you are diagnosed with severe acute pancreatitis à ADMIT TO ICU!!
CLASSIFY: Clinical+Biochemical vs. CT-based
1. Ranson criteria: One of the first. See section below. Should know this one!!
§ Know “GALAW” and “C HOBBS” (see below)
§ Was originally developed for Gallstone pancreatitis only. BUT the current one is for NON-GALLSTONE
§ Limitations:
i. Problem is that this takes 48 hours to obtain the score
ii. Also a one-time score. Only takes a snapshot in one moment of the film
2. Glasgow system
3. APACHE II (Acute Physiologic And Chronic Health Evaluation 2)

§ Was NOT developed for pancreatitis
§ Can use for anybody with any disease condition. Eg. Used commonly in ICU
§ Takes into account all the organ systems that can be affected by any disease condition
§ Advantage: More accurate than Ranson score. Can be done at any point at any time
§ Disadvantages: Problem with APACHE is that it is cumbersome and difficult to remember all. (There are online calculators for this)
o Also has parameters that require lab measurement in hospital setting
§ Score of 8 or more indicates severe
Assessing Severity with CT
1. Historical information: Balthazar score was the first CT staging system -- described in the 80s -- Did not include necrosis. Hence a new
scoring system was developed:
2. *** CT Severity Index (CTSI)
Other above MBBS level severity assessment tools:

§ BISAP: Less parameters but still need a lab
§ HAPS:
Ranson’s Criteria: Prognostic Indicator of Mortality in Pancreatitis NOT due to Gallstones (GALAW and C HOBBS)
At Admission During First 48 h
G: Blood Glucose >11 mmol/L (>200 mg/dL) (with no history of C: Serum Calcium <2 mmol/L (<8 mEq/L)
hyperglycemia) H: Hematocrit drop >10%
A: Age >55 O: Arterial PO2 <60 mmHg
L: Serum LDH >350 IU/L B: Base deficit >4 mmol/L (>4 mEq/L)
A: AST >250 IU/L B: BUN rise >1.8 mmol/L (>5 mg/dL)
9
W: WBC >16 x 10 /L S: Estimated fluid Sequestration >6 L
§ Difficult course if 2 criteria present

§ High mortality if ≥3 criteria present
§ ≤2 criteria = <5% mortality

§ ≥7 criteria = >99% mortality
§ Multiple other prognostic indices available, more accurate than Ranson but difficult to remember (e.g. APACHE)
TREATMENT
§ First confirm the diagnosis (amylase/CT) and assess severity (Ranson’s/Apache II)
§ Severe cases must be managed in ICU due to high mortality from pulmonary, renal and abdominal complications
Treatment is initially and mainly non-operative
1. NPO: Resting the pancreas by removing stimuli for secretion: NGT: Nasogastric aspiration is started IF the patient is vomiting.
2. IV fluid replacement with colloid or blood transfusion, to treat shock AND establish a diuresis. In less severe cases, electrolyte and water
replacement alone
a. Monitoring: U Cath or CVP: Beware third spacing of fluid, monitor urine output carefully
3. Nutritional support: Enteral vs. Parenteral
a. NJT or TPN: TPN may be instituted early in severe cases. Good evidence that nasojejunal feeding may be superior to TPN in the
absence of an ileus. Enteral also cheaper
b. An enteral feeding route is preferred. Feeding via nasojejunal tube. REASON for jejunal: To give “POST-PYLORIC” feeds. This will
avoid stimulating the pancreas as food gets in below the level of the duodenum and sites that will stimulate the activity of pancreas
c. Enteral always preferred when possible. Contraindications to enteral feeding in SAP:
i. Gut failure
ii. Prolonged ileus
iii. Complex pancreatic fistulae
d. Difference between a nasogastric and nasojejunal tube:
i. Major difference: A nasojejunal tube is a weighted tube. Has a piece of metal at the tip. If a nasogastric was placed in
the intestine it would be ejected by reverse peristalsis.
4. Analgesia: traditionally with pethidine to avoid the sphincter spasm associated with morphine.
5. Antibiotics: CONTROVERSIAL EXCEPT IN DOCUMENTED INFECTION (e.g. co-amoxiclav) commenced in severe cases and if the
pancreatitis is associated with gallstones. Prophylactic antibiotics NOT shown to reduce infected necrosis or mortality in acute necrotizing
pancreatitis
a. Aspirate necrotic areas of pancreas to diagnose infection; drain if infected
6. Prophylaxis against gastric erosions with sucralfate or an H2-receptor antagonist (e.g. ranitidine) or PPI (e.g. omeprazole).
---
7. ± Endoscopic sphincterotomy performed early in the admission à MAY be indicated in severe gallstone pancreatitis; dilated common
bile duct on ultrasound associated with deranged liver function tests also represents an indication for urgent ERCP and sphincterotomy.
8. NB: Re: Stopping progression of damage: Attempts at treatment with drugs that reduce pancreatic enzyme activation (e.g. aprotonin) or
secretion (e.g. probanthine or atropine) are of no proven benefit
9. Close monitoring and follow clinically and CT/ultrasound to exclude complications
10. Treat complications

---
11. Chief role of surgery is to drain fluid/abscesses or excise necrotic tissue (operative debridement/“necrosectomy”) in the case of
infected pancreatic necrosis (try to delay for >2 wk to allow demarcation between viable and necrotic tissue!!!). Surgery avoided during acute
attack
12. In the case of gallstone pancreatitis à cholecystectomy should be performed as soon as the patient recovers from the acute attack,
preferably during the same admission (3 to 5 days after pancreatic inflammation resolves)
THEN: Prevention of recurrence of acute pancreatitis:
1. Abstinence from alcohol

2. Cholecystectomy for the prevention of recurrent gallstones
a. Perform a "same admission cholecystectomy" where possible after the first episode of acute pancreatitis. But MUST assess the
gall bladder for stones first!!!
MUST KNOW: Why should early cholecystectomy be performed on patients with gallstone pancreatitis?
§ Pancreatitis will recur in ~33% of patients within 8 weeks (so always perform early interval cholecystectomy and IOC in 3 to 5
days when pancreatitis resolves)
COMPLICATIONS
LOCAL vs. SYSTEMIC
LOCAL
1. Pseudocysts and peripancreatic collections: follow if asymptomatic, drain if symptomatic or growing
*Pseudo cyst = Persistent encapsulated fluid collection after ~5 weeks of acute pancreatitis
§ Not a true cyst (hence, pseudo) àBecause it has no epithelial lining

§ “Pseudo” because: Wall is formed by inflammatory fibrosis, NOT epithelial cell lining
§ Formed secondary to pancreatic duct disruption
§ Patients complain of persistent pain, vomiting, abdominal mass and weight loss
§ There is persistent elevated amylase
§ Ultrasound is very good for diagnosis

§ CT scan is excellent as delineates anatomical site and relation to surrounding structures
§ ERCP will demonstrate duct disruption – can use stenting
§ MRCP becoming favoured
§ Angiography if there is bleeding into cyst à Perform embolization

o May rupture, haemorrhage, pancreatic fistula/ascites, infection and abscess
§ Most acute ones resolve (~50%)

§ If persistent > 6 weeks and > 6 cm àthen surgery- Cystogastrostomy or cystojejunostomy
§ If bleeding à Angiography with embolization
§ Endoscopic drainage
§ Percutaneous drainage
§ Management: Observation OR Drain: choice of endoscopic, percutaneous under radiological guidance, or surgical
2. Infected necrosis/abscesses: antibiotics + percutaneous drainage, endoscopic vs. Surgical
3. Bleeding: (1) gastric varices if splenic vein thrombosis, (2) pseudoaneurysm of vessels in areas of necrosis, especially splenic artery, (3)
duodenal ulcer related to compression of duodenum by enlarged pancreas
4. Splenic/mesenteric/portal vein rupture or thrombosis: No effective therapy described, anticoagulation not proven, hazardous
SYSTEMIC
1. Hypovolaemia and shock
2. Coagulopathy/DIC
3. Renal Failure
4. Respiratory failure (ARDS)
5. Rare: diabetes mellitus – from severe attack with pancreatic necrosis
6. Severe hypocalcaemia
7. Hyperglycaemia
Indications for surgery in acute pancreatitis

• Unclear diagnosis
• Deterioration or Failure to improve
• Infective necrosis or pancreatic abscess
• Pseudocysts
• Cholecystectomy and duct drainage
Dr. Roberts: Complications and their management
1. PANCREATIC NECROSIS (STERILE VS. INFECTED)

• *** Routine use of prophylactic antibiotics in pancreatic necrosis is NOT recommended ***
• ALSO: Not any antibiotic can penetrate pancreas
• Carbapenems can penetrate
** If there are signs of an infected necrosis à Need culture!!

• Do a CT-guided fine-needle aspiration.
• Then start broad-spectrums until results return à then culture-directed abx when results available
• Must give IV abx for infected necrosis
*** Surgical intervention is NOT done for sterile necrosis!!!!!!!

• Only recommended for infected necrosis OR persistent SAP
• Called a necrosectomy
• NOTE WELL: Reason this is not commonly done is because of risk of pancreatic insufficiency from excess resection of pancreatic tissue
and even total pancreatectomy
• MUST LEAVE DRAINS after à Cannot leave the fluid with the active enzymes in the patient!!!
Surgical Recall Summary:

How is the diagnosis made?
§ Abdominal CT with IV contrast; dead pancreatic tissue does not take up IV contrast and is not enhanced on CT scan (i.e., doesn’t “light up”)
What is the treatment:

§ Sterile? Medical management
§ Suspicious of infection? CT-guided FNA
§ Toxic, hypotensive/confirmed infection? Operative débridement
1
Consequences of removal of the pancreas/total pancreatectomy :
• Brittle diabetes:
• Etc.
• Consider everything produced by the pancreas
2. PSEUDOCYSTS
o Fluid collection in the lesser sac bound by stomach in front and pancreas behind
o Most are asymptomatic: Most < 6 cm will spontaneously resolve (~50%). Rarely require surgery
o > 6 cm may require intervention:
Options:
1. Percutaneous aspiration: Problem with this is it is usually a temporary solution as the fluid continues to refill. Even if a drain is placed,
still has risks associated with passage of the enzyme rich pancreatic fluid à May form fistulae and…
2. Internal drainage
a. Endoscopically
b. Surgically: Open or laparoscopic: May anastomose them to the stomach or to the jejunum and allow them to drain
o Called cystogastrostomy, cystojejunostomy, cystoduodenostomy
3. Resection
ALSO: Biopsy of the cyst wall to rule out a cystic carcinoma, which is a differential diagnosis (e.g., cystadenocarcinoma)
Complications of pseudocysts
§ Compresses stomach and other viscera – hinders filling and causes easy satiety
§ Bleeding into cavity – Blood vessels of post-abd wall
§ Sepsis
SURGICAL TUTOR ON PSEUDOCYSTS

Pseudocysts
§ Fibrous walled peri-pancreatic fluid collection
§ Present for more than 1 month
§ No epithelial lining. Fluid has high amylase content
§ Acute fluid collections are not pseudocysts
§ 35% patients with pancreatitis develop peri-pancreatic fluid collections
§ More than 50% resolve spontaneously over a 3 month period
§ Complication rate increases after 6 weeks
§ Diagnosis may be suggested by persistent elevation of serum amylase
§ Planned intervention at 6 weeks
Classification of pseudocysts
§ Type 1 - normal duct anatomy. No fistula between duct and cyst
§ Type 2 - abnormal duct anatomy - No fistula
§ Type 3 - abnormal duct anatomy and fistula
Investigation of pseudocysts
§ Ultrasound will allow assessment of changes in the size of the cyst
§ Endoscopic ultrasound increasingly used
§ CT to define relationship to adjacent organs
§ ERCP to define duct anatomy
3 Treatment options
A. Percutaneous drainage
§ Ultrasound or CT guided
§ 80% successful in type 1 cyst
§ Less successful if fistula to duct present
§ Occasionally associated with pancreatic abscess or fistula
B. Endoscopic drainage + insertion of pigtail catheter

§ Transpapillary stent via ERCP (pseudocyst must communicate with pancreatic duct)
§ or transmural
C. Surgical/Operative drainage
§ Cystogastrotomy
§ Roux Loop Cystojejunostomy
§ Allows adequate internal drainage
§ Biopsy cyst wall to exclude cystadenocarcinoma
§ Mortality similar to percutaneous drainage ( 5%)
§ Lower recurrence rate (approximately 5 vs. 20%)
Surgical Recall CRITICAL points!!:

What is the waiting period before a pseudocyst should be drained?
• It takes 6 weeks for pseudocyst walls to “mature” or become firm enough to hold sutures and most will resolve in this period of time if they
are going to
What is the treatment for pseudocyst with bleeding into cyst?

• Angiogram and embolization
What is the differential diagnosis of a pseudocyst?

• Cystadenocarcinoma, cystadenoma
What must be done during a surgical drainage procedure for a pancreatic pseudocyst?
• Biopsy of the cyst wall to rule out a cystic carcinoma (e.g., cystadenocarcinoma)
What is the most common cause of death due to pancreatic pseudocyst?

• Massive haemorrhage into the pseudocyst
A sentinel loop is a sign seen on an X-ray that indicates localized ileus from nearby inflammation. Simply put, it is the dilatation of a segment of large or small intestine.
An isolated distended loop of bowel is seen near the site of injured viscus or inflamed organ. This loop is called a "sentinel loop." The local distention of that intestinal loop
is due to local paralysis and accumulation of gas in the intestinal loop.
In acute pancreatitis, the sentinel loop is usually seen in left hypochondrium, while in acute cholecystitis, it is seen in the right hypochondrium. In acute appendicitis, the
sentinel loop is seen in right iliac fossa.
The colon cut-off sign describes gaseous distension seen in proximal colon associated with with narrowing of the splenic flexure in cases of acute pancreatitis.
This appearance results from inflammatory process extending from the pancreas into the phrenicocolic ligament via the transeverse mesocolon
Prognosis for patients living without a pancreas is very poor. Without the endocrine hormones (glucagon, insulin, somatostatin, and pancreatic
polypeptide) or the exocrine enzymes (trypsin, chymotrypsin, pancreatic lipase and amylase) a patient would be on a lengthy regimen of medications
and would be severely limited in his or her diet
Chronically patients have an increased daily caloric requirement, not wholly explained by moderate steatorrhoea. Despite persistent
malabsorption, deficiencies in fat-soluble vitamin, magnesium, and trace element serum levels can be prevented in most patients. Pancreatogenic
diabetes is characterized by (1) absence of the major glucoregulatory hormones insulin and glucagon, (2) instability, and (3) frequent hypoglycemia,
with the latter parameters improving with rigorous home glucose monitoring
Pathology of Acute Pancreatitis – From Harold Ellis Text (Inserted by Anggelos)
Acute pancreatitis differs from other inflammatory conditions because of the

autodigestion that may result from liberation of digestive enzymes. The pancreas is normally
protected from autodigestion by storing its enzymes in intracellular zymogen granules before
secreting them as proenzymes. Trypsin, for example, is secreted as trypsinogen and
converted to trypsin by the action of enterokinase in the gut. Trypsin itself then cleaves other
proenzymes, thus activating them. One such enzyme is phospholipase A which, in
pancreatitis, is involved in cell wall damage and fat necrosis along with pancreatic lipase.
The mechanisms initiating autodigestion are multiple. Duodenopancreatic reflux is an

important factor that may occur as a result of injury to the papilla following endoscopic
cannulation, trauma or surgery in this region, or as a result of damage to the sphincter
owing to the recent passage of a stone (hence the strong association of pancreatitis and
biliary calculi). Duodenal fluid containing enterokinase then refluxes into the duct, activating
the pancreatic proenzymes. Duodenal reflux can be shown experimentally to produce
pancreatitis, and may be a common factor that underlies many of the aetiological associations
mentioned above.
As inflammation proceeds, local infarction may occur as arterioles thrombose, and

more proenzymes leak out of the necrotic cells to be activated. Once started, pancreatitis can
be rapidly progressive, with widespread autodigestion not only confined to the pancreas. As
inflammation and autodigestion progress, liquefying necrotic material and inflammatory
exudate collect in the lesser sac. This fluid, walled off by the stomach in front and necrotic
pancreas behind, is the pancreas pseudocyst, and commonly appears from day 10 onwards.
General Surgery
Pancreatic Cancer Notes – ALSO ADD A SECTION ON PERIAMPULLARY CANCERS – See the lecture from the good lectures folder
Source: Sabiston, Toronto, (LAST PAGE OF THIS DOC HAS VERY BRIEF ANATOMY SUMMARY FROM SURGICAL RECALL)
June 2014
*** PDAC = Pancreatic Ductal Carcinoma***

INCIDENCE
§ 9th most common cancer
§ 4th most common cause of cancer death
§ Mean age = 72
§ Males slightly more than female (M > F, 1.3:1)
§ *Dismal prognosis: < 5% 5-year survival
§ ~90% die in 1 year of diagnosis
SITES (Harold Ellis Lecture Notes):

§ 60% head (AND 1/3 of those in head are periampullary (so 20%))
§ 25% body
§ 15% tail
RISK FACTORS
A. Non-modifiable
1. Risk increases with age - Mean age 72 years
2. Males slightly more than female (1.3:1)
3. Hereditary forms (see below) – (But sporadic more common!)
B. Modifiable/Environmental
1. Smoking - is the most notable risk factor: 2-5x increased risk, most clearly established risk factor
***Controversial risk factors:
§ Heavy alcohol use
§ Chronic pancreatitis
§ Diabetes
§ Obesity
§ Partial gastrectomy, cholecystectomy
§ High fat/low fibre diets
NOTE WELL: Hereditary forms

1. Lynch syndrome (HNPCC)
2. FAP-APC gene (chromosome 5q21)
3. Peutz-Jeghers syndrome
4. BRCA 2
5. Familial pancreatitis
6. Cystic fibrosis - CFTR gene
PATHOGENESIS OF SPORADIC
Like many other cancers, a sequential pathway observed from pancreatic intraepithelial neoplasia (PanIN) to invasive cancer (PDAC)
PATHOLOGY
§ Ductal adenocarcinoma: Most common type (75-80%); exocrine pancreas
§ Intraductal papillary mucinous neoplasm (IPMN)
§ Other: Mucinous cystic neoplasm (MCN), acinar cell carcinoma, islet-cell (insulinoma, gastrinoma, VIPoma, glucagonoma, somatostatinoma)
CLINICAL PRESENTATION
PRICIPLES: DEPENDS ON SITE. Periampullary and head vs. body and tail
Classify: Features due to 1. Primary mass 2. Direct spread 3. Distant metastasis 4. Paraneoplastic syndromes 5. Constitutional symptoms
1. Local effects of primary mass:

• Defining presenting symptom for periampullary tumours is jaundice!
o “Painless unremitting jaundice” frequently described
o **However a significant number present with pain and jaundice - Arising in epigastrium and radiating to the back
• Weight loss is very common presentation!! - Affects > 50%

• For body and tail: Vague mid-epigastric pain and weight loss more significant at presentation. Tend to present later and usually
inoperable!! < 10% have jaundice!!!
Physical exam - Often unremarkable aside from jaundice

• Courvoisier’s sign: Palpable, distended gall bladder – ONLY in 1/3 of patients!!!!!
o First described by Swiss surgeon Courvoisier in 1890
o He noted that choledocholithiasis is commonly associated with a shrunken, fibrotic gall bladder
2. Symptoms and signs of spread:
1. Direct spread
§ CBD - Jaundice
§ Duodenum - Occult bleeding or obstruction
§ Portal vein - Portal HTN and ascites
§ IVC – Bilateral leg oedema
2. Lymphatic
§ Adjacent lymph nodes
§ Widespread lymphatic spread:
o Virchow’s node - Left supraclavicular lymphadenopathy
o Sister Mary Joseph node - Periumbilical lymphadenopathy
3. Haematogenous
§ Liver (hepatomegaly, ascites) and then lung
§ Ascites
4. Transcoelomic
§ Peritoneal seeding
§ In these cases a rectal tumour may be palpable on DRE - Blumer's shelf
3. Paraneoplastic syndrome
§ Trousseau’s syndrome: Migratory thrombophlebitis
4. Constitutional symptoms
§ Fever, weight loss, night sweats
INVESTIGATIONS
GENERAL BLOODWORK vs. SPECIFIC IMAGING
A. LAB EVALUATION
1. CBC – Anaemia
2. LFTs including coagulation profile (esp. PT)
3. Tumour markers are appropriate at initial evaluation:
1. CA 19-9 (Carbohydrate antigen 19-9) – most sensitive for PDAC
• 79% sensitive, 82% specific
2. CEA
3. Alpha fetoprotein
4. Just to note: Serum amylase is very rarely elevated!!!
B. IMAGING STUDIES
1. Multi detector CT scan with contrast is investigation of choice for suspected pancreatic cancer. MUST KNOW uses:
a. *Allows accurate determination of level of biliary obstruction
b. *Detect regional or metastatic disease (nodes and vasculature + liver and lung)
c. *Defines the operability of the tumour
d. *Can guide fine needle aspiration
• *** For suspected periampullary pathology a TRIPHASIC CT (noncontrast, arterial and portal venous) with 3 mm slicing should
be routine. Reason: Widely available and excellent sensitivity (85%)
*** NOTE VERY WELL: Following CT scan, patients classified into:

1. Resectable (20%)
2. Borderline resectable
3. Unresectable
*** Resectable = No evidence of SMV or portal vein involvement and preserved fat plane around the SMA and coeliac artery branches ***
2. ERCP frequently used because of its ability to perform biopsy and to palliate jaundice
• “Double-duct sign” classic – Dilatation of CBD and main pancreatic duct
• (Palliative biliary stenting. Can also stent via PTC)
• *** BUT NOTE WELL: ERCP should be reserved for cases needing therapeutic or palliative intervention as other imaging
modalities provide superior diagnostic abilities without the invasiveness!!!!
3. MRCP if detailed assessment of luminal pancreaticobiliary anatomy required
4. EUS becoming more widely used

§ Probably most important to provide tissue diagnosis by use of FNA especially in patients undergoing neoadjuvant chemo (EUS-FNA)
§ Has ability to STAGE: assess regional lymph nodes and local extent of spread
§ BUT NOTE WELL: Has NOT been shown to provide any significant benefit over CT alone despite this
§ Ellis: EUS is a "key step in defining operability of tumour"
5. Abdominal ultrasound can evaluate CBD BUT CANNOT GIVE ADEQUATE VIEW OF PANCREAS DUE TO DUODENAL GAS!!!
STAGING (MUST ACTUALLY KNOW)

AJCC-TNM
§ T1 - Tumour limited to pancreas, 2 cm or smaller
§ T2 - Tumour limited to pancreas, but > 2 cm
§ T3 - Extends beyond pancreas but WITHOUT coeliac axis or SMA involvement
§ T4 - Extends beyond pancreas WITH coeliac axis or SMA involvement (i.e. unresectable primary)
§ (N = 0 or 1. M = 0 or 1)
*** NOTE WELL: Individuals with stage 3 (T4) or stage 4 (mets) are NOT candidates for immediate surgery
*** NOTE VERY WELL: Following CT scan, patients classified into:

1. Resectable
2. Borderline resectable
3. Unresectable
*** Resectable = no evidence of SMV or portal vein involvement and preserved fat plane around the SMA and coeliac artery branches ***
TREATMENT
Depends on stage and may be CURATIVE vs. PALLIATIVE
Based on Operability and Resectability (Consider size, location, vessel involvement, spread)
A. CURATIVE
Surgical resection is the only potentially curative treatment. Only for stage I and II
+ Adjuvant chemotherapy (Gemcitabine + FOLFIRINOX)
A. Resectable (20% of pancreatic cancer)
§ No involvement of liver, peritoneum or vasculature (hepatic artery, coeliac axis, SMA, SMV, portal vein, IVC,
aorta), no distant metastasis
§ Whipple procedure (pancreaticoduodenectomy) for cure – 5% mortality
§ If carcinoma of mid-body and tail of pancreas: Distal pancreatectomy ± splenectomy, lymphadenectomy
B. Borderline resectable
§ Tumours that ABUT the SMA, hepatic artery, celiac artery, SMV, portal vein,
***BUT NOTE WELL (Surgical Recall):

***Is portal vein or SMV involvement an absolute contraindication for resection?
§ NO—can be resected and reconstructed with vein interposition graft at some centers
Other mentions:
• MUST KNOW: Adjuvant chemotherapy widely accepted – 5-FU based regimen (FOLFIRINOX) +/- GEMCITABINE
improves survival
• Neoadjuvant chemotherapy with or without radiation for pancreatic ca is becoming increasingly common
o Despite many benefits and rationales however, no studies have shown an improvement in overall survival for patients who receive
neoadjuvant
• Usefulness of radiotherapy highly controversial
B. PALLIATIVE
For non-resectable (palliative à relieve pain, obstruction)
Most body/tail tumours are not resectable (due to late presentation)
Relieve biliary/duodenal obstruction with endoscopic stenting or double bypass procedure (choledochoenterostomy + gastroenterostomy)
MAIN POINT: Essentially, can either BYPASS or STENT both the CBD obstruction AND/OR the duodenal obstruction
1. Interventional radiology
2. Endoscopic (Stenting)
a. CBD: Via either ERCP or PTC (Self expanding metal stents > plastic stents)
b. Duodenal obstruction can now also be treated by endoscopic stenting
3. Surgical:
Bypass operations, single vs. double
a. For bile flow: Choledochojejunostomy
b. Duodenal bypass: Gastrojejunostomy
4. Severe pain: Opiates, splanchnicectomy, coeliac blockade
5. Chemotherapy (gemcitabine + FOLFIRINOX), radiotherapy – only slightly increase survival
SUMMARY
CURATIVE (15-20%) PALLIATIVE (80-85%)

Goals: 1. Palliate obstruction & 2. Palliate pain
A. HEAD/PERIAMPULLARY 1. Endoscopic stents

Whipple’s Procedure (Pancreaticoduodenectomy) a. Bile duct: Via ERCP or PTC (Metal > Plastic)
(~25% complication rate) b. Duodenum: Endoscopic stenting
Take: (Self-expanding Nitinol stents preferred!!)

1. Distal stomach (sometimes) (Nitinol is a metal alloy of NIckel and TItanium)
2. Entire duodenum
2. Bypass (Single or double. Double = both)
3. Pancreatic head and neck a. Bile duct: Choledochojejunostomy
b. Duodenum: Gastrojejunostomy
4. Common bile duct
5. Gallbladder 3. Pain
a. Opiates
Then reconstruct/reanastomose: b. Coeliac plexus block
1. Gastrojejunostomy
2. Choledochojejunostomy 4. Chemo: Gemcitabine + FOLFIRINOX
3. Pancreaticojejunostomy (Reimplant pancreatic duct into jejunal
roux loop)
B. MID-BODY AND TAIL
Distal pancreatectomy ± splenectomy, lymphadenectomy
Followed by ADJUVANT CHEMO WITH FOLFIRINOX +/-

GEMCITABINE
PROGNOSIS
§ Most important prognostic indicators are lymph node status, size > 3 cm, perineural invasion (invasion of tumour into microscopic nerves of
pancreas)
§ Overall 5-yr survival is 1%
§ 20% 5-yr survival following resection
§ Median survival for unresectable disease: 8-12 mo if locally advanced, 3-6 mo if metastatic
Know about Whipple’s procedure – SEE HAROLD ELLIS DESCRIPTION
***Why must the duodenum be removed if the head of the pancreas is removed?
§ They share the same blood supply (gastroduodenal artery)
What maneuver is used to mobilize the duodenum and pancreas and evaluate the entire pancreas?
§ Kocher maneuver: Incise the lateral attachments of the duodenum and then lift the pancreas to examine the posterior surface
Steps of a Whipple Resection

(Pancreaticoduodenectomy):
1. Assessment of metastatic disease (all peritoneal surfaces)
2. Mobilization of the duodenum and head of the pancreas with identification of the superior mesenteric vein
3. Mobilization of the stomach and proximal duodeum, transection of the stomach or proximal duodenum
4. Dissection of the hepatoduodenal ligament with skeletonization of the porta hepatis
5. Cholecystecomy and division of the bile duct
6. Mobilization and division of the proximal jejunum
7. Transection of the pancreatic neck and division of any remaining attachments
8. Reconstruction of gastrointestinal continuity: pancreaticojejunostomy, hepaticojejunostomy, gastro(duodeno)jejunostomy
Puestow procedure: Side-to-side anastomosis of the pancreas and jejunum (pancreatic duct is filleted open) [NB this is NOT what the above image
demonstrated – the above image shows and end to end anastomosis of pancreas and jejunum)
BRIEF ANATOMY SUMMARY
The 2 pancreatic ducts are:

1. The main duct of Wirsung
2. The accessory duct of Santorini
Blood supply to the head of pancreas:

1. Coeliac trunk à gastroduodenal à
a. Anterior superior pancreaticoduodenal artery
b. Posterior superior pancreaticoduodenal artery
2. Superior mesenteric artery à

a. Anterior inferior pancreaticoduodenal artery
b. Posterior inferior pancreaticoduodenal artery
3. Splenic artery à
a. Dorsal pancreatic artery
General Surgery
Acute GI Haemorrhage
Source: Sabiston
INTRODUCTION
Can originate from almost any region of the GI tract, including the pancreas, liver, and biliary tree.
Slightly more common in men than women
Management of these patients is frequently multidisciplinary, involving emergency medicine, gastroenterology, intensive
care, surgery, and interventional radiology.
• The importance of EARLY SURGICAL CONSULTATION in the care of these patients cannot be
overemphasized
Ultimately, 5% to 10% of admitted patients require operation intervention
Most patients with an acute GI hemorrhage stop bleeding spontaneously
> 5% mortality. Significantly higher in those initially hospitalized for other reasons
Haemorrhage can originate from ANY REGION OF THE GI TRACT and is typically classified based on its location
relative to the ligament of Treitz.
• NOTE WELL: Upper GI haemorrhage (from proximal to the ligament of Treitz) accounts for > 80% of
cases of acute bleeding
NOTE:
• Peptic ulcer disease and variceal haemorrhage are the most common causes of UGIB
• Diverticula and angiodysplasias are the most common causes of LGIB (Most lower GI bleeding is from the
colon)
o In < 5% of patients, the small intestine in responsible!!!
Obscure bleeding is defined as haemorrhage that persists or recurs after negative endoscopy.
Attempts to localize the source should NEVER precede appropriate resuscitative measures
APPROACH TO THE PATIENT

Rapid initial assessment
• Resuscitation is initiated with stabilization of the patient’s hemodynamic status and the establishment of a means
for monitoring ongoing blood loss.
• A careful history and physical examination should provide clues to the cause and source of the bleeding
• Specific investigation should proceed to refine the diagnosis.
INITIAL ASSESSMENT
ABCs: Adequacy of the patient’s airway and breathing take first priority. Once these are ensured, the patient’s hemodynamic
status becomes the dominant concern
Continuous reassessment of the patient’s circulatory status determines the aggressiveness of subsequent evaluation and
intervention
Severity of the haemorrhage can be generally determined based on simple clinical parameters.
Hypotension (systolic blood pressure < 90 mm Hg in the supine position)
• In patients without shock, postural changes should be elicited by allowing the patient to sit up with his or her
legs dangling for 5 minutes.
• A fall in DBP of > 10 mm Hg OR an **elevation of the pulse of > 20 beats/min again reflects at least a 20%
blood loss.
The haematocrit (PCV) is NOT useful for assessing the degree of haemorrhage in the acute setting because the
proportion of red blood cells and plasma initially lost is constant.
• The haematocrit level does not fall until plasma is redistributed into the intravascular space and resuscitation with
crystalloid solution is begun.
***Similarly, the absence of tachycardia may be misleading; some patients with severe blood loss may actually
have bradycardia secondary to vagal slowing of the heart.
• Hemodynamic signs are less reliable in older patients and patients taking beta blockers.
RESUSCITATION
The more severe the bleeding, the more aggressive the resuscitation.
• The single leading cause of morbidity and mortality in these patients is multiorgan failure related to inadequate initial or
subsequent resuscitation. Intubation and ventilation should be initiated early if there is any question of respiratory
compromise.
In patients with evidence of hemodynamic instability or those in whom ongoing bleeding is suspected, two large-bore
IV lines should be placed, preferably in the antecubital fossae!.
• Unstable patients should receive a 2-liter bolus of crystalloid solution, usually lactated Ringer’s, (which
most closely approximates the electrolyte composition of whole blood. The response to the fluid resuscitation should be
noted)
Blood should immediately be sent for:

1. Group and crossmatch,
2. Hematocrit,
3. Platelet count,
4. Coagulation profile,
5. Routine chemistries, and liver function tests.
A Foley catheter should also be inserted for assessment of end-organ perfusion.

• In older patients and patients with significant cardiac, pulmonary, or renal disease, placement of a central venous
or pulmonary artery catheter should be considered for closer monitoring
Decision to transfuse blood depends on the response to the fluid challenge, age of the patient, whether concomitant
cardiopulmonary disease is present
• Hematocrit may take 12 to 24 hours to equilibrate fully
• In general, the hematocrit should be maintained > 30% in older adults and above 20% in young,
otherwise healthy patients.
Similarly, the propensity of the suspected lesion to continue bleeding or rebleed must play a role in this decision. For example,
esophageal varices are likely to continue to bleed and transfusion might be considered earlier than if a Mallory-Weiss tear, which has a
low rebleeding rate, is considered to be the culprit. In general, packed red blood cells are the preferred form of transfusion although
whole blood, preferably warmed, may be used in scenarios of massive blood loss
HISTORY AND PHYSICAL EXAMINATION
Obviously, the characteristics of the bleeding provide important clues. The time of onset, volume, and frequency are
important in estimating blood loss.
Hematemesis, melena, and hematochezia are the most common manifestations of acute hemorrhage.
• Hematemesis is the vomiting of blood and is usually caused by bleeding from the upper GI tract although, rarely,
bleeding from the nose or pharynx can be responsible.
o It may be bright red or older and therefore take on the appearance of coffee grounds.
• Melaena, the passage of black, tarry, and foul-smelling stool, generally suggests bleeding from the upper GI tract
o Although the melanotic appearance typically results from gastric acid degradation which converts
haemoglobin to haematin, and from the actions of digestive enzymes and luminal bacteria in the small
intestine, blood loss from the distal small bowel or right colon may have this appearance,
particularly if transit is slow enough.
o NOTE: Melena should not be confused with the greenish character of the stool in patients on iron
supplements.
o **One way to distinguish these two is by performing a guaiac test, which tests negative in those on iron
supplementation.
• Hematochezia refers to bright red blood from the rectum that may or may not be mixed with stool
Medical history may provide clues to the diagnosis:
• Antecedent vomiting may suggest a Mallory-Weiss tear, whereas weight loss raises the specter of malignancy.
• Antecedent epigastric distress may point to a peptic ulcer
• Previous aortic surgery suggests the possibility of aortoenteric fistula.
• A history of liver disease prompts a consideration of variceal bleeding
Medication use may also be revealing:

• A history of ingestion of salicylates, NSAIDs, SSRIs is common, particularly in older patients. These
medications are associated with GI mucosal erosions
• NOTE WELL: GI bleeding in the setting of anticoagulation therapy, warfarin or low-molecular-weight heparin,
is STILL USUALLY THE RESULT OF GI PATHOLOGY and should not be ascribed to the anticoagulation
alone.
Physical examination may also be revealing:

• The oropharynx and nose can occasionally simulate symptoms from a more distal source and should always be
examined
• Epigastric tenderness is suggestive, but not diagnostic, of gastritis or peptic ulceration.
• The stigmata of liver disease, including jaundice, ascites, palmar erythema, and caput medusae, may suggest
bleeding related to varices, although these patients commonly bleed from other sources as well
LOCALIZATION
Subsequent management of the patient with acute GI hemorrhage depends on localization of the site of the bleeding
REMEMBER: Although melena is usually from the upper GI tract, it can be the result of bleeding from the small bowel
and/or colon!!
One approach to distinguishing these possibilities is the insertion of a nasogastric (NG) tube and examination of
the aspirate.
NOTE: Although hematemesis is usually diagnostic of an upper GI bleed, the NG tube is still useful to assess the rate of
ongoing bleeding and to begin to remove blood from the stomach to permit endoscopy.
• If the aspirate is positive, this effectively localizes the lesion. The presence of red blood or a coffee grounds
appearance suggests an upper GI source. Testing for occult blood is rarely necessary.
IMPORTANT POINT: The return of bile from a gastric aspirate suggests that the duodenum has been sampled.
• Although a bilious (if it is not bilious, you cannot exclude a duodenal bleed) & nonbloody, gastric aspirate
generally excludes the upper GI tract, these findings can occasionally be misleading. One study found that only 6 of
10 yellow-green nasogastric aspirates actually tested positive for bile
Upper endoscopy under these circumstances is highly accurate for identifying an upper GI lesion
To maximize efficacy, early endoscopy should be performed within 24 hours, even in stable patients
POINT: There is little argument that in an UNSTABLE patient, an URGENT ENDOSCOPY is often required,
• BUT in those with overt sign of bleeding BUT STABLE, an endoscopy within 6 or 12 hours has NOT BEEN
SHOWN to be of any additional benefit to endoscopies performed within 24 hours
ALSO NOTE VERY WELL: Esophagogastroduodenoscopy (EGD) in the urgent or emergent setting is associated with:
1. Reduced accuracy, often because of poor visualization, and a

2. Significant increase in the incidence of complications, including aspiration, respiratory depression, and GI
perforation, when compared with elective procedures
TREATMENT
Depending on the source of the bleeding, a variety of therapeutic options are available. These include:
1. Pharmacologic
2. Endoscopic
3. Angiographic
4. Surgical
Angiographic techniques are somewhat more generic and include selective angiography with infusion of a vasoconstrictor, typically vasopressin, or
embolization. Embolic agents include temporary materials such as gelatin sponge (Gelfoam; Pharmacia & Upjohn, Pfizer, New York) and autologous
clot or permanent devices such as coils
ACUTE UPPER GI HAEMORRHAGE

Upper GI bleeding refers to bleeding that arises from the GI tract proximal to the ligament of Treitz; it accounts for
almost 80% of significant GI hemorrhage.
KNOW THIS WELL:

The causes of upper GI bleeding are best categorized as NONVARICEAL (80%) OR VARICEAL (20%) sources
(bleeding related to portal hypertension)
The nonvariceal causes account for approximately 80% of this bleeding, with peptic ulcer disease being the most
common.
In the remaining 20% of patients, most of whom have cirrhosis, portal hypertension can lead to the development of:
1. Gastroesophageal varices (>90%),
2. Isolated gastric varices, or
3. Hypertensive portal gastropathy, any of which can be the source of an acute upper GI bleed.
ANOTHER VERY IMPORTANT POINT:
Although patients with cirrhosis are at high risk of developing variceal bleeding, nonvariceal sources
account for most upper GI bleeds, even in these patients with cirrhosis (who should STILL BE
ASSUMED to have variceal bleeding)
Endoscopic identification of the source of bleeding also permits an estimate of the risk of subsequent or persistent
haemorrhage
Although the best tool for localization of the bleeding source is an EGD, this intervention is associated
with increased risk and poor visualization in the acute setting, which may offset some of its benefits
Aggressive lavage of the stomach with room temperature normal saline solution prior to the procedure can be
helpful.
Also, evidence has suggested that a single bolus injection of IV erythromycin, which stimulates gastric emptying, can
significantly improve visualization
SPECIFIC CAUSES OF UGIB

NONVARICEAL
PEPTIC ULCER DISEASE (PUD)
(PUD) still represents the most frequent cause of upper GI hemorrhage, accounting for ~40% of all cases
• Approximately 10%-15% of patients with PUD develop bleeding at some point in the course of their disease.
• Bleeding is the most frequent indication for operation!!! and the principal cause for death in PUD!!!
Bleeding develops as a consequence of peptic acid erosion of the mucosal surface. Although chronic blood loss is
common with any ulcer, significant bleeding typically results when there is involvement of an artery of the submucosa or,
with penetration of the ulcer, an even larger vessel.
• POINT: Although duodenal ulcers are more common than gastric ulcers, gastric ulcers usually
bleed
• POINT: Most significant hemorrhage occurs when duodenal or gastric ulcers penetrate into
branches of the gastroduodenal artery or left gastric arteries, respectively
TREATMENT
Patients with clinical evidence of a GI bleed should receive an endoscopy within 24 hours and, while awaiting this
procedure, they should be treated with a PPI
After the index endoscopy, treatment strategies depend on the appearance of the lesion at endoscopy.
• Endoscopic therapy is instituted if bleeding is active OR, when bleeding has already stopped, if there is a
significant risk of rebleeding
The Forrest classification was developed in an attempt to assess this risk based on endoscopic findings and stratify the
patients into low-, intermediate-, and high-risk groups.
• Endoscopic therapy is recommended in cases of active bleeding as well as those with a visible vessel (Forrest I to
IIa).
• In case of an adherent clot (Forrest IIb), the clot is removed and the underlying lesion evaluated.
• Ulcers with a clean base or black spot, secondary to hematin deposition, are generally not treated endoscopically
Medical Management
In cases of a confirmed peptic ulcer bleed, PPIs have been shown to reduce the risk of rebleeding
Therefore, patients with a suspected or confirmed bleeding ulcer should be started on a PPI
In patients who are taking ulcerogenic medications such as NSAIDs or SSRIs, and present with a bleeding GI lesion, these
agents should be stopped. In those taking NSAIDs, more specific cycloxygenase-2 (COX-2) inhibitors, which are
associated with reduced ulceration, HAD BEEN a promising alternative.
• BUT affecting the popularity of these medications have been population-based studies showing that not all COX-
2 inhibitors result in a decreased incidence of upper GI complications
Endoscopic Management
Once the bleeding ulcer has been identified, effective local therapy can be delivered endoscopically to control the
hemorrhage. Available endoscopic options include epinephrine injection, heater probes, and coagulation, as well as the
application of clips
• Epinephrine injection alone is associated with a high rebleeding rate; standard practice is to provide combination
therapy
• Electrocoagulation, or laser or argon plasma coagulation (APC).
• A combination of injection with thermal therapy achieves hemostasis in 90% of bleeding PUDs
Rebleeding of an ulcer is associated with a significant increase in mortality
In those who rebleed, the role of a second attempt at endoscopic control has been controversial but has been validated.
Although this will fail in 25% of patients, who will then require emergent surgery
Most clinicians would now encourage a second attempt at endoscopic control before subjecting the patient to surgery.
Surgical Management
Approximately 10% of patients with bleeding ulcers still require surgical intervention for effective
hemostasis
The clinical factors to consider are shock and a low hemoglobin level at presentation. At the time of endoscopy, although
the Forrest classification is the most important indicator of rebleeding risk, the location and size of the ulcer
are also significant.
• Ulcers larger than 2 cm, posterior duodenal ulcers, and gastric ulcers à Significantly higher risk of
rebleeding.
Indications for surgery were traditionally based on the blood transfusion requirements. Increased blood transfusions are
clearly associated with increased mortality
The first priority at operation should be control of the hemorrhage. Once this is accomplished, a decision must be made
regarding the need for a definitive acid-reducing procedure. Each of these steps varies, depending on whether the lesion is
a duodenal or gastric ulcer.
DUODENAL ULCER
First step in surgery for a duodenal ulcer is exposure of the bleeding site
Hemorrhage can typically be controlled initially with pressure and then direct suture ligation with nonabsorbable suture.
A posterior ulcer eroding into the pancreaticoduodenal or gastroduodenal artery may require suture ligation of the vessel proximal and
distal to the ulcer
Once the bleeding has been addressed, a definitive acid reducing operation should be considered. With the identification of the role of
H. pylori infection in duodenal ulcer, the usefulness of such a procedure has been questioned, based on the argument that simple
closure and subsequent treatment for infection should be sufficient to prevent recurrence
GASTRIC ULCER
For a bleeding gastric ulcer, again, control of bleeding is the immediate priority. Although it may initially require gastrotomy and
suture ligation, this alone is associated with a high risk of rebleeding of almost 30%. In addition, because of a 10% incidence of
malignancy, gastric ulcer resection is generally indicated.
ESOPHAGITIS
The esophagus is infrequently the source for significant hemorrhage. When it does occur, it is most commonly the
result of esophagitis. Esophageal inflammation secondary to repeated exposure of the esophageal mucosa to the acidic
gastric secretions in gastroesophageal reflux disease (GERD) leads to an inflammatory response that can result in chronic
blood loss.
DIEULAFOY’S LESION
Dieulafoy’s lesions are vascular malformations found primarily along the lesser curve of the stomach
within 6 cm of the gastroesophageal junction, although they CAN OCCUR ELSEWHERE IN THE GI
TRACT.
• They represent rupture of unusually large vessels (1 to 3 mm) found in the gastric submucosa. Erosion of the
gastric mucosa overlying these vessels leads to haemorrhage
Application of thermal or sclerosant therapy is effective in 80% to 100% of cases
GASTRIC ANTRAL VASCULAR ECTASIA (GAVE)

Also known as watermelon stomach, gastric antral vascular ectasia (GAVE) is characterized by a collection of dilated
venules appearing as linear red streaks converging on the antrum in a longitudinal fashion, giving it the appearance of a
watermelon.
HAEMOBILIA
Haemobilia is often a difficult diagnosis to make. It is typically associated with trauma, recent instrumentation of
the biliary tree, or hepatic neoplasms.
• This unusual cause of GI bleeding should be suspected in anyone who presents with hemorrhage, right upper
quadrant pain, and jaundice
HEMOSUCCUS PANCREATICUS
Another rare cause of upper GI bleeding is bleeding from the pancreatic duct. This is often caused by erosion of a
pancreatic pseudocyst into the splenic artery. It presents with abdominal pain and hematochezia.
BLEEDING RELATED TO PORTAL HYPERTENSION
Upper GI bleeding is a serious complication of portal hypertension, most often in the setting of cirrhosis
Haemorrhage related to portal hypertension is usually the result of bleeding from varices
Most common in the distal 3-5 cm of oesophagus and can reach sizes of 1 to 2 cm.
Although these varices are most commonly seen in the esophagus, they may also develop in the stomach and
haemorrhoidal plexus of the rectum.
Portal hypertensive gastropathy, diffuse dilation of the mucosal and submucosal venous plexus of the stomach
associated with overlying gastritis, is an incompletely understood entity in which the stomach acquires a snakeskin-like
appearance, with cherry red spots.
KNOW THIS: Gastroesophageal varices develop in approximately 30% of patients with cirrhosis and
portal hypertension and 30% in this group develop variceal bleeding
Variceal hemorrhage is associated with an increased risk of rebleeding, increased need for transfusions, longer hospital
stay, and increased mortality. Hemorrhage is frequently massive, accompanied by hematemesis and hemodynamic
instability
TREATMENT
VERY GOOD Image at end presents an algorithm for management.
Central venous pressure monitoring is indicated for most of these patients and early admission to an ICU should be
considered.
Defects in coagulation are common and should be aggressively corrected. A significant percentage of patients with
variceal bleeding have underlying sepsis
• 7-day course of a quinolone will lower the risk of rebleeding. Thus, patients with variceal bleeding
should be given an empirical course of a broad-spectrum antibiotic
MEDICAL MANAGEMENT
Pharmacologic therapy to reduce portal hypertension
• Vasopressin produces splanchnic vasoconstriction and has been shown to reduce bleeding significantly
• Somatostatin or its synthetic analogue, octreotide, is the vasoactive agent of choice
ENDOSCOPIC MANAGEMENT
• Early EGD is critical to evaluate the source of bleeding because more than 50% of bleeding is caused by
nonvariceal sources
• If bleeding esophageal varices are identified, sclerotherapy and variceal banding have been shown to control
hemorrhage effectively
These endoscopic approaches, sometimes with up to three treatments over 24 hours, control the haemorrhage in up to 90%
of patients with oesophageal varices
OTHER MANAGEMENT
In patients for whom pharmacologic or endoscopic therapy fails to control the hemorrhage:
• Balloon tamponade can be successful in temporizing the hemorrhage. The Sengstaken-Blakemore tube
consists of a gastric tube with oesophageal and gastric balloons
• Balloon tamponade is reserved for patients with massive haemorrhage to permit more definitive therapies.
In cases of refractory variceal bleeding that cannot be controlled endoscopically:
• EMERGENT PORTAL DECOMPRESSION is indicated. This is required in approximately 10% of patients
with variceal bleeding.
• Transjugular intrahepatic portosystemic shunt (TIPSS): Although randomized studies have shown
equivalence between a transjugular intrahepatic portosystemic shunt (TIPSS) and surgical shunting in these
refractory cases, it is usually achieved by means of a percutaneous TIPSS.
Isolated gastric varices are managed much the same way as oesophageal varices, although endoscopic therapy tends to be
less successful
PREVENTION OF REBLEEDING
Once the initial bleeding has been controlled, prevention of recurrent haemorrhage should be a priority.
IF no further treatment is undertaken, approximately 70% of patients will have a further bleed within 2
months.
The risk of rebleeding is highest in the initial few hours to days following a first episode.
1. Medical therapy to prevent recurrence includes:
a. A nonselective beta-blocker, such as nadolol, and
b. An antiulcer agent, such as a PPI or sucralfate.
2. These are combined with endoscopic band ligation repeated every 10 to 14 days until all varices have been
eradicated.
KNOW THIS COMPLETELY. FULL SUMMARY:
LOWER GI BLEED
ACUTE LOWER GASTROINTESTINAL HAEMORRHAGE
When compared with upper GI hemorrhage, lower GI bleeding is a much less frequent reason for hospitalization—LGIB
accounts for ~20% of GI bleeding
In more than 95% of patients with lower GI bleeding, the source of haemorrhage is the
colon.
Cause is often age-related:
• Specifically, vascular lesions and diverticular disease affect all age groups but have an increasing incidence in
middle-aged and older adults.
• In the pediatric population, intussusception is most commonly responsible, whereas
• Meckel’s diverticulum must be considered in the differential diagnosis in the young adult
DIAGNOSIS
Lower GI bleeding typically presents with haematochezia, which can range from bright red blood to old clots. If the
bleeding is slower or from a more proximal source, lower GI bleeding often presents as melena
Diagnostic evaluation is further complicated by the observation that in up to 40% of patients with lower GI bleeding,
more than one potential source for bleeding is identified. If more than one source is identified, it is critical to confirm the
responsible lesion before initiating aggressive therapy
ALGORITHM FOR THE EVALUATION OF LOWER GI HAEMORRHAGE AT END OF DOCUMENT.
Once resuscitation has been initiated, the FIRST STEP IN THE WORKUP IS TO RULE OUT ANORECTAL
BLEEDING WITH A DIGITAL RECTAL EXAMINATION, ANOSCOPY, AND/OR SIGMOIDOSCOPY.
With significant bleeding, it is also important to eliminate an upper GI source. RECALL: An NG aspirate that contains
bile and no blood effectively rules out upper tract bleeding in most patients.
When emergent surgery for life-threatening haemorrhage is being contemplated, preoperative or intraoperative EGD is
usually appropriate.
Subsequent evaluation depends on the magnitude of the haemorrhage.

With major and/or persistent bleeding, the workup should progress depending on the patient’s hemodynamic stability. The
truly unstable patient who continues to bleed and requires ongoing aggressive resuscitation belongs in the operating room
for expeditious diagnosis and surgical intervention.
When hemorrhage is intermediate, resuscitation and hemodynamic stability permit a more directed evaluation and
therapeutic intervention. Colonoscopy is the mainstay here because it allows visualization of the pathology and
therapeutic intervention in colonic, rectal, and distal ileal sources of bleeding.
The usual adjuncts to colonoscopy include a tagged RBC scan and angiography. If these modalities are not diagnostic, the
source of the hemorrhage is considered obscure; such lesions and their evaluation are considered in the last section of this
chapter.
Colonoscopy
Colonoscopy is most appropriate in the setting of minimal to moderate bleeding; major hemorrhage interferes
significantly with visualization and the diagnostic yield is low.
Polyps, cancers, and inflammatory causes can frequently be seen. Unfortunately, angiodysplasias are often difficult to visualize,
particularly in the unstable patient with mesenteric vascular constriction. Diverticula are identified in most patients, whether or not
they are the source of the hemorrhage. Despite these limitations, the diagnostic yield in experienced hands is reasonable. For
example, some studies have reported that colonoscopy is successful in identifying the bleeding source in up to 95% of patients.
Most of the bleeding is secondary to angiodysplasias or diverticuli
Radionuclide Scanning
Radionuclide scanning with technetium-99m (99mTc–labeled RBC) is the most sensitive but least accurate method
for localizing GI bleeding.
• With this technique, the patient’s own red cells are labeled and reinjected. The labeled blood is extravasated into
the GI tract lumen, creating a focus that can be detected scintigraphically
• The RBC scan can detect bleeding as slow as 0.1 mL/min and is reported to be more than 90% sensitive.
Unfortunately, the spatial resolution is low and blood may move retrograde in the colon or distally in the small
bowel. Reported accuracy of localization is in the range of only 40% to 60% and it is particularly inaccurate for
distinguishing right-sided from left-sided colonic bleeding
Mesenteric Angiography
Selective angiography, using the superior or inferior mesenteric arteries, can detect hemorrhage in the range of 0.5 to 1.0
mL/ min but is generally only used for the diagnosis of ongoing hemorrhage. It can be particularly useful in identifying
the vascular patterns of angiodysplasias. It may also be used for localizing actively bleeding diverticula. In addition, it has
therapeutic capabilities. Catheter-directed vasopressin infusion can provide temporary control of bleeding, permitting
hemodynamic stabilization, although as many as 50% of patients will rebleed when the medication is discontinued. It can
also be used for embolization.
Typically, such therapy is reserved for patients whose underlying condition precludes surgical therapy. Unfortunately,
angiography is associated with a significant risk of complications, including hematoma, arterial thrombosis, contrast
reaction, and acute renal failure.
Treatment
Therapeutic approaches with lower GI bleeding are clearly dependent on the lesion identified. The criteria for surgery are
similar to those for upper GI hemorrhage,
Specific Causes of Lower GI Bleeding

COLONIC BLEEDING
DIVERTICULAR DISEASE
In the United States, diverticula are the most common cause of significant lower GI bleeding
In the past, diverticula were thought to be rare in patients younger than 40 years but is now an increasingly common
diagnosis in this age group.
Bleeding generally occurs at the neck of the diverticulum and is believed to be secondary to bleeding from the vasa recti
as they penetrate through the submucosa. Of those that bleed, more than 75% stop spontaneously, although approximately
10% will rebleed within a year and almost 50% within 10 years.
The best method of diagnosis and treatment is colonoscopy, although success is sometimes limited by the large amount of
bleeding. If the bleeding diverticulum can be identified, epinephrine injection may control the bleeding. Electrocautery
can also be used and, most recently, endoscopic clips have been successfully applied to control the hemorrhage. If
bleeding ceases with these maneuvers or ceases spontaneously, expectant management may be appropriate; however, this
requires clinical judgment based on the amount of the hemorrhage and any comorbidities, particularly cardiac disease. If
none of these maneuvers is successful or if hemorrhage recurs, angiography with embolization can be considered.
Superselective embolization of the bleeding colonic vessel has gained popularity, with high success rates (> 90%),
although the risk of ischemic complications continues to be of concern. Under these circumstances, colonic resection is
indicated. Certainty of the site of bleeding is critical. Blind hemicolectomy is associated with rebleeding in more than
50% of patients
Subtotal colectomy does not eliminate the risk of recurrent hemorrhage and, when compared with segmental resection, is
accompanied by a significant increase in morbidity, particularly diarrhea in older patients, in whom the remaining rectum
may never adapt. Mortality of emergent subtotal colectomy for bleeding is almost 30%
ANGIODYSPLASIA
In some reports, hemorrhage secondary to these vascular lesions accounts for up to 40% of lower GI bleeding; however,
most recent reports have noted the incidence to be much lower. Angiodysplasias of the intestine, also referred to as
arteriovenous malformations (AVMs), are distinct from hemangiomas and true congenital AVMS. They are thought to be
acquired degenerative lesions secondary to progressive dilation of normal blood vessels within the submucosa of the
intestine. Angiodysplasias have an equal gender distribution and are almost uniformly found in patients older than 50
years. These lesions are notably associated with aortic stenosis and renal failure, especially in older patients. The
hemorrhage tends to arise from the right side of the colon, with the cecum being the most common location, although they
can occur in the rest of the colon and small bowel. Most patients present with chronic bleeding but, in up to 15%,
hemorrhage may be massive. Bleeding stops spontaneously in most cases, but approximately 50% will rebleed within 5
years.
These lesions can be diagnosed by colonoscopy or angiography. During colonoscopy, they appear as red stellate lesions
with a surrounding rim of pale mucosa and can be treated with sclerotherapy or electrocautery. Angiography demonstrates
dilated, slowly emptying veins and, sometimes, early venous filling. If these lesions are discovered incidentally, no further
therapy is indicated. In acutely bleeding patients, they have been successfully treated with intra-arterial vasopressin,
selective gel foam embolization, endoscopic electrocoagulation, or injection with sclerosing agents. If these measures fail,
or bleeding recurs and the lesion has been localized, segmental resection, most commonly a right colectomy, is effective
NEOPLASIA
Colorectal carcinoma is an uncommon cause of significant lower GI hemorrhage but is probably the most important one
to rule out because more than 150,000 Americans are diagnosed annually with this type of cancer. The bleeding is usually
painless, intermittent, and slow in nature and is frequently associated with iron deficiency anemia
The best diagnostic tool is colonoscopy. If the bleeding is attributable to a polyp, it can be treated with endoscopic therapy
ANORECTAL DISEASE
The major causes of anorectal outlet bleeding are internal hemorrhoids, anal fissures, and colorectal neoplasia. Although
hemorrhoids are the most common of these entities, they only account for 5% to 10% of all acute lower GI bleeding. In
general, anorectal hemorrhage is low-volume bleeding that presents as bright red blood per rectum, which is seen in the
toilet and on the toilet paper. Most hemorrhoidal bleeding arises from internal hemorrhoids; these are painless and often
accompanied by prolapsing tissue that reduces spontaneously or has to be reduced manually by the patient. Anal fissure,
on the other hand, produces painful bleeding after a bowel movement; bleeding is only occasionally the main symptom in
these patients.
Because anorectal disease is common, a careful investigation to rule out all other sources of bleeding, especially
malignancy, is imperative before lower GI bleeding can be attributed to such pathology. Anal fissure can be treated
medically with stool-bulking agents (e.g., psyllium [Metamucil]), increased water intake, stool softeners, and topical
nitroglycerin ointment or diltiazem to relieve sphincter spasm and promote healing. Internal hemorrhoids should be
treated with bulking agents increased dietary fiber, and adequate hydration. Office-based interventions, including rubber
band ligation, injectable sclerosing agents, and infrared coagulation, have also been used. If these measures fail, surgical
hemorrhoidectomy may be needed. Most anorectal bleeding is self-limited and responds to dietary and local measures.
COLITIS
Inflammation of the colon is caused by a number of disease processes, including inflammatory bowel disease (e.g.,
Crohn’s disease, ulcerative colitis, indeterminate colitis), infectious colitis (0157:H7 Escherichia coli, cytomegalovirus
[CMV], Salmonella, Shigella, and Campylobacter spp., and Clostridium difficile ), radiation proctitis after treatment for
pelvic malignancies, and ischemia. Ulcerative colitis (UC) is more likely than Crohn’s disease to present with GI
bleeding.
Medical therapy with steroids, 5- aminosalicylic acid (ASA) compounds, immunomodulatory agents, and supportive care
are the mainstays of treatment. Surgical therapy is rarely indicated in the acute setting unless the patient develops a toxic
megacolon or hemorrhage refractory to medical management.
Chron’s:
Medical management consists of steroids, antibiotics, immunomodulators and ASA compounds. Because Crohn’s disease
is a relapsing and remitting disease, surgical therapy is used as a last resort. Massive colonic hemorrhage complicates
ulcerative colitis in up to 15% of affected patients, whereas it only occurs in 1% of those with Crohn’s colitis
Infectious colitis can cause bloody diarrhea. The diagnosis is usually established from the history and stool culture
Radiation proctitis has become more common in the last 30 or 40 years as the use of radiation to treat rectal cancer,
prostate cancer, and gynecologic malignancies has increased.
Flexible endoscopy reveals the characteristic bleeding telangiectasias. Treatment consists of antidiarrheals, hydrocortisone
enemas, and endoscopic APC. In cases of persistent bleeding, ablation with 4% formalin solution usually works well
Mesenteric Ischaemia
Mesenteric ischemia can be secondary to acute or chronic arterial or venous insufficiency. Predisposing factors include
preexisting cardiovascular disease (e.g., atrial fibrillation, congestive heart failure, acute myocardial infarction), recent
abdominal vascular surgery, hypercoagulable states, medications (e.g., vasopressors, digoxin), and vasculitis. Acute
colonic ischemia is the most common form of mesenteric ischemia. It tends to occur in the watershed areas of the splenic
flexure and rectosigmoid colon, but can be right-sided in up to 40% of patients. Patients present with abdominal pain and
bloody diarrhea. CT will often show a thickened bowel wall. The diagnosis is generally confirmed with flexible
endoscopy, which reveals edema, hemorrhage, and a demarcation between the normal and abnormal mucosa. Treatment
focuses on supportive care consisting of bowel rest, IV antibiotics, cardiovascular support, and correction of the low-flow
state. In 85% of cases, the ischemia is self-limited and resolves without incident, although some patients develop a colonic
stricture. In the other 15% of cases, surgery is indicated because of progressive ischemia and gangrene. Marked
leukocytosis, fever, a fluid requirement, tachycardia, acidosis, and peritonitis indicate a failure of the ischemia to resolve
and the need for surgical intervention. During the surgery, resection of the ischemic intestine and creation of an end
ostomy is indicated
OBSCURE CAUSES OF ACUTE GASTROINTESTINAL HEMORRHAGE

Obscure GI hemorrhage is defined as bleeding that persists or recurs after an initial negative evaluation with an EGD and
colonoscopy. Obscure bleeding can be further subdivided into obscure-occult or obscure-overt bleeding. Obscure-occult
bleeding is characterized by iron deficiency anemia or guaiac-positive stools without visible bleeding. If initial upper and
lower endoscopy fail to identify a source for obscure-occult bleeding and the patient has no systemic signs of disease, she
or he is often treated with iron therapy and more than 80% resolve symptoms
Fortunately, obscure-overt bleeding is only responsible for about 1% of all cases of GI bleeding. The differential diagnosis
of obscure-overt bleeding is long and varied and includes small bowel lesions not previously described.
Treatment
Obscure GI hemorrhage requires a careful approach to diagnosis and management. Specific causes and their management
are listed below. Up to 25% of cases of obscure lower GI hemorrhage remain without a diagnosis and 33% to 50% of
patients will rebleed within 3 to 5 years
Specific Causes of Small Bowel Bleeding
ANGIODYSPLASIAS
Angiodysplasias are the most common cause of small intestinal bleeding, accounting for 40% of cases in older patients
and 10% in younger patients. Most small intestinal vascular ectasias appear to occur in the jejunum, followed by the ileum
and then the duodenum.
Endoscope-directed segmental small bowel resection is the treatment of choice. Occasionally, these lesions may be
diffuse; this may occur in hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu syndrome), acute renal failure, or
von Willebrand disease
NEOPLASIA
Small bowel tumors are not very common, but can be sources of occult or frank GI bleeding. Bleeding typically results
from erosion of the mucosa overlying the tumor. GISTs have the greatest propensity for bleeding. Small bowel tumors are
typically diagnosed by small bowel contrast series or spiral CT scanning. Treatment involves surgical resection
CROHN’S DISEASE
Patients with Crohn’s disease may also present with small bowel bleeding in association with terminal ileitis
It is diagnosed by small bowel contrast series, and initial treatment is medical
MECKEL’S DIVERTICULUM
Meckel’s diverticulum is a true diverticulum in that it contains all layers of the small bowel wall. It is a congenital
remnant of the omphalomesenteric duct, occurring in approximately 2% of the general population. Often, heterotopic
tissue is present at the base of the diverticulum. Bleeding from a Meckel’s diverticulum is usually from an ulcerative
lesion on the ileal wall opposite the diverticulum, resulting from acid production by ectopic gastric mucosa
Surgical management usually requires a segmental resection to incorporate the opposing ileal mucosa, which is typically
the site of bleeding.
DIVERTICULA
Unlike a Meckel’s diverticulum, small intestinal diverticula are false diverticula that do not involve all layers of the
bowel. Bleeding from small bowel diverticula can present a diagnostic challenge In cases of profuse bleeding,
angiography or intraoperative endoscopy may be used to identify the bleeding source
BOX 48-3 Differential Diagnosis of Obscure Gastrointestinal Bleeding
Upper GI Bleeding Small Bowel Bleeding • U lcerative colitis

Angiodysplasia Crohn’s disease • C rohn’s colitis
Peptic ulcer disease Meckel’s diverticulum • I schemic colitis
Aortoenteric fistula Lymphoma • R adiation colitis
Neoplasia Radiation enteritis • I nfective colitis
HIV-related causes Ischemia Solitary rectal ulcer
Dieulafoy’s lesion HIV-related causes Amyloidosis
Lymphoma Bacterial infection Lymphoma
Sarcoidosis Metastatic disease Endometriosis
Hemobilia Angiodysplasia Angiodysplasia
Hemosuccus pancreaticus NS AID-induced erosions Neoplasia
GAVE Colon Bleeding HIV-related causes
Metastatic cancer Colitis Hemorrhoids
General Surgery
GI Bleed
February 2015
Haemorrhage can originate from any region of the GI tract and is typically classified based on its location relative to the ligament of Treitz.
th
§ Ligament of Treitz: Suspensory ligament where 4 portion of the duodenum transitions to jejunum
aka Suspensory Ligament of the Duodenum
General Points
§ Peptic ulcer disease and variceal haemorrhage are the most common causes of UGIB
§ Diverticula and angiodysplasias are the most common causes of LGIB (Most lower GI bleeding is from the colon)
o In < 5% of patients, the small intestine in responsible!!!
§ Attempts to localize the source should NEVER precede appropriate resuscitative measures
UGIB (>80% of GI Bleed)

Upper gastrointestinal bleeding (UGIB) is defined as bleeding derived from a source proximal to the ligament of Treitz
Signs and symptoms related to the BLOOD LOSS, HYPOVOLAEMIA and the UNDERLYING CAUSE
Features: In order of decreasing severity of the bleed:

§ Haematochezia (massive UGIB) > haematemesis > coffee ground emesis > melena > occult blood in stool
§ UGIB often presents with haematemesis and melaena unless very brisk (then can present with hematochezia, hypotension, tachycardia)
RE: MELAENA
§ Passage of black, tarry, and foul-smelling stool, generally suggests bleeding from the upper GI tract (> 50 ml of blood required to have
melaena)
§ Although the melanotic appearance typically results from gastric acid degradation which converts haemoglobin to haematin, and from the
actions of digestive enzymes and luminal bacteria in the small intestine, blood loss from the distal small bowel or right colon may have
this appearance, particularly if transit is slow enough.
§ NOTE: Melena should not be confused with the greenish character of the stool in patients on iron supplements.
o **One way to distinguish these two is by performing a guaiac test, which tests negative in those on iron supplementation.
Test for fecal occult blood
FIRST, most important thing to determine clinically (So also use this to classify): à***
• Variceal vs. Non-variceal (And then can organize the non-variceal into Local (anatomically) vs. General)
The causes of upper GI bleeding are best categorized as NONVARICEAL (80%) OR VARICEAL (20%) sources
Wiki: People are usually stratified into having either variceal or non-variceal sources of upper GI hemorrhage, as the two have different treatment
algorithms and prognosis.
NON-VARICEAL CAUSES:
§ Peptic ulcer disease (PUD) remains the most common cause of UGIB overall! (30-50% of non-variceal bleeding) > Mallory-Weiss
(20%) > Gastritis (15%). See the rest in the list below
THE 3 CAUSES OF VARICEAL BLEED:

1. Gastroesophageal varices (>90%),
2. Isolated gastric varices (rare), or
3. Hypertensive portal gastropathy (< 5%)
IMPORTANT POINT: Although patients with cirrhosis are at high risk of developing variceal bleeding, nonvariceal sources account for most
upper GI bleeds, even in these patients with cirrhosis (who should STILL BE ASSUMED to have variceal bleeding)
Initial management with endoscopy; if fails, then consider surgery (Only ~10% require surgery!)
Note: PUD accounts for approximately 55% of severe UGI bleeding
LGIB (~20% of GI bleeding)

Bleeding from a source distal to the ligament of Treitz
In >95% of patients with lower GI bleeding, the source of haemorrhage is the colon
Cause is often age-related: Specifically

• Middle-aged and older adults: Vascular lesions and diverticular disease affect all age groups but have an increased incidence
• In the paediatric population: intussusception is most commonly responsible, whereas
• Meckel’s diverticulum must be considered in the differential diagnosis in the young adult
- Often presents with BRBPR unless proximal to transverse colon

- May occasionally present with melena (If bleeding is slower or from a more proximal source)
- Initial management with colonoscopy to detect and potentially stop source of bleeding
- Angiography, RBC scan to determine source as indicated
- Surgical intervention if no source found – obscure bleed
NB: 80% OF UGIB AND 90% OF LGIB STOP SPONTANEOUSLY
CAUSES OF GI BLEEDING
LOCAL vs. GENERAL
LOCAL
1. Epistaxis – Not actually GI bleed, but may mislead

2. Oesophagus
a. Reflux oesophagitis (associated with hiatus hernia – most common oesophageal cause);
b. Oesophageal varices (associated with portal hypertension)
c. Peptic ulcer
d. Tumours (benign and malignant)
e. Aorto-oesophageal fistula (generally post EVAR)
3. Stomach
a. Gastric ulcer (20%)
b. Acute erosions (small ulcers < 5 mm; associated with aspirin, other NSAIDs and corticosteroids);
c. Gastritis (20%) (generalized inflammation, appearing as red dots through the endoscope);
d. Mallory–Weiss syndrome – Mallory–Weiss syndrome or gastro-oesophageal laceration syndrome refers to bleeding from tears
(a Mallory-Weiss tear) in the mucosa at the oesophagogastric junction, usually caused by severe alcoholism, retching, coughing,
or vomiting. The tear involves mucosa and submucosa but NOT the muscular layer (contrast to Boerhaave syndrome which
involves all the layers). The mean age is more than 60 and 80% are men. Hyperemesis gravidarum, which is severe morning
sickness associated with vomiting and retching in pregnancy, is also a known cause of Mallory-Weiss tear
e. Gastric antral vascular ectasia (Rare, associated with cirrhosis)
f. Vascular malformation: Dieulafoy’s lesion (very rare)
g. Tumours (benign and malignant)
4. Duodenal causes
a. Duodenal ulcer
b. Vascular malformations
c. Tumour
d. Aorto-enteric fistulae. Fistulae are usually secondary to prior vascular surgery and usually occur at the proximal anastomosis
at the third or fourth portion of the duodenum where it is retroperitoneal and near the aorta
e. Haemobilia, or bleeding from the biliary tree (e.g. haemorrhagic cholecystitis)
f. Haemosuccus pancreaticus, or bleeding from the pancreatic duct (e.g. pseudocyst with haemorrhage)
g. Severe superior mesenteric artery syndrome
----------
5. Jejunum, Ileum and Ileocecal Junction
a. Meckel’s diverticulum (rare surgical management)
b. Crohn’s disease*
c. Tuberculosis of ileocecal junction
6. Large intestine
a. Diverticula
b. Angiodysplasia
c. Colorectal cancer*
d. Polyps* (surgical management if not amenable to colonoscopic polypectomy)
e. Ulcerative colitis* (subtotal colectomy if failure of medical management)
f. Crohn’s disease (less frequently presents with bleeding)*
g. Pancolitis (infectious, chemotherapy or radiation induced)
h. Mesenteric thrombosis/ischaemic bowel*
i. Bleeding post-gastrointestinal anastomosis
7. Rectum and anus

a. Haemorrhoids
b. Fissures
c. Rectal cancer*
d. Anal varices
e. Polyps* (surgical management if not amenable to polypectomy)
f. Crohn’s or ulcerative colitis*
g. Solitary rectal ulcer syndrome
GENERAL (Get from Ashman notes or haematology)
General causes of bleeding include haemophilia, leukaemia, anticoagulant therapy and thrombocytopenia.
• Bleeding disorders: Platelet (number vs. function) vs. Coagulation (Inherited vs. acquired)
• Drugs: Warfarin, Heparin, Aspirin, SSRIs etc.
• DIC
*While it is accepted that general bleeding diatheses do not cause bleeding by themselves, they alter the course of bleeding from a local lesion.
NOTE WELL: GI bleeding in the setting of anticoagulation therapy, warfarin or low-molecular-weight heparin, is STILL USUALLY THE RESULT OF
GI PATHOLOGY and should not be ascribed to the anticoagulation alone.
NOTE: Duodenal ulcers are more common than gastric ulcers, BUT the incidence of bleeding is identical for both (some sources say gastric
ulcer bleed more frequently). In most cases, the bleeding is caused by the erosion of an artery in the base of the ulcer.
ASSESSMENT AND INVESTIGATIONS

Severity of the haemorrhage can be generally determined based on simple clinical parameters. (See shock/haemorrhage table)
§ Hypotension (***systolic blood pressure < 90 mm Hg in the supine position)

o In patients without shock, postural changes should be elicited by allowing the patient to SIT up with his or her legs dangling for 5 minutes.
o A fall in SBP of > 20 mmHg, DBP of > 10 mmHg OR an **elevation of the pulse of > 20 beats/min again reflects at least a 20% blood loss.
§ The haematocrit (PCV) is NOT useful for assessing the degree of haemorrhage in the acute setting because the proportion of red blood cells and
plasma initially lost is constant.
o The haematocrit level does not fall until plasma is redistributed into the intravascular space and resuscitation with crystalloid solution is begun.
o Takes 12-24 hours to fully equilibrate
§ ***Similarly, the absence of tachycardia may be misleading; some patients with severe blood loss may actually have bradycardia secondary to
vagal slowing of the heart!!!
§ ***Haemodynamic signs are less reliable in older patients, diabetic patients (autonomic neuropathy) and patients taking beta-blockers.
MANAGEMENT (KNOW THIS)

APPROACH TO PATIENT (SABISTON)
1. RAPID INITIAL ASSESSMENT AND RESUSCITATION

(Securing the airway and stabilizing the patient’s haemodynamic status with appropriate monitoring)
§ A + B: Secure the airway. Intubation and ventilation early if respiratory compromise
§ C: Insert 2 16-gauge (minimum), upper extremity, peripheral IV lines – preferably antecubital fossa!
§ C: If pt unstable, 2-litre bolus of crystalloid (usually LR)
§ C: Replace each ml of blood loss with 3 mL of crystalloid fluid
§ C: Foley catheter placement for continuous evaluation of urinary output as a guide to renal perfusion
§ C: In older patients or those with severe coexisting medical illnesses, CV line OR pulmonary artery catheter insertion for monitoring
hemodynamic cardiac performance
§ Take blood immediately for CBC, GXM, platelets, PT, PTT, electrolytes, BUN, Cr, LFTs
§ Decision to transfuse: Based on response to fluid challenge, age, risk of rebleed. In general, the haematocrit should be maintained > 30% in
older adults and above 20% in young, otherwise healthy patients.
NB: The single leading cause of morbidity and mortality in these patients is multiorgan failure related to inadequate initial or subsequent resuscitation.
2. FOCUSED HISTORY AND EXAMINATION

(To determine possible cause and help quantify blood loss!!!)
§ Determine the characteristics of the bleed – time of onset, volume, frequency etc.
§ Then risk factors for possible causes
§ E.g. Hx of liver disease may suggest variceal bleeding, prior vomiting may suggest Mallory-Weiss tear
§ Medications: NSAIDS, salicylates, SSRIs common! + antiplatelets, anticoagulants
§ Remember to always examine the oropharynx and nose!!!
3. LOCALIZE THE BLEEDING

(SEE LAST PAGE FOR ALGORITHM)
1. NG tube aspiration FIRST. 3 purposes:
a. Diagnose upper GI bleed (Presence of red blood or coffee grounds)
b. Assess rate of ongoing bleeding
c. Remove blood from stomach to permit endoscopy
2. Endoscopy (Upper (EGD) or Lower (colonoscopy))
a. Identify source (best tool for localization) and estimate risk of rebleed or persistent bleed
b. To maximize efficacy, early endoscopy should be performed within 24 hours, even in stable patients
c. Urgent endoscopy if patient unstable!!!! If stable, perform within 24 hours!!
3. Other studies as needed (E.g. Angiography, tagged RBC scan, Meckel’s scan)
IMPORTANT POINT: The return of bile from a gastric aspirate suggests that the duodenum has been sampled. Therefore, a bilious & nonbloody,
gastric aspirate generally excludes the upper GI tract (if it is not bilious, you cannot exclude a duodenal bleed)
ALSO NOTE VERY WELL: Esophagogastroduodenoscopy (EGD) in the urgent or emergent setting is associated with:
*Reduced accuracy because of poor visualization (can aid with normal saline lavage prior OR IV erythromycin/metoclopramide), and a
*Significant increase in incidence of complications, including aspiration, respiratory depression, and GI perforation, when compared with elective
4. INITIATE SPECIFIC THERAPY
4 main therapeutic options are available depending on source of bleed:

1. Pharmacologic
2. Endoscopic (Must know the 4 options!!: *Epinephrine injection, *thermal or *electrocautery, *sclerosant injection, *endoscopic clips)
3. Angiographic (Must know (2)!!: Infusion of a *vasoconstrictor (usu. vasopressin) or *embolization (e.g. with coils or gelatin sponges))
4. Surgical
For high-risk peptic ulcer patients, start high-dose IV PPI
INDICATIONS FOR SURGERY

1. Failure of medical management
2. Haemodynamic instability despite vigorous resuscitation
3. Prolonged bleeding requiring transfusion of > 3-6 units PRBCs
4. Recurrent haemorrhage after initial stabilization procedures with up to two attempts of endoscopic hemostasis
5. Hypovolemic shock
UPPER GI BLEED SPECIFIC CAUSES

1. PUD: SEE MANAGEMENT OF BLEEDING PEPTIC ULCER IN PUD SUMMARY NOTES!
2. DIEULAFOY’S LESION
§ Vascular malformations found primarily in stomach within 6 cm of the gastroesophageal junction, although they CAN OCCUR
ELSEWHERE IN THE GI TRACT.
§ They represent rupture of unusually large vessels (1 to 3 mm) found in the gastric submucosa. Erosion of the gastric mucosa overlying these
vessels leads to haemorrhage
§ Application of thermal or sclerosant therapy is effective in 80-100% of cases
3. GASTRIC ANTRAL VASCULAR ECTASIA (GAVE)

§ Also known as watermelon stomach. Characterized by a collection of dilated venules appearing as linear red streaks converging on the
antrum in a longitudinal fashion, giving it the appearance of a watermelon.
4. HAEMOBILIA
§ Difficult diagnosis to make. It is typically associated with trauma, recent instrumentation of the biliary tree, or hepatic neoplasms.
§ Unusual cause of GI bleeding & should be suspected in anyone who presents with haemorrhage, right upper quadrant pain, and jaundice
5. HEMOSUCCUS PANCREATICUS
§ Another rare cause of upper GI bleeding is bleeding from the pancreatic duct. This is often caused by erosion of a pancreatic pseudocyst
into the splenic artery. It presents with abdominal pain and haematochezia.
6. VARICEAL BLEEDING
§ Varices most common in the distal 3-5 cm of oesophagus and can reach sizes of 1 to 2 cm.
§ KNOW THIS: Gastroesophageal varices develop in approximately 30% of patients with cirrhosis and portal hypertension and 30% in
this group develop variceal bleeding
§ Haemorrhage is frequently massive, accompanied by hematemesis and hemodynamic instability
MANAGEMENT OF VARICEAL BLEEDING

Re: The algorithm above
§ Medical management reduces the portal HTN. Vasopressin à Very effective. Produces splanchnic vasoconstriction
§ Somatostatin or its synthetic analogue, octreotide is the vasoactive agent of choice
§ 7-day course of a quinolone lowers the risk of rebleeding
§ The endoscopic approaches, sometimes with up to three treatments over 24 hours, control the haemorrhage in up to 90% of patients with
oesophageal varices
In patients for whom pharmacologic or endoscopic therapy fails to control the hemorrhage:
• Balloon tamponade can be successful in temporizing the hemorrhage. The Sengstaken-Blakemore tube consists of a gastric tube with
oesophageal and gastric balloons
• Balloon tamponade is reserved for patients with massive haemorrhage to permit more definitive therapies (Emergent portal
decompression via TIPS or surgical shunt)
PREVENTION OF REBLEEDING IN VARICEAL BLEEDING
Once the initial bleeding has been controlled, prevention of recurrent haemorrhage should be a priority.
IF no further treatment is undertaken, approximately 70% of patients will have a further bleed within 2 months.
The risk of rebleeding is highest in the initial few hours to days following a first episode.
1. Medical therapy to prevent recurrence includes:
a. A nonselective beta-blocker, such as nadolol, and
b. An antiulcer agent, such as a PPI or sucralfate.
2. These are combined with endoscopic band ligation repeated every 10 to 14 days until all varices have been eradicated.
LOWER GI BLEED INVESTIGATION

(ALGORITHM FOR MANAGEMENT AT END OF DOCUMENT)
CRUCIAL RULE #1: Once resuscitation has been initiated, the FIRST STEP IN THE WORKUP IS TO RULE OUT ANORECTAL
BLEEDING WITH A DRE, ANOSCOPY, AND/OR SIGMOIDOSCOPY.
CRUCIAL RULE #2: With significant bleeding, it is also important to eliminate an upper GI source. RECALL: An NG aspirate
that contains bile and no blood effectively rules out upper tract bleeding in most patients.
Subsequent evaluation depends on the magnitude of the haemorrhage:

§ With major and/or persistent bleeding, manage based on the patient’s haemodynamic stability. The truly unstable patient who continues to
bleed and requires ongoing aggressive resuscitation à OT FOR IMMEDIATE DIAGNOSIS and surgical intervention
§ Intermediate haemorrhage à resuscitation and hemodynamic stability permit a more directed evaluation and therapeutic intervention.
Colonoscopy is the mainstay here because it allows visualization of the pathology and therapeutic intervention in colonic, rectal, and distal ileal
sources of bleeding.
The usual adjuncts to colonoscopy include a tagged RBC scan and angiography. If these modalities are not diagnostic, the source of the hemorrhage
is considered obscure; such lesions and their evaluation are considered in the last section of this chapter.
1. COLONOSCOPY
§ Colonoscopy is most appropriate in the setting of minimal to moderate bleeding; major hemorrhage interferes significantly with visualization
and the diagnostic yield is low
§ Some studies have reported that colonoscopy is successful in identifying the bleeding source in up to 95% of patients.
2. RADIONUCLIDE SCANNING (Tagged RBC scan)

Radionuclide scanning with technetium-99m (99mTc–labeled RBC) is the most sensitive but least accurate method for localizing GI bleeding
§ With this technique, the patient’s own red cells are labeled and reinjected. The labeled blood is extravasated into the GI tract lumen, creating a
focus that can be detected scintigraphically
§ The RBC scan can detect bleeding as slow as 0.1 mL/min and is reported to be more than 90% sensitive. Unfortunately, the spatial
resolution is low and blood may move retrograde in the colon or distally in the small bowel. Reported accuracy of localization is in the range of
only 40% to 60% and it is particularly inaccurate for distinguishing right-sided from left-sided colonic bleeding
3. MESENTERIC ANGIOGRAPHY
§ Selective angiography, using the superior or inferior mesenteric arteries, can detect hemorrhage in the range of 0.5-1.0 mL/ min but is
generally only used for the diagnosis of ongoing hemorrhage. It can be particularly useful in identifying the vascular patterns of
angiodysplasias. It may also be used for localizing actively bleeding diverticula.
§ In addition, it has therapeutic capabilities:
1. Catheter-directed vasopressin infusion can provide temporary control of bleeding, permitting haemodynamic stabilization
2. It can also be used for embolization
§ Typically, such therapy is reserved for patients whose underlying condition precludes surgical therapy. Unfortunately, angiography is
associated with a ***significant risk of complications, including haematoma, arterial thrombosis, contrast reaction, and acute renal failure
LOWER GI BLEED – SPECIFIC CAUSES
1. DIVERTICULAR DISEASE
§ Bleeding generally occurs at the neck of the diverticulum and is believed to be secondary to bleeding from the vasa recti as they penetrate
through the submucosa.
INV:
§ Best method of diagnosis and treatment is colonoscopy
MGMT:
1. Colonoscopic: If the bleeding diverticulum can be identified, epinephrine injection may control the bleeding. Electrocautery can also be
used and, most recently, endoscopic clips have been successfully applied to control the haemorrhage.
2. Angiographic: If none of these maneuvers is successful or if haemorrhage recurs, angiography with embolization can be considered. (High
success rate)
3. Surgery: Under some circumstances, segmental colonic resection is indicated. Certainty of the site of bleeding is critical. “Blind
hemicolectomy” is associated with rebleeding in more than 50% of patients!!!
2. ANGIODYSPLASIA
§ Angiodysplasias of the intestine, also referred to as arteriovenous malformations (AVMs), are distinct from haemangiomas and true congenital
AVMS. They are thought to be acquired degenerative lesions secondary to progressive dilation of normal blood vessels within the
submucosa of the intestine
§ M=F. Age > 50
INV:
§ The haemorrhage tends to arise from the right side of the colon, with the caecum being the most common location, although they can occur
in the rest of the colon and small bowel
§ Lesions can be diagnosed by colonoscopy or angiography.
o Colonoscopy à Red stellate lesions with a surrounding rim of pale mucosa and can be treated with sclerotherapy or electrocautery.
o Angiography à Dilated, slowly emptying veins
MGMT:
1. If discovered incidentally, no further therapy is indicated.
2. Colonoscopic and Angiographic: Acutely bleeding patients have been successfully treated with intra-arterial vasopressin, selective gel
foam embolization, endoscopic electrocoagulation, or injection with sclerosing agents.
3. Surgery: If these measures fail, or bleeding recurs and the lesion has been localized, segmental resection, most commonly a right
colectomy, is effective
3. MESENTERIC ISCHAEMIA
§ Mesenteric ischaemia can be secondary to acute or chronic & arterial or venous insufficiency.
§ ***Predisposing factors include

1. Preexisting cardiovascular disease (e.g., atrial fibrillation, congestive heart failure, acute myocardial infarction),
2. Recent abdominal vascular surgery,
3. Hypercoagulable states,
4. Medications (e.g., vasopressors, digoxin), and
5. Vasculitis
§ Patients present with abdominal pain and bloody diarrhoea
INV:
§ CT will often show a thickened bowel wall
§ Sigmoidoscopy/colonoscopy: The diagnosis is generally confirmed with sigmoidoscopy/colonoscopy, which reveals oedema, haemorrhage,
and a demarcation between the normal and abnormal mucosa.
MGMT:
§ Treatment focuses on supportive care consisting of bowel rest, IV antibiotics, cardiovascular support, and correction of the low-flow state. In
85% of cases, the ischaemia is self-limited and resolves without incident, although some patients develop a colonic stricture.
**In the other 15% of cases, surgery is indicated because of progressive ischaemia and gangrene**
§ Marked leukocytosis, fever, a fluid requirement, tachycardia, acidosis, and peritonitis indicate a failure of the ischaemia to resolve and the need for
surgical intervention. During the surgery, resection of the ischaemic intestine and creation of an end ostomy is indicated
Classification of Hemorrhage
Class 1 : 500 ml - 750 ml loss

Class 2 : 750 ml - 1500 ml loss
Tachyacrdia, sweating, decrease urine
Class 3 : 1500 ml - 2L loss

Dyaphoresis, hypertension
Class 4 : 2L -
Shock, no urine
General Surgery
Peptic Ulcer Disease Summary Points. MUST USE FULL NOTES FOR BACKGROUND AND EXPLANATIONS
Source: Toronto, Harold Ellis, Other
February 2015
AETIOLOGIES OF PUD
• NB: NSAID negative, H. pylori negative ulcers becoming more commonly recognized
• Others: CMV, ischaemic, idiopathic
• Alcohol: damages gastric mucosa but rarely causes ulcers
• Peptic ulcer associated with tobacco, cirrhosis of liver, COPD and chronic renal failure
H. PYLORI-INDUCED PUD
PATHOPHYSIOLOGY
§ H. pylori: Gram-negative, helical, microaerophilic, flagellated rod that resides ONLY on (but does not invade) the gastric
mucosa
§ ***Acid secreted by parietal cells (stimulated by vagal acetylcholine, gastrin, histamine) necessary for most ulcers
MUST KNOW: POSSIBLE OUTCOMES OF H. PYLORI INFECTION
1. Gastritis (non-erosive) in 100% of patients but asymptomatic

2. Peptic ulcer in 15% of patients
3. Gastric malignancy:
a. Gastric carcinoma AND
b. Mucosal associated lymphomatous tissue (MALT) lymphoma in 0.5% of patients
4. Most are asymptomatic but still worthwhile eradicating to lower future risk of peptic ulcer/gastric malignancy and prevent
spread to others (mostly children <5 yr of age)
Modified Johnson classification for GASTRIC ulcers.

I. Lesser curve, incisura.
II. Body of stomach, incisura + duodenal ulcer (active or healed).
III. Prepyloric. (II & III associated with acid hypersecretion)
IV. High on lesser curve near gastroesophageal junction.
V. Medication-induced (NSAID/acetylsalicylic acid), anywhere in stomach
ADD THE MECHANISMS OF H. PYLORI PEPTIC ULCERATION HERE – SEE FULL NOTES
INVESTIGATIONS
CLASSIFY: RADIOLOGIC + ENDOSCOPY + H. PYLORI DETECTION
1. Routine labs
2. Diagnosis of H. pylori infection (SEE BELOW)
3. Upper GI contrast studies: Barium meal – Demonstrates barium in crater of ulcer
a. Single contrast – Detects only 50% of ulcers
b. Double contrast – Detects 80-90%
i. Malignancy suggested in GASTRIC ulcer if:
1. Elevated ulcer
2. Heaped up edges producing “meniscus sign”
3. > 2cm in size
4. No associated duodenal ulcer
4. Upper GI endoscopy – Direct visualization, allows biopsy, therapeutic in the setting of GI bleed or obstruction
a. Must perform 4 QUADRANT BIOPSY on all GASTRIC ulcers to rule out malignancy. DU biopsy not necessary
Diagnosis of H. pylori infection

H. pylori testing should also be done in ALL patients with suspected PUD
INVASIVE vs. NON-INVASIVE
Test Sensitivity Specificity Comments
Non-invasive Tests
13
1. C-Urea breath test 90-100% 89-100% Affected by PPI therapy (false negatives)
2. Serology 88-99% 89-95% Can remain positive long after treatment/eradication
3. Stool antigen test 95-97% 94-98% Useful for diagnosing acute infection
Invasive Tests (require endoscopy
with antral biopsy)
1. Histology (gold standard) 93-99% 95-99% Gold standard; affected by PPI therapy (false negatives)
2. Rapid urease test (on biopsy) 89-98% 93-100% Rapid
3. Microbiology culture 98% 95-100% Research only
CARBON-13 UREA BREATH TEST = The urea breath test is the method of choice to document eradication!!!
Serology cannot be used as it remains elevated for > 1 year
MANAGEMENT
PRINCIPLE: Management depends on the underlying aetiology! PUD has become largely a medical disease with the
discovery of H. pylori and eradication therapies. Surgery is now reserved for complications and intractability
MEDICAL VS. SURGICAL
A. MEDICAL MANAGEMENT is the mainstay of uncomplicated PUD
4 categories
1. Lifestyle modification – Stop NSAIDS, aspirin, smoking, alcohol, coffee
2. H. pylori eradication – If H. pylori is present. Triple or quadruple therapy. NOTE VERY WELL: Remember test for
eradication about 6 weeks after Rx!!!
3. Acid reduction: Antisecretory OR neutralization
a. Antacids – neutralizes acid
b. H2 receptor antagonists – Famotidine is most potent of all
c. PPIs – THE MOST POTENT ANTISECRETORY AGENTS
i. MOA: Inhibits parietal cell H+/K+-ATPase pump which secretes acid
ii. NB: PPIs require an acidic environment within the gastric lumen to become activated; thus, using
antacids or H2 receptor antagonists in combination with PPIs could have deleterious effects
4. Increase mucosal barrier
H. pylori eradication therapy

Therapy is twofold in its approach, combining antibiotics against H. pylori with acid reduction medications.
NOTE: Main goal is to lower recurrence. Eradication of H. pylori has shown recurrence rates as low as 2%
This includes an antisecretory agent, now most commonly a PPI, although histamine antagonists are still used, along with two
antibiotics, usually amoxicillin with clarithromycin or metronidazole, given for a 2-week course.
Triple therapy for 7-14 d (Hp-Pac®):

1. Amoxicillin 1 g bid +
2. Clarithromycin 500 mg bid
3. PPI bid (e.g. lansoprazole 30 mg bid) +
• 80% success rate
Quadruple therapy for 10-14 d:

1. Tetracycline 500 mg qid +
2. Metronidazole 250 mg qid
3. PPI bid +
4. Bismuth subsalicylate 525 mg qid +
• Only recommended as first line therapy if resistance to clarithromycin or metronidazole is high, or in patients
with recent or repeated exposure to these drugs
• Levofloxacin can replace metronidazole or tetracycline
5-15% of cases are resistant to all known therapies
B. SURGICAL
Elective surgery for PUD is almost non-existent. Surgery now reserved primarily for complications (20% of cases) OR failure of medical
management
Basic principles:
o Gastric ulcers: Treat by removing ulcer + GASTRIN-secreting zone of antrum (recall that the G cells are found in the
antrum). Traditionally by Billroth I gastrectomy. Now more commonly by antrectomy + Roux-en-Y gastroenterostomy
(preferred), the latter to limit bile reflux
o Duodenal ulcers: Treat by removing the bulk of the ACID-secreting area of stomach (body and lesser curvature) and
reestablish gastric drainage via a Roux-en-Y gastroenterostomy
Indications for surgery: INTRACTABILITY vs. COMPLICATIONS
1. Intractable PUD (rare)

2. Haemorrhage (10%) – severe if from the gastroduodenal artery
3. Gastric Outlet Obstruction (2%) (secondary to acute inflammation (mechanical + functional obstruction) OR chronic
inflammation (fibrosis and stenosis)) Non-bilious, stale food. Dehydration, sucussion splash
st
4. Perforation (2%) (usually anterior and 1 pt of duodenum) (BUT highest mortality ~15%)
5. Penetration (2%) (posterior – may penetrate into pancreas – what is the difference from perforation)
6. FOR GASTRIC ULCERS: Dyslpasia or carcinoma – it is uncertain whether the ulcer actually predisposes to carcinoma or if
ulcers are so common that the apparent relationship is incidental
• Intractability is defined as failure of an ulcer to heal after an initial trial of 8 to 12 weeks of therapy OR if patients
relapse after therapy has been discontinued. This is unusual for duodenal ulcer disease in the H. pylori era.
• RE: GASTRIC ULCERS: ALWAYS operate if fails to heal completely, even if biopsy negative: could be primary
gastric lymphoma or adenocarcinoma
• ***Benign gastric ulcers that persist must be evaluated for malignancy
I. INTRACTABILITY (RARE) – DEFINITIVE ACID LOWERING OPERATIONS:
PRINCIPLES:
1. Reduce gastric acid secretion. “Acid-lowering” procedure
a. Vagotomy reduces the cephalic phase! Antrectomy reduces the antral phase!
2. Restore gastric drainage (Pyloroplasty (Heineke-Mikulicz pyloroplasty) OR a Billroth procedure)
Options (May be OPEN or LAPAROSCOPIC):
1. Vagotomy only (decrease acid output by ~50%)

a. Truncal vagotomy - division of the left and right vagus nerves above the hepatic and celiac branches. Interferes with
gastric emptying so MUST BE ACCOMPANIED BY A DRAINAGE PROCEDURE, either *gastrojejunostomy or
*pyloroplasty
o ***Heineke-Mikulicz pyloroplasty: Longitudinal incision through all layers of the pylorus, sewing closed in a transverse
direction to make the pylorus nonfunctional
b. Highly selective vagotomy (aka. parietal cell vagotomy) – If the branches of the vagus that supply the pyloric
sphincter (the nerves of Latarjet) are left intact, the remaining vagal fibres can be divided without the necessity of
gastric drainage. Divides only the vagus nerves supplying the acid-producing portion of the stomach within the corpus
(body) and fundus. Developed after recognition that truncal vagotomy, in combination with a drainage procedure or
gastric resection, adversely affects the pyloric antral pump function.
2. Vagotomy + Antrectomy (decrease acid output by ~85%)
o Antrectomy (eliminates hormonal stimulation from the antrum) is generally NOT performed for duodenal ulcers and is
more commonly done for gastric ulcers
o Antrectomy requires reconstruction of GI continuity that can be accomplished by a:
§ Gastroduodenostomy (Billroth I procedure) OR (see images on last page of Billroth reconstruction)
§ Gastrojejunostomy (Billroth II procedure)
o For benign disease, gastroduodenostomy is generally favored because it avoids the problem of retained antrum
syndrome, duodenal stump leak, and afferent loop obstruction associated with gastrojejunostomy after resection
SEE LAST PAGE FOR THE DIFFERENT BILLROTH OPERATIONS EXPLANATION
Laparoscopic peptic ulcer operations (SURGICAL TUTOR)

1. Thoracoscopic truncal vagotomy and pyloric stretch
2. Truncal vagotomy and pyloric stretch
3. Highly selective vagotomy
4. Posterior truncal vagotomy and selective anterior vagotomy
5. Posterior truncal vagotomy and anterior seromyotomy
RE: Diagnosis and Treatment of GASTRIC ULCERS
The diagnosis and treatment of gastric ulceration generally mirror that for duodenal ulcer disease.
The significant difference is the possibility of malignancy in a gastric ulcer.

This critical difference ALWAYS demands that cancer be ruled out via biopsy in acute and chronic presentations of gastric ulcer
disease
The presentation of a nonhealing gastric ulcer in the H. pylori era should raise serious concerns about the presence of an
underlying malignancy
Toronto Notes: Procedures for gastric ulcers

• Distal gastrectomy with ulcer excision: Billroth I or Billroth II
• Vagotomy and pyloroplasty only if acid hypersecretion (rare)
• Wedge resection if possible or biopsy with primary repair
COMPLICATIONS
I. HAEMORRHAGE: SEE END OF THIS DOCUMENT!!!
II. PERFORATION
• Perforation most common in the first part of the duodenum
• Sudden onset of pain. Acute abdomen: Rigid, diffuse guarding, ileus
• ERECT CHEST X-RAY – Pneumoperitoneum: Free air under diaphragm (70%) of cases. I.E. REMAINDER DO NOT HAVE
DEMONSTRABLE AIR
• CT MORE SENSITIVE TO DETECT INTRAPERITONEAL FREE GAS and exclude common differentials
EMERGENT SURGICAL INTERVENTION. Options:

§ Preoperative preparation
o Fluid resuscitation with CVP or Swan Ganz monitoring
o Analgesia
o Antibiotics
o Nasogastric intubation
**May be: Open vs. Laparoscopic

1. Oversewing of bleeding ulcer
§ Use 2/0 synthetic absorbable
For larger perforations:
2. Graham patch repair (Graham-Steele repair)– plication of ulcer and omental patch (MOST COMMON)
3. Antrectomy and Billroth II reconstruction
• After repair, the stomach is decompressed until bowel activity returns

• Also, initiate H. pylori eradication
Surgical tutor: After oversewing:

§ Thorough wash out and irrigation of peritoneal cavity with 0.9% saline
§ If unable to find perforation open the less sac
§ Remember that multiple perforations can occur
§ If closure secure and adequate toilet then a drain is not required
§ Prepyloric ulcer behave as duodenal ulcers
§ ***All gastric ulcers require biopsy to exclude malignancy
§ Definitive ulcer surgery probably not required
§ 50% patients develop no ulcer recurrence
§ Postoperatively patients should receive H. pylori eradication therapy
III. GASTRIC OUTLET OBSTRUCTION

• NG decompression and correction of hypochloraemic, hypokalemic metabolic alkalosis
• Medical management initially: high dose PPI therapy
• Surgical resection if obstruction does not resolve: either Billroth I, pyloroplasty or gastrojejunostomy
MANAGEMENT OF BLEEDING PEPTIC ULCERS

1. OGD to explore upper GI tract (see image below)
2. Establish risk of rebleeding/continuous bleed

a. Clinical risk factors: increased age (>60), bleeding diathesis, history of PUD, comorbid disease, hemodynamically
unstable
b. Endoscopic signs of recurrent bleeding (active bleeding, visible vessel, clot, red spot) - more predictive than
clinical risk factors
• If high risk, consider ICU admission
• Interventional radiology: angiography with embolization/coiling

• Surgery: if severe or recurrent bleeding, hemodynamically unstable, or failure of endoscopy and IR:
o Oversewing of bleeding ulcer ± pyloroplasty
HAEMORRHAGE (Sabiston)
(PUD) still represents the most frequent cause of upper GI hemorrhage, accounting for ~40% of all cases
• Approximately 10%-15% of patients with PUD develop bleeding at some point in the course of their disease.
• Bleeding is the most frequent indication for operation!!! and the principal cause for death in PUD!!!
Bleeding develops as a consequence of peptic acid erosion of the mucosal surface. Although chronic blood loss is common with any ulcer, significant
bleeding typically results when there is involvement of an artery of the submucosa or, with penetration of the ulcer, an even larger vessel.
• POINT: Although duodenal ulcers are more common than gastric ulcers, gastric ulcers usually bleed
• POINT: Most significant hemorrhage occurs when duodenal or gastric ulcers penetrate into branches of the gastroduodenal artery
or left gastric arteries, respectively
TREATMENT
Patients with clinical evidence of a GI bleed should receive an endoscopy within 24 hours and, while awaiting this procedure, they should be treated
with a PPI
After the index endoscopy, treatment strategies depend on the appearance of the lesion at endoscopy.
• Endoscopic therapy is instituted if bleeding is active OR, when bleeding has already stopped, if there is a significant risk of rebleeding
MUST KNOW: The Forrest classification was developed in an attempt to assess this risk based on endoscopic findings and stratify the patients into
low-, intermediate-, and high-risk groups.
• Endoscopic therapy is recommended in cases of active bleeding as well as those with a visible vessel (Forrest I to IIa).
• In case of an adherent clot (Forrest IIb), the clot is removed and the underlying lesion evaluated.
• Ulcers with a clean base or black spot, secondary to hematin deposition, are generally not treated endoscopically
Medical Management
In cases of a confirmed peptic ulcer bleed, PPIs have been shown to reduce the risk of rebleeding. Also start empirical H. pylori therapy
Therefore, patients with a suspected or confirmed bleeding ulcer should be started on a PPI
In patients who are taking ulcerogenic medications such as NSAIDs or SSRIs, and present with a bleeding GI lesion, these agents should be stopped. In
those taking NSAIDs, more specific cycloxygenase-2 (COX-2) inhibitors, which are associated with reduced ulceration, HAD BEEN a promising
alternative.
• BUT affecting the popularity of these medications have been population-based studies showing that not all COX-2 inhibitors result in a
decreased incidence of upper GI complications
Endoscopic Management
Once the bleeding ulcer has been identified, effective local therapy can be delivered endoscopically to control the hemorrhage. Available endoscopic
options include epinephrine injection, heater probes, and coagulation, as well as the application of clips
• Epinephrine injection alone is associated with a high rebleeding rate; standard practice is to provide combination therapy
• Electrocoagulation, or laser or argon plasma coagulation (APC).
• A combination of injection with thermal therapy achieves hemostasis in 90% of bleeding PUDs
Rebleeding of an ulcer is associated with a significant increase in mortality
In those who rebleed, the role of a second attempt at endoscopic control has been controversial but has been validated.
Although this will fail in 25% of patients, who will then require emergent surgery
Most clinicians would now encourage a second attempt at endoscopic control before subjecting the patient to surgery.
Surgical Management: Dr. East: Principle: Undersew the ulcer THEN may or may not do a definitive procedure. If
GU à Also biopsy
Approximately 10% of patients with bleeding ulcers still require surgical intervention for effective hemostasis
The clinical factors to consider are shock and a low hemoglobin level at presentation. At the time of endoscopy, although the Forrest classification is
the most important indicator of rebleeding risk, the location and size of the ulcer are also significant.
• Ulcers larger than 2 cm, posterior duodenal ulcers, and gastric ulcers à Significantly higher risk of rebleeding.
Indications for surgery were traditionally based on the blood transfusion requirements. Increased blood transfusions are clearly associated with
increased mortality
The first priority at operation should be control of the hemorrhage. Once this is accomplished, a decision must be made regarding the need for a
definitive acid-reducing procedure. Each of these steps varies, depending on whether the lesion is a duodenal or gastric ulcer.
DUODENAL ULCER
First step in surgery for a duodenal ulcer is exposure of the bleeding site
Hemorrhage can typically be controlled initially with pressure and then direct suture ligation with nonabsorbable suture.
A posterior ulcer eroding into the pancreaticoduodenal or gastroduodenal artery may require suture ligation of the vessel proximal and distal to the ulcer
Once the bleeding has been addressed, a definitive acid reducing operation should be considered!!! (SEE ABOVE). With the identification of the
role of H. pylori infection in duodenal ulcer, the usefulness of such a procedure has been questioned, based on the argument that simple closure and
subsequent treatment for infection should be sufficient to prevent recurrence
GASTRIC ULCER
For a bleeding gastric ulcer, again, control of bleeding is the immediate priority. Although it may initially require gastrotomy and suture ligation, this alone
is associated with a high risk of rebleeding of almost 30%. In addition, because of a 10% incidence of malignancy, gastric ulcer resection is
generally indicated
RE: SURGICAL REMOVAL OF INTRACTABLE ULCERS AND GASTRIN-SECRETING TISSUE
Partial gastrectomy was occasionally used for patients where medical management had failed to heal a benign gastric ulcer or to treat
repeated recurrences. The operation had the dual role of removing the ulcer and the gastrin-secreting mucosa. The classic gastrectomy
for chronic gastric ulcer was known as the Billroth I type (Billroth, 1881) and involved removing the distal two-thirds of the stomach.
The gastric remnant was then anastomosed to the first part of the duodenum. The standard partial gastrectomy for duodenal ulcers was
a Polya-type gastrectomy (Polya, 1911), also involving resection of the distal two-thirds of the stomach but anastomosing the cut end
of the stomach to the side of a loop of proximal jejunum (gastro-jejunostomy). This is also known as a Billroth II operation. The cut
end of the duodenum (duodenal stump) was closed and the ulcer left in situ to heal.
Numerous variations on gastrectomy have been described over the years, but the essential difference is whether the gastric remnant is
anastomosed to the duodenum (Billroth I-type) or to a jejunal loop (Polya-type). In general, partial gastrectomy was highly effective in
relieving symptoms and preventing recurrence of peptic disease, but long-term side-effects were a serious problem affecting 30–40% of
patients.
General Surgery
Diverticular Disease Notes
Source: Sabiston, Toronto Notes, Dr. East
March 2015
DIVERTICULAR DISEASE
DEFINITION AND INCIDENCE
A diverticulum is an abnormal outpouching of the wall of a hollow organ. In this case the colon
• True diverticulum à Composed of all layers of the intestinal wall (E.g. Meckel’s diverticulum)
• False diverticulum aka. Pseudodiverticulum à Mucosa only
Colonic diverticula = False, pulsion diverticula of the colon consisting of herniations of mucosa through the muscular layers of the colon at sites of
penetration of the muscular wall by arterioles (anatomically weak points) i.e. Where vasa recta penetrate the circular muscular layer – these
sites are on the *mesenteric side of the antimesenteric taeniae (see image on last page)
The terms diverticulosis and diverticular disease refer to the PRESENCE of colonic diverticula
(Look up pulsion vs. traction diverticulum)
RISK FACTORS
Not fully elucidated. Thought to be mainly:
LIFESTYLE (DIETARY) & MUSCLE WALL WEAKNESS
LIFESTYLE: Interesting point:
***No specimens of colonic diverticulosis are present in anatomic or medical museums in Europe before the industrial revolution à
th
**Diverticulosis was initially observed in the first decade of the 20 century à
1. ↓ Fiber consumption by North Americans and in Western Europe (↓ consumption of unprocessed cereals)
a. Explanation in pathogenesis below
b. **Supporting the low-fibre diet aetiology, diverticulosis is RARE in sub-Saharan blacks who have a high fibre diet BUT common in blacks
in Johannesburg (South Africa) who consume a low-fibre diet
2. Also, ↑ sugar and meat consumption by the general population are factors largely responsible for the appearance of diverticulosis.
MUSCLE WALL WEAKNESS

1. Aging!!!: Diverticulosis also related to aging – RARE in < 30 years old
a. But at least 2/3 of Americans will have developed colonic diverticula by age 80
2. Connective tissue disease: (e.g. Ehler-Danlos, Marfan’s)
INCIDENCE
§ 5-50% of Western population, lower incidence in non-Western countries
§ M=F
§ Prevalence is age dependent: <5% by age 40, 30% by age 60, 65% by age 85
§ 95% involve sigmoid colon (site of highest pressure)
PATHOGENESIS
Colonic diverticula = Herniations of mucosa through the muscular layers of the colon at sites of penetration of the muscular wall by arterioles
(anatomically weak points) i.e. Where vasa recta penetrate the circular muscular layer – these sites are on the *mesenteric side of the
antimesenteric taeniae.
§ *NOTE WELL: Because there are no perforating vessels on the antimesenteric side of the colon, diverticulae only form between
mesenteric taeniae!!!
***This close relationship between artery and diverticulum is responsible for the massive haemorrhage that can occasionally complicate
diverticulosis***
**Often there is a striking hypertrophy of the muscular layers of the colonic wall associated with diverticulosis
Ø Diverticula most commonly affect the sigmoid colon –

o 95% of cases overall involve sigmoid colon (65+30%) (Sigmoid is site of highest pressure, and has smallest lumen!!)
o Sigmoid ALONE in 50-65% of patients!
o Sigmoid colon + another segment = 30%
Ø Next most common = descending (~40%).
Ø Caecum = 7%
Ø Entire colon in 5-10%
MUST KNOW THIS EXPLANATION:

• High fibre diets result in large volume of stool in colonic lumen. Therefore LESS contractile pressure needs to be generated to propel faeces
forward. In these cases, colonic pressure is only slightly higher than atmospheric pressure.
• With DECREASED FIBRE, there is DECREASED STOOL BULK in the lumen and requires INCREASED COLONIC PRESSURES to propel
faeces.
• High intraluminal pressures thought to be responsible for the herniations of mucosa at anatomically weak points. Dr. East: i.e. sites
of penetration of vasa recta AND where longitudinal muscle is deficient (e.g. between taeniae)
• Almost never occur in the rectum (where longitudinal layer is reconstituted)
Clinical features of diverticulosis

• Uncomplicated diverticulosis: Asymptomatic (70-80%)
• Episodic abdominal pain (often LLQ), bloating, flatulence, constipation, diarrhoea
• Absence of fever/leukocytosis
• No physical exam findings or poorly localized LLQ tenderness
Complications:
• Diverticulitis (15-25%): 25% of which are complicated (i.e. abscess, obstruction, perforation, fistula)
• Bleeding (5-15%): PAINLESS rectal bleeding, 30-50% of massive lower GI bleeds
• Diverticular colitis (rare): diarrhoea, haematochezia, tenesmus, abdominal pain
DIVERTICULITIS
Important points à UNDERTAND THEM!!!:
Sabiston: Diverticulitis is a result of PERFORATION of a colonic diverticulum, which may be MICROPERFORATION (initially) or
MACROPERFORATION. (Me: So the term perforated diverticulitis is actually redundant??)
NOTE: The term diverticulitis is a MISNOMER as the disease is actually extraluminal PERICOLIC infection resulting from
extravasated faeces through the perforation.
PERIDIVERTICULITIS is actually the more appropriate term to describe this infectious process. The infection is as a result of the perforation.
(Me: So the condition is not simply inflammation of the diverticulum itself??)
Pathogenesis (Toronto)
• Erosion of the wall by increased intraluminal pressure or inspissated food particles/faecalith à inflammation and focal necrosis à micro or macroscopic
perforation
• Usually mild inflammation with perforation walled off by pericolic fat and mesentery; abscess, fistula or obstruction can ensue
• Poor containment results in free perforation and peritonitis!!
CLINICAL FEATURES
FIRST PRINCIPLE: Depends on severity of inflammation and whether or not complications are present; hence ranges from asymptomatic to
generalized peritonitis
CLASSIFY: UNCOMPLICATED vs. COMPLICATED
Approach the answer by starting with the uncomplicated presentation, then the added features for each possible complication
A. UNCOMPLICATED
HISTORY (THINK ALL THE GI SYMPTOMS!!!)
• Patients usually complain of LEFT LOWER QUADRANT PAIN (as sigmoid is most common site).
o May radiate to back, hypogastrium (hindgut structure), left groin.
• Alterations in bowel habits also common (Constipation, diarrhoea)
• Nausea, vomiting
• Fever, chills
• Urinary symptoms!! (Due to adjacent inflammation)
• Rectal bleeding is NOT usually associated – as it is an infectious inflammatory process
PHYSICAL FINDINGS
Depend on SITE of perforation + AMOUNT OF CONTAMINATION
GENERAL
§ Fever and leukocytosis if perforated
ABDOMEN
• Most common finding is TENDERNESS OF LEFT LOWER ABDOMEN
• May be voluntary guarding of left abdominal wall musculature (look up voluntary vs. involuntary guarding)
• Tender mass suggests a phlegmon or abscess
• NOTE: Abdominal wall distension may be detected if there is associated ileus or SBO secondary to the inflammatory process
DRE
• NOTE: Rectal/vaginal exam may reveal a tender, fluctuant mass typical of a pelvic abscess
B. COMPLICATIONS (25% OF CASES):

1. Abscess: Palpable tender abdominal OR rectal mass
2. Fistula: Colovesical (most common), coloenteric, colovaginal, colocutaneous
3. Colonic obstruction: **Due to scarring and stricturing from repeated inflammation!!
4. Bleeding
5. Free perforation: à Generalized peritonitis (Faeculent vs. Purulent)
o Features include involuntary guarding, rebound tenderness, absent bowel sounds due to ileus
DIAGNOSIS
Must distinguish sigmoid diverticulitis from cancer!!:

The surgical approach to diverticulitis is significantly different than that required for a perforated sigmoid cancer and as such if urgent
operation is needed, effort should be made to exclude cancer diagnosis.
• Limited sigmoidoscopy may be helpful here – only useful to exclude rectal ca. due to its reach
• Air should NOT be insufflated through scope: Possible increased colonic pressure may force more bacteria through perforation and
into peritoneal cavity
Diagnosis can usually be presumed by careful history and exam and it is reasonable to START ANTIBIOTICS based on this alone.
INVESTIGATIONS
GENERAL LABORATORY VS. SPECIFIC IMAGING VS. AFTER RESOLUTION
A. GENERAL
1. CBC
a. Leucocytosis. More marked if perforation
B. SPECIFIC IMAGING
1. Plain erect and supine AXR and erect CXR:

a. Localized diverticulitis (ileus, thickened wall, SBO, partial colonic obstruction)
b. Free air may be seen in 30% with perforation and generalized peritonitis
2. CT – (TEST OF CHOICE!!!) preferred over MRI. MANY Uses:

97% sensitive, 99% specific
a. Reveals location and extent of infection + inflammation
b. Presence of abscess
c. Sympathetic involvement of other organs with secondary complications such as ureteral obstruction
d. Bladder fistula (Colovesical fistula)
e. ALSO – THERAPEUTIC for CT-guided percutaneous abscess drainage
10% of diverticulitis cannot be distinguished from carcinoma
3. MRI
4. Abdominal U/S – Offers many of the advantages of CT, including the percutaneous drainage
5. Water-soluble contrast enema – Use has been diminished considerably!!! – Due to advantages of non-invasive tests. Also, enema
carries RISK of extravasation of more bacteria
• Many surgeons believe the risks outweigh the potential benefits
• Saw-tooth pattern (colonic spasm)
• Water-soluble contrast only (e.g. Gastrografin®). NEVER barium – risk of barium fecal peritonitis. Still a risk of any contrast
material causing aggravation either way
o Re: Water-soluble contrast: Diatrizoic acid (or its anionic form, diatrizoate), also known as amidotrizoic acid, or 3,5-diacetamido-2,4,6-
triiodobenzoic acid, is a radiocontrast agent containing iodine.
o Trade names include Hypaque, Gastrografin and Urografin, the latter being a combination of the sodium and meglumine salts.
C. DON’T FORGET: ~3 weeks after resolution of acute episode:

Purpose of elective evaluations: ESTABLISH EXTENT OF DISEASE and RULE OUT OTHER DIAGNOSES (polyps, malignancy):
• Colonoscopy or barium enema and flexible sigmoidoscopy
HINCHEY CLASSIFICATION OF PERFORATED DIVERTICULITIS:
• Stage I: Pericolic or mesenteric abscess

• Stage II: Walled-off pelvic abscess
• Stage III: Purulent peritonitis
• Stage IV: Faecal peritonitis
MANAGEMENT
Treatment must be individualized based on severity
Depends on if COMPLICATED or UNCOMPLICATED
Many guidelines exist: Toronto Notes summary then Sabiston details:

Toronto Notes Summary:
• UNCOMPLICATED: CONSERVATIVE MANAGEMENT
o Outpatient: Clear fluids only until improvement and antibiotics (e.g. ciprofloxacin and metronidazole) 7-10 d to cover gram negative
rods and anaerobes (e.g. B. fragilis)
o Commence high fibre diet
o HOSPITALIZE IF: Severe presentation, inability to tolerate oral intake, significant comorbidities, fail to improve outpatient management
o Treat with NPO, IVF, IV antibiotics (e.g. IV ceftriaxone + metronidazole, ampicillin, gentamicin), analgesia
• MUST KNOW: INDICATIONS FOR SURGERY:

1. Hinchey stage 3-4
2. Unstable patient with peritonitis
3. After 1 uncomplicated attack if: (a) immunosuppressed, (b) abscess needing percutaneous drainage
4. Consider after 2 or more attacks, recent trend is toward conservative management of recurrent mild/moderate attacks
5. Complications: Generalized peritonitis, free air, abscess, fistula, obstruction, haemorrhage, inability to rule out colon cancer on
endoscopy
6. Failure of medical management
• Surgical procedures (in most cases):
o Emergency or complex cases: Hartmann procedure: colon resection + Colostomy and rectal stump à ***Colostomy reversal in
3-6 mo
o Elective cases OR minimal contamination of the abdominal cavity: consider colon resection + primary anastomosis
UNCOMPLICATED DIVERTICULITIS à
PRINCIPLE: CONSERVATIVE MANAGEMENT +/- ELECTIVE SURGERY AFTER ACUTE ATTACK!!
Definition of uncomplicated diverticulitis:

Diverticulitis not associated with:
1. Free perforation
2. Obstruction
3. Fistula formation
- May be treated with antibiotics on an outpatient basis (Know the abx for the enteric organisms)
o 7-10 days. MUST COVER GRAM-NEGATIVE RODS AND ANAEROBES
- Commence high fibre diet
- Also, clear fluids only until improvement (why?)
INDICATIONS FOR ADMISSION IF UNCOMPLICATED:

Severe presentation, inability to tolerate oral intake, significant comorbidities, fail to improve outpatient management
Significant increased pain (localized peritonitis) à
1. Admission
2. NPO
3. IVF
4. IV antibiotics (e.g. IV ceftriaxone + metronidazole, ampicillin, gentamicin)
5. Analgesia (Pethidine NOT morphine)
6. Commence high fibre diet – No evidence for reversal of disease, but may stabilize it
NOTE WELL:
• AVOID MORPHINE because of increased colonic pressure associated with its use!!!
• PETHIDINE (MEPERIDINE) more appropriate analgesic - reported to decrease intraluminal pressure
***After symptoms have subsided for at least 3 weeks, INVESTIGATIONS to establish presence of diverticula AND exclude cancer:
1. Preferred test is COLONOSCOPY
2. Barium enema can demonstrate extent of diverticular disease but a sigmoid cancer may be hidden my numerous contrast filled diverticula –
significantly diminishes value of BE
First attack of uncomplicated diverticulitis that responds to antibiotics is generally treated NON-OPERATIVELY by starting a high-fibre diet
Chances of a second attack in these cases are < 25%
NEXT POINT: RE: FOLLOW-UP ELECTIVE SIGMOIDECTOMY

• Some surgeons recommend elective sigmoidectomy after recovery in younger patients (< 50) due to theoretical risk of
recurrence
• Other studies contradict this and suggest they should be managed in the same way as older patients
CONTROVERSIAL:
Surgical management considered if patient suffers recurrent attacks of diverticulitis. GENERALLY RECOMMENDED THAT SIGMOIDECTOMY BE
OFFERED AFTER 2 UNCOMPLICATED ATTACKS of diverticulitis – to prevent a future complicated episode needing emergency operation
• Another study suggested after 4 episodes instead of 2
• ** BUT Reconsidered in light of newer evidence that suggests pt with more than 2 episodes are not at risk for poorer outcomes and
morbidity and mortality are not significantly different. SO there is now a trend toward conservative management of each episode
NEXT POINT: Diverticulitis in the immunocompromised à Elective sigmoidectomy after a single attack should be considered
because of their decreased ability to combat infection
Growing trend:
Use of laparoscopic approach in ELECTIVE surgery (sigmoidectomy) for diverticulitis
- Most studies reveal a shorter hospital stay of 2-3 days compared to those undergoing standard midline incision
COMPLICATED DIVERTICULITIS (25%)

Complications (25% of cases)
1. Localized abscess (pericolic or pelvic)
2. Fistula
3. Free intraperitoneal perforation
4. Generalized peritonitis
5. Obstruction
6. Massive bleeding
7. Diverticulitis-associated colitis
*MASSIVE BLEEDING
§ Erosion of adjacent nutrient artery
§ Complicates 5% of cases of diverticulosis
§ Responsible for 55% of cases of lower GI bleed
§ Occurs from right sided diverticula more commonly than on left (about 75%, despite higher prevalence of diverticula on left)
§ Almost never associated with clinical inflammation
§ Stops spontaneously in >90% of cases
§ High recurrence rate (about 25%)
Diagnosis
§ MUST RULE OUT RECTAL BLEEDING BY SIGMOIDOSCOPY FIRST BEFORE OPERATING!!!
§ Must rule out upper GI bleeding by NG tube or gastroscopy
§ Try to localize bleed point by selective angiography, radionuclide scan or colonoscopy
§ Localization may not be successful or may be unwise.
Management
§ Settles spontaneously > 90% of time
§ Resection of affected segment if localization successful
§ Resection of entire colon and ileo-rectal anastomosis if localization unsuccessful or unwise
*ABSCESS
§ Usually confined to the pelvis
§ ***Significant pain, fever and leukocytosis
§ Abdominal or pelvic or rectal exam may detect tender, fluctuant mass
§ CT/MRI/US confirms the diagnosis and location
§ If small (< 2cm) à should be drained à preferred method is percutaneous CT/US guided draining
o Occasionally via rectum through a transanal approach
o Adequate drainage + antibiotics usually results in rapid improvement
§ Offer elective surgery after patient has completely recovered – usually ~ 6 wks after drainage
§ At this time, usually feasible to excise the diseased sigmoid colon and fashion and anastomosis between descending colon and rectum, thus
avoiding a colostomy
§ Major cause of recurrent diverticulitis is failure to remove the entire abnormally thickened bowel that is associated with the disease completely
§ Only the colon that is thickened and brittle (usually entire sigmoid) needs to be resected
*FISTULA
§ Relatively frequent complication of diverticulitis
§ May occur between colon and SKIN (spontaneous or resulting from percutaneous abscess drainage), bladder, vaginal, small bowel
§ ** Cure will not be achieved until the source of infection is eradicated by excising the diseased sigmoid colon!!!
§ Diverticulitis is a more common cause of fistula between bladder and colon than Chron’s disease or cancer!!!
§ Sigmoid-vesicular fistulae more common in men than women. REASON: Uterus prevents sigmoid from adhering to bladder.
§ Symptoms of sigmoid-vesicular fistula: PNEUMATURIA (air from urethra at end of micturition), FECALURIA, recurrent UTI
o Possible urosepsis in men
§ Reliable test to confirm fistula: CT SCAN – may demonstrate AIR IN THE BLADDER
o Barium enema very low sensitivity < 50%
§ ***MUST confirm diagnosis before definitive operation!
§ COLONOSCOPY to exclude colon ca or Chron’s disease as the cause. Very different treatment
§ Initial treatment of any fistula caused by diverticulitis: CONTROL THE INFECTION AND REDUCE THE ASSOCIATED INFLAMMATION
§ Rarely a cause for emergency surgery
§ Administer antibiotics
§ Definitive treatment: Diverticulitis fistulas usually treated with a ONE-STAGE operation – take down fistula and excise sigmoid colon.
Then anastomose rectum and descending colon.
§ The bladder usually heals on its own as the defect is usually so small – Just put in a Foley catheter or suprapubic cystostomy for 7
days. Larger defects à closure with absorbable sutures OR Graham’s patch
*GENERALIZED PERITONITIS
§ Requires immediate operative intervention
§ Pts have diffuse abdominal tenderness, voluntary and involuntary guarding over entire abdomen
§ Signs of generalised sepsis à increased WBC, fever, tachycardia, hypotension (look up septic shock and types of shock lecture)
§ CT scan à free intraperitoneal air
MANAGEMENT
§ In these cases, NOT safe to restore a primary anastomosis due to high risk of anastomotic breakdown in the hostile and infectious
environment
§ ***Proper surgical procedure is HARTMANN’S OPERATION – resect the diseased sigmoid colon, construct a colostomy using descending
colon, suture the divided end of rectum closed -> Hartmann’s operation – Named after Henri Hartmann – French surgeon in 1921
o This is the most common procedure used in this case
§ Also irrigate peritoneal cavity
§ Cover with IV antibiotics.
§ Can take down colostomy usually after at least 10 weeks when patient fully recovered then fashion an anastomosis between descending
colon and rectum
§ ***NOTE: Recent reports of successful treatment of acute complicated diverticulitis by laparoscopic lavage and IV abx
without resecting diseased segment FOR UP TO HINCHEY 3 BUT the Hartmann’s is still the preferred operation at this
time
*OBSTRUCTION
§ 2 circumstances cause obstruction in diverticulitis

1. Narrowing of sigmoid because of the muscular hypertrophy of the bowel wall à stricture à rarely causes obstruction. But may make it
impossible to distinguish from ca on radiology
2. More common à SMALL BOWEL OBSTRUCTION assc with the infectious and inflammatory aspect of diverticulitis. SB may adhere to
an abscess or phlegmon. Treatment in this case: NG tube to relive upper intestinal secretions. Treat infection with antibiotics and
percutaneous drainage of abscess
General Surgery
Acute Appendicitis and Appendicular Mass
Sources: Toronto Notes, Harold Ellis
February 2015
EPIDEMIOLOGY
§ 6% of population
§ M>F
§ 80% between 5-35 yr of age
§ Most common abdominal emergency!!!
PATHOGENESIS
KNOW THIS: LUMINAL OBSTRUCTION (MOST, BUT NOT ALL CASES) à Bacterial overgrowth à Inflammation/swelling à Increased intraluminal
pressure à Veins occluded first due to their lower pressure, followed by arteries à Localized ischaemia (as the appendix is supplied by ***end-arteries,
which are branches of the appendicular branch of the ileocolic artery (contained in the mesoappendix). Once thrombosed, gangrene is inevitable)
à Gangrene/perforation à Localized abscess (walled off by omentum) OR peritonitis
No strict time relationship for this chain of events. May perforate in < 12 hours or even > 3-4 days
***POINT: Acute appendicitis is relatively RARE at both extremes of age. Reasons:

§ Infants: Have a wide-mouthed and well-drained appendix
§ Old age: Lumen of appendix is almost obliterated
AETIOLOGIES (REMEMBER: Related to AGE group!!)

[PRINCIPLE: ANYTHING THAT CAUSES OBSTRUCTION OF THE LUMEN! Red = common causes. Others uncommon to rare]
§ Children or young adult:

o *Hyperplasia of lymphoid follicles (initiated by infection)
§ Adult:
o *Fecalith (hard mass of dry faeces that can obstruct the appendix)
o *Fibrosis/stricture
o *Obstructing tumour (**carcinoid tumour near its base, **caecal tumour, **ascending colon tumour)
§ Other causes:
o *Parasites
o *Foreign body
NOTE VERY WELL: Appendicitis can occur in the non-obstructed appendix!! Due to direct infection of the lymphoid follicles from the
appendix lumen OR in some cases, **haematogenous infection!!! (e.g. the rare streptococcal appendicitis)
CLINICAL FEATURES
§ Most reliable feature is progression of signs and symptoms

§ Abdominal pain then anorexia, nausea and vomiting
o ***Abdominal pain classic pattern: Pain initially periumbilical; constant, dull, poorly localized, then shifts after ~6 hours to RIF, well
localized pain over McBurney’s point
o REASON: This is due to progression of disease from visceral irritation (causing referred pain from structures of the embryonic
midgut, including the appendix) to localized irritation of parietal structures
§ Low grade fever (38.C), **rises if perforation!!!
§ Important: Common for patient to admit to one or more previous milder episodes of the pain. Referred to as “grumbling appendix”: [Due to
appendiceal colic and not necessarily inflammation (In text and mentioned by Dr. East)]
§ DON’T FORGET: ALSO Depending on the various positions of the appendix:

o Pelvic à Urinary frequency, dysuria due to bladder irritation
o Retroileal à Constipation, diarrhoea or tenesmus
o Look up others
***WITH PERFORATION: May be a temporary remission or even cessation of pain!!! as tension in the distended organ is
relieved!!! Followed by the more severe and more generalized pain as general peritonitis develops
SIGNS
A. GENERAL
§ Toxic appearance, painful distress
§ Fever and tachycardia common
§ Tongue often coated + fetor oris
B. ABDOMEN
§ Signs of LOCAL OR GENERAL PERITONITIS: Guarding, rebound tenderness. (If answering a question on appendicitis presentation, MUST
mention McBurney’s sign and that there are a number of other signs and call some names, but make sure go to DRE findings!!!)
§ Late cases: Features of generalized peritonitis: Diffuse tenderness, rebound, guarding, rigidity, absent bowel sounds
Other signs
1. McBurney’s sign: Inferior appendix: Maximal pain at a point 1/3 on an imaginary line drawn from the ASIS to the umbilicus
2. Rovsing’s sign Inferior appendix: Tenderness in the right iliac fossa on palpation of the left iliac fossa
3. Iliopsoas sign: Retrocaecal appendix: (i.e. the appendix rests on the course of the right psoas muscle): (RLQ pain on passive
hyperextension of hip or flexion of RIGHT hip against resistance)
4. Obturator sign: Pelvic appendix: (RLQ pain with internal and external rotation of the flexed RIGHT hip)
5. Dunphy’s sign: Sharp pain in right iliac fossa elicited by coughing
6. Markle sign: Pain elicited in a certain area of the abdomen when the standing patient drops from standing on toes to the heels with a jarring
landing. Has a sensitivity of 74%
7. Pointing sign
C. DRE (IMPORTANT): Right wall tenderness if pelvic appendix OR if pus in pouch of Douglas
COMPLICATIONS:
1. Gangrene and perforation (especially if >24 h duration) à Peritonitis
a. NB: the risk of rupture in the first 24 hours of onset is 25%!
2. Abscess
3. Phlegmon
INVESTIGATIONS
CLASSIFY: GENERAL LABORATORY + IMAGING
BUT FIRST NOTE that the diagnosis is most often made clinically!!!
A. LABORATORY:
1. CBC: Mild neutrophil leukocytosis with left shift (may have normal WBC counts)
a. Higher leukocyte count with perforation
2. β-hCG to rule out ectopic pregnancy!!!
3. Urinalysis to evaluate for pyelonephritis or renal calculus. But can have mild haematuria and pyuria in appendicitis with pelvic inflammation resulting in
inflammation of the ureter!!!
B. IMAGING:
1. Upright CXR, AXR: usually nonspecific
a. Free air if perforated (very rarely)
b. Calcified fecalith (only seen in 5% of cases!!!),
c. RLQ ileus
d. Sentinel loops
e. Loss of psoas shadow
2. Ultrasound:
a. May visualize appendix, AND helps rule out gynaecological causes
b. Overall accuracy 90-94% - can rule in but CANNOT rule out appendicitis (if > 6 mm, SENS/SPEC/ NPV/PPV 98%)
3. CT scan:
a. Overall accuracy 94-100%, optimal investigation
b. Thick wall, appendiceal diameter > 6 mm, periappendiceal fluid, appendicolith (aka. fecolith), inflammatory changes
DIFFERENTIAL DIAGNOSIS
Classify based on: ABDOMINAL vs. UROGENITAL vs. GYNAECOLOGIC causes

OR: Based on age group (sort them out)
Intraabdominal causes (ALL acute abdomen causes are acute appendicitis differentials!!!)
1. *Mesenteric adenitis (children)
2. *Meckel’s diverticulitis
3. *Acute bowel obstruction
4. *Acute Crohn’s ileitis
5. Perforated peptic ulcer
6. Acute cholecystitis
7. Gastroenteritis (in GE, the vomiting precedes the pain. In appendicitis, pain classically precedes vomiting)
8. Pancreatitis
9. Volvulus
10. Diverticulitis BUT more common on left (but if sigmoid mobile enough, may cause RIF pain)
UG tract causes
1. Acute pyelonephritis
2. Ureteric colic
3. Testicular torsion
Gynaecologic emergencies
1. Ruptured ectopic pregnancy
2. PID
3. Acute salpingitis
4. Ruptured ovarian cyst
5. Ovarian torsion
6. Mittelschmerz
TREATMENT
PRINCIPLE: Traditional treatment of acute appendicitis is appendicectomy; nowadays performed at laparoscopy!
BUT recent evidence supports role of conservative management that may be suitable for up to 80% of cases. Must meet certain
requirements. Now adopted as gold standard in some cases
1. Resuscitate, correct electrolyte abnormalities
2. Surgery (traditionally gold standard, 20% mortality with perforation especially in elderly) + antibiotic coverage
RE: APPENDICECTOMY:
LAPAROSCOPIC vs. OPEN (see comparison below)
Complications: spillage of bowel contents, pelvic abscess, enterocutaneous fistula
Names of appendicectomy incisions:

1. Lanz (aka. McArthur-McBurney) – Transverse incision in right iliac fossa
2. Gridiron (aka. Davis Rockey) – Oblique appendicectomy incision in right iliac fossa
RE: ANTIBIOTIC PROPHYLAXIS

§ Antibiotic prophylaxis is given preoperatively (No post-op antibiotic unless perforated!!!)
o Antibiotics to cover gram negatives and anaerobes
o Metronidazole preferred
o Can also use clindamycin or fluoroquinolones or Augmentin
o Can use gentamicin but moving away from these drugs due to otoxicity and nephrotoxicity
nd rd th
o Other choices: 2 /3 or 4 generation cephalosporin for aerobic gut organisms
o Zosyn® (Piperacillin + tazobactam) is considered more high power. Don't usually go straight to this
DR. EAST: RE: ROLE OF NON-OPERATIVE MANAGEMENT IN ACUTE APPENDICITIS.

§ Up to 80% of cases can be managed this way!!
§ Was considered malpractice until about 2 years ago
§ It is now acceptable and standard of care in some places!!!
§ Criteria
1. Must have a CT scan and demonstrate there is NO FECOLITH and
2. No evidence of generalized peritonitis suggesting perforation
DR. EAST: RE: APPENDIX MASS

§ "Appendix mass" is also a diagnosis
§ In these circumstances, the inflamed appendix is walled off by adhesions to the omentum with or without an abscess. Immediate
surgery is difficult and dangerous, with risk of damage to adjacent bowel.
§ MUST do an ultrasound in the case of appendix mass. May be an ABSCESS or PHLEGMONOUS mass
§ Initial treatment is conservative!! (Close monitoring + antibiotics)

1. Careful monitoring of patient general condition, temperature and pulse.
2. Commence metronidazole.
3. On this regimen, 80% of appendix masses resolve.
4. Whether to perform an interval appendectomy 3 months later is controversial
§ If it is a phlegmonous mass:
o DO NOT TAKE TO SURGERY. TREAT NONOPERATIVELY. If operate, great risk of spreading pus and causing generalized peritonitis
o (Prefer the term non-operative as opposed to conservative. As there are conservative surgeries)
§ For abscess
1. Can either use radiologic percutaneous drainage of the abscess
2. OR place a drain surgically.
o Some surgeons may look for the appendix. Debatable
3. AND antibiotics x 14 d
4. ± interval appendicectomy in 6 wk (controversial)
PROGNOSIS
Mortality rate: 0.08% (non-perforated), 0.5% (perforated appendicitis)
DDX OF RIGHT ILIAC FOSSA MASS

§ Appendix abscess or appendix mass
§ Caecal carcinoma
§ Chron’s disease
§ Very distended gall bladder
§ Pelvic kidney or renal transplant
§ Ovarian tumour or tubal mass
§ Aneurysm of any of the iliacs
§ Ileocecal tuberculosis
§ Psoas abscess –now rare
Additional level information
LAPAROSCOPIC VS. OPEN APPENDECTOMY

Laparoscopic Surgery (the usual)
1. Wound infection less likely
2. Intra-abdominal abscesses 2 times more likely
3. Reduced pain on POD #1
4. Reduced hospital stay by 1.1 d
5. Sooner return to normal activity, work and sport
6. Costs outside hospital are reduced
Open Surgery (the usual)

1. Shorter duration of surgery
2. Lower operation costs
Overview:
Diagnostic laparoscopy and laparoscopic appendicectomy appear to be advantageous over open appendicectomy, particularly for young
female patients and obese patients.
MODIFIED ALVARADO SCORE FOR ACUTE APPENDICITIS

1 point per:
§ Migratory right Iliac fossa pain (1 point)
§ Anorexia (1 point)
§ Nausea/vomiting (1 point)
§ Tenderness in right Iliac fossa (2 points)
§ Rebound tenderness in right Iliac fossa (1 point)
§ Fever >37.5°C (1 point)
§ Leukocytosis (2 points)
Ø 0-3 = low risk, discharge to return if no improvement

Ø 4-6 = moderate risk, admit, observe, repeat examinations
Ø Male 7-9 = appendectomy
Ø Female (not pregnant) 7-9 = diagnostic laparoscopy ± appendectomy
Effect of Delay to Operation on Outcomes in Adults with Acute Appendicitis

Arch Surg 2010;145:886-892
Purpose: To examine the effect of delay to appendectomy on morbidity and mortality among adults with appendicitis.
Method: Retrospective cohort study with the main exposure being time to operation, and main outcomes being 30-d overall morbidity and serious
morbidity/mortality.
Results: Of 32,782 patients in the study, 75.2%, 15.1%, and 9.8% underwent surgeries within 6 h, 6-12 h, and >12 h of admission, respectively.
Differences in operative duration and length of postoperative stay were statistically significant but not clinically meaningful. No significant differences
were observed in adjusted overall morbidity or serious morbidity/mortality. Duration from surgical admission to anesthesia induction was not predictive in
regression models for either outcomes.
Conclusions: Delay of appendectomy for acute appendicitis among adults does not adversely affect outcomes.
Surgical Recall:
What vessel provides blood supply to the appendix?
§ Appendiceal artery (end artery) —branch of the ileocolic artery
Name the mesentery of the appendix.

§ Mesoappendix (contains the appendiceal artery)
How can the appendix be located if the cecum has been identified?
§ Follow the taenia coli down to the appendix; The taeniae converge on the appendix
General Surgery
Mechanical Bowel Obstruction
Sources: Toronto Notes, Surgical Recall, Some Sabiston, etc.
February 2015
Points on Pathogenesis
• Obstruction of bowel due to whatever cause à Proximal dilatation + distal decompression

• Note well: May take 12-24 h to decompress, so this explains any passage of faeces and flatus that may occur after the onset of obstruction
• Also important: Bowel wall oedema and disruption of normal bowel absorptive function à Increased intraluminal fluid à Transudative fluid loss into
peritoneal cavity, electrolyte disturbances
• The 2 mechanisms of vascular compromise in BO (Ellis) – Add them here. Remember as usual it is the venous outflow that becomes compromised
first, followed by the arterial inflow
Clinically:
4 Cardinal features of intestinal obstruction:

st
1. Abdominal pain (colicky or constant if strangulated) – usu. 1 symptom. SBO (midgut) à Periumbilical. LBO (hindgut) à Suprapubic
2. Abdominal distension à More marked in LBO or distal SBO
3. Vomiting à Early in SBO, late ± faeculent in LBO
4. Obstipation (Constipation only if incomplete – patient will still be able to pass flatus)
Must differentiate between:

1. Mechanical obstruction and ileus, and
Characterize obstruction as
2. Acute vs. Chronic
3. Small vs. Large bowel
4. Partial vs. Complete (Constipation vs. Obstipation to differentiate!!)
5. Open loop vs. Closed loop
6. Strangulating vs. non-strangulating
7. With vs. without perforation
VERY IMPORTANT TABLE: Features differentiating SBO, LBO and Paralytic Ileus:
SBO LBO PARALYTIC ILEUS
Nausea, Vomiting Early, may be bilious Late, may be faeculent Present
Abdominal Pain Colicky Colicky Minimal or absent
Abdominal Distension Depends on if distal or proximal Marked Usually mild

§ Mild if proximal SBO
§ More marked if distal
Constipation Present Present Present
Bowel sounds Normal or increased Normal or increased Reduced to absent. INCREASED in

BUT Absent if secondary ileus (e.g. due BUT Absent if secondary ileus (e.g. some cases
to perforation) due to perforation)
Other May have visible peristalsis May have visible peristalsis
Abdominal x-ray Erect: Air-fluid levels Erect: Air-fluid levels Air throughout small bowel and
findings colon
Supine: Supine:
1. Distended bowel is usually central 1. Distended bowel usually peripheral
à “Picture frame” appearance
2. Complete rings: “Ladder” pattern or
“stacked coins” appearance (plicae 2. Incomplete rings/haustrations due to
circularis a.k.a. valvulae taeniae coli
conniventes)
3. Proximal distention (> 6 cm) + distal
3. Proximal distention (> 3 cm) decompression
4. *No colonic gas 4. *No small bowel air IF competent

ileocecal valve
Sigmoid volvulus à Omega or Coffee

bean sign
Clinical Features unique to LBO
• ***Open loop (10-20%) (Safer):
o Incompetent ileocecal valve allows relief of colonic pressure as contents reflux into ileum
o Therefore clinical presentation similar to SBO
• ***Closed loop (80-90%) (Dangerous):

o Competent ileocecal valve, resulting in proximal and distal occlusions
o Massive colonic distention à increased pressure in caecum (largest and most distensible) à bowel wall ischemia à necrosis à
perforation
COMPLICATIONS OF COMPLETE OBSTRUCTION
1. Strangulation of bowel (10% of bowel obstructions) = surgical emergency:

• MUST KNOW!!!: Clinical features (To differentiate simple vs. strangulated obstruction)!!!
1. Change in character of pain from colicky to continuous ache, hematemesis, melena (if infarction)
2. Fever, tachycardia, leukocytosis, toxic appearance, raised CRP
3. Features of peritonitis: Abdominal tenderness, rebound tenderness, involuntary guarding, rigidity (later)
4. Bowel sounds becoming reduced or absent reflecting peritonism
Other:
2. Perforation: secondary to ischemia and luminal distention

3. Septicemia
4. Hypovolemic shock (due to third spacing)
INVESTIGATIONS
General laboratory vs. Radiological investigations
(Probably start with radiological in exam)
A. RADIOLOGICAL:
1. Plain radiographs of CHEST and ABDOMEN

a. Erect CXR or left lateral decubitus (LLD) to rule out free air, usually seen under the right hemidiaphragm
b. Abdominal x-ray (Erect and supine) to confirm diagnosis and determine SBO vs. LBO vs. ileus (See comparison in table above)
• If ischaemic bowel look for: Free air, pneumatosis, thickened bowel wall, air in portal vein, dilated small and large bowels, thickened or
hose-like haustra (normally finger-like projections)
• NOTE WELL: SUPINE ABDDOMINAL FILMS ARE THE MOST IMPORTANT IN B.O!!!
2. CT scan with ORAL water-soluble contrast!!!: Most used in developed countries!. Provides information on level of obstruction,
severity, *cause – important to r/o closed loop obstruction, especially in the elderly
3. Less used: Upper GI series/small bowel series for SBO (if no cause apparent, i.e. no hernias, no history of previous surgeries)
4. If suspect LBO, consider a rectal water-soluble enema without bowel prep! (Gastrografin® for PO/PR; Hypaque® for IV) rather than
barium enema (can thicken and cause complete obstruction)
a. NB: Unlike usual barium enema, no pre-examination laxative is given because of risk of exacerbating the obstruction and
possibly causing perforation
b. NB: If the ileocecal valve is competent and the obstruction is in the small bowel, the study will be normal!!
May consider ultrasound or MRI in pregnant patients
B. LABORATORY:
1. CBC:
a. Haematocrit (haemoconcentration) to assess degree of dehydration (only evident after 12-24 hours!)
b. IF strangulation: leukocytosis with left shift, (also lactic acidosis, elevated LDH (late signs))
2. U&Es:
a. Fluid AND electrolyte abnormalities!
b. BUN & creatinine elevated in pre-renal renal failure secondary to significant third spacing of fluids!!
3. ABG: Metabolic alkalosis due to frequent vomiting

4. Amylase elevated!!! – Remember to look over the causes of elevated amylase
Rule from Toronto Notes sidebar:

Patients presenting with a SBO in setting of “virgin” abdomen should have surgery ASAP – EXCEPTION: malignant obstruction from history
and imaging.
Causes of SBO in a “virgin” abdomen… Fill out this list:
1.. Hernia
2…
In a non-virgin abdomen – adhesional SBOs resolve spontaneously with NG decompression 70% of time.
TREATMENT
FIRST POINT TO MAKE: Acute BO is invariably an urgent problem that requires emergency surgical intervention,
with 2 possible exceptions!!!
“Never let the sun rise or set on (small) bowel obstruction”
Classify answer: PREOPERATIVE PREPARATION + OPERATIVE TREATMENT
A. PREOPERATIVE
1. ABCs: - Adequate resuscitation prior to surgery is vital. Surgery in under resuscitated patient is associated with increased mortality!!!
2. Stabilize vital signs, fluid and electrolyte resuscitation (with normal saline/Ringer’s first, then with added potassium AFTER fluid
deficits are corrected AND renal function is satisfactory)
3. NG tube + suction to: 1. Relieve vomiting, 2. Prevent aspiration and 3. Decompress small bowel by prevention of further distention by
swallowed air
4. Foley catheter/CVP line to monitor in/outs
5. Antibiotic therapy commenced IF strangulation is likely
B. AT OPERATION
1. Inspection of bowel to determine “viability”. 4 signs of non-viability:

1. Loss of peristalsis
2. Green or black appearance (purple may be salvageable)
3. Loss of the normal sheen
4. Loss of arterial pulsation in the supplying mesentery
• (If there is “doubtful bowel” – can reassess it in a few minutes after wrapping in a warm wet pack!!!!! If extensive doubtful bowel,
may actually plan a “second-look” laparotomy in 48 hours to reassess necessity of extensive bowel resection)
2. General principles:
a. Small bowel can be resected + anastomosed primarily because of its excellent blood supply!!!
b. For LBO, managed differently because of poorer blood supply and intraluminal bacteria so primary anastomosis very liable to
leak if obstruction
• Right sided lesions (proximal to splenic flexure) may be treated with resection of obstructing lesion + primary ileocolic
anastomosis
• Left sided lesions managed by resection of obstructing segment + temporary double-barreled colostomy (and mucus fistula)
OR if distal end cannot reach, Hartmann’s procedure.
o Can consider primary colo-colic anastomosis. BUT must lavage bowel first by passing a catheter through the appendix
stump. To help minimize the risk of leak with this, may bring out a temporary defunctioning loop ileostomy!!!
2 POSSIBLE EXCEPTIONS TO THE RULE FOR ABSOLUTE OPERATIVE INTERVENTION, AND ATTEMPT OF
CONSERVATIVE MANAGEMENT:
1. SBO with history of abdominal/pelvic surgery (especially (but not only) within 30 days of abdominal surgery!!!) à conservative
management (likely to resolve) à surgery if no resolution in 48-72 h or complications (BUT, an increase in pain OR rising pulse OR any
features of strangulation are enough to abandon conservative treatment and reexplore the abdomen!!)
2. When distinction from postoperative paralytic ileus is uncertain
***Conservative management entails “drip and suck” method. IV fluid (drip) and NG aspiration and GI rest (suck), AND close monitoring of
vitals and serial abdominal exams!!!!***
Other cases for possible trial of medical management n SBO (according to Toronto Notes)
• Crohn’s and carcinomatosis
NB: Volvulus requires sigmoidoscopic or endoscopic decompression followed by operative reduction if unsuccessful
• If successful, consider sigmoid resection on same admission
Caecal volvulus can be a true volvulus or a caecal ‘bascule’ – both need surgical treatment
RE: SBO
If asked for the causes of SBO, start with:
“The 3 most common causes of SBO are __, __ and __. The others can be classified into intraluminal, intramural, extrinsic”
Top 3 causes in order:

1. Adhesions (~75%) [LBO from adhesions are extremely rare]
2. Incarcerated or strangulated hernias (not just hernia!)
3. Cancer/Neoplasms
Then classify the others (know them well):
A. Intraluminal
a. Intussusception
b. Gallstone “ileus”
B. Intramural
a. Crohn’s
b. Radiation stricture
c. Adenocarcinoma
C. Extramural
a. Adhesions
b. Incarcerated hernia
c. Peritoneal carcinomatosis
Prognosis: Mortality: non-strangulating <1%, strangulating 8% (25% if >36 h), ischemic = up to 50%
RE: LBO
Top 3 causes in order:

1. Cancer
2. Diverticulitis
3. Volvulus
Others
A. Intraluminal
a. Faecal impaction
B. Intramural
a. Adenocarcinoma
b. Diverticulitis (Not usually the acute setting, but rather the associated stricturing and fibrosis from long-standing, recurrent
diverticulitis)
c. IBD stricture (Crohn’s and less commonly UC)
d. Radiation stricture
C. Extramural
a. Volvulus
b. Adhesions
Prognosis
Overall mortality: 10%
Caecal perforation + feculent peritonitis: 20% mortality
Toronto Notes box:

In a patient with clinical LBO consider impending perforation when:
§ Cecum ≥12 cm in diameter
§ Tenderness present over caecum
Know about closed loop obstruction: E.g. LBO with competent ileocecal valve, volvulus. The loop can fill but valvular mechanism prevents emptying.
RE: VOLVULUS (GO TO GS36 IN TORONTO NOTES AND EDIT THIS)

Most common sites: Sigmoid colon > Caecum > Small intestine.
But stomach and gallbladder volvulus may occur!!!
Sigmoid Volvulus
Plain abdominal radiograph: “Coffee-bean” sign or “omega sign”
Management:
1. Pass a flatus tube via a sigmoidoscope into the sigmoid colon. Often untwists early volvulus
a. If this fails, untwist at laparotomy
b. If successful, still elective resection of redundant sigmoid loop (preferably same admission)
2. If gangrene has occurred, excise affective segment and bring out ends as a double-barrelled colostomy (Paul-Mikulicz procedure)
So ALL patients with sigmoid volvulus get laparotomy at some point!!!
SURGICAL RECALL – MUST KNOW THESE:
What are classic electrolyte/acid-base findings with proximal obstruction?

§ Hypovolemic, hypochloraemic, hypokalemia metabolic alkalosis
What tests can differentiate partial from complete bowel obstruction (SBO?)?
§ CT with ORAL contrast, small bowel follow-through
*What is superior mesenteric artery (SMA) syndrome?

§ Seen with weight loss—SMA compresses duodenum, causing obstruction
Intraoperatively, how can the level of obstruction be determined in patients with SBO?
§ Transition from dilated bowel proximal to the decompressed bowel distal to the obstruction
What is the most common indication for abdominal surgery in patients with Crohn’s disease?
§ SBO
What may cause SBO if patient is on warfarin?

§ Bowel wall haematoma
What is the #1 cause of SBO in adults (industrialized nations)?

§ Postop adhesions
What is the #1 cause of SBO around the world?

§ Incarcerated hernias
What is the #1 cause of SBO in children?

§ Hernias
What classic saying is associated with complete SBO?

§ “Never let the sun set or rise on complete SBO”
What condition commonly mimics SBO?

§ Paralytic ileus (AXR reveals gas distention throughout, including the colon)
What tumor classically causes SBO due to “mesenteric fibrosis”?

§ Carcinoid tumor
Re: Small bowl tumours:
What is the most common benign small bowel tumor?

§ Leiomyoma
What is the most common malignant small bowel tumor?

§ Adenocarcinoma
What is the differential diagnosis of malignant tumors of the small intestine?

1. Adenocarcinoma (50%)
2. Carcinoid (25%)
3. Lymphoma (20%)
4. Sarcomas (<5%)
What is the workup of a small bowel tumor?

§ UGI with small bowel follow-through, enteroclysis, CT scan, enteroscopy
What is the treatment for malignant small bowel tumor?

§ Resection and removal of mesenteric draining lymph nodes
*What malignancy is classically associated with metastasis to small bowel?

§ Melanoma
General Surgery
Paralytic Ileus and Colonic Pseudo-obstruction
February 2015
Paralytic (or adynamic or neurogenic) ileus can be defined as a state of atony of the intestine.
Principal clinical features are the same as mechanical EXCEPT PAIN IS MINIMAL OR ABSENT
1. ABSENCE of intestinal movements and hence ABSENCE OF COLICKY PAIN
2. Abdominal distension
3. Vomiting
4. Obstipation
AETIOLOGIES
ACUTE
1. Peritonitis/Intraabdominal sepsis – Possibly due to toxic paralysis of the myenteric plexus
2. Metabolic (uraemia) + Electrolyte disturbances (Na, decreased K, Ca)
3. Drug-induced (opiates, narcotics, anticholinergics, psychotropics)
4. Postoperative –
• Some degree of paralytic ileus occurs after EVERY laparotomy
• Complex aetiology including sympathetic overaction, bowel manipulation, potassium depletion if vomiting, associated
peritoneal irritation, and the associated stomach and large bowel atony that occurs after every abdominal operation for ~24-
48 hours
• The distension is probably due to swallowed air
• Paralytic ileus that persists for more than 48 hours postop probably has some other causative factor!!!!!
5. C. difficile
CHRONIC
1. Neurologic disease (enteric NS, CNS, PNS)
2. Scleroderma
Effects in short (similar to mechanical obstruction):

1. Severe fluid, electrolyte and protein loss into gut lumen and via vomitus
2. Gross gaseous distension of gut mainly from swallowed air that cannot pass, which impairs blood supply and allows toxin absorption
CLINICAL FEATURES
Paralytic ileus is most common in the postop stage of peritonitis or of major abdominal surgery
Features as above. Remember pain is not present APART FROM the discomfort of the laparotomy wound and the abdominal distension
Examination: Abdomen distended, tender and silent
PLAIN ABDOMINAL X-RAY: Gas in SMALL AND LARGE BOWEL ± fluid levels on erect
Harold Ellis:
“The paralytic ileus may merge insidiously into a mechanical obstruction produced by adhesions or bands following abdominal surgery, and
an important, often extremely difficult, differential diagnosis lies between these two conditions. The diagnosis is important, since paralytic
ileus is treated conservatively whereas mechanical obstruction usually calls for urgent operation.”
Differentiating paralytic ileus from mechanical obstruction is based on the following criteria:
1. Pain – Paralytic is relatively painless
2. Bowel sounds – An absolutely silent abdomen is diagnostic of paralytic ileus
3. Timing – If flatus was passed before then the obstruction occurs, likely to be mechanical
4. Duration – Paralytic usually lasts 24-48 hours (may go up to ~4 days)
5. X-ray appearance –
• A plain x-ray of the abdomen showing a localized loop of distended small intestine without gas shadows in the colon or rectum is strongly
suggestive of mechanical obstruction, in contrast to the diffuse appearance of gas throughout the small and large bowel in paralytic
ileus.
TREATMENT
PROPHYLAXIS VS. ESTABLISHED CASE
A. BEST TREATMENT IS PROPHYLAXIS!!!

• Biochemical imbalance is corrected preoperatively.
• The bowel is handled gently at operation.
• Postoperatively, gastric distension due to air swallowing may require nasogastric suction
B. BUT FOR ESTABLISHED CASES
1. NG decompression – remove swallowed air
2. NPO
3. IV fluid and electrolyte therapy – careful electrolyte monitoring
4. Consider TPN for prolonged ileus
5. Pethidine preferred for pain relief over other opioids as it has less effect on intestinal motility
6. Phenothiazine for nausea
7. Look for and correct underlying causative abnormalities (e.g. sepsis, medications, electrolytes),
8. Post-op: gastric and small bowel motility returns by 24-48 h, colonic motility by 3-5 d
If ileus stubborn/prolonged à consider pharmacologic therapy (efficacy uncertain)

9. Motility agents eg. metoclopramide (dopamine antagonistà stimulates GASTRIC emptying) and erythromycin (stimulates motilin receptor)
10. Current interest in novel therapies such as gum chewing and pharmacologic therapy (opioid antagonists)
OGILVIE’S SYNDROME
Acute pseudo-obstruction with distention of colon without mechanical obstruction in distal colon
Arises in bedridden patients with serious extraintestinal illness or trauma (spine/pelvic fractures, intestinal ischaemia, ureteric colic)
PATHOPHYSIOLOGY
Exact mechanism unknown, likely autonomic dysregulation à possibly:
1. Sympathetic deprivation to colon,
2. Unopposed parasympathetic tone, and
3. Interruption of sacral parasympathetic tone to distal bowel
Usually, the small bowel is unaffected and peristalsis continues and passes intestinal contents into the colon. The large
bowel is atonic, so the colon, in particular the caecum, distends enormously, becomes ischaemic and, if unrelieved, will
perforate
• First presents with abdominal distention (>90%) ± tenderness

• Later symptoms mimic true obstruction
ASSOCIATIONS
• Most common: trauma, infection, cardiac (MI, CHF)
• Disability (long term debilitation, chronic disease, bed-bound nursing home patients, paraplegia),
• Drugs (narcotic use, laxative abuse, polypharmacy),
• Other (recent orthopedic or neurosurgery, post-partum, electrolyte abnormalities including hypokalemia, retroperitoneal hematoma, diffuse
carcinomatosis)
INVESTIGATIONS
• AXR: Caecal dilatation – if diameter ≥12 cm, increased risk of perforation
TREATMENT
• Treat underlying cause (electrolyte imbalances etc.)
• NPO, NG tube
• Decompression of colon. Methods:
o Rectal tube, colonoscopy
• Pharmacologic: Neostigmine (cholinesterase inhibitor). AVOID LAXATIVES AS THEY MAY PRECIPITATE PERFORATION
• Surgical decompression (ostomy/resection) uncommon
• Surgery (extremely rare): if perforation, ischemia or failure of conservative management
PROGNOSIS
Most resolve with conservative management
Toxic Megacolon – See Toronto Notes

General Surgery
Enterocutaneous Fistulae
Sources: Surgical Tutor, Surgical Recall, Toronto Notes
March 2015
FISTULAE IN GENERAL (TORONTO NOTES)
Definition
§ Abnormal communication between two epithelialized surfaces (e.g. enterocutaneous, colovesical, aortoenteric, entero-enteric)
Aetiology
§ Inflammatory states (e.g. infection, IBD (especially Crohn’s), diverticular disease, abscess)
§ Iatrogenic/surgery (e.g. anastomotic leak, radiation)
§ Foreign object erosion (e.g. gallstone, graft)
§ Neoplastic
§ Congenital, trauma
Investigations
§ Ultrasound, CT scan, fistulogram
§ Small bowel or barium enema will define state of intestine or distal obstruction
§ ALSO: Measure amount of drainage from fistula!!
Treatment
§ Decrease secretion: octreotide/somatostatin/omeprazole
§ Surgical intervention: dependent upon etiology (for non-closing fistulas); uncertainty of diagnosis
MUST KNOW: Why Fistulae Stay Open

Popular acronym: “HIS FRIENDS”
§ High output fistula (> 500 cc/day)
§ Intestinal destruction (> 50% of circumference)
§ Short segment fistula < 2.5 cm
§ Foreign body
§ Radiation
§ Infection
§ Epithelialization (i.e. Mucocutaneous continuity has developed, or e.g. colostomy)
§ Neoplasm
§ Distal obstruction (most common)
§ Steroids (may inhibit closure, usually will not maintain fistula)
ENTEROCUTANEOUS FISTULAE
An abnormal communication between the GI tract and skin
Simple fistula = direct communication between gut and skin
Complex fistula = fistula with associated abscess cavity
CLASSIFICATION
Enterocutaneous fistulas are classified in the following manner:

§ High output: Output greater than 500mL per 24 hours
§ Moderate output: Output between 200 and 500 mL per 24 hours
§ Low output: output less than 200 mL per 24 hours.
Moderate- or high-output fistulas are usually related to the small bowel.
Fistulae, particularly if high output (>500 ml/day) cause:

1. Skin irritation and excoriation
2. Dehydration
3. Electrolyte and acid-base imbalance
4. Malnutrition
5. Sepsis
§ Associated with anastomotic leaks, and intra-abdominal and pelvic abscesses from enteric contamination.
§ Also, cutaneous sepsis from irritation of the abdominal wall by the enteric effluent is also common.
AETIOLOGY (same as for general fistulae)
§ Inflammatory states (e.g. infection, IBD (especially Crohn’s), diverticular disease, abscess)
§ Iatrogenic/surgery (e.g. anastomotic leak!!!)
§ Neoplastic
§ Radiation
§ Trauma to bowel/colon
IMAGING
Important to “determine anatomy of fistula”:
• Fistulography will define tract
• Small bowel or barium enema will define state of intestine or distal obstruction
• US and CT scan to detects and to define abscess cavities
• MUST ALSO MEASURE OUTPUT TO DETERMINE FLUID VOLUME REPLACEMENT
MANAGEMENT
USUALLY CONSERVATIVE management initially:
Reason: ~50% will close spontaneously, but the other 50% require operation and resection of the involved bowel segment
Conservative management consists of:

(TIP: THINK OF ALL THE PROBLEMS CAUSED BY FISTULAE AND HOW TO ADDRESS EACH)
1. Correction of fluid and electrolyte loss

§ Require careful fluid balance
§ Restoration of blood volume
§ Somatostatin: Somatostatin analogues such as sandostatin reduce fistula output, facilitate skin care and may contribute to the closure of
fistulas, especially those of biliary or pancreatic origin.
2. Correction of acid-base imbalance

§ H2 Antagonist, proton pump inhibitor to reduce gastric secretions
§ Somatostatin analogues (e.g. Octreotide) to reduce GI and pancreatic secretions
3. Nutritional support
§ NPO and possibly an nasogastric tube
§ Malnutrition corrected with either parenteral or enteral nutrition
§ Complete bowel rest is useful in the initial management until stabilization and evaluation is complete, especially
if there is underlying sepsis and the fistula output is high. Gradually, enteric nutrition can be initiated.
§ BUT, enteral nutrition can be given distal to fistula!!!
§ Total parenteral nutrition given via Dacron-cuffed tunneled feeding line
§ Radiological screening to ensure tube in correct site
4. Skin protection
§ Upper GI contents are very corrosive
§ With higher fistula output, care of the skin surrounding the fistula is best accomplished by sump drainage of the fistula and application
of various skin-protective preparations.
§ Care is taken to avoid skin maceration, cellulitis and cutaneous necrosis à Makes any subsequent surgical therapy is more difficult.
§ An enterostomal therapist should be involved with the care of these patients
5. Control of sepsis
§ Drain any abscess cavities (percutaneously, guided by CT or U/S)!
§ Uncontrolled sepsis remains the major cause of mortality in these patients. Sometimes an exploratory laparotomy may be performed to
drain abscesses that are not accessible to percutaneous drainage
§ Antibiotics usually avoided
§ If there is clinical evidence of sepsis with swinging fever and leucocytosis, broad-spectrum antibiotics covering Gram-negative organisms
and anaerobes are prescribed after preliminary work-up for sepsis (i.e. urine culture, blood culture and examination of the wound). Use of
antibiotics should be judicious and guided by the cultures and sensitivity studies.
PROGNOSIS
Ø 60% will close in one month once sepsis has been controlled with conservative treatment
Ø Mortality associated with fistula is still at least 10%
Ø Surgery should be considered if fistula does not close by 30-40 days
Enterocutaneous fistulas will not close if:

• There is total discontinuity of bowel ends
• There is distal obstruction
• Chronic abscess cavity exists around the site of the leak
• Mucocutaneous continuity has occurred
Fistulas are less likely to close if:

• They arise from disease intestine (e.g. Crohn's Disease)
• They are end fistulae
• The patient is malnourished
• They are internal fistulas
General Surgery
Inflammatory Bowel Disease
February 2015
Inflammatory bowel disease: Term generally used to denote 2 diseases of unknown cause with similar genetic characteristics: Ulcerative colitis
and Chron’s disease
BUT in ~10-15% of patients with IBD confined to colon, clear distinction cannot be made and the disease is labeled indeterminate colitis. May also
have mixed colitis
DIFFERENCES BETWEEN ULCERATIVE COLITIS AND CHRON’S DISEASE

(Mostly from Prof. Hanchard lecture)
CLASSIFY ANSWER: DIFFERENCES MAINLY PATHOLOGICAL (BELOW). HOWEVER ALSO RADIOGRAPHIC AND MANAGEMENT
DIFFERENCES
ULCERATIVE COLITIS CHRON’S DISEASE
1. GENETICS: HLA-DR2 mutations GENETICS: NOD2/CARD15 mutations on chromosome 16

2. Typically lesions involve mucosa and submucosa only Transmural
3. Always involves rectum (Proctitis is actually the hallmark of UC) Rectum involved in 50%
4. Can only involve rectum and colon Can affect anywhere in GI tract
5. Terminal ileum reported to be involved in 10% (But this is not true Terminal ileum involved in 30%
involvement. Rather “backwash ileitis” from caecal involvement!!!)
6. Anal lesions in 25% Anal lesions in 75%
7. Disease is in contiguity (starts in rectum and extends in a continuous Disease discontinuous (Multiple, separate, sharply delineated “skip
fashion to involve all or part of the colon) lesions” are characteristic)
Also contributes to the “cobblestone appearance”; due to patchy
distribution of the disease in which the disease tissue is depressed below
the level of the normal mucosa
8. Characteristic microscopic feature: CRYPT ABSCESS Pathognomonic microscopic feature: NONCASEATING GRANULOMA
9. Mucosa granular and ulcerated but NO fissuring Mucosa discretely ulcerated and fissuring
10. NO fistulas (makes sense since the inflammation is confined to the Fistulas in 10% (between loops of bowel, bladder, vagina, abdominal
mucosa and wont involve adjacent organs) skin)
11. Serosa normal; no creeping fat Serosa inflamed; “creeping fat” present (mesenteric fat extending
around serosa)
12. Colon shortened because muscle changes; fibrous strictures rare Colon shortened because of fibrosis; fibrous strictures common (esp. of
terminal ileum and require resection)
13. Inflammatory polyposis (PSEUDOPOLYPS) common Inflammatory polyposis UNcommon
ULCERATIVE COLITIS
INCIDENCE/EPIDEMIOLOGY
§ More common than Chron’s!!!!
§ More common in developed countries – relatively unusual in Asia, Africa and South America. Whites > Blacks
§ All ages are susceptible, BUT more commonly affects patients < 30 years
o **A small secondary peak in the incidence occurs in the 50s!!
§ Male = Female !!!
RISK FACTORS/CAUSE
CLASSIFY: GENETIC VS ENVIRONMENTAL
**Cause of UC is unknown (Idiopathic), BUT:
*Suspected risk factors:
st
1. FAMILY HISTORY of IBD is a significant risk factor!! (15% have a 1 degree relative)
a. 2 genetic abnormalities associated with UC – involve variations in DNA repair genes. Patients with UC have variations in alleles of
group HLA-DR2.
2. ALTERED IMMUNOLOGICAL RESPONSE to external AND host antigens = CURRENT theory of the cause of IBD!!!
a. Other studies have shown: Defective cell-mediated immunity, impaired chemotaxis and abnormalities of helper and suppressor T-cells may
be involved in the pathogenesis.
3. INFECTIOUS AGENTS incl. C. difficile and C jejuni have been implicated in causing sustained immune response BUT also not confirmed
4. DIETARY FACTORS incl. *low fiber intake, *high refined sugars, *cows milk BUT none have been shown to play a definitive role.
a.Its prevalence in industrialized countries and increased incidence in those who migrate from low-risk to high-risk areas suggest an
environmental influence
5. OCPs Both UC and Chron’s more common in women using OCPs!
Protective Factors
1. SMOKING may confer a PROTECTIVE effect against developing UC, AND may also be THERAPEUTIC – nicotine has been reported to
induce remission in some cases
a. This is in contrast to Chron’s which is more common in smokers and may be aggravated by smoking**
2. Patients who have had APPENDISECTOMY also appear to be at DECREASED RISK for UC.
PATHOLOGIC FEATURES
GROSS vs. HISTOLOGIC
A. GROSS APPEARANCE
UC is a disease in which the major pathologic process involves the mucosa and submucosa of the colon SPARING the muscularis
**The DIAGNOSTIC CHARACTERISTIC OF UC IS CONTINUOUS, UNINTERRUPTED INFLAMMATION OF THE COLONIC MUCOSA, BEGINNING
IN THE DISTAL RECTUM AND EXTENDING PROXIMALLY FOR A VARIABLE DISTANCE**
1. Despite the name, ulceration is NOT always present, esp. in early disease:
***In fact, the typical gross appearance of UC is hyperaemic mucosa
2. THE RECTUM IS INVARIABLY INVOLVED with the inflammatory process (30% confined to rectum):
- Rectal involvement (PROCTITIS) IS THE HALLMARK OF THE DISEASE and the diagnosis should be seriously questioned if the
rectal mucosa is not affected
3. The inflammation extends in a CONTINUOUS FASHION for a variable distance into the more proximal colon
4. The ENTIRE COLON, including (caecum and appendix) may be affected in UC
- In contrast to Chron’s, UC DOES NOT involve the terminal ileum EXCEPT in cases of “backwash ileitis” (ileal mucosa appear inflamed
in presence of extensive proximal colon involvement)
5. COLONIC STRICTURES can occur in 5-12% of patients with chronic UC.
- NOTE VERY WELL: CANCER MUST BE EXCLUDED!! as the cause of any colonic stricture occurring in the setting of UC (Even though most
are benign)
**3 important features suggestive of malignant strictures in UC**:

1. Appearance later in the course of UC (60% after 20 yrs vs. 0% after 10 yrs!)
2. Location proximal to splenic flexure (86% malignant)
3. Large bowel obstruction caused by the stricture
B. HISTOLOGIC APPEARANCE
Typical microscopic finding of UC = Inflammation of MUCOSA AND SUBMUCOSA

- Most characteristic lesion is the CRYPT ABSCESS (neutrophils fill and expand the lumen of involved crypts of Lieberkuhn) BUT they
are not specific (may also be seen in Chron’s or infectious colitis)
IMPORTANT: The inflammatory process in UC spares the muscular coats of the colon, which differentiates it from Chron’s disease, which is
characterized by transmural inflammation, or involvement of all layers of the intestinal wall.
- EXCEPTION: HOWEVER, in rare cases of severe inflammation characteristic of toxic megacolon in
patients with UC, all layers of the colon may be involved
CLINICAL FEATURES
CHRONIC, RELAPSING PATTERN IN MOST PATIENTS. CONTINUOUS PATTERN IN 10-15%
CLASSIFY: INTESTINAL vs. EXTRA-INTESTINAL MANIFESTATIONS
A. INTESTINAL (remember UC is mainly rectal, so almost all the rectal complaints)

1. Rectal bleeding common in UC (Hallmark feature – 90%) – may also be present in Chron’s BUT usually not as severe
2. Both may present with diarrhoea ± passage of mucus (mucorrhoea)
3. Patients with UC tend to have more TENESMUS, URGENCY, INCONTINENCE than those with Chron’s – likely because UC is invariably
associated with distal proctitis
4. Acute abdominal discomfort, esp. with defecation – BUT less severe than in patient with Chron’s
5. Tender abdominal mass is suggestive of a phlegmon or abscess – more commonly associated with Chron’s
6. Perianal disease is UNCOMMON in UC (25%) – whereas it may be the only presenting feature in Chron’s (75%)
B. EXTRA-INTESTINAL
Systemic: Fever, anorexia, weight loss, fatigue in severe cases
A. Rheumatologic (Known as the enteropathic arthritides)

1. Peripheral Arthritis (~20%) – esp. of knees, ankles, hips and shoulders. Usu. assc with increased activity of intestinal disease
2. Ankylosing spondylitis (~3-5%)
3. Sacroileitis
B. Dermatologic
4. Erythema nodosum (~10-15%)
5. Pyoderma gangrenosum – usu. on pretibial region – Erythematous plaque that ulcerates
C. Ocular
6. Anterior uveitis (vision threatening)
7. Episcleritis (benign)
D. Hepatobiliary
8. ***Primary sclerosing cholangitis (PSC) (5-8%) – Mostly men. Higher risk of colon cancer. PSC may be asymptomatic and diagnosed
only by lab tests or may present with symptoms of obstructive jaundice and abdominal pain.
• Disease is progressive and ultimately fatal unless liver transplantation is undertaken!!!
• Colectomy has NO EFFECT on the course of the disease!!!
#1-7 typically improve or resolve after colectomy
MUST KNOW: RISK FOR CARCINOMA

UC confers an increased risk for colorectal carcinoma. Carcinomas arising from UC tend to be highly aggressive!!!
MUST KNOW: Most important risk factors:

1. Prolonged duration of disease
2. “Pancolonic” disease
3. Severity of the inflammation
4. Continuously active disease
• MUST KNOW THIS STATISTIC: ~5% risk of developing colon cancer at 10 years; then, risk increases 1-2% per year; thus,
an incidence of ~20% after 20 years of the disease (~30% at 30 years)
• Cumulative risk for cancer increases with duration of disease: 25% at 25 years and 65% at 40 years
• Patients with disease of left colon only have a lower risk of carcinoma than patients with entire colon involvement (pancolitis)
• A colonic stricture in a patient with UC must be presumed carcinoma until proved otherwise. If malignancy cannot be ruled out by
endoscopy, the presence of a stricture is an indication for operative intervention
KNOW THIS WELL: American Cancer Society guidelines recommend surveillance colonoscopy every 1-2 years,
beginning 8 years after the onset of pancolitis and 12-15 years after the onset of left-sided colitis.
(Traditionally 10 random biopsy specimens were recommended. Now up to 30 is suggested)
• When high-grade dysplasia is found and has been confirmed by a second independent pathologist, proctocolectomy should be recommended.
INVESTIGATIONS
No single confirmatory test
ENDOSCOPY VS. RADIOGRAPHY VS. BIOPSY
1. Endoscopic examination of the colon and rectum is essential in the diagnosis of IBD
a. In acute phase/exacerbation!!: Proctosigmoidoscopy ONLY is often sufficient as the rectum is invariably inflamed in
patients with UC (Complete colonoscopy offers little additional info in the acute setting and increases risk for perforation!!!)
§ The presence of diffuse, confluent symmetrical disease from the dentate line proximally is consistent with UC
b. Full colonoscopy should be carried out after the disease is under control
IF colonoscopy cannot be done à Radiography:
2. Barium enema – May be normal. Characteristic features: 1. Featureless bowel (loss of haustral markings and shortening). 2. Pseudopolyps
3. CT colonography – has replaced barium enema for this purpose!!
BUT both still contraindicated in severe disease (require bowel prep, etc.)!!
4. Multiple mucosal biopsy specimens from serial sites to confirm diagnosis
ALSO VERY IMPORTANT TO REMEMBER: To exclude other conditions

(The top 2 differentials are Chron’s and infectious colitis, so as such à)
1. Upper GI contrast series with small bowel follow-through should be obtained to rule out the possibility of small bowel
involvement, which would suggest Chron’s disease
2. ***Stool samples (GS/C) Infectious conditions that mimic UC include colitis caused by C. difficile, entamoeba histolytica, C. jejuni and
salmonella enteritidis.
MANAGEMENT
CLASSIFY: MEDICAL vs. SURGICAL
MEDICAL THERAPY (MAINSTAY OF MANAGEMENT!!)
MAINSTAYS OF MEDICAL MANAGEMENT. Can be grouped into 3 broad categories:
1. Aminosalicylates [5-ASA derivatives] (ORAL or TOPICAL (ENEMA) Eg. Sulfasalazine)

2. Corticosteroids (ORAL, IV or TOPICAL (ENEMA). Eg. Prednisone, hydrocortisone, budesonide)
3. Immunomodulatory drugs (Eg. 6-mercaptopurine, azathioprine)
1. Aminosalicylates
- Most common therapy in the treatment of MILD TO MODERATE UC
- Sulfasalazine used – composed of a molecule of 5-aminosalicylic acid (5-ASA) linked to sulfapyridine
o ***Use is limited by its toxicity, mainly due to the sulfapyridine part. Newer 5-ASA drugs less toxic as they do not contain this!!!!
- Can treat active disease at higher doses and play a role in maintaining remission at lower doses
2. Corticosteroids
- Highly effective in treatment of ACUTE ATTACK/ACTIVE UC and can be administered orally, IV or topically through enemas
- MOA: Block phospholipase A2 thereby decreasing prostaglandins and leukotrienes
- Side effects preclude long-term therapy with steroids
- (Side effects of steroid therapy include – HTN, DM, osteoporosis, increased susceptibility to infection)
- IV methylprednisolone – high dose to remit acute attack
- Hydrocortisone enemas 2-3 times/day often effective in treating disease limited to rectum and left colon – benefits include less
absorption so less systemic side effects
- Budesonide has been shown to be as effective as prednisolone with far fewer side effects, including much less adrenal suppression
3. Immunomodulatory medications (mostly for steroid-sparing)

- Often used in the LONG-TERM MANAGEMENT of patients with UC
- 6-mercaptopurine (purine analogue) and its precursor azathioprine act by causing chromosome breaks and inhibiting proliferation of
rapidly dividing cells such as lymphocytes.
- Advantages: Both are useful in inducing remission in patients refractory to 5-ASA, and they allow steroids to be tapered or minimized
- Side effects: Include reversible bone marrow suppression and pancreatitis
- Cyclosporine may be used but typically reserved for severe acute UC and refractory Chron’s disease due to severe side effects
4 INDICATIONS FOR SURGERY
KNOW WELL!! Include:
1. Intractable disease (MOST COMMON INDICATION)

2. Fulminant colitis, especially with toxic megacolon
3. Massive bleeding
4. High grade dysplasia or carcinoma (Detected by biopsy)
A. ELECTIVE SURGICAL PROCEDURES

Point: (Operation MUST BE TOTAL (PAN-) PROCTOCOLECTOMY, not segmental. Because of invariable recurrence)
The 3 elective surgical options for UC include:

1. Restorative proctocolectomy with IPAA (Ileal pouch anal anastomosis) – Risk of POUCHITIS!!
2. Total proctocolectomy with (Brooke) ileostomy
3. Total proctocolectomy with a (Kock) continent ileostomy (Kock pouch)
B. BUT in emergency!!: Total colectomy and ileostomy with Hartmann closure of the rectum, (rectal preservation)
POST-OPERATIVE CARE
A contrast enema is performed approx. 10 weeks postop to ensure an intact IPAA. If the enema shows a leak, the contrast examination is
repeated in 6 weeks. If the radiograph shows no leak, the diverting ileostomy is closed.
*Segmental colectomy for UC, in contrast to Chron’s disease, has been shown to be an inadequate procedure for controlling disease à invariably
results in the recurrence of disease in the remaining colon within a short time and is contraindicated
(Re: Total colectomy with continent ileostomy: Single-chambered reservoir is fashioned by suturing several limbs of ileum together after the
antimesenteric border has been divided (acts as replacement of the rectum). A valve is then created from the outflow tract that provides obstruction to
the pouch contents (continence). Between 2-4 times daily, the patient introduces a tube through the valve to evacuate the pouch. Major problem with the
Kock pouch is the high complication rate necessitating reoperation in 50% of patients)
SEE FULL NOTES FOR SURGICAL MANAGEMENT OF TOXIC MEGACOLON AND BLEEDING
COMPLICATIONS
Think all the extraintestinal manifestations, strictures, colorectal carcinoma and toxic megacolon with danger of perforation
CHRON’S DISEASE
***Originally described as regional ileitis
BUT may affect ANY segment of the GI tract FROM MOUTH TO ANUS
• 15% have disease limited to the colon
EPIDEMIOLOGY
§ Similar to UC, there is a bimodal age distribution: with

a. Peaks between ages 15 and 30 years and a second smaller peak between 55 and 80 years of age
§ Male = Female
§ More common among Caucasians, Ashkenazi Jews!
AETIOLOGY/RISK FACTORS
Aetiology is unknown
GENETIC + ENVIRONMENTAL
A. GENETIC
§ Family history
§ NOD2/CARD15 gene, located on chromosome 16, significant role in Crohn’s disease
B. ENVIRONMENTAL
IMMUNOLOGICAL THEORIES: Three prevalent theories include:

1. Response to a specific infectious agent
2. A defective mucosal barrier allowing an increased exposure to antigens, and
3. An abnormal host response to dietary antigens
§ MYCOBACTERIUM PARATUBERCULOSIS, has been isolated in up to 65%

§ SMOKING is risk factor for Crohn’s disease and, after intestinal resection, the risk of recurrence is greatly increased in smokers.
§ OCPs: Increased risk in patients taking OCPs.
PATHOLOGIC FEATURES
A. GROSS APPEARANCE
1. Crohn’s disease is a transmural, predominantly submucosal inflammation characterized by a thickened colonic wall.
2. The affected mucosa observed by endoscopy is often described as having a cobblestone appearance. In severe disease, the bowel wall may be
entirely encased by creeping fat
3. Normal mucosa may intervene between areas of inflammation, causing skip lesions characteristic of the disease.
4. Deep linear ulcers that resemble railroad tracks or bear claws.
5. Most common locations = ILEUM + ASCENDING COLON
B. HISTOLOGIC APPEARANCE
Transmural inflammation, submucosal oedema, lymphoid aggregation and, ultimately, fibrosis.

§ MUST KNOW!!: The pathognomonic histologic feature of Crohn’s disease is the NONCASEATING GRANULOMA, a
localized, well-formed aggregate of epithelioid histiocytes surrounded by lymphocytes and giant cells (50% of pts)
MUST KNOW: RE: CANCER

• The risk for development of carcinoma of the colon is not as high as the risk in long-standing, chronic ulcerative colitis, BUT it is
present; therefore, patients with chronic active disease require periodic colonoscopic surveillance and biopsy. The presence of high-grade
dysplasia is an indication for colectomy.
CLINICAL FEATURES
CLASSIFY: GASTROINTESTINAL VS. EXTRAINTESTINAL
A. GASTROINTESTINAL
1. Characteristic triad!! of symptoms—abdominal pain, diarrhoea, and weight loss— most common presentation
– mimics that of viral gastroenteritis or irritable bowel syndrome
2. Other constitutional symptoms may include anorexia, fever, AND recurrent oral aphthous ulcers
3. Features of anal disease (30-50%)

a. Including anal fistulas, fissures, strictures, oedematous skin tags, and erosion of the anoderm
b. Anal disease in a patient with colitis suggests a diagnosis of Crohn’s disease because primary anal disease is unusual in patients with
ulcerative colitis.
4. ALSO: Features of fistulae!!!

a. Enteroenteric
b. Enterovesical
c. Enterovaginal
d. Enterocutaneous
B. EXTRAINTESTINAL
A. Rheumatologic (CD > UC)
1. Peripheral Arthritis– esp. of knees, ankles, hips and shoulders. Usu. assc with increased activity of intestinal disease
2. Ankylosing spondylitis
3. Sacroileitis
B. Dermatologic (CD > UC)

1. Erythema nodosum
2. Pyoderma gangrenosum – usu. on pretibial region – Erythematous plaque that ulcerates
C. Ocular (CD > UC)

1. Uveitis (vision threatening)
2. Episcleritis (benign)
D. Hepatobiliary
1. Cholelithiasis – In patients with ileal Chron’s or ileal resection. Due to interruption of the enterohepatic circulation
2. *Primary sclerosing cholangitis (PSC) – Mostly men. Higher risk of colon cancer. PSC may be asymptomatic and diagnosed only
by lab tests or may present with symptoms of obstructive jaundice and abdominal pain.
• Disease is progressive and ultimately fatal unless liver transplantation is undertaken!!!
• Colectomy has NO EFFECT on the course of the disease!!!
E. Urologic
1. Urolithiasis (urinary tract calculi) – especially following ileal resection
2. Fistulae
F. Others
1. Vitamin deficiencies – B12 (absorbed in terminal ileum), ADEK (require bile salts to aid absorption. Bile salts lost in ileal disease/resection)
INVESTIGATIONS
ENDOSCOPIC vs. RADIOLOGIC vs. BIOPSY
**MAIN PRINCIPLE: WANT TO VISUALIZE BOTH UPPER AND LOWER GI TRACT!!!
The differential diagnosis of Crohn’s colitis includes ulcerative colitis and various infectious agents
A. ENDOSCOPIC (Upper and Lower GI) + BIOPSY

1. Colonoscopy: Early disease; is the more sensitive diagnostic modality. The disease is often patchy in distribution
a. ± Gastroscopy
b. Dr. East: Capsule endoscopy à NEWER TECHNOLOGY. Also, double balloon endoscopy??
B. RADIOLOGIC (Upper and Lower GI)

2. Double-contrast enema may provide useful information in making the diagnosis and determining the extent of the disease.
• Characteristic radiologic findings in Crohn’s colitis are skip lesions, contour defects, longitudinal and transverse ulcers, a cobblestone-like
mucosal pattern, strictures, terminal ileitis (lead-pipe appearance), thickening of the haustral margin, and irregular nodular defects.
3. Small bowel series (Barium follow-through) OR enteroclysis should be performed in all patients with suspected Crohn’s disease or
ulcerative colitis. Involvement of the small intestine strongly favors the diagnosis of Crohn’s disease
§ Findings: *Narrowing (“string sign of Kantor”), *Aphthous ulcers, *Cobblestoning, *Fistulae
4. CT/MR enterography to visualize SMALL bowel
5. Biopsy samples should be obtained. However, unless a granuloma is identified, distinguishing between the two diseases may still be difficult.
6. ***Stool should be sent for culture and examined for ova and parasites
MANAGEMENT
MEDICAL VS. SURGICAL
LIFESTYLE MODIFICATION - Smoking cessation
A. MEDICAL THERAPY (MAINSTAY OF MGMT AS SURGERY IS NOT CURATIVE!!!)

INVOLVES: INDUCTION OF REMISSION and MAINTENANCE
The medical treatment of Crohn’s disease is similar to that of ulcerative colitis and includes
1. Aminosalicylates (mild colonic disease)
2. Corticosteroids (Oral prednisone in exacerbation. IV methylprednisolone if severe)
3. Immunomodulatory medications (Most often for maintaining remission. Most commonly used as steroid-sparing agents. Need > 3
months) (e.g., 6-MP, azathioprine, cyclosporine).
4. Biologics: One immunomodulatory drug that deserves mention in the treatment of Crohn’s disease is INFLIXIMAB, a monoclonal anti–
TNF-α antibody designed to block the TNF-α receptor in an effort to decrease inflammation. Infliximab is given as an IV infusion to treat
Crohn’s disease in steroid-dependent or intractable patients
B. SURGICAL MANAGEMENT – PRINCIPLE:

MUST KNOW: Surgery is NOT curative as Chron’s is a pan-GI disease. Because of this an important principle in the surgical
treatment of Crohn’s disease is to resect only enough intestine to improve symptoms or correct complications
Surgery generally reserved for complications such as fistulae, obstruction, abscess, perforation, bleeding and for medically refractory disease
INDICATIONS FOR SURGERY:
1. Intractability (MOST COMMON)

2. Intestinal obstruction (SBO)!!! (SECOND MOST COMMON!)
3. Intra-abdominal abscess
4. Fistulas
5. Fulminant colitis +/- Toxic megacolon

6. Massive bleeding
7. High-grade dysplasia or cancer
8. Growth retardation
SURGICAL PROCEDURES
1. Resection and anastomosis/stoma if active or subacute inflammation, perforation, fistula

§ Resection margin only has to be free of gross disease (microscopic disease irrelevant to prognosis!!) [ileocecal resection, total
colectomy/proctocolectomy with stoma, segmental colectomy]
2. Stricturoplasty – FOR SHORT STRICTURES: Widens lumen in chronically scarred bowel: relieves obstruction without resecting bowel
(contraindicated in acute inflammation)
Complications of Treatment
1. Short bowel syndrome (diarrhea, steatorrhoea, malnutrition)
§ If <50% or <200 cm of functional small intestine, risk of short bowel syndrome
Complications of ileal resection:

2. Gallstones (if terminal ileum resected, decreased bile salt resorption à increased cholesterol precipitation)
3. Kidney stones (MUST KNOW: Loss of calcium in diarrhea à increased oxalate absorption à hyperoxaluria à Stones)
4. Fistulas
§ At least 50% clinical recurrence within 5 yr; 85% within 15 yr; endoscopic recurrence rate even higher
§ 40% likelihood of second bowel resection, 30% likelihood of third bowel resection
MAINTAINING REMISSION OF CROHN’S DISEASE AFTER RESECTION
• Options include treatment with 5-ASA compounds, antibiotics, and the thiopurines azathioprine and 6-MP
• Prophylaxis is typically begun within 2 weeks after surgery
COMPLICATIONS
1. Intestinal obstruction/perforation
2. Fistula formation
3. Malignancy (lower risk compared to UC)
a. Surveillance colonoscopy same as ulcerative colitis (see above) if more than 1/3 of colon involved
General Surgery
Hernia and Inguinoscrotal Swellings
Sources: Toronto Notes, Surgical Recall, Harold Ellis, etc.
February 2015
DEFINITION
A hernia is a protrusion of an organ or a part of an organ through a defect in the wall of the cavity in which it is contained, into an abnormal position.
§ The wall can be the abdominal wall, muscle fascia, diaphragm or foramen magnum
INCIDENCE
§ Inguinal: Peak incidence is 50s

§ M:F = 9-12:1
§ Lifetime risk of developing a hernia: Males 20-25%, Females 2%
§ Account for approximately 10% of general surgical workload
§ Most common surgical disease of males
ANATOMY (MORE POINTS AT END OF DOCUMENT)

Most hernias have a sac of parietal peritoneum. Most common abdominal wall hernias in order of frequency:
1. 50% Indirect inguinal hernia (incidence in men = ~5%)
2. 25% Direct inguinal hernia (incidence in men = ~1%)
3. 5% are femoral (more common in women than men because of the wider pelvis (85% are in females!))
4. Umbilical and Paraumbilical
5. Incisional - Ventral hernia at site of wound closure, may be secondary to wound infection
6. Ventral and epigastric
Re: Inguinal hernias: 60% occur on the right, 20% on the left and 20% bilateral
HESSELBACH’S TRIANGLE BOUNDARIES

§ Lateral: Inferior epigastric vessels actually the Medial boarder of the Inferior Epigastric Vein. It is a branch of the External Epigastric Vein
§ Inferior: Inguinal ligament
§ Medial: Lateral margin of rectus sheath
(Floor consists of internal oblique and the transversus abdominis muscles)
INGUINAL CANAL
§ 4 cm long
§ Passes downward from lateral to medial, deep to superficial.
§ From the internal (deep) inguinal ring to the external (superficial) inguinal ring
§ Parallel to and directly above the inguinal ligament
§ Anatomical landmark of the deep ring is 1-2 cm above the midpoint of the inguinal ligament (i.e. 1-2 cm above the femoral pulse)
§ Transmits the spermatic cord in men, round ligament in women. And the ilioinguinal nerve
Borders:
1. Anterior: Skin > superficial fascia > External oblique aponeurosis cover the full length. Internal oblique covers lateral 1/3
2. Superior: Lowermost arching fibres internal oblique and transversus abdominus
3. Posterior: Fascia transversalis laterally. Conjoint tendon medially (common aponeurotic insertion of internal oblique and transversus abdominus)
4. Inferior: Inguinal ligament (aka. Poupart’s ligament)
CONTENTS OF THE SPERMATIC CORD (8)

1. Vas deferens
2. Artery to vas deferens (branch of inferior vesical artery)
3. Testicular artery (artery is branch of the abdominal aorta)
4. Testicular pampiniform venous plexus
5. Testicular lymphatics
6. Cremaster muscle
7. Genital branch of genitofemoral nerve (Nerve to cremaster)
8. Cremasteric artery (branch of inferior epigastric artery)
9. ± hernia sac
***NOTE WELL: The ilioinguinal nerve LIES ON TOP OF (not in) the spermatic cord, but is in the inguinal canal!!!
FEMORAL CANAL
§ ~1.5 cm in length.
§ Lies at the medial extremity of the femoral sheath. Borders:
1. Anterior: Inguinal ligament
2. Medial: Sharp edge of the lacunar part of the inguinal ligament (Gimbernat’s ligament)
3. Posterior: Pectineal ligament of Astley Cooper
4. Lateral: Femoral vein
§ Contains a plug of fat and the lymph node of Cloquet

§ Acronym: “NAVEL” [Lateral to medial: Nerve, Artery, Vein, Empty space, Lymph node]
RISK FACTORS/AETIOLOGY
Hernias occur at sites of weakness in the abdominal wall
A. CONGENITAL ABNORMALITIES
§ (e.g. patent processus vaginalis, failure of complete closure of the umbilical scar) i.e. Indirect Inguinal and Umbilical hernias
§ Also, connective tissue disorders (e.g. Marfan’s syndrome, Ehler-Danlos syndrome)
B. ACQUIRED ABNORMALITIES
“Hernias should be thought of as portents of other disease conditions”. 2 main factors:
I. Activities which increase intra-abdominal pressure:
§ Chronic cough: E.g. chronic bronchitis
§ Constipation E.g. due to colon cancer
§ Straining on urination E.g. BPH or prostate cancer
§ Ascites
§ Pregnancy
§ Obesity
§ Heavy lifting
II. Abdominal weakness

a. Age, malnutrition, connective tissue diseases
o
b. Previous abdominal surgery (2 to poor healing as a result of infection, haematoma formation, poor technique, damage to nerves
leading to paralysis of abdominal wall muscles)
c. Previous hernia repair
FOR INCISIONAL HERNIA (Patient factors vs. Surgical factors)

A. PATIENT FACTORS
1. Wound infection
2. Haematoma formation
3. General poor wound healing factors (e.g. malnutrition, comorbidities)
4. Obesity
5. Respiratory complications (esp. with cough)
B. SURGICAL FACTORS
1. Poor surgical technique
2. Type of incision (e.g. midline laparotomy incision vs. small laparoscopy incision)
3. Damage to nerves leading to paralysis of abdominal wall muscles
4. Placement of drains
- Occurs through the scar from a previous operation

- 1% of all transparietal abdominal incisions result in a hernia
- Account for 10% of all abdominal wall hernias
- Partial dehiscence of all deep fascial layers occurs
- BUT skin remains intact
- *Most develop within a year of surgery
- Symptoms are often minimal with cosmetic appearance the main concern
- Most are wide necked but strangulation can occur
- If surgery is required, the following should be considered
o Fascial closure or mayo-type repair using sutures
o A 'keel repair' using sutures
o A mesh repair using polypropylene or PTFE: Mesh can be placed as a sublay, onlay or inlay
o The results with mesh are superior to suture repairs
CLASSIFYING HERNIAS
1. Reducible – Usually painless, Has a cough impulse
2. Irreducible (Incarcerated) – Irreducible hernia, not necessarily strangulated. No cough impulse
3. Strangulated: Vascular supply of protruded viscus is compromised (ischaemia) due to constriction by the neck of the sac
§ Venous drainage from the sac contents is compromised first!! Then arterial
§ Order of frequency of strangulation: Femoral > Indirect inguinal > Direct inguinal
§ (SURGICAL EMERGENCY: Requires emergency repair as gangrene and subsequent perforation are imminent)
CLINICAL FEATURES
A. Non-strangulated
§ Mass of variable size, may spontaneously reduce when supine or manually reduce
§ Often painless
§ Transmits palpable impulse with coughing or straining This is a cough inpulse
B. If strangulation supervenes (Must can reel these off rapid):

1. Severe pain in hernia
2. Features of intestinal obstruction! (Colicky abdominal pain, distension, vomiting, obstipation)
3. Examination of hernia:
a. Tender, tense hernia
b. Cannot be reduced and has no cough impulse
c. Overlying skin becomes inflamed and oedematous (rubor, calor, dolor, etc)
4. May have other features of mechanical obstruction incl. increased bowel sounds
As ischaemia progresses to gangrene and perforation à Patient becomes febrile, toxic and features of generalized peritonitis develop (guarding,
rebound tenderness, rigidity, absent bowel sounds)
COMPLICATIONS
1. Incarceration: Irreducible
2. Strangulation: Irreducible with resulting ischemia
§ 10% patients with strangulation give no previous history of a hernia
§ Operative mortality remains at approximately 10% (10x greater than for elective repair)
§ Small, new hernias more likely to strangulate
§ Femoral (~40% risk) >> indirect inguinal > direct inguinal (~3% risk)
§ Intense pain followed by tenderness
§ Intestinal obstruction, gangrenous bowel, sepsis
§ Surgical emergency – GO DIRECTLY TO OT FOR REPAIR
§ DO NOT ATTEMPT TO MANUALLY REDUCE hernia if septic or if contents of hernial sac gangrenous
DIRECT VS. INDIRECT VS. FEMORAL

Indirect inguinal: Enters the internal (deep) inguinal ring and traverses the inguinal canal
Direct inguinal: Pushes through the posterior wall of the inguinal canal medial to the inguinal ring (i.e. within Hesselbach’s Triangle)
“Although clinically it is usually quite easy to tell the difference between the two types of inguinal hernia, the ultimate differentiation can only be made at
operation: the inferior epigastric vessels demarcate the medial edge of the internal ring; therefore, an indirect sac will pass lateral, and a direct hernia
medial, to these vessels”
Inguinal vs. Femoral: If an indirect inguinal hernia protrudes through the external ring, it can be felt to lie above and medial to the pubic tubercle and
is thus differentiated from a femoral hernia, which emerges through the femoral canal below and lateral to this landmark”
Indirect inguinal Direct inguinal Femoral
Epidemiology Most common hernia in BOTH men and 1% of all men Affects mostly females (85%)
women
Males > females
Origin/Anatomy Originates in deep inguinal ring Through Hesselbach’s triangle Into femoral canal, below inguinal ligament
Lateral to inferior epigastric artery Medial to inferior epigastric artery but may override it
Often descends into scrotal sac Usually does not descend into scrotal Medial to femoral vein within femoral canal
(or labia majora!!!) sac
Aetiology Congenital (persistence of the processus ALWAYS ACQUIRED ALWAYS ACQUIRED
vaginalis) OR Acquired
Risk of Common Extremely rare Highest
strangulation
Extends into Often Extremely rare
scrotum
Reduces on lying Not readily Spontaneously
Recurrence after Uncommon <1% More common (3-4%)
surgery Depends on choice of repair
OTHER/SPECIAL TYPES OF HERNIAS
1. Incisional hernia – (See above) Hernia through an incisional site. Most common cause is wound infection
2. Umbilical hernia – Hernia through the umbilical ring. In adults associated with ascites, pregnancy and obesity
3. Epigastric hernia – Ventral hernia through the linea alba above the umbilicus
4. Spigelian hernia – Ventral hernia through linea semilunaris (aka. “spontaneous lateral ventral hernia”)
5. Pantaloon hernia – A direct and an indirect inguinal hernia coexist; they bulge on either side of the inferior epigastric vessels like the legs of a
pair of pantaloons.
6. Richter’s hernia – Only part of bowel circumference (usually anti-mesenteric border) is incarcerated or strangulated so may not be obstructed –
THE RISK: A strangulated Richter’s hernia may self-reduce and thus be overlooked, leaving a gangrenous segment at risk of perforation
7. Maydl’s – Maydl's hernia (Hernia-in-W) is a rare type of hernia and may be lethal if undiagnosed. The hernial sac contains two loops of bowel
with another loop of bowel being intra-abdominal. A loop of bowel in the form of 'W lies in the hernial sac and the centre portion of the 'W
loop may become strangulated, either alone or in combination with the bowel in the hernial sac. It is more often seen in men, and predominantly on
the right side. Maydl's hernia should be suspected in patients with large incarcerated herniae and in patients with evidence of intra-abdominal
strangulation or peritonitis. Postural or manual reduction of the hernia is contra-indicated as it may result in non-viable bowel being missed.
8. Littre's hernia – A Meckel's diverticulum lies within the hernial sac. Littré's hernia occurs most commonly in a femoral or inguinal hernia
Reduction En Masse - a complication of inguinal hernia where it is reduced (and looks like all bowel has returned to peritonium) but a loop of bowel remains trapped
inside the peritoneal sac
9. Sliding hernia: The sac of the ordinary indirect inguinal hernia is formed entirely by parietal peritoneum. When part of the wall of the sac is
formed by a viscus, the hernia is called a sliding hernia. Often the medial wall of the sac of an indirect inguinal hernia is formed partially by
bladder and it’s overlying peritoneum. This is usually true in direct hernias. Such conditions cause no great additional problems in repair and will not
be considered here. However, when the posterior wall of the sac is formed by the bowel and its overlying visceral peritoneum, it is a true sliding
indirect inguinal hernia. The repair may be difficult and does require careful consideration.
10. Parastomal hernia – Hernia adjacent to a stoma (e.g. colostomy)
11. Obturator hernia – Rare. Hernia through the obturator canal or foramen, which is a normal anatomical structure between the obturator groove on
the inferior aspect of the superior pubic ramus and superior border of the obturator membrane. F > M
12. Cooper’s hernia – Hernia through the femoral canal and tracking into the scrotum or labia majus
13. Amyand’s hernia – Hernia sac containing ruptured appendix (Think: Amyand’s = Appendix)
Lumbar Hernias:
14. Petit’s hernia – (Rare) hernia through Petit’s triangle (a.k.a. inferior lumbar triangle) (Think: petite = small = inferior)
15. Grynfeltt’s hernia – Hernia through Grynfeltt-Lesshaft triangle (superior lumbar triangle)
INVESTIGATIONS
§ Physical examination usually sufficient
§ Herniography?
§ Ultrasound
§ CT (CT required for obturator hernias, internal abdominal hernias and Spigelian femoral hernias in obese patients)
MANAGEMENT
“Management options depend on if uncomplicated or strangulated”
Uncomplicated: CONSERVATIVE vs. SURGICAL
Strangulated: SURGICAL EMERGENCY
I. UNCOMPLICATED
A. CONSERVATIVE/OBSERVATION
1. Observation is acceptable for small asymptomatic inguinal hernias
2. Truss: A truss or some form of hernia support may be used to provide symptomatic relief for large uncomplicated hernias in elderly unfit
patients and those who decline surgery
3. MUST Advise patient that if it becomes irreducible or if features of strangulation develop, return to hospital!
B. SURGICAL
§ CAN BE EITHER TENSION-FREE (HERNIOPLASTY) vs. TENSION (HERNIORRHAPHY)
§ AND repair may be done OPEN or LAPAROSCOPIC
§ Most repairs are now done using tension free techniques – a plug in the hernial defect and a patch over it or patch alone
Hernioplasty chosen over Herniorrhaphy because it is a tension free technique
IMPORTANT: Surgery aims to (i) reduce the hernial contents, (ii) excise the sac (herniotomy) in most cases, and (iii) repair and
close the defect, either by approximation of adjacent tissues to restore the normal anatomy (herniorrhaphy), OR by insertion of
additional material (hernioplasty). The site of the hernia must be marked clearly on the skin during consultation with the patient
before induction of anaesthesia so that no mistake is made about its location.
Indications: *Prevent strangulation and evisceration, *symptomatic relief, *cosmesis; if asymptomatic can delay surgery
Terms to know:
1. Herniorrhaphy - refers to repair of the posterior wall of the inguinal canal behind the spermatic cord (by one of several methods), together
with repair of the external oblique aponeurosis in front of the cord. Strong nonabsorbable sutures are used.
§ Shouldice repair - The weakened transversalis fascia is incised along the line of the inguinal canal and repaired in an overlapping
fashion (i.e. it is imbricated or plicated). The deep inguinal ring is closed snugly around the cord. The internal oblique and transversus
(conjoint tendon) are approximated to the deep aspect of the inguinal ligament.
§ Bassini repair - The conjoint tendon is sutured onto the inguinal ligament. **Optional: A J-shaped incision, known as a ‘Tanner
slide’, is made in the anterior rectus sheath to enable the conjoint tendon to ‘slide’ down towards the inguinal ligament without tension.
o Recurrence rate = 10-30%!!!
§ FOR FEMORAL HERNIAS: McVay repair: (The conjoint tendon is sutured onto the Cooper’s ligament) Repair of inguinal hernia by
approximating the transversus abdominis aponeurosis and the conjoint tendon to Cooper’s ligament (which is basically the superior
pubic bone periosteum)
2. Hernioplasty (reinforcement of the posterior inguinal canal wall with a synthetic mesh) is required for large hernias and hernias in the
middle-aged and elderly with poor abdominal wall musculature. The Lichtenstein tension-free mesh repair is an example of hernioplasty
3. CHILDREN ONLY: Herniotomy alone (removal of the hernial sac only - surgical correction of a hernia by cutting through a band of tissue that constricts it.) alone is adequate for an indirect
inguinal hernia in children in whom the abdominal wall muscles are normal. Formal repair of posterior wall of the inguinal canal is not required.
Lichtenstein vs. Bassini vs. Shouldice repair:

• Lichtenstein repair is tension-free – a mesh repair
• Bassini repair is under tension – Conjoint tendon attached to inguinal ligament
• Shouldice repair is under tension (not done locally) – The transversalis fascia has to be stretched (the transversalis fascia is imbricated) and
the transversus abdominis and internal oblique is approximated to the inguinal ligament
Shouldice & Lichtenstein now regarded as 'gold standard' as judged by low risk of recurrence. Both have a recurrence rate of < 1%
Shouldice repair actually has a lower recurrence rate than Lichtenstein!!!
Other repairs (From lecture)

§ Coopers ligament repair: conjoint tendon to inguinal ligament and coopers ligament.
§ Halstead Repair: the cord is brought anteriorly
§ Darn
RE: OTHER MESH REPAIRS (LECTURE)/Surgical Recall

Lichtenstein repair
Stoppa (Surgical Tutor)
IPOM (intraperitoneal onlay mesh)
TAPP (Trans abdominal preperitoneal mesh repair) Laproscopic method
TEPA (Trans extra peritoneal mesh repair) Laproscopic method
RE: Laparoscopic approach:

§ Not appropriate for large or irreducible hernias
§ Advantages: reduced post-operative pain and earlier return to work.
§ Disadvantages: increased risk of femoral nerve and spermatic cord damage, risk of developing intraperitoneal adhesions with the
transperitoneal procedure, and greater cost and duration of the operation. Initial experience indicates that recurrence rates are similar to those
associated with open operations.
II. STRANGULATED HERNIAS

STANDARD = LAPAROTOMY + TENSION REPAIR
***RECENT EVIDENCE SUGGESTS MESH REPAIR IS EQUALLY ACCEPTABLE
§ Standard surgical approach to suspicion of a strangulated hernia is a LAPAROTOMY. ***This is because you expect that bowel will need to be
resected. NOTE: Suspect strangulation even if only mild tenderness present.
§ POINT: In the case of a strangulated hernia the placement of a prosthetic hernia repair may possibly place patient at higher risk of infection and
breakdown of the bowel anastomosis. Hence Bassini repair preferred
§ NOTE: Emerging body of evidence suggests can go ahead with the mesh anyway unless there is gross infection.
A trial suggested that mosquito nets can actually replace or be superior to standard mesh used in hernia repair in terms of effectiveness. Criticism of
these studies is that they have been short-term studies. Advantage: MUCH cheaper
ADVICE AFTER SURGERY

Patients require analgesia for the first few days. They should avoid straining and lifting for about 4 weeks after surgery, and avoid very heavy
physical work for about 6–8 weeks. The average length of stay off work is approximately 2–4 weeks after open repair and 1–2 weeks after
laparoscopic repair. If hernioplasty is done, the 2-4 weeks is the time needed for the cells to grow through the fenestrated mesh - Dr. Roberts KPH
POSTOPERATIVE COMPLICATIONS
1. Recurrence (15-20%):
§ Risk factors: recurrent hernia, age >50, smoking, BMI >25, poor pre-op functional status (ASA ≥3 – see Anesthesia, A3), associated
medical conditions: type II DM, hyperlipidemia, immunosuppression, any comorbid conditions increasing intra-abdominal pressure
§ Less common with mesh/"tension-free" repair
2. Scrotal haematoma (3%):

§ Painful scrotal swelling from compromised venous return of testes
§ Deep bleeding: may enter retroperitoneal space and not be initially apparent
§ Difficulty voiding
3. Nerve entrapment:
§ Ilioinguinal (causes numbness of inner thigh or lateral scrotum)
§ Genital branch of genitofemoral (in spermatic cord)
Iliohypogastic
4. Stenosis/occlusion of femoral vein:
§ Acute leg swelling
5. Ischaemic colitis?/orchitis
6. Urinary retention Borders of the Femoral Ring

A. False Ring
B. True Ring
RE: FEMORAL HERNIA MANAGEMENT (SURGICAL TUTOR)
§ All uncomplicated femoral hernias should be repaired as an urgent elective procedure
§ Three classical approaches to the femoral canal have been described
1. Low (Lockwood)
2. Transinguinal (Lotheissen)
3. High (McEvedy)
§ Irrespective of approach used the following will be achieved
a. Dissection of the sac
b. Reduction / inspection of the contents
c. Ligation of the sac
d. Approximation of the inguinal and pectineal ligaments
FEW MORE SURGICAL DETAILS

Bassini repair is an alternative to Lichtenstein repair locally. This is often preferred to repair strangulated hernia where bowel has to be resected.
Placing a prosthetic such as mesh may increase the risk of infection and anastomotic breakdown.
Wikipedia: The Bassini technique is a "tension" repair, in which the edges of the defect are sewn back together, without any mesh. In the Bassini
technique, the conjoint tendon (formed by the distal ends of the transversus abdominis and internal oblique muscles) is approximated to the inguinal
ligament and closed. Today, Bassini's main interest is historical. Hernias repaired with the Bassini technique have a 30% recurrence rate, which is
generally caused by tension on the tissues pulling the edges together without mesh.
Recovery is slower than with tension-free Hernioplasty due to more swelling at the operative site. Due to the slower recovery, this technique is
generally only used if a mesh repair would be inadvisable. For example, patients that require removal of part of their intestine due to strangulation
may experience infection and further problems if mesh is used, so the Bassini Repair technique is recommended.
Shouldice repair not done locally.
The Shouldice technique is the mainstream suture-based repair. It is a relatively difficult four-layer reconstruction of fascia transversalis. High success
rate and low rate of recurrence.
DIFFERENTIAL DIAGNOSIS OF INGUINOSCROTAL SWELLING
Whenever one considers the differential diagnosis of a mass situated in a particular area, a two-stage mental process is required: first, what are the
anatomical structures in that particular region, and, second, what pathological entities may arise therefrom?
In considering the groin, let these possibilities pass through your mind: Differential Diagnosis of Testicular Swelling
1. The hernial orifices: Testicular Swelling with PAIN
a. Inguinal hernia 1. Epididimytis
b. Femoral hernia 2. Orchitis
2. The testicular apparatus: 3. Testicular trauma
a. Hydrocele of the cord 4. Testicular torsion
b. Ectopic testis 5. Incarcerated scrotal hernia
c. Testicle torsion 6. Testicular tumor
3. The vein: saphena varix
Testicular Swelling without PAIN
4. The artery: femoral aneurysm
1. Hydrocele
5. The lymph nodes: lymphadenopathy due to infection, neoplasm or lymphoma 2. Spermatocele
6. The psoas sheath: psoas abscess 3. Varicocele
7. The skin and subcutaneous tissues: lipoma, liosarcoma 4. Indirect inguinal hernia
8. Haematoma, seroma, abscess 5. Hematocele
6. Testicular tumor
Dr. East: Is it important to know whether hernia is direct or indirect?
§ From perspective of repair, it is not important. Indirect hernias encroach on and weaken Hesselbach’s triangle and direct hernias do the same to
the deep ring. THEREFORE ALL INGUINAL HERNIA REPAIRS ADDRESS BOTH DEFECTS SIMULTANEOUSLY. That is, the repair is the
same whether the hernia is direct or indirect.
§ From perspective of risk of incarceration, it is important only if patient is very infirm and you would like to avoid surgical repair. Indirect hernias
are more likely to incarcerate than direct hernias. Indirect hernias should always be repaired. However, direct hernias may be left alone in an
infirm, unfit patient because they are unlikely to incarcerate.
Sliding hernia (Surgical Recall)

--
Surgical Recall: Common OT inguinal hernia questions
What is the first identifiable subcutaneous named layer?

§ Scarpa’s fascia (thin in adults)
What is the name of the subcutaneous vein that is ligated?

§ Superficial epigastric vein
What happens if you cut the ilioinguinal nerve?

§ Numbness of inner thigh or lateral scrotum; usually goes away in 6 months
From what abdominal muscle layer is the cremaster muscle derived?

§ Internal oblique muscle
From what abdominal muscle layer is the inguinal ligament (a.k.a. Poupart’s ligament) derived?
§ External oblique muscle aponeurosis
To what does the inguinal (Poupart’s) ligament attach?

§ Anterior superior iliac spine to the pubic tubercle (NOT symphysis)
Which nerve travels on the spermatic cord?

§ Ilioinguinal nerve
Why do some surgeons deliberately cut the ilioinguinal nerve?

§ First they obtain preoperative consent and cut so as to remove the risk of entrapment and postoperative pain
What is the hernia sac made of?

§ Peritoneum (direct) or a patent processus vaginalis (indirect)
What attaches the testicle to the scrotum?

§ Gubernaculum
What is the most common organ in an inguinal hernia sac in men?

§ Small intestine
What is the most common organ in an inguinal hernia sac in women?

§ Ovary/Fallopian tube
What lies in the inguinal canal in the female instead of the VAS?
§ Round ligament
Where in the inguinal canal does the hernia sac lie in relation to the other structures?
§ Anteromedially
What is a “cord lipoma”?

§ Preperitoneal fat on the cord structures (pushed in by the hernia sac); not a real lipoma; remove surgically, if feasible
What nerve is found on top of the spermatic cord?

§ Ilioinguinal nerve
What nerve travels within the spermatic cord?

§ Genital branch of the genitofemoral nerve
What is the major difference in repairing a pediatric indirect inguinal hernia and an adult inguinal hernia?
§ In babies and children it is rarely necessary to repair the inguinal floor; repair with “high ligation” of the hernia sac
General Surgery
Gastric Carcinoma, GIST and Gastric Lymphoma
Source: Toronto Notes, Harold Ellis, Surgical Recall, Dr. East
February 2015
GASTRIC CARCINOMA
EPIDEMIOLOGY
• Most common age group = 50-60 yr
th th
• Male > female = 1.5:1. 4 most common cancer in Jamaican men and 5 most common in women
• Incidence of adenocarcinoma <10 (U.S.) vs. 60 (Japan, Korea) per 100,000 (incidence highest in Asia and Latin America)
• Incidence has decreased by 2/3 in past 50 yr
• Genetic alteration seen in > 50% of gastric cancer is P53
RISK FACTORS (MUST KNOW!!)
A. ENVIRONMENTAL
1. H. pylori infection, causing chronic atrophic gastritis (6-9 fold risk) (However <1% of those infected will go on to gastric
cancer)
2. Nationality – Gastric ca. much more common in Japan. Important: However this is NOT thought to be genetic as incidence
declines in Japanese immigrants to America
3. Smoked food/meats, nitrosamines – common in Japan
4. Smoking
5. Alcohol
B. GENETIC
1. Blood type A
2. HNPCC: Hereditary nonpolyposis colorectal cancer
3. HDGC: Hereditary diffuse gastric carcinoma
C. PREDISPOSING MEDICAL CONDITIONS

1. Chronic gastric ulcer
2. Gastric polyps (adenomatous)
3. Pernicious anaemia associated with achlorhydria and chronic atrophic gastritis
4. Previous partial gastrectomy (>10 yr post-gastrectomy, 2-3 fold increase)
5. Hypertrophic gastropathy
MICROSCOPIC PATHOLOGY: ALL ARE ADENOCARCINOMAS with varying degrees of differentiation
MACROSCOPIC PATHOLOGY
§ 1/3 diffusely involves the stomach. ¼ involve pyloric region.
§ *Ulcers more common on lesser than greater curvature. BUT an ulcer on the greater curvature is more likely malignant
§ More common proximally
§ Remainder fairly evenly distributed throughout the rest of the organ
§ MUST KNOW: THE 4 PATHOLOGIC APPEARANCES:
1. Malignant ulcer with raised edges (75%)
2. Polypoid/fungating
3. Colloid tumour
4. Leather bottle stomach (linitis plastica) (10%) – aka. diffuse infiltrating
CLINICAL FEATURES
FIRST POINT: Often asymptomatic until late , insidious or late onset of symptoms (Weight loss is the most common symptom):
Clinical suspicion:
§ Ulcer fails to heal
§ Lesion on greater curvature of stomach or cardia
Classify the presentation of all cancers in this way:

1. Local Effects of tumour
• Vague epigastric pain
• Epigastric mass
• Early satiety
• Abdominal symptoms (may be relieved by PUD treatment): burping, nausea, vomiting, dyspepsia, dysphagia (proximal ca)
• *Occasionally haematemesis and/or melaena
• *Perforation
2. Features due to direct spread

• Oesophagus: Dysphagia (if the gastric ca is proximal)
• Duodenum: Vomiting esp. in antral tumours with pyloric obstruction
• Transverse colon: Bowel obstruction, Gastrocolic fistula à Faecal vomiting!!
• Can also spread to pancreas (pain radiates to back), abdominal wall, transverse mesocolon and transverse colon
3. Features due to distant metastasis

a. Lymphatic:
o Left supraclavicular nodes of Virchow (Troisier’s sign)
o Sister Mary Joseph nodule
o Irish’s left axillary nodes
b. Haematogenous:
o Liver – Jaundice, hepatomegaly, ascites
o Lungs
o Bone
c. Transcoelomic: Peritoneal seeding à Ascites
o Implantation in both ovaries à Bilateral Krukenberg tumours
o Rectal (Blumer’s) shelf
4. Paraneoplastic syndromes
• Chronic DIC leading to Trousseau’s sign (migratory thrombophlebitis)
• Haemolytic anaemia
• Membranous glomerulonephritis
5. Constitutional symptoms
• Anorexia, weight loss, anaemia
**MUST, MUST KNOW: Signs of Metastatic Gastric Carcinoma

1. Virchow’s node: Left supraclavicular node
2. Blumer’s shelf: Mass in pouch of Douglas (peritoneal mets deposit anterior to the rectum)
3. Krukenberg tumour: metastases to ovary
4. Sister Mary Joseph node: umbilical lymph node metastases
5. Irish’s node: left axillary nodes
Principal DDx is benign gastric ulcer
Other ddx for gastric tumours:

o Malignant: Adenocarcinoma, GIST, lymphoma,
o Benign: Benign gastric ulcer, gastric polyp, leiomyoma, leiomyosarcoma, carcinoid, ectopic pancreatic tissue, gastrinoma
5 COMMON DISEASES WITH A SIMILAR CLINICAL PICTURE – slight lemon-yellow tinge, anaemia, weight loss
1. Carcinoma of stomach
2. Carcinoma of caecum
3. Carcinoma of pancreas
4. Pernicious anaemia
5. Uraemia
Form an important quintet and must always be considered together
INVESTIGATIONS
GENERAL VS. SPECIFIC (Diagnosis + Staging)
1. CBC – anaemia
2. CEA – elevated in 30% of cases
*DIAGNOSIS
1. Barium meal – Alleged 90% accuracy but probably lower

2. OGD and multiple biopsies; Biopsy lesion itself + 4 quadrant biopsy
*STAGING (search for direct spread and mets)
1. CT chest/abdomen/pelvis – Assess nodal and metastatic spread

2. EUS to assess preoperative T-stage and N-stage, local spread
3. Staging laparoscopy – Assess primary, local invasion into adjacent organs, small peritoneal and liver mets that CT may
miss, sample ascites for cytology if present
The presence of even small metastasis means the patient has incurable disease
MANAGEMENT
As with almost all cancers, management depends on the stage and may be:
CURATIVE VS. PALLIATIVE
A. CURATIVE (partial or total gastrectomy with extensive lymph node clearance ± neoadjuvant and adjuvant chemotherapy)
1. Proximal OR midbody lesions:

• Total gastrectomy and oesophagojejunostomy, [and Roux-en-y reconstruction (with or without pouch)]
• With D1 lymph node dissection (i.e. nodes along greater & lesser curvature)
• RE: Proximal gastrectomy? - NO!!! NOT generally acceptable as Mortality & Morbidity higher
2. Distal lesions:
• Distal gastrectomy with Billroth II reconstruction: Wide margins (> 5 cm), en bloc removal of omentum and lymph
nodes. (Never use a Billroth I for gastric cancer!)
NOTE: MUST RESECT A MINIMUM OF 16 LYMPH NODES FOR ADEQUATE LYMPH NODE CLEARANCE
NOTE: FOR STAGE II AND III, AS WITH MOST GI CANCERS, FOLLOW WITH ADJUVANT CHEMOTHERAPY +/- RADIATION
B. PALLIATIVE
(If distant mets or peritoneal implants) – 10-15% are inoperable at presentation
A. Stenting (Most common)
1. Stenting of the pylorus for gastric outflow obstruction
2. Stenting also used for unresectable carcinoma at the cardiac/oesophageal end producing dysphagia
B. Surgery
1. Palliative gastric resection to decrease bleeding and relieve obstruction, enables the patient to eat
2. Gastroenterostomy for irremovable obstructive lesions of the pylorus
C. Chemoradiation
1. Radiation therapy
2. Studies are showing larger role for chemotherapy
FOLLOW-UP (DR. EAST + DR. PLUMMER)

Dr. Plummer: Somewhat controversial as if recurrent disease is detected by any modality, in the vast majority of cases
nothing curative can be done for the patient.
May consider:
§ History & examination every 4 months for 1 year, then every 6 months for 2 years, then every year
§ Annual endoscopy?
§ Annual CT scan?
Surgical Recall Pointers:

When should splenectomy be performed?
§ When the tumor directly invades the spleen/splenic hilum or with splenic hilar adenopathy
Define “extended lymph node dissection.”

§ Usually D1 and D2:
§ D1 are perigastric LNs (along the greater and lesser curvature)
§ D2 include: splenic artery LNs, hepatic artery LNs, anterior mesocolon LNs, anterior pancreas LNs, crural LNs
What is the adjuvant treatment?

§ Stages II and III: postoperative chemotherapy and radiation
PROGNOSIS
Overall 5-year survival in US is 25%. 50% in Japan.
Reason for better survival in Japan: Aggressive screening and capturing early cancers.
• Stage IA: 71%

• Stage IIA: 45%
• Stage IIIA: 20%
• Stage IV: 4%
GASTROINTESTINAL STROMAL TUMOUR (GIST)

Most common mesenchymal neoplasm of GI tract. May be BENIGN or MALIGNANT
Arise from interstitial cells of Cajal (cells associated with Auerbach’s plexus. The pacemaker cells of the GI tract, which
coordinate peristalsis). Previously thought to be leiomyomas and leiomyosarcomas
Can occur anywhere along the GI tract but most common in stomach (50%) and proximal small intestine (25%)
Surgical Recall: Sites: GI tract—“esophagus to rectum”—most commonly found in stomach (60%) > small bowel (30%), duodenum
(5%) > rectum (3%) > colon (2%) > oesophagus (1%)
75-80% associated with tyrosine kinase (c-KIT) mutations
EPIDEMIOLOGY
• M=F
• Usually age > 40
Typically present with (basically the LOCAL effects of a gastric tumour i.e. USU NO SPREAD OR METS):
• Vague abdominal mass,
• Feeling of abdominal fullness, early satiety if large enough, or
• Obstruction or
• Secondary symptoms of bleeding and anemia
• **Often discovered incidentally on CT, laparotomy or endoscopy**
RISK FACTORS
• Neurofibromatosis type IA (von Recklinghausen’s disease)
• Carney’s triad: GISTs, paraganglioma, and pulmonary chondroma
AETIOLOGY
Aetiology is unclear, but they are associated with type 1 neurofibromatosis in some cases.
• The pathogenesis is a spontaneous mutation in the c-kit gene, which normally codes for a membrane receptor (c-kit/CD117),
which is the receptor for a growth factor called stem cell factor
• The c-kit mutation results in a continuous signal for cell growth from this receptor (even without the growth factor being attached to
it), which is mediated via a tyrosine kinase in the intracellular domain of the receptor molecule.
• Some GISTs arise from mutations in platelet-derived growth factor α receptor (PDGFA); occasional cases demonstrate an
inherited predisposition.
INVESTIGATIONS
1. Endoscopy with biopsy – detects tumour
2. CT – may also detect tumour
3. EUS – Can be used to confirm the nature of the polyp and its origin from the muscular layer of the stomach wall
4. PET scan – To diagnose distant mets
5. Tumour marker – C-KIT (CD117 antigen)
6. NOTE VERY WELL RE BIOPSY:

• Pre-operative biopsy: controversial, but useful for indeterminate lesions:
o NOT recommended IF index of suspicion for GIST is already high
o Percutaneous biopsy is NOT recommended due to high friability and risk of peritoneal spread!!
o The presence of the c-kit protein (CD117) on the cell surface is almost diagnostic
NB:
• Most small GISTS (< 5 cm) have a low mitotic rate and behave like benign tumours
• Larger GISTS (> 5 cm) have a more malignant phenotype and require adjuvant chemotherapy
MANAGEMENT
• ± Neoadjuvant chemotherapy
• Surgical resection (without lymphadenectomy)
• ± Adjuvant chemotherapy (IMATINIB!!!!!)
A. If < 2cm: Monitor with serial endoscopy and resect if growing or symptomatic
B. If > 2cm: Surgical Resection

• Wide excision is the treatment of choice
• Lymphadenectomy is NOT recommended (as GISTs rarely metastasize to lymph nodes)
C. Chemotherapy – IMATINIB – For advanced disease (mets) or high-risk GIST

• Neoadjuvant and/or adjuvant
• Molecular targeted chemotherapy with imatinib mesilate (Glivec), an inhibitor of the c-kit tyrosine kinase, is very effective.
• Can be either given prior to surgery to shrink a large tumour in order to make it operable or given postoperatively to treat
metastases or when complete resection was not possible.
GASTRIC LYMPHOMA (DR.EAST)

About 10-15% of gastric malignancies
Stomach must be exclusive or predominant site of disease for it to be called gastric lymphoma
Stomach is most common site (70%)
Causative agent is H. pylori
Pathology
1. Large B-cell lymphoma
2. MALT lymphoma (low grade B-cell lymphoma) – some (but not all) caused by H. Pylori infection
3. Burkitt’s lymphoma (Epstein-Barr virus)
4. Other
Symptoms similar to adenocarcinoma

Diagnosis
§ Endoscopy & biopsy
§ Staging (and search for non-gastric sites) should be performed since this has implications for treatment
Treatment
Early MALT lymphomas:
§ H. Pylori eradication and endoscopic follow-up
§ Molecular markers predict which will respond to anti-H. Pylori Rx and which will not (but prohibitively expensive).
§ Radiation in refractory cases
Surgery? (considered unnecessary by some)
Chemoradiation with H. pylori eradication is mainstay

General Surgery
Post-gastrectomy and Post-vagotomy Syndromes
Sources: Toronto Notes, Dr. East, Harold Ellis
February 2015
Postoperative complications
§ Acute
o Bleeding
o Infection
o Delayed gastric emptying
§ Chronic
o Postgastrectomy syndromes
POSTGASTRECTOMY SYNDROMES
CLASSIFICATION/OUTLINE: (Dr. East):
A. Secondary to gastric resection

1. Metabolic disturbances
a. Iron deficiency anaemia
b. Megaloblastic anaemia
c. Impaired fat absorption à Steatorrhoea
d. Osteoporosis
e. Weight loss
2. Small stomach syndrome
B. Secondary to destruction of the pyloric mechanism

1. Early dumping syndrome
2. Late dumping syndrome
C. Secondary to Billroth II Reconstruction

1. Afferent loop syndrome
2. Efferent loop syndrome
3. Blind loop syndrome
4. Alkaline reflux gastritis
5. Retained antrum syndrome
D. Secondary to Vagotomy (Postvagotomy syndromes)

1. Diarrhoea
2. Stomal ulceration
3. Gastric atony
4. Cholelithiasis
A. SECONDARY TO GASTRIC RESECTION

1. Small stomach syndrome – Feeling of fullness after moderate sized meal
2. Metabolic disturbances (worse in women)

§ Weight loss
§ Anaemia: Iron or B12 deficiency – HCl required for iron absorption. Intrinsic factor (IF) needed for B12. Both normally
secreted by gastric parietal cells
§ Impaired fat absorption: Inadequate mixing of food with bile salts and pancreatic enzymes with ingested fat (due to
duodenal bypass) à Steatorrhoea
§ Osteoporosis: Decreased calcium absorption from bypassed duodenum
B. SECONDARY TO DESTRUCTION OF THE PYLORIC MECHANISM

Dumping Syndrome:
1. Early dumping syndrome

§ Occurs within 30 mins post-prandial
§ Occurs because of rapid passage for food of high osmolarity from the stomach to small bowel/jejunum – this
results in rapid shift of ECF into small bowel (temporary reduction in circulating blood volume) causing bowel
distension & hypotension
§ GI symptoms – Nausea, vomiting, bloating, abdominal pain, diarrhea

§ CVS symptoms – Tachycardia, diaphoresis, dizziness, fainting after food (due to the rapid hypovolaemia and
subsequent sympathetic overdrive response)
§ TREATMENT:
§ A. Dietary measures & reclining after eating
a. Frequent feedings of small meals
b. Avoid foods with large amounts of sugar and fat (high osmolarity)
c. Separate liquids from solids during meal (avoid washing down meals)
d. Sandostatin (somatostatin analogue) works BUT must be administered parenterally
§ B. Surgery is last resort – interposition of antiperistaltic jejunal segment between stomach and small bowel to delay
gastric emptying
2. Late dumping syndrome

§ 2-3 hours after meals
§ Also due to rapid gastric emptying, high glucose content in meal and consequent acute hyperglycemia.
§ Reactive insulin output overshoots, resulting in subsequent hypoglycemia
§ Symptoms are those of hypoglycemia (i.e. Autonomic and neuroglycopaenic – Diaphoresis, tremor, dizziness,
tachycardia, confusion)
§ Treatment – Same options as early dumping, with emphasis on reducing carbohydrate intake. Also pectin with acarbose
C. SECONDARY TO BILLROTH II RECONSTRUCTION

1. Afferent Loop Syndrome
§ Accumulation of bile and pancreatic secretions causes intermittent mechanical obstruction and distention of afferent
limb, with intermittent, explosive discharge of contents into stomach
§ Clinical features: (Features of intestinal obstruction!!) Early postprandial distention, RUQ pain, nausea, bilious vomiting,
anaemia
§ Diagnosed by HIDA scan
§ Treatment: Surgery (conversion to Roux-en-Y increases afferent loop drainage)
2. Efferent loop syndrome
§ Obstruction from adhesions or internal hernia

§ Symptoms and treatment as for small bowel obstruction
3. Alkaline reflux gastritis
§ Due to emptying of the afferent loop of a Polya gastrectomy into the stomach remnant à Hypersensitivity of
stomach remnant to bile
§ Associated with bilious vomiting
§ Diagnosed (and differentiated from afferent loop syndrome) by HIDA scan
§ Treatment: Surgery (conversion to Roux-en-Y increases afferent loop drainage)
4. Blind loop syndrome
§ Bacterial overgrowth of colonic Gram-negative bacteria in afferent limb

§ Clinical features: anemia/weakness, diarrhea, malnutrition, abdominal pain and hypocalcemia
§ Treatment: Broad-spectrum antibiotics, surgery (conversion to Billroth I)
5. Retained antrum syndrome

§ Residual antral mucosa in duodenal stump à Perpetually bathed in high pH (alkaline) duodenal juices
§ Sustained high secretion of gastrin causing recurrent ulceration
§ Diagnosed by technetium scan
§ Treat with PPI
§ Convert Billroth II to Billroth I if Rx fails
D. SECONDARY TO VAGOTOMY (POSTVAGOTOMY SYNDROMES)
1. Diarrhoea
§ Autonomic dysfunction of small bowel
§ Aggravated by early dumping
§ Usually self limited and requires only therapy, including cholestyramine
§ Antiperistaltic jejunal interposition if all else fails
§ Incidence reduced by performing highly selective vagotomy without drainage
2. Gastric atony
§ Often acute and self limited but may be chronic
§ Treated with prokinetic agent (metoclopramide or erythromycin)
3. Cholelithiasis
§ Secondary to impaired gallbladder emptying due to the disruption of the neural (vagal) aspect
General Surgery
Intestinal and Vascular Anastomoses
Sources: Surgical Tutor
February 2015
Gastrointestinal anastomoses
§ Anastomoses can be fashioned in various ways
o End-to-end
o End-to-side
o Side-to-side
§ Anastomoses heal in three phases
Lag phase (day 0-4)

Acute inflammatory responses occurs
Anastomosis has no intrinsic strength
Fibroplasia phase (day 3-14)

Fibroblasts proliferate
Immature collagen is laid down
Maturation phase (beyond 10 days)

Collagen is remodelled
Strength of anastomosis is increased
Factors influencing anastomotic healing

§ Anastomotic technique is required to maintain apposition until collagen is laid down
§ Anastomoses show serosal healing and require:
o Maintenance of apposition
o Good blood supply
o Tension free
§ Anastomotic leak or failure my occur if:
o Distal obstruction
o Peri-anastomotic sepsis
o Per-anastomotic haematoma
o Hypotension
o Hypoxia
o Jaundice
o Corticosteroids
o Uraemia
§ Any anastomotic technique should:
o Promote primary healing by accurate alignment of the divided bowel
o Cause minimal disruption of the local vasculature
o Incorporate minimum amount of foreign material
o Not implant malignant cells at the anastomosis
o Not enhance the risk of metachronous tumours
No evidence to suggest that hand-sewn are superior to stapled anastomoses
Anastomotic techniques
§ Conventional methods
o Hand-sewn
o Stapled
§ Novel techniques
o Compression rings
o Tissue glues
Two layered technique

§ Classic teaching of GI anastomoses
o Inner continuous all layer catgut suture
o Outer seromuscular interrupted silk
§ Produced serosal apposition and mucosal inversion
§ Inner layer believed to be haemostatic but also strangulates mucosa
Single layered technique

Modern teaching of GI anastomoses
Interrupted seromuscular absorbable (e.g. 3/0 Vicryl on round bodied needle)
Incorporates strong submucosal layer
Minimal damage to submucosal vascular plexus
Stapled anastomoses
Side to side anastomosis with linear staplers (e.g. GIA 60)
End to end anastomosis with circular devices (e.g. CEEA)
Stapled anastomoses reduced radiologically detected anastomotic leaks
Associated with increased rate of anastomotic strictures
Drainage of anastomosis
Drainage of anastomoses is controversial
No evidence that the use of a drain reduced leak rate for anastomoses above pelvic brim
Drain may increase risk of anastomotic leak
Biliary and urological anastomoses

Always use absorbable sutures
Nonabsorbable sutures risk stone formation
Vascular anastomoses
Always use nonabsorbable.
Prolene most often used
2/0 on aorta
4/0 on femoral artery
General Surgery
Colorectal Cancer and Screening (Last page has ileoanal pouch summary)
Sources: Sabiston, Toronto Notes, Dr. P. Roberts lecture, Dr. East lecture
February 2015
Outline of Contents:
1. General information
2. Colonic polyps
3. Hereditary colon cancer syndromes
4. Sporadic colon cancer (Starts on page 6) – everything up to management and follow-up
5. Screening (Page 10-12)
6. IPAA + Pouchitis
GENERAL INFO
THERE ARE 3 FORMS OF COLON CANCER (More detail in long notes)
1. Hereditary (e.g. FAP, HNPCC) – Family history, young age at onset, extraintestinal tumors. **Mutation in ALL cells of the individual
2. Familial – Relatively recent concept, a more subtle form of inheritance
• NOTE: First-degree relative of a patient with colon ca before age 50 is TWICE as likely to develop the cancer
3. Sporadic – Absence of family history, usu. older population (60-80), usually an isolated lesion. **Mutation only in the tumor itself
But in both hereditary and sporadic, the genetics of colon cancer initiation and progression are similar
The most common form of colorectal cancer is sporadic, without an associated strong family history.
ADENOMA CARCINOMA SEQUENCE

(MUST SEE LONG NOTES FOR MORE DETAIL)
Colorectal cancer genetics revolutionized in 1988 when the genetic changes involved were first described, from benign adenomatous polyp to invasive
carcinoma
Since then, tumor suppressor genes, DNA mismatch repair genes and proto-oncogenes that contribute have been identified.
The Fearon-Vogelstein adenoma-carcinoma model of colorectal neoplasia is one of the best-known models of carcinogenesis. Damage to these
genes important in the sequence of tumor progression
• Sequence of tumour initiation and progression explained by adenoma-carcinoma sequence involving damage to protooncogenes and tumor
suppressor genes
• Accepted by almost all authorities (see my long notes for support of the theory, if there is time)
• Colorectal cancers evolve through a progression of benign polyps to invasive carcinoma
• (BUT!!! there have been a few rare documented cases of colonic cancers arising DENOVO from normal mucosa)
• 10-year time span for the progression of an adenomatous polyp to a cancer.
• Earliest genetic change: The APC gene is a tumour suppressor gene located on chromosome 5q21. The earliest mutation in the adenoma-
carcinoma sequence occurs in this gene! --> Mutations in K-ras gene which causes formation of polyps --> p53 mutations which
increases expression of COX that aids in the formation of carcinoma IT IS FOR THIS REASON WHY ASPIRIN IS SAID TO REDUCE THE
INCIDENCE OF COLERECTAL CANCER AS IT WORKS AGAINST THE COX PATHWAY
• Earliest phenotypic change is known as “aberrant crypt formation”
Colonic epithelial cells lose the normal progression to maturity and cell death and begin proliferating in an increasingly uncontrolled manner. With this uncontrolled proliferation, the cells accumulate
on the surface of the bowel lumen as a polyp. With more proliferation and increasing cellular disorganization, the cells extend though the muscularis mucosae to become invasive carcinoma.
COLORECTAL POLYPS
DEFINITION
• Polyp: mass projecting into the lumen of the bowel above the surface of the intestinal epithelium
• Sessile (flat) or pedunculated (on a stalk)
• 50% found in the rectosigmoid region, 50% are multiple
EPIDEMIOLOGY
• 30% of the population have polyps by age 50 (40% by age 60, 50% by age 70)
CLINICAL FEATURES
• **Usually asymptomatic, do not typically bleed, tenesmus, intestinal obstruction, mucus
• Usually detected during routine endoscopy or familial/high risk screening
GOOD POINT!!!: The incidence of invasive carcinoma in a polyp is dependent on its size and histologic type
• (Polyps < 1 cm have < 5% incidence of Ca. Villous polyps > 2 cm have 50% chance of developing carcinoma.)
TYPES (MUST KNOW)
3 Classifications of polyps:
1. Gross appearance – Sessile vs. pedunculated
2. Histologic appearance – For adenomatous polyps only!!!!: Tubular (65-80%) > tubulovillous (20%) > villous (10%)
3. Neoplastic vs. Non-neoplastic
--
1. Non-neoplastic:
A. Hyperplastic: most common non-neoplastic polyp
B. Inflammatory “pseudopolyps”: associated with IBD, no malignant potential
C. Mucosal polyps: small <5 mm, no clinical significance

D. Submucosal polyps: lymphoid aggregates, lipomas, leiomyomas, carcinoids
2. Neoplastic:
A. Hamartomatous: Juvenile polyps (large bowel), Peutz-Jeghers syndrome (small bowel) – Rare, Autosomal Dominant: combination
of hamartomatous polyps of intestinal tract from stomach to rectum, and hyperpigmentation of lips and buccal mucosa. Also
increased risk of extraintestinal malignancies; breast, ovary, cervix, thyroid, bladder, pancreas, etc.)
• ***Malignant risk due to associated adenomas!! (large bowel)
• ***Low malignant potential à most spontaneously regress or autoamputate
B. Adenomatous: Premalignant, often carcinoma in situ:

• Some may contain invasive carcinoma (“malignant polyp” – 3-9%): invasion into muscularis
• MUST KNOW: Malignant potential (% that contain cancer): villous (40%) > tubulovillous (20%) > tubular (5%)
FROM DR. ROBERTS:

Ø Also have serrated polyps. This one don't reach textbook yet
Ø **NOTE: Advanced polyps are those > 10 mm (1 cm) in size. They have an exponentially higher risk of transformation and MUST be removed.
INVESTIGATIONS
• Colonoscopy is the gold standard for diagnosis and treatment of colonic polyps
• CT colonography: increasing in availability; patients still require bowel prep and will require colonoscopy if polyps are identified
• Other: Flexible sigmoidoscope if polyps are detected, proceed to colonoscopy for examination of entire bowel and biopsy.
Virtual colonoscopy AKA CT COLONOGRAPHY uses x-rays to produce 2d and 3d images of the colon
TREATMENT
MUST KNOW: Indications for intervention:
1. Symptoms
2. Malignancy or risk of malignancy (i.e. adenomatous polyps)
Options: Endoscopic polypectomy vs. Segmental colectomy
Usually, pedunculated polyps may be removed at colonoscopy using a snare. Sessile polyps pose some difficulty and may require segmental
colectomy
• Endoscopic removal of entire growth (polypectomy)

• Surgical resection for those **invading into muscularis (high risk of malignancy) and those **too large to remove endoscopically
• Follow-up endoscopy 1 yr later, then every 3-5 yr (i.e. CANCER SCREENING BEGINS FOR THE PATIENT)
HEREDITARY COLON CANCER SYNDROMES

LIST
CLASSIFY: HNPCC vs. Adenomatous vs. Hamartomatous
A. HNPCC (AD) – MOST COMMON - (MLH and MSH genes chromosome 2, 3, 7) – 70-80% malignancy risk! ~3-5% of all colon cancers!
B. Adenomatous
1. FAP (AD) – APC gene (100% malignancy risk! ~0.5% of colon cancers) and its variants:
a) Classic FAP
b) Attenuated FAP (AFAP)
c) Gardner’s syndrome
d) Turcot syndrome
2. MAP (AR) – (MYH associated polyposis) – similar to FAP, but no FAP mutation (MYH gene instead)
C. Hamartomatous
1. Peutz-Jeghers syndrome – 2-10% risk (STK11 chromosome 19)
2. Multiple polyposis coli
3. Familial juvenile polyposis
4. Cowden’s disease - PTEN (chromosome 10)
5. Bannayan-Zonana syndrome - (PTEN – chromosome 10)
NB:
§ Osteomas usu present as visible + palpable prominences in skull, mandible, and tibia of individuals with FAP. They are almost always benign
§ Desmoid tumors can present in the retroperitoneum and abdominal wall. Often locally invasive
INVESTIGATIONS
1. Genetic testing (80-95% sensitive , 99-100% specific) (see sidebar)
a. If no polyposis found à Still annual screening from puberty to age 50, then routine screening
b. If polyposis or APC gene mutation found à Annual colonoscopy and consider surgery;
§ ALSO consider upper endoscopy to evaluate for gastric, duodenal and periampullary tumours
Management of FAP
KNOW THIS BACK AND FRONT, INSIDE OUT
FIRST CRUCIAL POINT TO MAKE: FAP is Intestinal AND Extraintestinal. So removal of the colon and rectum and LOWER GI
surveillance is not enough!!! Must do surveillance of the other at risk sites and intervene where necessary
Treatment summary:
§ “PROPHYLACTIC Surgery” indicated by age 17-20
§ OPTIONS (MUST KNOW):
1. Restorative proctocolectomy with IPAA (most commonly recommended)
2. Total proctocolectomy with permanent ileostomy
3. Total colectomy with ileorectal anastomosis
o See the advantages and disadvantages of this option below
§ Doxorubicin-based chemotherapy
§ NSAIDs for intra-abdominal desmoids
RE: THE GASTRIC, DUODENAL AND PERIAMPULLARY RISK:

§ ***Upper GI surveillance every 2 years after age 30 + endoscopic polypectomy if possible for all duodenal adenomas (the
gastric polyps are usually non-neoplastic)
§ Whipple’s pancreaticoduodenectomy for early ampullary cancer
Surgical treatment of patients with FAP is directed at removal of ALL affected colonic and rectal mucosa. Restorative proctocolectomy with IPAA
= most commonly recommended operation.
Alternative approach:
Total abdominal colectomy with ileorectal anastomosis - was used extensively before the development of the technique of IPAA and has certain
advantages. If an FAP patient has relatively few polyps in the rectum, consideration may be given to this option.
§ Advantages: It is technically a simpler operation to perform and the pelvic dissection is avoided. This eliminates the potential complication of injury
to the autonomic nerves that could result in impotence
§ Disadvantages are that the rectum remains at high risk for the formation of new precancerous polyps, a proctoscopic examination is required
every 6 months to detect and destroy any new polyps, and there is a definite increased risk for cancer arising in the rectum with the passage of
time.
Re: The extraintestinal cancers

§ Polyps of the stomach and duodenum are not uncommon in patients with FAP.
o ***The gastric polyps are usually hyperplastic and do not require surgical removal.
o ***However, the duodenal and ampullary polyps are generally neoplastic and require attention.
§ A reasonable surveillance program is for UPPER GI surveillance every 2 years after the age of 30 years and endoscopic polypectomy, if
possible, to remove all large adenomas from the duodenum.
HNPCC
HNPCC is the most frequently occurring hereditary colorectal cancer syndrome in the United States and Western Europe!!
MUST KNOW: AD inheritance , mutation in a DNA mismatch repair gene (MSH2, MSH6, MLH1) resulting à microsatellite
genomic instability and à subsequent mutations
Accounts for approximately 3% of all cases of colorectal cancer
MUST KNOW: Dr. Henry Lynch described the 4 prominent features of the syndrome including:
1. Onset of cancer at a relatively young age (mean = 44 years)

2. Proximal distribution (70% à right colon!!!)
3. Increased number of synchronous and metachronous cancers
4. Predominance of mucinous or poorly differentiated (signet cell) adenocarcinoma (BUT STILL BETTER PROGNOSIS!!)
Two hereditary syndromes were initially described:
1. Lynch I syndrome is characterized by cancer of the proximal colon occurring at a relatively young age
2. Lynch II syndrome à colorectal AND EXTRACOLONIC CANCERS, including cancers of [breast, endometrial, ovarian],
[gastric, small intestinal], pancreatic, and [ureteral and renal pelvic] origin.
BUT NO GENETIC DIFFERENCES HAVE BEEN FOUND BETWEEN THE 2
DIAGNOSIS
The mainstay of the diagnosis of HNPCC is a detailed family history!!!
Clinically identifying HNPCC:
MUST KNOW: 3 common clinical criteria for diagnosis of HNPCC:
1. Amsterdam 1 criteria: This one did not account for extra intestinal cancers
2. Amsterdam 2 addresses this
3. Bethesda guidelines
Before the genetic mechanisms underlying the Lynch syndromes were understood, the syndromes were defined by the Amsterdam Criteria, which
required three criteria for the diagnosis:
(3, 2, 1 for memory)
st
1. Colorectal cancer in three 1 degree relatives
2. Involvement of at least two generations
3. At least one affected individual < 50 years at diagnosis
These requirements were recognized as being too restrictive, and the modified Amsterdam Criteria expanded the cancers to be included to not
only colorectal but also endometrial, ovarian, gastric, pancreatic, small intestinal, ureteral, and renal pelvic cancers. Further liberalization for
identifying patients with HNPCC occurred with the introduction of the Bethesda criteria
OTHER INVESTIGATIONS
1. Genetic testing (80% sensitive) – Colonoscopy mandatory even if negative

a. Refer for genetic screening individuals who fulfill EITHER the Amsterdam Criteria OR the revised Bethesda Criteria
2. Colonoscopy (starting age 20) annually
3. Surveillance for extracolonic lesions
OTHER POINTS
Should be remembered that as many as 20% of newly discovered cases of HNPCC are caused by spontaneous germline mutations, so a family history
may not accurately reflect the genetic nature of the syndrome.
Colorectal cancer, or an HNPCC-related cancer, arising in a person younger than 50 years should raise the suspicion of this syndrome. Genetic
counseling and genetic testing can be offered
MANAGEMENT OF HNPCC
Treatment summary:
Still controversial
FIRST CRUCIAL POINT: Unlike FAP, role for prophylactic colectomy is NOT universally accepted. General summary of recommendation:
1. Before cancer, close surveillance – Start colonoscopy at 20, repeat every 2 years until 35. Then repeat every year
a. In women from 25, periodic vacuum curettage, pelvic ultrasound and CA-125 levels
2. When colon cancer detected, procedure of choice: Total colectomy and ileorectal anastomosis + annual proctoscopy (because
rectum remains at risk)
a. DON’T FORGET: In women with no further plans for childbearing à prophylactic TAH/BSO recommended
• NOTE WELL: Obvious that the slow evolution from benign polyp to invasive cancer is NOT a feature of the pathogenesis in HNPCC
patients, and this phenomenon of accelerated carcinogenesis mandates frequent (annual) colonoscopic examinations. Even with annual
colonoscopic examinations, there is a documented risk for colon cancer but, when a cancer arises while the patient is under a vigorous surveillance
program, the cancer stage is usually favorable
• Role of prophylactic colectomy for patients with HNPCC has been considered in some cases, but this has NOT received universal
acceptance.
• It is an interesting but well-documented fact that the prognosis is better for cancer patients with HNPCC than for non-HNPCC patients with cancer of
the same stage.
PEUTZ JEGHERS
Autosomal dominant syndrome characterized by the combination of hamartomatous polyps of the intestinal tract AND hyperpigmentation of the
buccal mucosa, lips, and digits
• Rare
• Increased (2% to 10%) risk for cancer of the intestinal tract, with cancers reported throughout the intestinal tract, from the stomach to the
rectum.
• There is also an increased risk for EXTRAINTESTINAL MALIGNANCIES, including cancer of the [breast, ovary, fallopian tubes, cervix],
[gallbladder, bile ducts, pancreas], thyroid, lung and testicles.
• Reasonable to survey the colon endoscopically every 2 years, and patients should be screened periodically for malignancies of the breast, cervix,
ovary, testicle, stomach, and pancreas.
MYH-ASSOCIATED POLYPOSIS
Recessive inheritance
Phenotype resembling FAP but no discoverable FAP mutation

Mutations found instead in the MYH gene – responsible for repairing oxidative DNA damage. The mutations promote defects in the APC gene producing
polyps and tumors à MYH associated polyposis (MAP)
Mutation has been characterized in Northern European, Indian and Pakistani populations.
§ The MYH phenotype is highly variable and for now management should follow guidelines established for FAP and AFAP.
MULTIPLE POLYPOSIS COLI

Autosomal dominant syndrome
• Predominately hamartomas, but the hamartomas may contain adenomatous elements, and adenomatous polyps also are common
• Increased cancer risk in afflicted individuals, with a malignant potential of at least 10% in patients with multiple juvenile polyps
• Increased risk for both GI and extraintestinal cancer. The syndrome is usually discovered because of GI bleeding, intussusception
• Patients with numerous polyps should be treated with abdominal colectomy, ileorectal anastomosis, and frequent endoscopic surveillance of the
rectum. If the diffuse form of polyposis involves the rectal mucosa, consideration should be given to restorative proctocolectomy with IPAA.
SPORADIC COLON CANCER

NB: Colon or large intestine is 1.5 m (5 feet). Rectum is 15 cm (5 inches)
INCIDENCE
§ Most common form of colorectal cancer
§ Risk for colorectal cancer increases with age. > 90% of new cases diagnosed in patients > 50
§ NOTE: First-degree relative of a patient with colon ca before age 50 is TWICE as likely to develop the cancer
§ 3% synchronous
§ Synchronous tumour = > 1 tumour occurring at the same time (or detected < 6 months after finding the initial lesion)
§ Metachronous tumour: A previous colonic neoplasm increases the risk of a second tumour (*One anonymous source: lesion appearing > 6
months after finding the initial lesion)
RISK FACTORS
NOTE: Most patients have no specific risk factors
CLASSIFY: MODIFIABLE VS. NON-MODIFIABLE
A. NON-MODIFIABLE
1. Age 90% > 50 (dominant risk factor in sporadic cases), mean age is 70
2. Genetic:
st
a. Family history of CRC, especially 1 degree relative under age 50 (i.e. “Familial colon cancer”)
b. Hereditary colon cancer syndromes: FAP, HNPCC (i.e. “Hereditary colon cancer”)
3. Colonic conditions:
a. Adenomatous polyps (MUST KNOW à Especially if >1 cm, villous, multiple)
b. IBD (MUST KNOW à Especially for UC: Risk is 5% at 10 years, then 1-2% per year thereafter)
4. Previous colorectal cancer (also gonadal or breast)
5. Diabetes mellitus and acromegaly (***insulin and IGF-1 are growth factors for colonic mucosal cells)
B. MODIFIABLE
1. Diet (High fat, red meat, low fibre)
2. Smoking
AETIOLOGY AND PATHOPHYS (SEE ABOVE)

CLINICAL FEATURES
FIRST POINT: Often asymptomatic. When symptomatic, depends on site of lesion in colon and morphology
Left colon (35%)

Pathology: Annular, often constrictive invasive lesions
Symptoms:
1. Altered bowel habits: Constipation most common ± overflow/spurious diarrhoea (alternating bowel patterns)
2. Features of partial/complete LBO: Abdominal pain, decreased stool caliber (pencil-shaped stools in circumferential lesions)
3. Mucus PR: Some tumours are mucin-secreting adenocarcinomas. Patient will very likely be **hypokalemic à (The mucous contains large
amount of potassium)
4. Bright-red blood PR (haematochezia)
5. Sigmoid cancers may present with features of a colovesical or colovaginal fistula!!!
Right colon (25%)

Pathology: Exophytic lesions with occult bleeding.
§ Symptoms: Weight loss, weakness, features of anaemia, melaena, rarely obstruction
§ Signs: Fe-deficiency anemia, RLQ mass (10%), altered blood PR
NB: CRC has been “migrating” to the right side of the colon. In the past 40 years, the incidence of cancer in the right colon has increased in
comparison to cancer arising in the left colon and rectum.
Rectum 30% - Arise in distal 15 cm of large bowel

Pathology: Ulcerating
§ Symptoms: Haematochezia = most common. Obstruction, tenesmus, other features of left sided lesions
§ Signs: Palpable mass on DRE (reveals the tumour in 90% of cases), BRBPR
Other general features:

FEATURES OF SPREAD
1. Direct extension
2. Lymphatic – Local lymphatics, Sister Mary Joseph’s nodule, Left supraclavicular node (Virchow’s node, aka. Troisier’s sign), Left axillary
nodes (Irish’s node)
3. Haematogenous (liver most common, lung, bone, brain; tumour of distal rectum à IVC à lungs) ~20% have liver mets at diagnosis!
4. Transcoelomic: Peritoneal seeding (Called carcinomatosis peritonei if extensive): Krukenberg (ovary), Blumer’s shelf (pelvic cul-de-sac)
Iron deficiency anaemia in any male or nonmenstruating female should lead to a search for a source of bleeding from the GI tract
Although “obstructive symptoms” are usually associated with cancers of the left colon, ANY advanced colorectal cancer can cause a change in bowel
habits and intestinal obstruction
20% patients have distant metastatic disease at time of presentation
Surgical Tutor: 40% of cancers present as a surgical emergency with either obstruction or perforation
INVESTIGATIONS
GENERAL VS. DIAGNOSTIC VS. STAGING
A. GENERAL LABORATORY:
1. CBC
2. U&Es – Possible hypokalaemia, if mucin-secreting adenocarcinoma
3. LFTs – Assess possible liver mets
4. CEA (Carcinoembryonic antigen)
§ NB: Not all colon cancer produce CEA
§ (Preoperative for baseline, > 5 ng/mL have worse prognosis)
§ NB: ULN for CEA is 4. Expect 0 or near 0. Can use for surveillance in selected patients who had preoperative elevation.
B. DIAGNOSTIC:
1. Colonoscopy with biopsy (GOLD STANDARD for diagnosis of colon ca). 2 purposes:
a. Look for synchronous/metachronous lesions (3-5% of patients);
b. Biopsy of the tumor to verify the diagnosis
2. Alternative: Double contrast barium enema (“apple core” lesion) WITH sigmoidoscopy
§ BUT colonoscopy is generally performed even after a cancer is detected by barium enema to obtain a biopsy and to detect (and
remove) small polyps that may be missed by the contrast study!
If a patient is FOBT +ve, or has microcytic anemia or has a change in bowel habits, do colonoscopy
NOTE VERY WELL: In patients with tumors causing complete obstruction, the diagnosis is best established by resection of the tumor without the
benefit of preoperative colonoscopy. A water-soluble contrast enema (investigation of choice) is often useful in such circumstances to establish the
anatomic level of the obstruction
C. STAGING
1. CT chest, abdomen, pelvis – GOLD STANDARD for staging. The top 3 sites of colon cancer mets are #1 Liver, #2 Lungs, #3 Peritoneum
2. CT head only if lesions suspected
3. Bone scan only if lesions suspected
MUST NOTE WELL: FOR RECTAL CANCER: ALSO pelvic MRI or endorectal ultrasound to determine T and N stage. Rectal ca has
requirement for precise characterization of the cancer with respect to proximity to the anal sphincters and the extent of invasion, as
determined by depth of penetration into the bowel wall and spread to adjacent lymph nodes.
ALSO: Precise location of the rectal tumor is best determined by examination with a rigid proctosigmoidoscope – DONE EVEN IF DIAGNOSED
AT COLONOSCOPY because the flexible proctosigmoidoscope may not accurately measure the exact distance from the tumor to the anal sphincter!!
The depth of penetration can be estimated by digital rectal examination (superficially invasive tumors are mobile, whereas the lesions become tethered
and fixed with increasing depth of penetration), and EUS or MRI with endorectal coil can provide a fairly accurate assessment of the extent of invasion of
the bowel wall
STAGING
1. Dukes’ criteria
2. Modified Dukes’ criteria
3. AJCC-TNM (American Joint Committee on Cancer)
*** BUT Remember adequate staging requires CT Chest, Abdomen, Pelvis!!!

*** For rectal ca. may add MRI and endorectal ultrasound!!!
DUKES’ CLASSIFICATION
Developed in 1932 by Dr. Cuthbert Dukes, a pathologist at St. Mark’s Hospital in London that was later modified.
§ The classification was developed for rectal cancer!!!, but it was generally also used to describe the stage of colon cancer.
The Dukes classification is simple to remember and is still frequently used:

A. Dukes’ stage A cancer is confined to the bowel wall
B. Stage B cancer penetrates the bowel wall
C. Stage C cancer indicates lymph node metastases
o Doctors from the Mayo Clinic, established a distinction between tumors that partially penetrated the muscularis propria (B1) and those that fully
penetrated this layer (B2).
o Further separated the tumors that had invaded lymph nodes but did not penetrate the entire bowel wall (C1) from tumors that invaded lymph nodes
and did penetrate the entire wall (C2).
o Doctors from the Cleveland Clinic added stage D for tumors with distant metastasis.
o All these modifications in various combinations are still in use and are often called the MODIFIED DUKES CLASSIFICATION.
RE: DUKES’: 5-year survival - 90%, 70% and 30% for Stages A, B and C respectively
The classification in used in the US was developed by the American Joint Committee on Cancer (AJCC). This classification, known as the TNM
Combines clinical info obtained preoperatively with data obtained during surgery and after histologic examination of the specimen
TNM Staging of Colorectal Carcinoma (AJCC/IUCC 2010)

Primary Tumour (T) Regional Lymph Nodes (N) Distant Metastasis (M)
T0 No primary tumour found N0 No regional node involvement M0 No distant metastasis
Tis Carcinoma in situ N1 Metastasis in 1-3 regional nodes M1 Distant metastasis
T1 Invasion into submucosa N2 Metastasis in 4 or more regional
T2 Invasion into muscularis propria nodes
T3 Invasion through muscularis propria and into serosa
T4 Invasion into adjacent structures or organs
MANAGEMENT
Colon cancer
Principles: Management depends on the stage of the tumour AND
the objectives of management for colon cancer may be CURATIVE or PALLIATIVE:
Re: Goals of curative (KNOW THIS WELL) – May be LAPAROSCOPIC OR OPEN

1. RADICAL colectomy: Wide resection of the primary cancer with adequate (5 cm) margins
2. Regional lymphadenectomy (at least 12 nodes!)
3. Restoration of continuity of the GI tract by anastomoses (with sutures or staples), or colostomy
4. Adjuvant chemotherapy (FOLFOX, FOLFIRI, FOLFIRINOX) can be considered for stage II or III (5FU+leucovorin based regimens)
§ NB: ADJUVANT CHEMOTHERAPY DOES NOT IMPROVE SURVIVAL IN STAGE 1!!!
Re: Palliative
§ Presence of hepatic metastasis does NOT preclude resection of the primary tumour. REASONS: Resection of the primary may still provide
excellent PALLIATION wrt obstruction and bleeding AND if the metastatic disease in the liver is resectable, the patient may yet be cured
Colonic stenting is now available for obstructing tumours to relieve obstruction prior to resection OR for palliation in unresectable tumours. In the
former, this allows decompression as well as bowel preparation, which reduces the leak rate of a primary anastomosis at operation. Helps to
avoid needing a Hartmann’s operation!!!
More surgical details:

1. Before elective operations, the bowel MAY be prepared by giving a low residue diet and enemas. Oral purgatives are no longer given because of
the potential dehydration. (BUT NOTE THAT there is NO evidence that bowel prep decreases infections!!!)
2. Perioperative prophylactic antibiotics (e.g. gentamicin and metronidazole) are given (before incision)
3. Operative access is achieved laparoscopically, OR by laparotomy, usually via a midline incision
4. The affected segment of bowel is removed with a margin of normal bowel, usually 5 cm clear each side of the tumour. There must be a good
blood supply to the cut ends of bowel to ensure healing so, in practice, lines of resection are determined by the distribution of mesenteric
blood vessels. For example, ascending colon lesions are treated by removing the whole right colon (right hemicolectomy), as the right
colic artery must be ligated in order to remove a section of the right colon
5. A wedge-shaped section of colonic mesentery is removed with the bowel. This contains the primary field of lymph node drainage. If there are
other obvious lymph node metastases, these are usually included in the resection specimen
6. MUST FULLY UNDERSTAND THESE PRINCIPLES: RECTAL CANCERS are a special case!!! The preferred operation is a
sphincter-saving anterior resection of rectum; provided the lower edge of the tumour is 1–2 cm above the anal
sphincters, the sphincter can usually be preserved. This operation involves excising the tumour with an appropriate length of bowel
plus an intact envelope of fat around it (the mesorectum containing local lymph nodes). The proximal end of bowel is then anastomosed to
the distal stump. Alternatively, a pelvic reservoir is created using a J-pouch technique. This has been shown to reduce the frequency and urgency
of defaecation without increasing surgical complications. A temporary defunctioning ileostomy or colostomy is sometimes used to aid healing of a
low anastomosis.
§ If the sphincter is involved, the entire rectum and anus has to be removed via an abdominoperineal resection (APR), with the
proximal end of bowel brought out as a permanent colostomy
7. Postoperatively, an ‘enhanced recovery’ program may be employed to encourage early eating and mobilisation. These have been shown to
lower complication rates and shorten hospital stays Care is taken to not spread tumour by unnecessary palpation
8. The extent of resection is determined by the location of the cancer, its blood supply and draining lymphatic system, and presence or absence of
direct extension into adjacent organs. The cancer-bearing portion of colon is removed according to vascular distribution of segment
9. To restore the continuity of the GI tract, an anastomosis is fashioned with sutures or staples, joining the ends of the intestine (small or
large). **It is important that both segments of the intestine used for the anastomosis have an excellent blood supply and that there be
no tension on the anastomosis
Possible procedures (**Know what parts of colon and which vessels are taken in each)
1. Right hemicolectomy – Procedure of choice for lesions in caecum, ascending colon and hepatic flexure
§ Resect bowel from 4-6 cm proximal to ileocecal valve, to the portion of transverse colon supplied by right branch of middle colic artery
§ Anastomose terminal ileum and transverse colon
2. Extended right hemicolectomy – most transverse colon lesions
§ Anastomose terminal ileum and proximal left colon
§ Divide right and middle colic arteries at their origin and remove right and transverse colon supplied by these vessels
3. Left hemicolectomy – for descending colon tumours
§ Resect from splenic flexure to rectosigmoid junction
4. Sigmoid colectomy – sigmoid colon lesions
5. Subtotal colectomy (with ileosigmoid anastomosis)
6. Total colectomy
§ Remove entire colon from ileum to rectum
§ Fashion ileorectal anastomosis
o Indicated for patients with multiple primary tumors, for individuals with HNPCC, and occasionally for those with completely obstructing
sigmoid cancers.
o Loss of the absorptive and storage capacity of the colon from this procedure causes an increase in stool frequency. Patients < 60 generally
tolerate this well, with gradual adaptation of the small bowel mucosa, and an acceptable stool frequency of 1-3 movements daily.
o In older individuals, however, abdominal colectomy may result in significant chronic diarrhoea
*** NOTE: Proper surgery requires a minimum of 12 lymph nodes. ***
Treatment of stage IV patients depends on the location and extent of the metastases. Isolated hepatic or pulmonary lesions may be amenable to
resection. Chemotherapy is indicated, with new agents complementing the 5-FU regimens that remain the keystone of therapy.
The newest agents that have been shown to be effective for metastatic disease and are being studied in the adjuvant setting are the
monoclonal antibodies bevacizumab
RE: LAPAROSCOPIC SURGERY:

§ Early studies raised concerns about port site recurrence
§ BUT recent studies suggest equivalent overall and disease-free survival
MUST KNOW: HOW TO MANAGE COLON CANCER THAT PRESENTS WITH COMPLETE OBSTRUCTION
4 ways to manage the situation of tumour causing complete obstruction:
(NB: Joining normal bowel to dilated bowel always has a high risk of anastomotic leak. Also risk of leak in unprepared bowel)
1. Primary anastomosis between the proximal colon and the colon distal to the tumor has been avoided in the past in the presence of obstruction
because of a high risk for anastomotic leak associated with this approach. Thus, such patients were usually treated by resection of the
segment of colon containing the obstructing cancer, closure of the distal sigmoid or rectum, and constructing a colostomy (Hartmann’s
operation)
2. Alternatives to this approach have been to resect the segment of left colon containing the cancer and then cleanse the remaining
colon with saline lavage by inserting a catheter through the appendix or ileum into the cecum and irrigating the contents from the colon. A
primary anastomosis between the prepared colon and rectum can then be fashioned without the need for a temporary colostomy.
3. A third approach occasionally used for obstructing cancers of the sigmoid colon is to resect the tumor and the entire colon proximal to the
tumor (hence removing the dilated segment) and fashion an anastomosis between the ileum and distal sigmoid colon (subtotal
colectomy and ileosigmoid anastomosis).
• This approach has the advantage of avoiding a temporary colostomy and eliminating the need to search for synchronous lesions in the colon
proximal to the cancer. However, patients treated by this approach may have more frequent bowel movements.
4. More recently, endoscopic techniques permit the placement of a stent introduced with the aid of a colonoscope that traverses the
obstructed tumor and expands, re-creating a lumen, relieving the obstruction, and permitting a bowel preparation and elective operation
with primary colorectal anastomosis.
Rectal Cancer
NOTE WELL: Although cause and pathogenesis of adenocarcinoma are similar throughout the large bowel, significant differences in the use of
diagnostic and therapeutic modalities separate colonic from rectal cancers.
This distinction is largely because of the confinement of the rectum by the bony pelvis
Re: Investigation
1. **The limited mobility of the rectum allows MRI to generate better images and increases its sensitivity.
2. **In addition, the proximity of the rectum to the anus permits easy access of ultrasound probes for more accurate assessment of the extent
of penetration of the bowel wall and the involvement of adjacent lymph nodes.
Re: Management
1. **The limited accessibility of the rectum, proximity to the urogenital organs and anal sphincters, and close association with the
autonomic nerves supplying the bladder and genitalia require special and unique consideration when planning treatment for cancer of the
rectum – surgical access is relatively difficult. Therefore, colon and rectal adenocarcinomas are discussed separately.
2. Furthermore, the biologic properties of the rectum, combined with its anatomic distance from the small intestine afforded by its retroperitoneal
pelvic location, provides an opportunity for treatment by radiation therapy. (SB cannot tolerate as high doses of radiation as LB without
complications such as radiation enteritis including stricture, haemorrhage and perforation)
--
Multimodality treatment employed for rectal cancer – though exact selection criteria is controversial
Principles
1. Neoadjuvant radiation or chemoradiation therapy (For stage II and III. In US, given for 5-6 weeks of radiation, then surgery 6-10 weeks
after completion of radiation)
§ Preop radiation shown to be superior to postop. Even if only given over 5 days, reduces recurrence and increases survival
§ Combine with 5FU-leucovorin based chemo often significantly downstages tumor
§ Up to 10-25% may experience a “complete clinical response”/cure with neoadjuvant chemoradiation
§ Downstaging may also help surgeon to preserve continence
2. Operation – See options below – Depends mainly on distance of tumour from anal verge - If anastomosis made, may bring out a diverting stoma
to protect it, and close after 10 weeks
§ Upper 1/3 – Anterior resection: Resect tumour with restorative anastomosis between sigmoid colon and lower rectum (also divide IMA and
left colic at highest level possible)
§ Middle 1/3 – Can usually be treated by anterior resection, if satisfactory distal clearance can be obtained – easier in women as wider pelvis
facilitates dissection
§ Lower 1/3 – < 5 cm from anal verge à usually treat by AP resection of rectum with terminal colostomy (also take IMA and left colic)
3. Adjuvant chemoradiation
§ Risk of local recurrence can be reduced by radiotherapy. Chemoradiotherapy produces a better outcome
§ Can be given either preoperatively or postoperatively
Palliation
Even if incurable, palliation best achieved, when possible, by excision of the primary tumour
In completely inoperable cases, chemoradiotherapy, diathermy or laser of the tumour (electrocoagulation or photocoagulation) may give temporary relief.
SABISTON: 6 types of operations:
1. Local excision: for select T1 lesions only
2. Transanal Endoscopic Microsurgery - If the tumor is confined to the submucosa (uT1, N0), excision by a transanal approach is an attractive
option
3. Fulguration - The technique of fulguration, which eradicates the cancer by using an electrocautery device that destroys the tumor by creating
a full-thickness eschar at the tumor site, requires extension of the eschar into the perirectal fat, thus destroying both the tumor and rectal wall
4. Low anterior resection of rectum (LAR): curative procedure of choice if adequate distal margins; uses technique of total mesorectal excision
a. LAR removes distal sigmoid and rectum with anastomosis of distal colon to anus.
b. Removes the portion of bowel containing the cancer and the mesorectum completely, which contains the lymphatic channels that
drain the tumor bed
c. The term LOW anterior resection indicates that the operation entails resection of the rectum below the peritoneal reflection through
an abdominal approach. (Anterior resection resects proximal rectum above the peritoneal reflection)
d. Risk of local recurrence reduced by performing total mesorectal excision (see Sabiston)
***For cancers involving the lower half of the rectum, the entire mesorectum, which contains the lymph channels draining the tumor bed, should be
excised in continuity with the rectum. This technique, total mesorectal excision, produces the complete resection of an intact package of the
rectum and its adjacent mesorectum, enveloped within the visceral pelvic fascia with uninvolved circumferential margins. The use of the technique
of total mesorectal excision has resulted in a significant increase in 5-year survival rates
Intestinal continuity is reestablished by fashioning an anastomosis between the descending colon and rectum, which has been greatly facilitated by the
introduction of the circular stapling device. After the colorectal anastomosis has been completed, it should be inspected with a proctoscope inserted
through the anus. If there is concern about the integrity of the anastomosis, or if the patient has received high-dose preoperative chemoradiation, a
temporary proximal colostomy or ileostomy should be made to permit complete healing of the anastomosis. The stoma can be closed in approximately
10 weeks if proctoscopy and contrast studies verify the integrity of the anastomosis. An end-to-end anastomosis between the descending colon and
distal rectum or anus may result in significant alteration of bowel habits attributed to the loss of the normal rectal capacity. Patients treated with this
operation often experience frequent small bowel movements (low anterior resection syndrome or clustering). This problem can be addressed by
fashioning a colonic J pouch as the proximal component of the anastomosis.
5. Abdominoperineal resection of rectum (APR): if adequate distal margins cannot be obtained (An anonymous source suggests this to be 2 cm
from the internal sphincter or rectal cancers < 8 cm from the anal verge! (Surgical Recall)); also includes a total mesorectal excision??
a. Involves the removal of distal sigmoid colon, rectum, and anus through abdominal and perineal incisions – permanent end
colostomy required
6. Sphincter-sparing abdominal perineal resection with coloanal anastomosis
FOLLOW UP
Currently there are no data suggesting optimal follow-up
Aimed at early detection of recurrence, treatable metastasis and metachronous (meaning new) cancer
MUST KNOW: One recommendation:
§ Colonoscopy at 1, 3, 5 years post surgery.
§ Also, CEA every 3 months for 2 years – monitor initial response to treatment AND assess recurrence
§ Consider periodic CT chest, abdomen, pelvis
Intensive follow-up improves overall survival
SCREENING FOR COLORECTAL CANCER

SCREENING IN GENERAL
CRC is a “good” candidate disease for screening. Must know screening for colon by heart! Know the procedures!
Criteria for screening:
1. DISEASE CRITERIA 2. TEST CRITERIA 3. INSTITUTIONAL CRITERIA
1. Disease must be common 1. Must be reasonably sensitive and specific 1. Must be able to cope with positive screening
2. Disease must be serious 2. Must be relatively cheap tests
3. Must be detectable precursor lesions 3. Must be readily available and easily
4. Long latent phase accessible
5. Treatment of precursor lesions must prevent 4. Must be convenient and acceptable to
the disease people
6. Treatment of early disease must reduce 5. Must be safe
morbidity and mortality
SPECIFIC TO CRC: American Cancer Society (ACS) Recommendations
WHO TO SCREEN: Screening is performed appropriate to risk!!:

1. For people at “AVERAGE RISK”: Start at 50 yo if no known risk factors & choose from the list below
2. Familial – 10 years before age at which first degree relative contracted disease OR 40 yo (whichever first) & colonoscopy every 5 years
3. Pre-cancerous disease require specific screening schedules (e.g. ulcerative colitis) or pre-emptive colectomy (e.g. FAP)
APPROACHES TO SCREENING (5 POSSIBLE TESTS):

1. Stool tests alone (gFOBT or FIT): Every year
2. Flexible sigmoidoscopy alone (no longer supported by ACS): Every 5 years
• Can increase flex SIG accuracy by combining with annual FOB or FIT
3. Double contrast BE: Every 5 Years
4. CT colonography: Every 5 years
5. Colonoscopy: Every 10 years
1. Faecal screening tests (gFOBT, FIT, sDNA):

NB: ACS: Recommend annual stool tests (preferably FIT) ONLY IF INVASIVE TESTS REFUSED!!!
A. Faecal occult blood [gFOBT: (guiac based faecal occult blood test)]: Focus on this one. Detects heme.
• Based on guiac impregnated paper slides that change colour in the presence of perioxidase activity from haemoglobin
• Low, sensitivity (<50% for cancer & only 7% for advanced adenoma)
• Low specificity: Only 10% of guaiac positive patients will have colon cancer
• Detection rate is better with several stool samples obtained on separate days
• *** Therefore: Consists of 3 tests done on 3 different days
MUST KNOW: Factors affecting results of FOB:
1. Not all polyps bleed. Approximately 1/3 of patients with colon ca. have negative FOB test
2. Patient needs to be on a diet low in peroxidase (no rare beef etc.) to avoid false positives
3. Certain medications: Iron, cimetidine, Antacids à false negative
• *** NB: Once positive MUST go on to colonoscopy
B. FIT (Faecal Immunochemical Test)

§ Detects globin (more specific for human Hb)
§ Better, less variable sensitivity and specificity than gFOBT
§ No dietary restrictions and less sampling of stool
§ Must be performed annually to maximize cumulative sensitivity
C. sDNA
§ Tests entire volume of 1 large stool for known DNA alterations in the adenoma-carcinoma sequence of colorectal carcinogenesis
§ Sensitivity and specificity better than stool blood tests
§ Expensive
§ Performance interval uncertain
2. Sigmoidoscopy:
NB: ACS: Flexible/rigid sigmoidoscopy by itself is NO LONGER A DEFENSIBLE RECOMMENDATION!!!
Office procedure; no sedation required
Bowel prep. similar to colonoscopy
Colonoscopy indicated if any significant polyps identified
Will miss as much as 50% of cancers
1. Flexible sigmoidoscope will take you up to splenic flexure. (About 70 cm)

• Note that cancer on the left side is more common BUT right side incidence is increasing. At least 50% of colon ca now out of reach
of sigmoidoscopy
2. Rigid sigmoidoscope: About 30-40 cm à Rectosigmoid junction
• Advantages: Can use to measure the length since rigid
3. Double-Contrast Barium Enema + Proctosigmoidoscopy:

(Single contrast: NOT used for screening à Used for emergency)
Double contrast:
• Widely available and relatively cheap
• Sensitivity and specificity very operator dependent
• Misses 60% of polyps ≥1cm and misses significant % of cancers
Patient needs bowel prep. Need to wash out all faeces
• Pass a u-cath through anus and blow up bulb
• Then instill barium
• Then instill air so barium coats the wall and can observe integrity of the lining
** NOTE: One advantage of proctosig over BE à can see a tumour at tip of anus.
Drawback of BE is that it would miss this as the contrast is instilled proximal to this (where the ucath is inserted)
** So BE is NOT good for assessment of distal rectum and anus!!!!
** Bottom line: A double contrast BE is never complete without proctosig!!
*** (And a proctosig is not complete without a DRE first)
4. Colonoscopy GOLD STANDARD

Advantages:
1. Highest sensitivity (95%) and specificity (but will miss 12% advanced adenomas and 5% of cancers)
2. Allows complete colon assessment – can pick up synchronous lesions (occur in 3-5%)
3. Allows biopsy + polypectomy
Disadvantages:
1. Expensive and therefore unaffordable by a large percentage of at-risk population
2. Requires uncommon skill & therefore not widely available
3. Requires sedation. (Flexible sig does not require this)
4. Requires bowel prep
5. Most dangerous screening method: Risk of haemorrhage and perforation
5. CT Colonography - newest technology

Looks this up. Note that it IS readily available in Jamaica
Advantages:
1. Sensitivity and specificity now close to colonoscopy
2. Doesn't require sedation and requires much less time than colonoscopy
3. LOWER risk of perforation. Remember must still prep bowel as well as CO2 must be introduced so there is still a risk of perforation. You have to
come from Clarendon or Portland to perforate a bowel by blowing too much air though.
4. Also can look at liver same time!! So can stage at same time.
Disadvantages:
1. Very expensive (requires multi-slice CT scanner) and not widely available
2. Requires bowel prep similar to colonoscopy
3. However still cant biopsy
4. High radiation exposure. Also, repeat every 5 years if normal so leads to significant cumulative radiation dose
5. Slightly lower sensitivity than colonoscopy
ILEO ANAL POUCHES AND POUCHITIS

Wiki: the ileal pouch-anal anastomosis (IPAA), also known as an ileo-anal pouch, restorative proctocolectomy, ileal-anal pullthrough, or
sometimes referred to as a j-pouch, s-pouch, w-pouch or an internal pouch (or Kock pouch), is a surgically constructed internal reservoir; usually
situated near where the rectum would normally be. The procedure retains or restores functionality of the anus with stools passed under voluntary control
of the patient.
POUCH DESIGN (Surgical Tutor)
Functional results of ileoanal pouch

§ Mean stool frequency is six per day
§ Perfect continence
o During day (90%)
o At night (60%)
§ Gross incontinence (5%)
Morbidity
50% develop significant complications:
§ Small bowel obstruction (20%)
§ Pouchitis (15%)
§ Genitourinary dysfunction (6%)
§ Pelvic sepsis (5%)
§ Fistula (5%)
§ Pouch failure (6%)
§ Anal stenosis (5%)
§ Larger capacity pouches reduce stool frequency
Pouchitis is inflammation of the ileal pouch (an artificial rectum surgically created out of ileal gut tissue in patients who have undergone a colectomy),
which is created in the management of patients with ulcerative colitis, indeterminate colitis, FAP, or, rarely, other colitides.
Ileal pouch-anal anastomosis following total proctocolectomy has become part of the standard surgical treatment for patients with ulcerative colitis or
familial adenomatous polyposis who require colectomy.
Patients with pouchitis typically present with bloody diarrhea, urgency in passing stools, or discomfort while passing stools. The loss of blood and/or
dehydration resulting from the frequent stools will frequently result in nausea. In fewer cases, pain can occur with pouchitis.
**There is no clinically approved treatment for pouchitis. First line treatment is usually with antibiotics (7-10 day course), specifically with
ciprofloxacin and metronidazole. Ampicillin or Piperacillin can also be considered as alternatives to empiric Ciprofloxacin and metronidazole)
Half of the chronic, unremitting pouchitis population will eventually require surgical treatment of the pouch.
General Surgery
Perianal diseases: LOOK UP ACTUAL CLINICAL IMAGES OF ALL THESE!!!! – MUST GO THROUGH SURGICAL RECALL
Sources: Dr. Leake Teaching, Dr. East lecture, Surgical Tutor, Toronto Notes
February 2015
Common peri-anal conditions include:
Benign/Non-neoplastic
1. Haemorrhoids
2. Anal fissure
3. Anorectal abscess
4. Fistula-in-ano
5. Pilonidal disease
6. Rectal prolapse
Neoplastic
1. Bowen’s disease
2. Paget’s disease
3. Basal cell carcinoma
4. Squamous cell carcinoma
5. Verrucous carcinoma
6. Adenocarcinoma
7. Melanoma
Common presenting complaints

1. Bleeding: Eg. Haemorrhoids, anal fissures, etc.
2. Anal pain
3. Itch
4. Faecal/mucus/purulent discharge
5. Prolapse
HAEMORRHOIDS
DEFINITION
• Dilated/engorged vascular and connective tissue cushions in the anal canal usually developing as a result of chronic
increases in intra-abdominal pressure. Haemorrhoids are NOT varicose veins!
Haemorrhoidal venous cushions are normal structures of the anorectum and are universally present unless a previous intervention has taken place.
They are located in the right anterior, right posterior and left lateral sections of the anal canal (based on the path of the superior
haemorrhoidal vessels) to fine-tune the continence mechanism (by closing off the anus completely).
Because of their rich vascular supply, highly sensitive location, and tendency to engorge and prolapse, haemorrhoidal venous cushions are common
causes of anal pathology
• Also called piles

• Most commonly 3, 7, 11 o’clock positions (With patient in lithotomy position)
• Affect 50% of population over the age of 50 years
• **Skin tags are NOT haemorrhoids. Skin tags arise from thrombosed haemorrhoids which may leave excess skin
RISK FACTORS
• Any chronic increase in intra-abdominal pressure: Chronic constipation, pregnancy, pelvic venous congestion, tenesmus,
obesity, portal hypertension, heavy lifting Pathophysiology (Simple)
There are 3 main types of varices:
CLASSIFICATION 1. Esophageal
2. Caput Medusa (Umbilical Vein)
Internal (Above) vs. External (Below) 3. Ano-rectal (Hemrrhoids)
Internal arise ABOVE the dentate line. Therefore usually PAINLESS. Further subclassified into 4 degrees: The dilation of these veins are due to Portal
HTN.
1. 1st degree: Bleed, Not prolapse through the anus
2. 2nd degree: Bleed + prolapse with straining. Spontaneous reduction There are 3 veins that drain the rectum:
1. Superior rectal v. (drains to Inferior
3. 3rd degree: Bleed + prolapse. Requires manual reduction Messenteric)
4. 4th degree: Bleed + permanently prolapsed. Cannot be manually reduced 2. Middle rectal v. (drains to Internal Iliac )
3. Inferior rectal v. (drains to Internal
Pudendal)
External arise BELOW the dentate line. PAINFUL (Covered in skin and have somatic nerve supply)
All the veins are connected but only the
Superior Mesenteric is connected to the Portal
System. Because of their connection, increase
in the SRV will cause engorgement of MRV
and IRV.
CLINICAL FEATURES
Internal:
1. PAINLESS rectal bleeding – Bright red (believed to be from AV shunts rather than veins) on defecation, wiping, or
spontaneously,
a. NOT mixed with stool (must ask in PR bleed history!!), but may coat it
b. Anaemia
2. Prolapse
3. Faecal discharge – Because of failure of the cushion mechanism to close off the anus completely & difficulty with hygiene)
4. Mucus discharge
5. Tenesmus (sensation of incomplete evacuation), rectal fullness – due to large internal hemorrhoids.
6. Pruritus
7. RE: Pain – Never associated with uncomplicated hemorrhoids. Associated with prolapsed, thrombosed internal hemorrhoids or
thrombosed external hemorrhoids
Examination:
0
§ Only 4 internal hemorrhoids, external hemorrhoids, and prolapsed thrombosed hemorrhoids visible on inspection
§ Digital rectal examination (mainly to rule out other conditions – uncomplicated hemorrhoids cannot usually be felt!)
3 Conditions in which a patient will deny a

INVESTIGATIONS DRE due to Pain - Dr. Fray
1. Thrombosed hemorrhoids
2. Peri-anal fissures
• Dr. Leake: Usually confirmed with flexible sigmoidoscopy (Sometimes rigid proctoscopy) 3. Peri-anal abcess
NOTE VERY WELL: MUST remember to rule out more serious causes (e.g. colon Ca.) in a person with haemorrhoids and rectal
bleeding, using colonoscopy. DO NOT assume it is due to the haemorrhoids
NOTE VERY WELL: (all patients with rectal bleeding over 25 should have sigmoidoscopy and all over 35 or with a family history of
colon cancer should have sigmoidoscopy & barium enema or colonoscopy to exclude colorectal cancer)
MANAGEMENT OPTIONS
DIET MODIFICATION VS. MEDICAL VS. SURGICAL
PRINCIPLES:
1. Depend on whether internal or external, and degree if internal, and whether complicated or uncomplicated
st nd rd th
2. 1 and 2 amenable to the more conservative approaches. Generally treatment of choice for 3 or 4 degree is
haemorrhoidectomy
A. DIET MODIFICATION
st nd
• Correct constipation: All patients should have a high-fibre diet. 25-35 g is often first line therapy for 1 and 2 degree
internal haemorrhoids (*most usually respond to this management. If not adequately managed, see below) A low residue diet is one with
reduced fiber
B. MEDICAL:
1. Steroid cream
2. Pramoxine/Pramocaine: A local anaesthetic also used as an antipruritic
External Haemorrhoids: In the acute setting: Laxatives/stool softeners + Analgesics + Ice (+/- steroid cream) Some also consider SITZ Baths. This
is done 2 to 3 times daily or after
passing feaces. This causes the
C. SURGICAL: relaxation of the sphincter, as it may
spasm.
1. Rubber band ligation:
Steroids are used to reduce
§ Can be done as outpatient inflammation and pruritus. Side effect
st nd
§ For 1 and 2 degree haemorrhoids is mucosal atrophy after long periods
of use.
§ Only for internal haemorrhoids due to the pain associated with external
§ Involves strangulating the excess tissue à Necrosis and sloughing
§ Usually limit to 2 bands per visit – more can lead to stenosis
2. Sclerotherapy:
• Causes fibrosis of the connective tissue around the vessels
• Sclerosants: Phenol in almond oil, and saline solutions, quinine
• Randomized trial of rubber band ligation and sclerotherapy have shown:
a. 90% success with rubber band ligation
b. 70% success with sclerotherapy
3. Photocoagulation
4. Haemorrhoidectomy
rd th
• Usually reserved for 3 and 4 degree haemorrhoids (treatment of choice) and those who do not respond to
banding
• 2 main indications:
1. Persisting, big prolapsing haemorrhoids
2. Persistent heavy bleeding
• Open (Milligan-Morgan procedure) vs. Closed (Ferguson) procedure

• NEWER: Stapled Haemorrhoidectomy (aka. PPH – Procedure for prolapsing haemorrhoids)
o Pros: Much less painful than a standard haemorrhoidectomy, reduced operating time, shorter hospital stay
o Cons: Slightly higher recurrence rate
Complications of haemorrhoidectomy
1. Bleeding (3%)
2. Secondary infection - May be reduced with oral metronidazole
3. Postoperative pain - Botulinum toxin injection may also reduce postoperative pain
4. Anal stenosis may develop if adequate skin bridges are not maintained
5. Urinary retention (10%)
RE: Prolapsed thrombosed internal hemorrhoids

- Analgesic/Stool softener/sitz baths (from German sitzen – to sit) and review after resolution for definitive treatment
- Emergency haemorrhoidectomy
RE: Thrombosed external hemorrhoids

- Incise & evacuate clot or excise hemorrhoid under LA if painful
- If pain subsiding, analgesic/stool softener/sitz baths
ANAL FISSURE
(Toronto Notes + Surgical tutor + Dr. East)
DEFINITION
• Tear of anal canal below dentate line (very sensitive squamous epithelium)
• Usually seen between 30-50 years
• 90% posterior midline (comparatively low blood flow), 10% anterior midline
• Anterior fissure more common in women than men – especially post partum
• **If multiple or off midline: consider other possible causes such as IBD, STIs (syphilis), TB, leukemia or anal carcinoma
• Repetitive injury cycle after first tear:
o Sphincter spasm occurs preventing edges from healing and leads to further tearing
o Ischaemia may ensue and contribute to chronicity
AETIOLOGY
Not fully understood. Theories:
1. Forceful dilation of anal canal: Large, hard stools and irritant diarrheal stools à Slices mucosa
2. ***Chronicity probably then results from reactive internal anal sphincter spasm à mucosal ischaemia secondary to
muscle spasm – THIS WOULD SUPPORT WHY THE TREATMENTS BELOW WORK
a. Probably not a 'tear' due to the passage of a hard stool (Pecten band theory)
b. 5% associated with chronic intersphincteric abscess
If multiple fissures or at unusual site (away from the ant or post midline) consider:
a. Crohn's Disease
b. Syphilis
c. Tuberculosis
Others risk factors: Anal sex, HIV infection, Habitual use of cathartics, childbirth, leukaemia
CLINICAL FEATURES
A. Acute fissure:
• Significant PAIN, especially on defecation (can be excruciating!!)
• With bright red bleeding on defecation or blood on tissue paper
• Purulent discharge
• Pruritus ani
Examination:
• Fissure often visible on parting of buttocks and/or a 'sentinel pile' (Linear ulcer with sentinel pile at apex on
inspection)
a. Sentinel pile: Thickened mucosa/skin at the distal end of an anal fissure that is often confused with a small
haemorrhoid
• Sphincter spasm on limited DRE
• DRE will be extremely painful à
• *DRE, barium enema, etc should be done but may have to be delayed or performed under anesthesia
• Treatment is conservative: Stool softeners, bulking agent, sitz baths (heals 90%)
B. Chronic fissure (i.e. > 6 weeks) (anal ulcer):

• Associated with increased intra-anal pressure
• Features of Chronicity: Triad: *Fissure > 6 weeks, *sentinel skin tags/pile, *hypertrophied anal papillae
• Treatment: Internal sphincter spasm must be addressed – Reversible chemical sphincterotomy OR
surgical sphincterotomy
What disease processes must be considered with a chronic anal fissure?

Crohn’s disease, anal cancer, sexually transmitted disease, ulcerative colitis, AIDS
TREATMENT
MEDICAL vs. SURGICAL
[OR Conservative vs. Chemical sphincterotomy vs. Surgical sphincterotomy]
Most acute fissures heal spontaneously
MEDICAL
A. Conservative: Excellent anal hygiene + Stool softeners + bulking agents + sitz baths + Topical anaesthesia à
• 50% heal with this
B. Chemical sphincterotomy (Mainly for chronic fissure):
• Topical nitroglycerin (0.2%) or nifedipine: Increases local blood flow, promoting healing and relieves sphincter spasm
• GTN is nitric oxide donor that relaxes internal anal sphincter
• Induces a 'reversible chemical sphincterotomy'
o Reduces anal resting pressure by 30–40%
• Heals > 70% fissures by 6 weeks with about a 10% risk of early recurrence
• Most common side effect is headache
• Similar results to GTN achieved with diltiazem
Alternative treatment:
• Botulinum toxin: Also produces a chemical sphincterotomy. Inhibits release of acetylcholine (ACh), reducing sphincter
spasm
SURGICAL
• Indication for surgery: Chronic fissure refractory to conservative/medical therapy
• 95% patients achieve prolonged symptomatic improvement
• 20% patients some degree of incontinence (faecal soiling or incontinent of flatus)
• Anal dilatation or lateral internal sphincterotomy are the two most common procedures
o Sphincterotomy more effective and has a reduced risk of incontinence
o Lateral sphincterotomy is the preferred technique
o Posterior sphincterotomy or fissurectomy should be avoided!
• Lateral internal anal sphincterotomy (most effective): Objective is to relieve sphincter spasm à increases blood flow and
promotes healing; but 5% chance of faecal incontinence therefore not commonly done
DR. EAST:
• Note that surgical sphincterotomy carries a risk of incontinence – all patients have transient incontinence for flatus and liquid
stool – permanent in about 5%.
• Most cases of anal fissure will be cured permanently by internal sphincterotomy
• Recurrences can usually be prevented by adopting high fiber diet and avoiding rushing to pass stool
• Recurrences may also be due to anal sex, Crohn’s disease, leukemia and HIV disease
ANORECTAL ABSCESS & FISTULAE

Anatomy of anal canal (Surgical Tutor)
§ Internal sphincter = smooth muscle
§ External sphincter = striated muscle
§ Mucosa of upper third of anal canal – no somatic sensation
§ Mucosa of lower two thirds of anal canal – somatic innervation from inferior rectal nerves
§ Anal glands occur in intersphincteric plane & open at level of dentate line
ANORECTAL ABSCESS
Infection in one or more of the anal spaces
Usually bacterial infection of blocked anal gland at the dentate/pectinate line

§ E. coli, Proteus, Streptococci, Staphylococci, Bacteroides, anaerobes
Dr. Leake:
Anal glands become obstructed à Infected à Abscess forms in intersphincteric plane à Extends in a particular
direction and eventually ruptures.
See “cryptoglandular hypothesis”
Classified depending on the direction in which it extends:
1. Intersphincteric
2. Perianal abscess (Spread vertically downward)
3. Ischiorectal abscess (Spread horizontally) à Patient usually more systemically unwell as larger space to fill with pus
4. Supralevator (Spread vertically upward) à Least common and unlikely to have any perianal manifestations
CLINICAL FEATURES
Classify: LOCAL vs. SYSTEMIC
A. LOCAL
1. Severe, throbbing pain
§ Worsens with basically everything à sitting, moving, ambulating, straining
2. Defecation difficult
3. Tender perianal or rectal mass on examination. Fluctuance usually not evident because of depth of pus
B. SYSTEMIC
1. Malaise
2. Sweating
3. Rigors
TREATMENT
MUST BE SURGICALLY DRAINED URGENTLY!!! – There is no room for non-surgical treatment
Especially dangerous in diabetics and immunosuppressed patients
As with all abscesses:
1. Incision and drainage + Appropriate antibiotics
Outcomes:
a. Curative in 50% of cases
st
b. ~50% develop anorectal fistulae (most within 1 6 months after surgery)!!
§ Initial surgery should simply be incision and drainage

§ Avoid looking for a fistula at initial surgery
§ Rectal EUA at approximately five days
§ Especially if gut related organisms on culture
§ 80% recurrent abscesses associated with a fistula
2. ***Indications for post-op IV antibiotics!!: Diabetic, heart murmur, immunosuppression or cellulitis

a. **Toronto: Antibiotics are NOT typically helpful in the treatment of perianal abscesses
**Recurrent perianal abscesses associated with Chron’s disease
FISTULA-IN-ANO
DEFINITION
An inflammatory tract with its internal os at the dentate line, and its external os on perianal skin
§ (Dr. Leake: Must know: Essentially an extension of an abscess resulting in an abnormal communication between the anal canal
and skin. Internal opening at anal gland site in anal canal (dentate line) à tract à external opening on perianal skin)
~50% of perianal abscesses become fistulae

***Other causes: Post-op, trauma, anal fissure, malignancy, radiation proctitis
CLASSIFIED BASED ON THE TRACT

Parks Classification is the most common classification used for fistulas-in-ano. This classification
system, demonstrated in the image below, defines 4 types of fistula-in-ano that result from
cryptoglandular infections: intersphincteric, transsphincteric, suprasphincteric, and extrasphincteric:
1. Interspincteric (70%) – Traverses the internal anal sphincter

2. Transsphincteric (25%) – Traverses both internal and external sphincter
3. Suprasphincteric (5%) – Internal only, ascends and circumvents external
4. Extrasphincteric (< 1%) - Extrasphincteric fistulae are usually not associated with
intersphinteric sepsis
Goodsall’s rule: Regards identifying the internal opening of a fistula-in-ano:

• Fistulas originating anterior to transverse line through the anus will course straight ahead/have a radial tract and exit anteriorly,
whereas fistulas which exit posterior to the transverse line will have a curved tract and originate in the midline
See another image at end of document
CLINICAL FEATURES
§ Presents as a non-healing sore inside the anus with recurrent abscess formation
§ Intermittent or constant purulent discharge from perianal opening
§ Pain
§ Palpable cord-like tract
§ Consider inflammatory bowel disease or neoplasia

§ Chron’s fistulae are usually multiple
IDENTIFICATION
1. Identify internal opening using Goodsall’s rule
2. Identify fistulous tract: Probing (DRE) or fistulography under anesthesia
INVESTIGATION (Surgical tutor)
• Clinical assessment + Proctoscopy

• MRI
• Endorectal Ultrasound
TREATMENT
Depends on whether the external anal sphincter is involved
Toronto Notes:
Surgery:
• Puborectalis is the key to future continence
• Fistulotomy: Unroof the tract from external to internal opening, allow drainage, heals by secondary intention
o Low lying fistula (does not involve external sphincter) à primary fistulotomy
o High lying fistula (involves external sphincter) à require 2 stage surgery. Staged fistulotomy with seton suture placed
through tract:
§ Promotes drainage
§ Promotes fibrosis and decreases incidence of incontinence
§ Delineates anatomy
§ Usually done to spare muscle cutting
Dr. Leake:
Simple:
1. Fistulotomy (***For intersphincteric and transsphincteric)
Complex
Investigate first: MRI or endorectal U/S. If external sphincter is involved, options include:
1. Seton placement – Involves tying a suture and tightening it regularly which slowly cuts… look up
2. Fibrin glue:
a. Obstructs the tract of the fistula (Prevents passage of stool through the abnormal opening)
b. Expensive, 60-70% success rate, no risk involved
3. Anorectal advancement flap may be considered: Take some rectal mucosa down, advancing it to cover the opening.
Very technical procedure
Postoperative
• Sitz baths, irrigation and packing to ensure healing proceeds from inside to outside
COMPLICATIONS
• Recurrence
• Rarely fecal incontinence
PILONIDAL DISEASE
TORONTO (SEE ST: http://www.surgical-tutor.org.uk/default-home.htm?specialities/general/pilonidal_sinus.htm~right)
DEFINITION
§ Chronic recurring abscess or chronic draining sinus in sacrococcygeal area
§ Dr. East: Sinuses and cysts high in the natal cleft
§ Associated with hairs – either a foreign body reaction to embedded hair or a disease of hair follicles
EPIDEMIOLOGY
§ Occurs most frequently in young men age 15-40 yr; rare in >50 yr
AETIOLOGY
§ Obstruction of the hair follicles in this area à formation of cysts, sinuses or abscesses
CLINICAL FEATURES
§ Asymptomatic until acutely infected, then pain/tenderness, purulent discharge, inspissated hair
TREATMENT
Acute abscess:
1. I&D (often performed by primary care doctors)
a. Wound packed open
b. 40% develop chronic pilonidal sinuses
2. Surgery:
Indication: failure of healing after I&D, recurrent disease, complex disease
a. Pilonidal cystotomy: Wide excision of sinus tract and cyst à Wound closed by either *secondary intention,
*primary closure with tissue flap, or *marsupialization (cyst edge sewn to surrounding tissue to leave sinus tract open)
Very resistant to treatment with recurrence common after all procedures
ANAL NEOPLASMS
TORONTO (SEE ST: http://www.surgical-tutor.org.uk/default-home.htm?specialities/general/anal_ca.htm~right)
1. ANAL CANAL
A. Squamous Cell Carcinoma (SCC) of Anal Canal (above dentate line)
§ Most common tumour of anal canal (75%)
§ Anus prone to human papilloma virus (HPV) infection, therefore at risk for anal squamous intraepithelial lesions (ASIL)
o High grade squamous intraepithelial lesion (HSIL) and low grade squamous intraepithelial lesion (LSIL) terminology used
§ Clinical features: anal bleeding, pain, mass, ulceration, pruritus; 25% asymptomatic
§ Treatment: chemotherapy ± radiation ± surgery
§ Prognosis: 80% 5-yr survival
B. Malignant Melanoma of Anal Canal

§ 3rd most common site for primary malignant melanoma after skin, eyes
§ Aggressive, distant metastases common at time of diagnosis
§ Treatment: wide excision or APR ± chemoradiation
§ Prognosis: <5% 5-yr survival
2. ANAL MARGIN
Clinical features and treatment as for skin tumours elsewhere
Squamous and basal cell carcinoma, Bowen’s disease (SCC in situ) and Paget’s disease
DR. EAST SUMMARY OF THE ANAL NEOPLASMS

Bowen’s disease
§ In-situ squamous cell carcinoma
§ Brownish macules
§ Treated by wide excision and flap closure
Paget’s disease
§ In-situ adenocarcinoma
§ Associated with underlying adenocarcinoma in 50% - 85% of cases
§ Eczematoid plaques with whitish-gray ulcerations or papillary lesions
Basal cell carcinoma

§ Nodular appearance as elsewhere on skin
Squamous cell carcinoma

§ Can be cured with combination radiation & chemotherapy
§ AP resection only for failed chemoradiation
Verrucous carcinoma
§ Squamous cell cancer arising in condyloma.
Adenocarcinoma
§ Arising from columnar epithelium in transitional zone or from anal glands or apocrine cells
Melanoma
§ May produce a mass, pain and bleeding and may be amelanotic.
General Surgery
Stomas – COMMON EXAM STATION – GET A LOT OF PICS, INCLUDING OF THE COMPLICATIONS
Sources: Harold Ellis, Toronto Notes, Oxford Handbook
February 2015
DEFINITION
§ A surgically created communication between a hollow viscus and the skin
§ May be permanent (e.g. when the distal bowel has been removed) or temporary (when there is possibility of restoring continuity at a later date)
“It is often necessary to divert the faecal stream to the anterior abdominal wall via a stoma”. The effluent is collected in a removable plastic bag attached
by adhesive to the abdominal skin. Stomas are named according to the part of the bowel opening on to the abdominal wall, i.e. ileostomy or colostomy.
The term urostomy is used for the ileal conduit that connects ureters to the skin surface in patients whose bladder has been removed. (The OSTOMY is
usually on the RIGHT SIDE because the RIGHT KIDNEY is SHORTER than the left)
CLASSIFICATION
Stomas may be classified as:
A. Permanent vs. Temporary (possibility of future restoration of continuity)
B. Loop vs. End vs. Double-barreled (Paul-Mikulicz)
C. Or based on segment of GI tract used
MUST KNOW ALL ABOUT: DEFUNCTIONING/DIVERTING STOMAS

A ‘defunctioning’ (loop) stoma (ileostomy or colostomy) may be used to “protect a more distal anastomosis” at particular risk of leakage or breakdown
by preventing intraluminal pressure rises AND by “diverting the faecal stream”.
Common indications are:

1. To protect a more distal anastomosis in the following scenarios:
a. A technically difficult “low rectal anastomosis” (flatus and faeces may leak through the anastomosis),
b. An anastomosis performed after resection of an obstructing lesion (distension may compromise the blood supply to the healing
anastomosis)
c. An emergency resection with primary anastomosis involving unprepared bowel, with contamination (solid faeces may remain impacted
in the lumen).
2. Decompress obstructed colon as a prelude to resection of and obstructing lesion
3. May also be used to ‘rest’ a more distal segment of bowel or perineum involved in an inflammatory process, by diverting the faecal
stream, even if no resection and anastomosis was performed. Examples include pericolic abscess, complex anorectal fistulae and major surgical
perineal wounds.
Reversing the temporary stoma to restore bowel continuity is often a relatively simple procedure, usually performed after 3–4 months. Some
surgeons perform a limited contrast enema to demonstrate anastomotic integrity before closing the stoma.
MAIN COMPONENTS OF STOMA APPARATUS
1. Collecting pouch or bag with an

2. Adhesive flange which adheres to the skin and keeps the pouch in position (NB: The flange is cut to fit the stoma closely and
3. any exposed skin is covered with a barrier paste!!!)
COMMON TYPES OF STOMA
Ileostomies and colostomies can be done by making an opening in a loop of colon (loop colostomy) or by dividing the colon and bringing out one end
(end colostomy)
1. ILEOSTOMY: may be ‘loop’ or ‘end’.

NB: “Brooke” ileostomy: Standard ileostomy that is folded on itself to protrude from the abdomen ~2 cm to allow easy appliance placement and
collection of succus
Identification: Usually positioned in RLQ, spouted, prominent mucosal folds, ileum is brought through rectus abdominus muscles
Indications:
REMEMBER TO CLASSIFY INTO:
1. Loop: (see above) To protect distal anastomosis (e.g. partial colectomy, formation or ileorectal pouch).
2. End: Usually after total proctocolectomy (e.g. ulcerative colitis, FAP, total colonic Hirschsprung’s disease)
Also note!!!:
§ Conventional ileostomy: Discharges small quantities of liquid material continuously, appliance required at all times (plastic bag attached to a
sheet of protective material)
§ Continent ileostomy: Reservoir is constructed from distal ileum, emptied by inserting catheter into stoma several times a day; rarely used, has
mostly been replaced by ileal pouch anal anastomosis (IPAA)
**Colostomies contrast with ileostomies by the nature of the effluent. Ileostomy effluent is very irritant and causes severe skin excoriation. For this
reason, an ileostomy is "spouted", to keep the effluent off the skin, in contrast to a colostomy, which is “flush to skin”**
2. COLOSTOMY: may be ‘loop’ or ‘end’.
Indications
§ Loop: (see above)
1. Decompress obstructed colon as a prelude to resection of an obstructing lesion
2. To divert faeces to protect a distal anastomosis after resection,
3. evacuate stool after distal colon or rectum is removed, rectal trauma, colovaginal or perianal fistula.
§ End: Removal of the distal colon and rectum (e.g. Hartmann’s procedure, AP resection)
Most common permanent colostomy is a sigmoid colostomy – expels stool once per day, no appliance required
Chronic paracolostomy hernia is a common complication
3. UROSTOMY + ILEAL CONDUIT:

One or both ureters are diverted to a short length of ileum, which is disconnected and brought to the skin (usually follows radical lower urinary tract
surgery).
§ (Ileal Conduit: Connection of ileum to one or both ureters proximally and abdominal wall distally to drain urine )
Identification: Spouted, prominent mucosal folds, dark pink/red, right-sided

§ Indistinguishable from ileostomy unless the output is seen!!!
Indications:
§ Usually follows radical lower urinary tract surgery (e.g. bladder resection for cancer)
4. GASTROSTOMY/DUODENOSTOMY/JEJUNOSTOMY:
Surgically or endoscopically created connection between the stomach/duodenum/jejunum and the anterior abdominal wall
Identification: Narrow caliber, flush to skin with little visible mucosa, usually at left upper quadrant. Fitted with indwelling tubes or access devices.
Indications: For feeding and/or drainage
OTHER STOMAS
1. Caecostomy or typhlostomy: loop stoma in the caecum.
2. Appendicostomy or caecostomy tube: used in paediatrics to allow administration of proximal enemas.
3. Cholecystostomy: communication between the gallbladder and anterior abdominal wall (drainage of gallbladder contents).
4. Nephrostomy: tube that exits through flank region and drains urine from the renal pelvis.
COMPLICATIONS (10%) – EDIT FROM ELLIS

All:
o
1. Obstruction: 2 to herniation, stenosis (skin and abdominal wall), adhesive bands, volvulus In - Ischemia
2. Retraction (fall in?) Retrospect - Retraction
3. Prolapse (fall out?) Portia - Prolapsed
4. Paracolostomy hernia Has - Hernia
Demonstrated - Dermatitis
Particularly ileostomy: Psychological - Psychosocial issues
5. Skin irritation/excoriation Stubbornness - Stenosis
6. Peri-ileostomy infection, abscess and fistula formation Hatred - High Output
7. High-output
Other:
8. Necrosis
9. Psychological problems
Other things to know:
Mucous Fistula
§ Connection of distal limb of colon to abdominal wall skin
Loop colostomy
§ The colon is brought to the surface and the antimesenteric border opened.
§ A rod or similar device is often used to stop the opened bowel loop from falling back inside.
§ A loop colostomy is used temporarily to divert faeces and is simple to reverse; more commonly nowadays, a loop ileostomy is preferred because
of the better blood supply to the bowel facilitating subsequent closure.
End colostomy
§ An end (or terminal) colostomy is fashioned by dividing the colon and bringing the proximal end to the surface.
§ It may be used as a definitive procedure in a patient undergoing total rectal excision, or following perforated diverticular disease in which the
diseased bowel is removed and gross faecal contamination makes performing a primary anastomosis to restore continuity undesirable.
§ In the latter, the distal bowel may be closed off and left within the abdomen (a Hartmann’s procedure) or brought to the surface at a separate
place as a mucous fistula.
Double-barreled colostomy
§ A double-barreled (Paul–Mikulicz) colostomy comprises proximal and distal ends of colon brought out adjacent to each other, rather like a loop
colostomy but with the intervening colon removed.
§ This type of colostomy is not commonly used because the distal bowel is usually too short, but it is useful in the treatment of sigmoid volvulus, in
which there is usually sufficient distal colon.
FOR OSCE EXAM: Inspection of a stoma

Use the following system to describe or identify a stoma.
1. IF it is very obvious what type of stoma it is from first glance, state it immediately and defend your reasons
2. Site?
3. Stoma bag covering?
4. Appearance:
a. Spouted or flush to skin?
b. Healthy mucous lining? What colour?
c. One orifice (end) or two (loop)?
5. Content (e.g. urine, formed stool, semi-formed or liquid stool).
a. Any other abdominal scars?
b. Any drains or healed stoma sites?
6. Look for evidence of complications:
a. Early: necrosis (black/brown discoloration), infection
b. Late: parastomal hernia, prolapse, stenosis, retraction, obstruction, skin erosions, bleeding.
MANAGEMENT OF A COLOSTOMY
§ In the first few weeks after performing a colostomy, the faecal discharge is semiliquid, but this gradually reverts to normal, solid stools.
§ The colostomy appliances, which are both waterproof and windproof, allow the patient to lead a normal life with little risk of leakage or unpleasant
odour.
§ Although there is obviously no sphincteric control of the colostomy opening, most patients find that they pass a single stool a day, usually after
breakfast.
§ This can be helped by preparations such as Fybogel or Celevac, which produce a bulky, formed stool.
§ Patients are best advised to avoid large amounts of vegetables or fruit, which may produce diarrhoea and excessive flatus.
When preparing to close a colostomy: NEVER reverse a colostomy without a barium or other study checking if there is a
distal obstruction or stricture
MUST KNOW: DIFFERENTIATING A COLOSTOMY FROM AN ILEOSTOMY FROM AN ILEAL CONDUIT:

1) Site: Either may be ANYWHERE, BUT:
a. Ileostomy usually right lower quadrant/iliac fossa and
b. Colostomy usually left lower quadrant/iliac fossa
2) Appearance:
a. Nipple/spout on ileostomy to keep effluent off the skin.
b. Colostomy usually flush with skin
3) Nature of the effluent: (Can observe in the colostomy bag à Is it more liquid or solidified? IN EXAM ALSO LOOK OUT FOR URINE IN THE
BAG IN THE CASE OF AN ILEAL CONDUIT!!!). Ileostomy effluent is very irritant and causes severe skin excoriation and possibly sepsis. For
this reason, an ileostomy is constructed with a spout to keep the effluent off the skin, in contrast to a colostomy, which is flush.
Why wait 1 year for attempt at reanastomosis and closure of an end colostomy?
• It takes a few months for scar tissue and adhesions to settle. Much greater risk of cutting bowel that has adhered to fascia etc and
enterocutaneous fistula formation if attempted before about 1 year.
COLOSTOMY BAG
Describe: It consists of a reservoir bag with an opening to put over the ostomy site. There is an adhesive potion for attachment of the bag and a vent for
filtering air (some don’t). Some have gradients at port for you to cut to a suitable size
Surgery Elective
Aneurysms
Sources: Dr. Hilary Brown, UHWI lecture, Toronto Notes, Harold Ellis
February 2015
DEFINITION
An abnormal, permanent dilatation of a vessel by at least 50% of the normal diameter (same as saying 1.5 times the normal
lumen)
§ Can have aneurysms of arteries, veins or ventricles

§ Aneurysms: May be TRUE (involves all layers of the vessel) or FALSE (Pseudoaneurysm – caused by trauma)
§ Morphology: Saccular (Spherical) vs. Fusiform (Spindle shaped) vs. Pseudoaneurysm
Involves part of wall Involves all the wall
Seen in Berry aneurysms Seen in the aorta
MUST KNOW: GENERAL CLINICAL FEATURES OF TRUE ANEURYSMS
FIRST POINT: Depend on size and site
§ See abdominal aortic aneurysms section below
§ When peripheral arteries involved, more common complaints are pulsatile mass or of acute distal ischaemia
***Examination findings:
§ Dilatation along the course of the artery
§ Pulsatile and expansile mass
§ May feel a thrill if feeding vessel has a narrow orifice
§ May auscultate a bruit
§ If AVM present à Machinery murmur
COMPLICATIONS
1. Rupture (See rupture risk for AAA in prognosis)
2. Thrombosis à Distal ischaemia
3. Embolism à Small à Digital ischaemia (“BLUE TOE” SYNDROME). Large à May threaten entire limb
4. Compression: On adjacent structures. AAA may cause back pain, sciatica, femoral vein compression common in femoral aneurysms
5. Infection: May cause aneurysm, OR aneurysm may become secondarily infected
NOTE WELL (From Dr. Hilary Brown): Different aneurysms have different tendencies:
1. AAA: Rupture
2. Splenic artery: Rupture
3. Popliteal artery: Thrombose. Some embolize
4. Subclavian aneurysm: Embolism
ABDOMINAL AORTIC ANEURYSMS

INCIDENCE
§ Most common in age > 65 (Average age = 75)
§ M > F [3-8:1]
§ BY FAR more common in white males
SITE
Most commonly in the abdominal aorta (50% abdominal aorta, 40% thoracic aorta, 10% ascending aorta)
1. Suprarenal (5%)
2. Infrarenal (95%)
§ Aortoiliac (30%)
CAUSES
1. Degenerative (atherosclerotic)
§ Most common cause of true aneurysms
§ Multifactorial: Genetic, inflammatory and proteolytic mechanisms all contribute
2. Traumatic
§ Can cause both true and false aneurysms
§ *Penetrating injury e.g. bullet or knife wound
§ **Iatrogenic during catheterization for angiography or angioplasty
3. Mycotic (usually suprarenal aneurysms)
§ Tertiary syphilis (thoracic aorta) – now uncommon
§ Salmonella, staph aureus (abdominal aorta) – more common
§ Also caused by mycotic emboli from infective endocarditis
§ Unusual bacteria and fungi in the immunocompromised
4. Connective tissue disorder (Marfan’s syndrome, Ehlers-Danlos syndrome)
5. Aortic dissection
6. Vasculitis
RISK FACTORS (NON-MODIFIABLE vs. MODIFIABLE)
1. Age > 65
2. Male (Male sex = higher incidence. BUT Females = rupture at a smaller diameter)
3. Family history of AAA
4. Connective tissue disease
5. HTN
6. Any atherosclerotic arterial disease (Peripheral arterial disease, coronary artery disease, cerebrovascular disease)
7. Smoking
8. Certain infections (e.g. syphilis)
NOTE WELL: Diabetes is NOT a risk factor!!! Some studies actually suggest diabetics have less aneurysms!
NOTE WELL (Dr. Hilary Brown): The ONLY things that increase RUPTURE RISK are:
1. COPD
2. SURGERY: ANY kind of surgery. Thought to be due to the release of various elastases in surgery.
OTHER INFO
Atherosclerotic aneurysms also common in iliac, popliteal & femoral arteries
40% of patients with infrarenal aortic aneurysm have an aneurysm elsewhere in aortic tree
Normal aorta size:

§ Women - 2 cm
§ Men - up to 3 cm
*** NOTE WELL: Threshold for intervention of AAA - 5.5 cm (supported by literature!!! – NOT 5 cm)
§ BUT Might intervene at a lower diameter in women
Dr. Hilary Brown: MUST KNOW: Rupture risk PER YEAR for AAA:
§ 5-6 cm - 5-10%
§ 6-7 cm - 10-15%
§ 7-8 cm - 15-20%
§ >8 cm - 25%
NOTE WELL: It adds on each year. So in 4 years an 8 cm aneurysm has 100% risk of rupture
CLINICAL FEATURES
CLASSIFY: May present due to LOCAL EFFECTS vs. ACUTE EXPANSION vs. COMPLICATIONS
FIRST POINT: Frequently asymptomatic (75%), detected incidentally on investigation for another condition
§ Common presentation – Due to acute expansion OR disruption of the arterial wall
§ History of risk factors and associated diseases – HTN, PVD, CAD, COPD, renal insufficiency
§ Symptoms/signs of generalized atherosclerosis (ischaemic heart disease, peripheral arterial occlusive disease, peripheral aneurysms)
A. LOCAL EFFECTS
1. Pain (chest, abdominal, flank, back)
2. Patient may have noticed a pulsatile swelling
B. ACUTE EXPANSION
1. Hypotension
2. Syncope
3. Distal pulses may be intact
C. COMPLICATIONS
1. Ruptured AAA (50% die and never reach hospital)
§ Rupture caries a high overall mortality (80%)
§ Severe back pain, radiation to the groin
§ Sometimes epigastric or Iliac fossa pain
§ Often, mass ceases to be pulsatile
§ Syncope
§ Generalized abdominal tenderness
§ **Rupture into surrounding structures à GI bleed (brisk haematemesis, melaena, aortoduodenal fistula), aortocaval fistula
§ Profoundly shocked on exam: Cold, clammy, tachycardia, hypotensive.
2. Distal embolization: (Acute limb ischaemia, “blue toe syndrome”)

3. Compression: Ureteric obstruction and hydronephrosis (Uncommon, often with inflammatory aortic aneurysm)
CLASSIC TRIAD of Ruptured AAA
1. Pain
2. Hypotension
3. Pulsatile abdominal mass
Airway or oesophageal obstruction, hoarseness (left recurrent laryngeal nerve paralysis), hemoptysis, or hematemesis (indicates thoracic or
thoracoabdominal aortic aneurysm)
§ Mass overlying or displacing the artery superficially, eg. palpable mass of pancreatic ca. may have a transmitted pulsation from the underlying
aorta, but will NOT be expansile
INVESTIGATIONS
GENERAL BLOODWORK vs. IMAGING
A. GENERAL BLOODWORK:
§ CBC, U&Es, creatinine, PTT, INR, GXM
B. IMAGING
1. AXR – May show calcification in the wall of the aneurysm (Lateral more useful)
a. ‘Eggshell’ pattern of calcification
2. Abdominal U/S (100% sensitive, up to ± 0.6 cm accuracy in size determination) –
a. Usually sufficient investigation for detection BUT not for operative planning
3. CT aortogram – (MUST PERFORM even if patient comes in with an ultrasound diagnosis)
§ ***Accurate delineation of size, extent of aneurysm, relationship to surrounding structures, evidence of leakage
§ Dr. Hilary Brown: U/S has a lot of inter-observer variability. NB: Aortogram always includes iliac and femoral! (From lung bases to thighs)
§ Also need to define anatomy of the aneurysm: Suprarenal, juxtarenal or infrarenal
§ Particularly useful for juxtarenal and suprarenal
4. MRA
5. Conventional angiography –
§ NOT NECESSARY
§ MUST KNOW: Underestimates size and extent of a true aneurysm (as it images the lumen which is usually narrowed by thrombus)
§ Also, may be dangerous as the guidewire or cannula may perforate the aneurysm wall
MANAGEMENT
FIRST POINT: Depends on location, size (i.e. rupture risk) and symptoms and life expectancy to decide:
CONSERVATIVE (WITH MONITORING) vs. SURGICAL
A. CONSERVATIVE
1. Watchful waiting, U/S every 6 mo to 1 yr depending on size and location
2. Cardiovascular risk factor reduction: smoking cessation; control of HTN, DM, and hyperlipidemia
3. Regular exercise
4. ADD TABLE WITH RECOMMENDATIONS FOR SCREENING (LOOK UP ONLINE IF THERE ARE NEWER)
B. SURGICAL
INDICATIONS:
1. When risk of rupture greater than or equal to risk of surgery (>5.5 cm [or 2x the normal lumen size])
§ Risk of rupture depends on
1. Size (> 5.5 cm)
2. Rate of enlargement (if > 0.4 cm/year)
3. Symptoms, comorbidities (COPD, surgery)
2. Symptomatic
3. Ruptured
4. Mycotic
5. Associated with acute Type A dissection or complicated Type B dissection
Elective AAA repair mortality 2-5%; [elective TAA repair mortality <10%] (highest with proximal aortic and thoracoabdominal repairs)
Consider revascularization for patients with CAD before elective repair of aneurysm.
MUST KNOW: CONTRAINDICATIONS:

1. Life expectancy <1 yr
2. Terminal disease (e.g. cancer)
3. Significant comorbidities (e.g. recent MI, unstable angina)
4. Decreased mental acuity
SURGICAL OPTIONS
(Dr. Hilary Brown: OPEN REPAIR (GRAFT) or ENDOVASCULAR REPAIR (EVAR))

NB. Bypass is NOT a standard procedure BUT is done by some
***FIRST, DON’T FORGET: PREOPERATIVE ASSESSMENT: Identify patient’s risk:

Investigations are based on the major complications of AAA surgery:
*** M.I and stroke. Therefore:
1. **ECG
2. Usually do a ***stress test
3. CXR
4. Some persons get a carotid ultrasound to ensure no unstable plaque. Not routine.
A. OPEN SURGERY (LAPAROTOMY OR RETROPERITONEAL) WITH GRAFT REPLACEMENT
Graft material: Prosthetic graft (e.g. Dacron) [LOOK UP ONLINE OR IN LECTURE]
Procedure summary:
1. Laparotomy
2. Clamp the aorta
§ Infra-renal aneurysms are much easier to deal with:
a. *** Reason: For the other 2 types (supra and juxta), the cross clamp needs to be placed proximal to renal arteries: Risk of renal failure.
Fortunately about 80% of times this is avoided.
3. Select a graft:
a. Dacron
b. PTFE
4. Fashion proximal anastomosis
5. Move the clamp down to the graft
6. Fashion distal anastomosis
§ Usually can use a tube graft if high enough
§ If not, use a bifurcated graft
§ This would be aortoiliac or aortobifemoral
*** NOTE VERY WELL: In most cases, the INFERIOR mesenteric artery (IMA) WILL branch off in the portion of aorta being replaced. This is
usually ligated or reimplanted
§ This is an important POST-OP concern
§ If the patient develops abdominal pain and bloody diarrhea it should suggest colonic ischemia!! This is because of interruption of IMA
§ If there is significant ischaemia with transmural colon necrosis, may have to take it out.
§ This should ALWAYS be in the back of your head
POSSIBLE COMPLICATIONS
EARLY:
1. Renal failure: The renal arterial ostia are often compressed when the aorta is clamped, thus rendering the kidneys ischaemic for the duration of
cross-clamping.
2. Arterial thrombosis
3. Distal embolization: Thrombus from the sac may disperse distally and block the small vessels in the foot and lower leg causing acute ischaemia,
in this context called ‘trash foot’
4. Spinal cord injury (paraparesis or paraplegia)
5. Impotence
6. Anastomotic rupture or bleeding
7. Myocardial infarction. Coronary artery disease is common in the population who develop aortic aneurysms. Cross-clamping the aorta during
surgery dramatically increases the peripheral resistance against which the heart must work, and this extra stress, coupled with the
metabolic stress that occurs when the legs are reperfused, may precipitate a myocardial infarct.
LATE:
1. Graft infection (Remember it is a foreign body)
2. Graft thrombosis
3. Aortoenteric fistula
4. Anastomotic (pseudo) aneurysm
B. ENDOVASCULAR REPAIR (STENT) - "EVAR" = ENDOVASCULAR AORTIC REPAIR

(TEVAR = Thoracic Endovascular Aortic Repair)
In the first world, 80% of aneurysm repairs are now done endovascular. High success rates in patients with suitable anatomy and
experienced centres
§ Much less physiological stress on patient. It has therefore expanded the selection candidates.
§ Most patients are in and out of hospital in 2-3 days. Has revolutionized the management of these patients
Involves:
§ Get femoral access with a needle and go up through one femoral artery
§ Use fluoroscopy to guide a stent to its desired location
§ Once at the level of the renal arteries, start opening the stent (for infra-renal aneurysm)
§ Then, go up from the other groin and interlock the stent with a “leg” on this current side as well with the main body of the stent
*** The blood in the aneurysm outside the stent thromboses.
Advantages:
§ Decreased *morbidity and mortality, *procedure time, *need for transfusion, *ICU admissions, *length of hospitalization, and *recovery time
Disadvantages:
§ Affordability: $5000-15000 USD for the stent. Very expensive. Only 7 done at UWI so far
o BUT the back-end causes are lower. Don't have to pay for ICU stay and less time loss at work (about 2 weeks usually)
§ *ENDOLEAK rates as high as 20-30%, *device failure increasing as longer follow-up periods are achieved
§ *Re-intervention rates 10-30%
§ *Radiation exposure (remember fluoroscopic guidance)
Harold Ellis: The prosthetic graft is introduced via a femoral artery and positioned across the aneurysm. It is secured in the normal diameter aorta above and below the
aneurysm with self-expanding stents. The aneurysm sac is thus excluded from aortic blood flow and any residual blood in the sac thromboses. When there is not a sufficient
length of normal diameter aorta below the aneurysm either a bifurcated graft is deployed with components via both femorals or a unilateral aortoiliac graft is deployed and a
subsequent femorofemoral bypass graft is performed
COMPLICATIONS
EARLY:
1. Immediate conversion to open repair
2. Arterial thrombosis
3. Arterial embolism
4. Iliac artery rupture
5. Groin haematoma
LATE:
1. Endoleak (must know about)
2. Graft kinking
3. Graft migration
4. Thrombosis
5. Rupture of aneurysm
Wikipedia: Endoleaks
An endoleak is a leak into the aneurysm sac after endovascular repair. (Persistent blood flow into the aneurysm sac). 5 types of endoleaks exist:
Type I - Perigraft leakage at proximal or distal graft attachment sites (near the renal and iliac arteries)
Type II - Retrograde flow from collateral branches such as the lumbar and inferior mesenteric arteries
Type III - Leakage between overlapping parts of the stent (i.e. connection between overlapping components) or rupture through graft material.
Type IV - Leakage through the graft wall due to the pores of the graft material
Type V - Expansion of the aneurysm sac without an identifiable leak. Also called "endotension".
RUPTURED AAA
In most patients reaching hospital, the rupture is contained by the retroperitoneum, helped by the hypotension following rupture. Injudicious fluid
replacement to restore normal blood pressure prior to surgery may lead to further bleeding and breaching of the retroperitoneum, resulting in
haemoperitoneum and exsanguination.
***Management of Ruptured AAA

1. ABCs (with cautious/judicious fluid replacement)
2. NO IMAGING (haemodynamically unstable)
3. Straight to OT – IMMEDIATE LAPAROTOMY (confirm diagnosis by laparotomy)
4. Crossmatch 10 units packed RBCs
POPLITEAL ANEURYSMS (SEE HAROLD ELLIS)
• Usually congenital
o Not the same risk factors as AAA
• 50% bilateral
• 25% will have AAA
• *** NOTE: Popliteal aneurysms thrombose and embolize. Patients who come in emergency room with acute leg ischaemia
outside context of trauma à Popliteal aneurysm until proven otherwise
• Detected on Physical exam
o Bounding, widened popliteal pulse.
• Need an ultrasound to r/o.
• Need to be fixed as will thrombose. HIGH amputation rate if not.
SPLENIC ARTERY ANEURYSM

These rupture
*** Problem with these is that they are at high rupture risk during pregnancy
Need to be fixed in women of child-bearing age
*** If it ruptures in pregnancy - maternal mortality is 50% and fetal mortality is 75%
General Surgery
Disorders of the Male Genitalia
Sources: Essential Surgery 5E, Dr. East
March 2015
MUST, MUST SEE SEPARATE NOTES ON EXAMINATION OF SCROTAL SWELLINGS

Outline of contents:
1. Information from Essential surgery (p. 1-6)
2. Dr. East’s summary points (p. 6)
3. Surgical Tutor (p. 7)
INTRODUCTION
Abnormalities of the scrotal contents include disorders of the testis or its coverings, the spermatic cord and inguino-scrotal
hernias. Distinguishing between them usually requires only clinical examination.
**Diagnoses that must not be missed are testicular tumours and testicular torsion. Other problems include inflammation,
hydrocoeles and cysts, maldescent and testicular trauma, as well as varicocoele.
A lump or swelling in the scrotum may be:

§ A solid or cystic mass arising from a component of scrotal contents or spermatic cord.
o These include testis, epididymis & epididymal appendage, vas deferens and pampiniform venous plexus
§ A collection of fluid in the tunica or processus vaginalis (hydrocoele)
§ An indirect inguinal hernia extending along the embryological path of testicular descent into the scrotum
SCROTAL PAIN
ACUTE PAIN – “ACUTE SCROTUM”
In acute scrotal pain, testicular torsion must be excluded since the torted testis can be saved if operation is performed
promptly; an exploratory operation is mandatory if torsion cannot be confidently excluded.
Torsion occurs mainly in adolescents but occasionally in young adults. Recurrent, incomplete torsion may cause transient episodes of
severe pain or poorly defined lower abdominal pain. In these cases, the anatomical relationship of the testis to the tunica
vaginalis is often abnormal so the testes lie horizontally rather than vertically when standing. These ‘bell-clapper’ testes are
susceptible to torsion.
The main differential diagnosis at all ages is acute epididymitis. Torsion of an epididymal appendage (hydatid of Morgagni)
produces symptoms similar to testicular torsion in children but less severe; surgical exploration is usually still required to exclude it. A
traumatic haematocoele also causes acute pain but the trauma or surgery that preceded it points to the likely diagnosis.
CHRONIC PAIN
§ Chronic scrotal pain is most often due to inflammation. It can often be traced to a vasectomy, although the cause is usually
obscure and treatment often ineffective.
§ Sperm leakage (sperm granuloma) following vasectomy may also cause chronic pain.
§ Pain is a feature of chronic bacterial epididymitis, which usually follows an acute episode.
Common causes of acute pain in the scrotum

1. Torsion of the testis
§ Sudden onset of unilateral scrotal pain with or without poorly localised abdominal pain
§ In early cases, the testis is high in the scrotum and exquisitely tender, and the cord is thickened; later these signs are often obscured by oedema
§ The opposite testis may lie horizontally (bell-clapper testis)
2. Torsion of the epididymal appendage (hydatid of Morgagni)

§ Nearly always in children
§ Sudden onset of unilateral scrotal pain; the testis hangs normally. There is a tenderness only at its upper pole and minimal overlying oedema
3. Acute epididymitis
§ Moderate or severe scrotal pain and tenderness with marked redness and oedema
§ Often preceded by symptoms of urinary tract infection; urine usually contains white cells, nitrites and organisms
4. Haematocoele following trauma or scrotal surgery (e.g. vasectomy)

§ History may be diagnostic although torsion is sometimes precipitated by trauma
INFLAMMATION OF THE EPIDIDYMIS AND TESTIS

EPIDIDYMITIS
Bacterial epididymitis is the most common inflammatory disorder of scrotal contents.

§ It is usually secondary to urethral infection that has ascended via the vas deferens!!!
§ The source is a urinary tract infection with coliforms (in the 50–65 age group) OR a sexually transmitted infection with
Chlamydia or Neisseria gonorrhoeae (common in the 15–30 age group).
§ Epididymitis is often incorrectly called orchitis or epididymo-orchitis. The testis is rarely infected, although the inflammation
surrounding epididymitis may cause testicular tenderness.
§ In epididymitis, pain usually begins acutely. It may present as a surgical emergency and be clinically indistinguishable
from testicular torsion.
§ On examination, the affected side of the scrotum and its contents are swollen, oedematous and tender, and the scrotal
skin can be red and warm (IE. THE FEATURES OF INFLAMMATION!)
§ It may be difficult to palpate testis and epididymis separately once infection is established!!
In a boy under 15, epididymitis must never be diagnosed in the absence of urinary symptoms, a
proven urinary infection or urethritis. Such an ‘acute scrotum’ must be explored to exclude torsion.
§ Treatment of acute epididymitis is initially with bed rest for analgesia and at least a month of an appropriate broad-
spectrum antibiotic.
§ The infecting organism is often not identified but attempts should be made to do so using urine cultures, blood cultures or
culture of urethral discharge after prostatic massage. Ofloxacin is often favoured on a ‘best-guess’ basis as it covers
Chlamydia and Gram-negative organisms.
§ Persistent or chronic epididymitis may cause the patient to suffer chronic scrotal tenderness. Chronic epididymitis may also
result from inadequate antibiotic treatment of an acute episode.
TUBERCULOUS EPIDIDYMITIS
§ Tuberculosis may involve the epididymis via bloodstream spread from a pulmonary or other focus. A tuberculous urinary tract
infection can spread to the epididymis, with swelling as the presenting complaint. Typically, the whole length of the epididymis
is thickened, non-tender and ‘cold’. In contrast to bacterial epididymitis, the epididymis can be readily
distinguished from the testis on palpation. If untreated, the testis may also become involved.
§ Diagnosis requires analysis of serial early morning urine specimens (EMUs) for mycobacteria or, more reliably, histological
examination of percutaneous needle biopsies. If tuberculosis is confirmed, a search must be made for pulmonary and urinary
tract disease
ORCHITIS
§ Primary bacterial orchitis is rare and may result from pyogenic infection in the genital tract or elsewhere.
§ Tertiary gummatous syphilis may involve the testis, producing diffuse non-tender enlargement. This is now
rare and there is usually a history of primary and secondary lesions. Sometimes a gumma is found unexpectedly during
investigation of a suspected testicular tumour.
§ Viral orchitis is most often caused by mumps. In post-pubertal males, bilateral mumps orchitis produces infertility in
50%; elevated follicle-stimulating hormone (FSH) blood levels following orchitis usually indicate the patient is infertile. Mumps
orchitis manifests 4–6 days after the onset of parotitis with extreme testicular tenderness and an inflammatory hydrocoele.
o Treatment is directed at symptomatic relief. Mumps has reappeared since the spurious MMR vaccine scare. Other
viruses affecting the testis include Coxsackie, human immunodeficiency virus (HIV), Epstein–Barr, varicella and, in
earlier times, smallpox.
HYDROCOELE (PRIMARY vs. SECONDARY)

PRIMARY HYDROCOELE (90%)
A hydrocoele is an excessive collection of fluid within the tunica vaginalis, i.e. in the serous space surrounding
the testis. Like the peritoneal cavity, the tunica normally contains a little serous fluid which is produced and reabsorbed at the same
rate
§ In infants and children, a hydrocoele is usually an expression of a patent processus vaginalis (PPV). In
some, the scrotal swelling disappears overnight, and is known as a communicating hydrocoele.
o Provided there is no hernia, hydrocoeles below the age of 1 year usually resolve spontaneously. For older
children, ligation of the PPV is required.
§ Primary hydrocoeles may develop in adulthood, particularly in the elderly, by slow accumulation of serous fluid,
presumably by impaired reabsorption. These can reach a huge size, containing several hundred millilitres of fluid but the
lesions are otherwise asymptomatic. The swelling is soft and non-tender and the testis cannot usually be palpated. The
presence of fluid is confirmed by transillumination
Note that a secondary hydrocoele may develop in response to testicular tumour or inflammation!! In most, the
hydrocoele is small and the testis can easily be palpated to reveal the primary abnormality.
Management
§ For symptomatic patients, a hydrocoele operation can be performed by everting the sac and oversewing the edges
(Jaboulay procedure) or plicating the sac (Lord’s method).
§ If the sac is thick, it is best excised (hydrocelectomy)
§ Alternatives include observation alone or periodic aspiration (rarely performed) if the patient is unsuitable for surgery.
§ NOTE WELL: If a testicular tumour is a possibility, a hydrocoele must not be aspirated as malignant cells can be disseminated
via scrotal skin to its lymphatic field.
HYDROCOELE OF THE CORD

§ Rarely, a hydrocoele develops in a remnant of the processus vaginalis somewhere along the course of
the spermatic cord. This hydrocoele also transilluminates, and is known as an encysted hydrocoele of the cord.
§ In females, a multicystic hydrocoele of the canal of Nuck sometimes presents as a swelling in the groin. It probably results
from cystic degeneration of the round ligament.
FOURNIER’S SCROTAL GANGRENE

§ Fournier’s scrotal gangrene is a form of necrotising fasciitis of genitalia and perineum and does NOT
involve the testes. There is often consequent systemic sepsis. The underlying causes are varied and include pre-existing
primary hydrocoele, genitourinary trauma, either accidental or iatrogenic, perirectal abscess and urethral stricture.
§ Predisposing factors include diabetes mellitus, corticosteroids, chemotherapy and alcohol abuse. The infecting
organism is principally an anaerobe but there is often synergistic aerobic infection. Treatment is urgent and includes IV
antibiotics and surgical excision of all necrotic tissue, with the wound left open to heal by secondary intention.
EPIDIDYMAL CYST AND SPERMATOCOELE

§ Multiple cysts can develop in the upper pole of the epididymis and present as a painless scrotal swelling.
Epididymal cysts affect a slightly younger age group than hydrocoeles. The testis can be palpated separately from the
cysts, which transilluminate.
§ Less common is a spermatocoele, a single cyst containing spermatozoa. Spermatocoeles usually occur in the
head of the epididymis and may present like a third testis. They are clinically similar to epididymal cysts but may or may not
transilluminate. Occasionally they occur in the spermatic cord and surgical excision may cause obstruction to passage of
sperm. If a patient wishes to remain fertile and the cysts are bilateral, excision may be contraindicated.
VARICOCOELE
§ A varicocoele represents dilatation and tortuosity of the pampiniform plexus of the spermatic vein in the
spermatic cord (basically remember varicose veins in spermatic cord)
§ The condition is much more common on the LEFT (90%) à may result from the different venous drainage of the two
sides: on the left, the testicular vein drains into the high-pressure renal vein, whereas the right testicular vein drains
directly into the inferior vena cava!!!
§ Varicocoele is common, affecting about 10% of young adult males.
§It is usually asymptomatic but is often discovered during examination for infertility.
o Varicocoele increases scrotal temperature, which may inhibit sperm function and cause possible loss of testicular
volume.
§ Varicocoele is best diagnosed if the patient is examined standing, when the varicocoele feels like ‘a bag of worms’
§ When lying flat, the distended veins often collapse and become impalpable.
§ Rarely, a varicocoele may be caused by an invading renal cell carcinoma obstructing the left renal vein.
o Such varicocoeles DO NOT collapse when the patient lies flat.
MANAGEMENT:
§ In adults, surgical treatment of varicocoele is only indicated for relief of pain or treatment of low sperm count (oligospermia).
§ In the child or adolescent, treatment may be advised to preserve spermatogenesis. The treatment of choice is
percutaneous embolization. Alternatively, surgical ligation can be performed laparoscopically or via an open
approach.
TESTICULAR TUMOURS
Testicular tumours are relatively uncommon, making up about 1.5% of male cancers, but they are the most common cancer in
men in their 20s and 30s. They are important because curative treatment is now available for most of them.
Testicular lymphatic drainage and the route of lymphatic metastases is towards intra-abdominal nodes and is
determined by the embryology of testicular descent. Note that this is different from scrotal skin, which drains
towards inguinal nodes.
§ Half have already metastasized by the time of presentation.

§ Undescended testes are at least 30 times more likely to turn malignant, although the individual risk is still low.
These tumours are usually seminomas.
More than 90% of primary testicular tumours are derived from germ cells, the rest being classified by the World Health
Organization as sex cord/gonadal stromal tumours. Germ cell testicular tumours are generally fast-growing, aggressive tumours that
metastasize to intra-abdominal lymph nodes and later via the bloodstream to the lungs.
Non-germ cell Leydig cell tumours, derived from the gonadal stroma, often present with excess hormone secretion rather than a
testicular lump. This causes precocious puberty in a child and testicular feminization in an adult.
Testes may be secondarily involved in more widespread malignancy such as lymphoma, CLL or, in children,
ALL. These rarely present as lumps but the surgeon may be asked to perform testicular biopsy as part of monitoring.
WHO histopathological classification of testicular tumours

1. Germ cell tumours (90%)
§ Seminoma (48%) – most common
§ Non-seminomatous GCT (42%)
a. Teratoma (most common)
b. Embryonal carcinoma
c. Yolk sac tumour
d. Choriocarcinoma
e. Mixed NSGCT
f. Mixed GCT
2. Sex cord/gonadal stromal tumours
§ Leydig cell tumour
§ Sertoli cell tumour
§ Mixed
3. Miscellaneous non-specific stromal tumours
§ Ovarian epithelial tumours
§ Tumours of the collecting ducts and rete testis
§ Lymphoma, leukaemia, secondary metastases
PATHOLOGY OF TESTICULAR TUMOURS

SEMINOMAS = MOST COMMON
§ More than half of malignant testicular tumours are seminomas, derived from spermatocytes. They occur predominantly
between the ages of 20 and 45 with a peak incidence at 35 years. The cut surface of a seminoma is typically pale,
creamy-white and homogeneous.
TERATOMAS
§ Teratomas are slightly less common than seminomas and their peak incidence is a decade earlier.
§ Teratomas may contain tissue from all germ cell layers: ectoderm, mesoderm and endoderm. Teratomas exhibit a wide range
of differentiation.
CLINICAL FEATURES OF TESTICULAR TUMOURS

§ A malignant testicular tumour usually presents as a painless, progressively enlarging testicular lump. If
the testicular capsule becomes involved, a secondary hydrocoele may appear but this is usually small and does not
hinder palpation.
§ Seminoma and teratoma both spread via lymphatics to para-aortic nodes at about the level of L1/2. Spread is then
proximally along the lymphatic chain then thoracic duct to supraclavicular nodes and the systemic circulation.
§ Lung secondaries are particularly common in teratomas.
A solid testicular lump must be assumed to be a tumour until proven otherwise.
The history is rarely helpful but may include an episode of trauma which merely drew attention to the lump. On examination,
the testis is either diffusely enlarged or contains a discrete lump which is firm and non-tender. Systemic examination may reveal
evidence of metastases. Malignant cervical nodes may be palpable but inguinal nodes are NOT involved unless the tumour
has spread to scrotal skin, which is rare except when biopsy or orchidectomy has been performed through a
scrotal incision.
§ Orchidectomy for suspected tumour should ALWAYS be carried out via an inguinal approach.
INVESTIGATION AND TREATMENT OF TESTICULAR TUMOURS
The outlook for treated testicular tumours, even with metastases, is often good.
Investigation and treatment usually take place in parallel. The aims are to confirm the diagnosis, detect any metastases and stage
the disease, then to treat according to the stage. The first investigation is scrotal ultrasonography. If this confirms a solid testicular
mass, surgical exploration is required. Preliminary staging investigations are usually performed next, including chest X-ray or CT (to
look for hilar node involvement and lung secondaries), CT abdomen and pelvis to assess retroperitoneal nodes and blood levels of
tumour markers (which must be measured before treatment).
Tumour markers contribute to diagnosis and staging and are useful for tracking residual or recurrent metastases because blood levels
correlate with tumour bulk. Serial postoperative measurements help monitor disease progress and the impact of therapy.
Tumour markers
1. Human chorionic gonadotrophin (beta-hCG) is secreted by syncytiotrophoblastic cells and levels may rise in any
tumour type, particularly poorly differentiated germ cell tumours.
2. Alpha-fetoprotein (AFP) is produced by yolk sac elements. About 75% of patients with metastatic teratoma have
elevated AFP levels but this marker is NOT expressed in seminoma.
3. Lactic dehydrogenase (LDH) is elevated in more than half the patients with metastatic seminoma.
Surgical exploration
Orchidectomy is the only appropriate treatment for the primary tumour and is usually performed as part of the
diagnostic process!!! The surgical approach is via an inguinal incision to avoid involving scrotal skin. The spermatic cord is
temporarily clamped to prevent venous spread of tumour cells and the testis is brought out for inspection and palpation. If the testis is
obviously malignant, orchidectomy is performed, dividing the cord at the internal inguinal ring. If there is diagnostic doubt, a testicular
biopsy is taken and examined immediately by frozen section before proceeding. The other testis is usually unaffected and can be
preserved. Further treatment is planned according to tumour type and stage.
MANAGEMENT OF SEMINOMA
For stage 1 seminoma, i.e. disease confined to the testis, some oncologists advise no further treatment after orchidectomy, although
carboplatin-based chemotherapy is occasionally recommended. Seminoma is very radiosensitive and radiotherapy can also play a role
for the primary, although it is not usually recommended by the European Association of Urologists in view of the high cure rate from
standard treatment. For stages IIa and b (i.e. abdominal lymphadenopathy up to 5 cm diameter), radical radiotherapy to the ipsilateral
(same side) para-aortic and iliac nodes gives a cure rate of about 95%. In stage IIb, chemotherapy is an alternative to radiotherapy
using etoposide and cisplatin (EP), or cisplatin, eposide, bleomycin (PEB).
LONG-TERM SURVEILLANCE
§ After chemotherapy, surgical debulking (‘salvage’) of residual lymph node masses is occasionally indicated. In the long term,
tumour markers and sequential CT scans are used to monitor the success of treatment. Recurrent disease can nearly always
be successfully treated by radiotherapy, chemotherapy or surgery.
FERTILITY
§ Many patients with testicular tumours are already subfertile at presentation, and chemotherapy is likely to further adversely
affect fertility. Patients need to be counselled carefully and, if required, semen can be collected and stored before treatment so
that artificial insemination or in vitro fertilisation may be performed later. However, the success rate is poor.
TORSION OF THE TESTIS OR EPIDIDYMAL APPENDAGE
TESTICULAR TORSION
In infants, the newly descended testis and its investing tunica vaginalis are mobile within the scrotum. These testes may undergo
extravaginal torsion which presents as a hard, swollen testis. Later in childhood, the testis becomes suspended in a near vertical
position, anchored by the spermatic cord and by attachments to the posterior scrotal wall. This attachment prevents rotation.
Minor anatomical variations can produce a narrow-based pedicle with a horizontal (‘bellclapper’) testicular lie, that allows the
testis to twist about its axis within the tunica (intravaginal torsion). When this occurs, pampiniform plexus veins become
compressed causing venous congestion. After a few hours, venous infarction occurs unless torsion is corrected.
Trauma during sport may sometimes initiate the process, and there have been reports of successful manual untwisting on the sports
field. In general, however, torsion is an emergency requiring prompt diagnosis and urgent surgical treatment to save the testis. Torsion
presents with a sudden onset of severe testicular pain often with poorly localized central abdominal pain (because the testis
retains its embryological nerve supply) and sometimes vomiting. In the early stages, the affected testis is tender, slightly swollen
and drawn up into the neck of the scrotum where the cord may be palpably thickened. With these features, the diagnosis is seldom in
doubt. At a later stage, the scrotal skin becomes red and oedematous, making accurate palpation difficult. At this point, torsion may be
difficult to distinguish from acute epididymitis and the scrotum must be explored surgically.
TORSION OF THE EPIDIDYMAL APPENDAGE (HYDATID OF MORGAGNI)

The hydatid of Morgagni is a small embryological remnant at the upper pole of the testis. This may undergo torsion and produce
symptoms similar to testicular torsion, out of proportion to the small size of the infarcted tissue. Infarction of the hydatid is of no
consequence except that it must be distinguished from testicular torsion.
MANAGEMENT OF SUSPECTED TESTICULAR TORSION
Differentiating between acute epididymitis and torsion can be difficult. If a firm diagnosis cannot be reached, surgical exploration is
mandatory. Investigations are of little value: radionuclide studies and Doppler ultrasound examination may be employed to show
testicular blood flow but results can be misleading.
Urgent operation is usually imperative as delay leads to testicular necrosis after about 8 hours. A scrotal incision is made and the testis
is examined and untwisted. If the testis is black and fails to recover its colour, it is necrotic and should be removed to prevent it inducing
a sympathetic contralateral orchiopathy. If some colour is restored, the testis is best left, although it may later atrophy. After untwisting,
the testis is sutured to the tunica vaginalis or placed in a surgically created dartos pouch to prevent recurrence. Both testes should be
secured as predisposition to torsion is usually bilateral
TRAUMA TO THE TESTIS
The testes may be injured during contact sports or fights. The dense fibrous capsule investing the testis (tunica albuginea) may remain
intact or it may split, but the testis is extremely painful in either case. If the tunica remains intact, a testicular haematoma results; if it
splits, the testicular parenchyma bursts and bleeds into the tunica vaginalis cavity, resulting in a haematocoele.
If pain is severe and persistent, the scrotum can be explored surgically. Pain from a haematoma can be relieved by incising the tunica
albuginea. Evacuating a haematocoele, however, may be impossible because blood infiltrates the tissues. If a haematocoele can be
evacuated, the tunica albuginea rupture is best repaired.
---
NOTES FROM DR. EAST
HYDROCELE:
Pathology
§ Idiopathic or primary (>90% of cases)
§ Secondary (to orchitis, testicular cancer)
**Communicating hydroceles do not occur in adults
Treatment:
1. Non-surgical – Sclerotherapy
2. Surgical – Jaboulay procedure, Lord’s procedure, or Hydrocelectomy
3. **Aspiration alone is not an acceptable treatment for idiopathic hydrocele. It always recurs and requires repeated
aspiration.
EPIDIDYMAL CYST (SPERMATOCELE)

§ Need not be treated at all in most cases. Should not be treated surgically in young patients.
§ Varicocele – aching towards end of day
§ Treated in most cases with supportive underwear
§ Needs surgical treatment if causing infertility
TESTICULAR TUMOR –
§ Seminoma most common.
§ Occurs mostly in young, Caucasian men (25 – 40, remember Lance Armstrong). VERY RARE IN BLACK MEN.
§ Undescended testis is major predisposing factor.
TESTICULAR TORSION
§ Acute, severe pain. Often comes on during sleep.
§ May untwist spontaneously and present as recurrent testicular pain
§ Associated with shortening of cord and bloody vaginalis fluid
§ Ultrasound diagnostic
§ Requires urgent surgery (must be done in <4hrs after onset) and fixation (orchidopexy) of both testes
§ i.e. Bilateral orchidopexy (must fix the other side as well)
§ Orchidectomy if black and necrotic
ACUTE ORCHITIS
§ May require incision of tunica albuginea to prevent necrosis
TORSION APPENDIX TESTIS
--
SURGICAL TUTOR
TESTICULAR TORSION
§ Common surgical emergency in adolescent boys
§ Peak incidence in second decade of life
§ A high insertion of tunica vaginalis ('Bell clapper testis') predisposes
§ Abnormality usually bilateral with contralateral testis also having horizontal lie
§ Usually presents with acute scrotal pain
§ May present with abdominal pain
§ Always examine in the scrotum in boys with abdominal pain
§ Urinary symptoms are uncommon
§ 50% have had previous episode of pain
§ Examination shows tender high-riding testis often with a small hydrocele
Management
§ Investigation usually not required
§ Testicular torsion is a clinical diagnosis requiring urgent surgical exploration
§ Diagnosis usually obvious
§ If testis infarcted - needs orchidectomy
§ If viability in doubt wrap in warm swab and wait
§ If viable both ipsilateral and contralateral side require an orchidopexy
Outcome
§ Approximately 60% of testes are salvageable
§ Re-examination at 6 months shows about 10% to be atrophic
§ Outcome best in those operated on with less than 6 hours symptoms
§ Beyond 12 hours salvage of testis less assured.
§ Long-term sub-fertility occasionally is a problem
§ Possibly due to an auto-immune response affecting both testes
EPIDIDYMITIS
§ Uncommon in adolescents - be wary about making the diagnosis
§ Usually has a more prolonged history, less pain and urinary symptoms
§ Tenderness is greatest over the epididymis
Idiopathic scrotal oedema

§ Usually occurs in boys less than 10 years old
§ Presents with scrotal redness and oedema
§ Pain is slight and testis feels normal
TORSION OF TESTICULAR APPENDIX

§ Presents with sudden testicular pain but often not severe
§ Hydrocele with tender appendage (hydatid of Morgagni) often apparent
§ If discovered during scrotal exploration appendage should be excised.
EXAMINATION OF A SCROTAL MASS
DR. EAST LECTURE:

Examination (preferably standing)
1. Inspection
2. Palpation
§ Can you get above it? (ie, can you clearly feel the cord structures unequivocally above the swelling?
§ Does it feel cystic or solid? Like a bag of worms?
§ Can you feel the testis? Is the testis normal? Is it exquisitely tender?
§ Transillumination: waste of time in dark skinned adults
A. IF YOU CAN GET ABOVE IT, IT IS A SCROTAL MASS. It is unlikely to be a hernia. DO NOT TRY TO REDUCE IT.
• Ultrasound may be used for definitive diagnosis
• MUST KNOW: Differential diagnosis Scrotal Masses:
o Not confined to scrotum:
1. Hernias
o Confined to scrotum
1. Epididymo-orchitis
2. Epididymal Cyst (Spermatocele) – cystic – yields watery or white fluid (contains seminal fluid)
3. Varicocele – bag of worms feel
4. Vaginal Hydrocele – cystic – yields straw coloured fluid
5. Testicular tumor – hard
6. Torsion testis
7. Chronic orchitis – firm to soft
8. Scrotal haematoma
9. Gumma
B. IF YOU CAN’T GET ABOVE IT, IT IS AN INGUINOSCROTAL MASS. It is likely to be a hernia.

• It is legitimate to ask patient to cough, but you will not see a cough impulse in a fully extended hernia
• It is also legitimate to attempt to reduce it but this may be impossible (1) in the standing position (2) because of chronic incarceration
• CAN ASK THE PATIENT IN EXAM IF HE CAN USUALLY PUT IT BACK IF YOU HAVE TROUBLE REDUCING IT
• CAN ALSO ASK THE PATIENT TO REDUCE IT FOR YOU IF YOU ARE HAVNG A HARD TIME BUT FEEL IT MAY BE REDUCIBLE
• **Inguinoscrotal hernias are always indirect – direct hernias never descend into the scrotum
§ If you can reduce it

1. Ask patient to cough again – you will usually see a cough impulse this time
2. Try to control hernia by putting one finger over the deep ring. If controlled, it is an indirect hernia. If it escapes medial to your finger
(through Hesselbach’s triangle) it is direct
Dr. East: Is it important to know whether hernia is direct or indirect?
§ From perspective of repair, it is not important. Indirect hernias encroach on and weaken Hesselbach’s triangle and direct hernias do the same to
the deep ring. THEREFORE ALL INGUINAL HERNIA REPAIRS ADDRESS BOTH DEFECTS SIMULTANEOUSLY. That is, the repair is the
same whether the hernia is direct or indirect.
§ From perspective of risk of incarceration, it is important only if patient is very infirm and you would like to avoid surgical repair. Indirect hernias
are more likely to incarcerate than direct hernias. Indirect hernias should always be repaired. However, direct hernias may be left alone in an
infirm, unfit patient because they are unlikely to incarcerate.
Complications of surgery
• Hematoma, infection
• Chronic groin pain (from nerve entrapment, either at surgery or more commonly as fibrous capsule/infiltrate contracts), ischemic orchitis
(from pampiniform plexus injury)
• What do you do if a mesh repair becomes infected?
- Open wound, expose mesh, dressings, antibiotics. In most cases, prolene mesh will not need to be removed.
- If infection persists, mesh needs to be removed. May be replaced by connective tissue xenograph (eg, Surgisis, which is pig collagen).
HYDROCELE
Pathology
§ Idiopathic or primary (>90% of cases)
§ Secondary (to orchitis, testicular cancer)
**Communicating hydroceles do not occur in adults
Treatment:
§ Non-surgical – Sclerotherapy
§ Surgical - Hydrocelectomy
§ **Aspiration alone is not an acceptable treatment for idiopathic hydrocele. It always recurs and requires repeated aspiration.
EPIDIDYMAL CYST (SPERMATOCELE) – Need not be treated at all in most cases. Should not be treated surgically in young patients.
VARICOCELE
§ Aching towards end of day
§ Treated in most cases with supportive underwear
§ Needs surgical treatment if causing infertility
TESTICULAR TUMOR
§ Seminoma most common.
§ Occurs mostly in young, Caucasian men (25 – 40, remember Lance Armstrong). VERY RARE IN BLACK MEN
§ Undescended testis is major predisposing factor.
TESTICULAR TORSION
§ Acute, severe pain. Often comes on during sleep.
§ May untwist spontaneously and present as recurrent testicular pain
§ Associated with shortening of cord and bloody vaginalis fluid
§ Ultrasound diagnostic
§ Requires urgent surgery (must be done in <4hrs after onset) and fixation (orchidopexy) of both testes.
ACUTE ORCHITIS
§ May require incision of tunica albuginea to prevent necrosis
TORSION APPENDIX TESTIS
--
SURGICAL TUTOR
Testicular torsion
§ Common surgical emergency in adolescent boys
§ Peak incidence in second decade of life
§ A high insertion of tunica vaginalis ('Bell clapper testis') predisposes
§ Abnormality usually bilateral with contralateral testis also having horizontal lie
§ Usually presents with acute scrotal pain
§ May present with abdominal pain
§ Always examine in the scrotum in boys with abdominal pain
§ Urinary symptoms are uncommon
§ 50% have had previous episode of pain
§ Examination shows tender high-riding testis often with a small hydrocele
Management
§ Investigation usually not required
§ Testicular torsion is a clinical diagnosis requiring urgent surgical exploration
§ Diagnosis usually obvious
§ If testis infarcted - needs orchidectomy
§ If viability in doubt wrap in warm swab and wait
§ If viable both ipsilateral and contralateral side require an orchidopexy
Outcome
§ Approximately 60% of testes are salvageable
§ Re-examination at 6 months shows about 10% to be atrophic
§ Outcome best in those operated on with less than 6 hours symptoms
§ Beyond 12 hours salvage of testis less assured.
§ Long-term sub-fertility occasionally is a problem
§ Possibly due to an auto-immune response affecting both testes
Epididymitis
§ Uncommon in adolescents - be wary about making the diagnosis
§ Usually has a more prolonged history, less pain and urinary symptoms
§ Tenderness is greatest over the epididymis
Idiopathic scrotal oedema

§ Usually occurs in boys less than 10 years old
§ Presents with scrotal redness and oedema
§ Pain is slight and testis feels normal
Torsion of testicular appendix
§ Presents with sudden testicular pain but often not severe
§ Hydrocele with tender appendage (hydatid of Morgagni) often apparent
§ If discovered during scrotal exploration appendage should be excised.
ESSENTIAL SURGERY: CLINICAL EXAMINATION OF SCROTAL LUMPS AND

SWELLINGS
A lump or swelling in the scrotum may be:
§ A solid or cystic mass arising from a component of scrotal contents or spermatic cord. These include testis, epididymis, epididymal
appendage, vas deferens and pampiniform venous plexus
§ A collection of fluid in the tunica or processus vaginalis (hydrocoele)
§ An indirect inguinal hernia extending along the embryological path of testicular descent into the scrotum
The origin of a scrotal lump
The first objective is to determine if the swelling arises in the groin, the spermatic cord or the scrotum and is achieved by palpating the cord
at the scrotal neck. In a hernia, the cord is broader than normal and the hernia can be shown to communicate with the abdominal cavity by a
cough impulse or by reducing the hernia. Spermatic cord swellings (varicocoele or cyst) are usually easily recognised. In purely scrotal
lumps, the spermatic cord is a normal diameter.
Testicular and epididymal lumps
With a scrotal abnormality, an attempt should be made to palpate testis and epididymis separately, and to determine their relationship to the
lump.
If the testis is enlarged or has a lump within it, this is a tumour until proven otherwise. Testicular swellings due to lymphoma, leukaemia or
granulomatous infections (e.g. tuberculosis or syphilitic gumma) may be softer but this is unreliable. Any testicular pathology may cause a
little fluid to accumulate in the tunica vaginalis producing a small secondary hydrocoele but this rarely interferes with testicular palpation.
Lumps in the epididymis (cysts, chronic epididymitis or, rarely, tuberculous granulomata) are discrete from, but attached to, an otherwise
normal testis. Tiny focal lumps in the epididymis are rarely clinically important. Infective lesions cause diffuse and usually painful thickening
of the epididymis, whereas epididymal cysts are almost always located at the upper pole. Epididymal cysts are filled with clear fluid and
therefore transilluminate. Transillumination is demonstrated by shining a strong beam of light through the scrotum in a partly darkened room.
If the lesion is fluid-filled, it will glow (except in the case of blood). About 10% of cysts in the epididymis, and most in the cord, are filled
with an opalescent fluid containing spermatozoa (spermatocoeles) which can also transilluminate.
General Surgery
Postoperative Complications (GO TO CH 22 SURGICAL RECALL AND EDIT THIS DOCUMENT)
Sources: Toronto Notes, Dr. L. Powell Class, etc.
February 2015
1. Fever
2. Wound complications
3. Urinary retention and renal complications
4. Respiratory complications
5. Cardiac complications
6. Intra-abdominal abscess
7. Paralytic Ileus
8. Delirium
POSTOPERATIVE FEVER
§ Defined as > 38.5 C or 101.5 F (Surgical Recall)
§ Fever does not necessarily imply infection particularly in the first 24-48 h post-op
§ Fever may not be present or is blunted if patient is receiving chemotherapy, glucocorticoids or immunosuppression
§ Timing of fever may help identify cause
Hours after surgery – POD #1 (IMMEDIATE):

1. Inflammatory reaction in response to trauma from surgery
2. Transfusion reactions. Reaction to blood products received during surgery
3. Malignant hyperthermia – (Anaesthetic complication that may occur intraop. Treat with DANTROLENE)
POD #1-2 (ACUTE):

1. Atelectasis (most common cause of fever on POD #1-2)
2. Aspiration pneumonitis
3. Early wound infection! (especially Clostridium (bronze-brown weeping wound), Group A Streptococcus – feel for crepitus and look for
“dishwater” drainage)
4. Transfusion reactions
5. Other: Addisonian crisis, *thyroid storm
POD #3-5 or 7 (SUBACUTE):

INFECTIONS more likely:
1. Surgical site infection
2. IV site/line infection
3. UTI
4. Bowel anastomotic leak (tachycardia, hypotension, oliguria, abdominal pain)

5. Septic thrombophlebitis
POD #8+ (DELAYED):

1. DVT/PE (NB: Can be anytime post-op!!!, most commonly POD #8-10)
2. Intra-abdominal/peritoneal abscess
3. Drug fever
4. Other: cholecystitis, peri-rectal abscess, URTI, infected seroma/biloma/hematoma, parotitis, C. difficile colitis, endocarditis
POD #1+ (drug fever)

Complete fever workup = Physical exam (look at wound, etc.), CXR, urinalysis, blood cultures, CBC
Treatment
§ Treat primary cause
§ Antipyrexia (e.g. acetaminophen)
WOUND/INCISIONAL COMPLICATIONS
WOUND CARE
§ ***Can have a shower POD #2-3 after epithelialization of wound (A sutured wound epithelializes after 24-48 hours)
§ ***Dressings can be removed POD #2 and left uncovered IF DRY
o MUST Examine wound if wet dressing, signs of infection (fever, tachycardia, pain)
§ ***Skin sutures and staples can be removed POD #7-10:

o Exceptions: Incision crosses crease (groin), closed under tension, in extremities (hand) or patient factors (elderly, corticosteroid use,
immunosuppressed) removed POD #14, earlier if signs of infection
§ Negative pressure dressings consist of foam and suction, promote granulation

o Ideal for large (grafted sites) or non-healing wounds (irradiated skin, ulcer)
o See VAC dressing notes (Vacuum assisted closure)
DRAINS (SEE SEPARATE NOTES)

Sometimes placed intra-operatively to prevent fluid accumulation (blood, pus, serum, bile, urine)
Can be used to assess quantity of third space fluid accumulation post-operatively
§ Potential route of infection, bring out through separate incision (vs. operative wound) to decrease risk of wound infection and remove as soon as
possible
Types of drains
§ Open (Penrose), higher risk of infection
§ Closed (Jackson-Pratt, hemovac) connected to suction
§ Pump (Davol) suction with airflow system to prevent obstruction
Monitor drain outputs daily (volume, colour, consistency, look for obstruction)
§ Drains should be removed once drainage is minimal (usually less than 30-50 ml/24 h)
§ Evidence does not support routine post-operative drainage of abdominal cavity
Drain Size (External diameter!): Measured by the unit French: French = diameter (mm) x 3 (NOT pi (3.14) as
commonly thought!!)
SURGICAL SITE INFECTION

AETIOLOGY
§ S. aureus, E. coli, Enterococcus, Streptococcus spp., Clostridium spp.
RISK FACTORS
SURGICAL FACTORS vs. PATIENT FACTORS
A. SURGICAL FACTORS
I. TYPE OF PROCEDURE:
1. Clean < 1.5%
§ (Elective surgery NOT entering resp/GI/biliary/GU tracts (not emergent, not traumatic), no acute inflammation)
§ Eg. Elective inguinal herniorrhaphy
2. Clean-contaminated < 3%
§ (Elective entering of resp/GI/biliary/GU tracts)
§ Eg. Cholecystectomy
3. Contaminated 5%
§ (Nonpurulent inflammation, gross spillage from GI, entry into biliary or GU tracts with infected bile/urine, penetrating trauma <4 h old)
§ Eg. Necrotic bowel resection
4. Dirty ~33-50%
§ (Purulent inflammation, pre-op perforation of resp/GI/biliary/GU tracts, penetrating trauma >4 h old)
§ Eg. Intra-abdominal abscess drainage
II. OTHERS: Procedures >2 h long, foreign bodies (drains, sutures, grafts), break in sterile technique, prolonged preoperative hospitalization
B. PATIENT FACTORS
1. Age
2. Immunocompromise: DM, steroids, immunosuppression
3. Malnutrition
4. Patient with other infections
5. Obesity
6. Traumatic wound
7. Haematoma, seroma
8. Burn
9. Radiation, chemotherapy
CLINICAL PRESENTATION
§ Typically fever POD #3-6 (BUT Streptococcus and Clostridium can present in 24 h)
§ [Features of inflammation: Dolor, rubor, calor, exudate]

§ Pain, blanchable wound erythema, induration, frank pus or purulosanguinous discharge, warmth
COMPLICATIONS
1. Abscess
2. Fistula, sinus tracts
3. Locally spreading infection à Myonecrosis or fascial necrosis (necrotizing fasciitis)
4. Systemic spread/sepsis
5. Impaired wound healing à

6. Wound dehiscence à
7. Hernia or
8. Evisceration
PROPHYLAXIS (MUST MUST KNOW)

Used to reduce the chance of surgical site infections
1. PRE-OP ANTIBIOTICS for most surgeries (cefazolin ± metronidazole or if β-lactam allergy, clindamycin ± gentamycin):
o Within 1 h PRE-incision; NB: can re-dose at 1-2 half lives (~q4-8h) in the OR
o Not required for low risk elective cholecystectomy, haemorrhoidectomy, fistulotomy, sphincterotomy for fissure
o Generally no need to continue prophylactic antibiotics postoperatively!!!, (i.e. Give for no more than 24 hours total!)
§ Reserve post-operative antibiotics for treatment of suspected or documented intra-abdominal infection
2. Other methods:
o Betadine/Chlorhexidine-alcohol wash of surgical site
o Normothermia (maintain patient temperature 36-38C during OR)
o Hyperoxygenation (consider FiO2 of 80% in OR)
o Hair removal should not be performed unless necessary; if so, clipping superior to shaving (Never use a razor!!)
o Consider delayed primary closure of incision for contaminated wounds
TREATMENT
1. Prevention!!
2. Examination of the wound!!!
a. Inspect
b. Compress adjacent areas to express any drainage
c. Swab drainage for C&S and Gram stain
3. Re-open affected part of incision, pack, heal by secondary intention

4. Debride necrotic and non-viable tissue
5. Antibiotics and demarcation of erythema ONLY IF cellulitis or immunodeficiency
WOUND HEMORRHAGE/HAEMATOMA
Secondary to inadequate surgical control of hemostasis
RISK FACTORS
§ Inherited or acquired bleeding tendencies: Anticoagulant therapy, coagulopathies, thrombocytopenia, DIC, severe liver disease,
myeloproliferative disorders,
§ Severe arterial hypertension, severe cough
§ More common with transverse incisions through muscle
CLINICAL FEATURES
§ Pain, swelling, discolouration of wound edges, leakage
§ Rapidly expanding neck hematoma can compromise airway and is a surgical emergency
TREATMENT
§ Pressure dressing
§ Open drainage ± wound packing (large hematoma only)
§ If significant bleeding, may need to re-operate to find source (often do not find a discrete vessel)
SEROMA
Fluid collection other than pus or blood
Treatment
Pressure dressing ± needle drainage
If significant may need to re-operate
WOUND DEHISCENCE
(TORONTO FIRST. SEE NOTES FROM DR. POWELL BELOW. MUST READ BOTH!!!)
Disruption of fascial layer, abdominal contents contained by skin only

§ 95% caused by intact suture tearing through fascia
CLINICAL FEATURES
Typically POD #1-3,
§ Most common presentation sigs: is serosanguinous drainage from wound, ± evisceration (disruption of all abdominal
layers and extrusion of abdominal contents – mortality of 15%)
§ Palpation of wound edge: should normally feel a “healing ridge” from abdominal wall closure (raised area of tissue under incision)
RISK FACTORS
Local: technical failure of closure, increased intra-abdominal pressure (e.g. COPD, ileus, bowel obstruction), hematoma, infection, poor blood supply,
radiation, patient not fully paralyzed while closing
Systemic: smoking, malnutrition (hypoalbuminemia, vitamin C deficiency), connective tissue diseases, immunosuppression, pulmonary disease, ascites,
poor nutrition, steroids, chemotherapy, obesity, other (e.g. age, sepsis, uremia)
Diabetes mellitus alone is not a risk factor
TREATMENT
§ Place moist dressing over wound with binder around abdomen and transfer to OT!!!
§ May consider conservative management with debridement of fascial and/or skin margins
§ Evisceration is a surgical emergency!! take patient for operative closure, use slowly absorbable suture ± retention suture
MUST KNOW: ABDOMINAL WOUND FAILURE (DR. POWELL NOTES)

Two levels of closure:
1. Fascial
2. Skin
Either can fail:

• Combination of both is called a “burst abdomen”
• Can be Partial vs. Complete
• Can be Concealed (Fascia only) vs. Revealed (Fascia + Skin)
“Dehiscence” usually refers to failure of the fascial closure (not skin)
CAUSES
PATIENT FACTORS vs. SURGEON FACTORS
PATIENT FACTORS:
LOCAL
1. Infection most common. Local vs. Systemic
2. Haematoma formation
3. Anything that raises IAP (COPD, bowel obstruction, ascites)
SYSTEMIC
4. Age
5. Nutritional factors (malnutrition à Vitamin C deficiency, hypoalbuminaemia, obesity)
6. Smoking
7. Immunocompromise: Steroids, immunosuppression (NB: DM alone is NOT a risk factor)
8. Connective tissue diseases
9. Patient general status and comorbidities
10. Reoperation
SURGEON:
1. Poor surgical technique
2. Choice of suture material
3. Handling of suture
4. Choice of needle: Only use a round-bodied needle.
*** Perhaps the only reasonable materials to close fascia are proline or PDS. PDS absorption time is about 6 months to a year. It is actually more
suitable than proline for abdominal wound closure as proline stays for 1000 years. This doesn't usually cause a problem though. Suture sinuses and
suture abscesses are possible problems but rare.
How to know when someone has abdominal wound failure:

Revealed vs. Concealed dehiscence
Concealed is when fascia alone dehisce
** NOTE: How to Dx concealed:

*Will see gauze stained “salmon pink” - (SEROSANGUINOUS DRAINAGE FROM WOUND) = Peritoneal fluid stained with blood - Pathognomonic
On removing dressing
Managing concealed:
1. MUST KNOW: Sterile dressing to wound + EARLY RETURN TO THEATRE FOR IMMEDIATE FASCIAL RECLOSURE (Reoperate –
resuture under GA)
2. Sometimes can make the decision to investigate the cause and once satisfied that operation is not needed can decide to address later. In
this case the surgeon accepts that there will be a massive ventral hernia. May not want to operate based on second hit hypothesis
3. NOTE WELL: Evisceration is a surgical emergency: take patient for operative closure, use slowly absorbable suture ± retention suture
*** Fascia takes about 6 months to one year to heal and remodel ***
Urinary and Renal Complications
URINARY RETENTION
May occur after any operation with general anesthesia or spinal anesthesia
More likely in older males with history of BPH, patients on anticholinergics
Clinical Presentation
§ Abdominal discomfort, overflow incontinence
§ Palpable bladder
§ Post-void residual urine volume >100 mL
Treatment
§ Foley catheter to rest bladder, then trial of voiding
OLIGURIA/ANURIA
Aetiology
Pre-renal vs. renal vs. post-renal:
§ Most common post-op cause is pre-renal ± ischaemic ATN
o External fluid loss: Haemorrhage, dehydration, diarrhoea
o Internal fluid loss: Third-spacing due to bowel obstruction, anastomotic leak, pancreatitis
Clinical Presentation
§ Urine output <0.5 ml/kg/h,
§ Increasing Cr, increasing BUN
Treatment
§ According to underlying cause; fluid deficit is treated with crystalloid (NS or RL)
Respiratory Complications
ATELECTASIS
Comprises 90% of post-op pulmonary complications
Clinical Features
Low-grade fever on POD #1, tachypnea, tachycardia
Decreased breath sounds, bronchial breathing, crackles
Risk Factors
COPD, smoking, obesity, elderly persons
Upper abdominal/thoracic surgery
Oversedation
Significant post-op pain, poor inspiratory effort
Treatment
Pre-operative prophylaxis
Smoking cessation (best if >8 wk pre-op)
Postoperative prophylaxis
Incentive spirometry, deep breathing exercise, chest physiotherapy, intermittent positive pressure breathing
Selective nasogastric tube decompression after abdominal surgery
Short-acting neuromuscular blocking agents
Minimize use of respiratory depressive drug,
Good pain control, early ambulation
PNEUMONIA/PNEUMONITIS
May be secondary to aspiration of gastric contents during anesthetic induction or extubation, causing a chemical pneumonitis
Risk Factors
Aspiration: general anesthetic, decreased LOC, GERD, full stomach, bowel/gastric outlet obstruction + non-functioning NG tube, pregnancy, seizure
disorder
Non-aspiration: atelectasis, immobility, pre-existing respiratory disease
Clinical Features
Productive cough, fever
Tachycardia, cyanosis, respiratory failure, decreased LOC
CXR: pulmonary infiltrate
Treatment
Prophylaxis: see atelectasis prophylaxis, pre-op NPO/NG tube, rapid sequence anesthetic induction
Immediate removal of debris and fluid from airway
Consider endotracheal intubation and flexible bronchoscopic aspiration
IV antibiotics to cover oral nosocomial aerobes and anaerobes (e.g. ceftriaxone, metronidazole)
PULMONARY EMBOLUS
Clinical Features
Unilateral leg swelling and pain (DVT as a source of PE), sudden onset SOB, tachycardia, fever
Most commonly POD #8-10, but can occur anytime post-op
Treatment
IV heparin, long-term warfarin (INR = 2-3) for 3 mo
Greenfield (IVC) filter if contraindications to anticoagulation
Prophylaxis: subcutaneous heparin (5000 units bid) or LMWH, compression stockings (T.E.D. Hose), pneumatic compression device
PULMONARY EDEMA
Aetiology
Cardiogenic vs. noncardiogenic
Circulatory overload: excess volume replacement, LV failure, shift of fluid from peripheral to pulmonary vascular bed, negative airway pressure, alveolar
injury due to toxins (e.g. ARDS)
ƒ.more common with pre-existing cardiac disease
Negative pressure pulmonary edema due to inspiratory efforts against a closed glottis upon awakening from general anaesthesia
Clinical Features
Shortness of breath, crackles at lung bases, CXR abnormal
Treatment (LMNOP)
Lasix
Morphine (decreases symptoms of dyspnea, venodilator and afterload reduction)
Nitrates (venodilator)
Oxygen + non-invasive ventilation
Position (sit patient up)
RESPIRATORY FAILURE
Cardiac Complications
Abnormal ECGs common in post-op period (compare to pre-op ECG)
Common arrhythmias: supraventricular tachycardia (SVT), atrial fibrillation (secondary to fluid overload, PE, MI)
MYOCARDIAL INFARCTION (MI)

Surgery increases risk of MI
Incidence:
0.5% in previously asymptomatic men >50 yr old
40-fold increase in men >50 yr old with previous MI
Risk Factors
Pre-op hypertension, CHF
Previous MI (highest risk ≤6 mo, but risk never returns to baseline)
Increased age
Intra-operative hypotension
Operations >3 h
Angina
Clinical Features
Majority of cases on day of operation or POD #3-4 (shifting of third space fluid back into intravascular compartment)
Often silent without chest pain, may only present with new-onset CHF (dyspnea), arrhythmias, hypotension
General Surgery
Venous Disease of the Lower Limb
Sources: Toronto Notes, Surgical Tutor, Dr. Hall Class. MUST ALSO READ NOTES FROM DR. POWELL CLASS
February 2015
Outline:
1. Varicose veins (Superficial venous insufficiency)
2. Deep Venous Insufficiency
3. (Need to read DVT medicine notes)
4. Venous ulceration
VARICOSE VEINS
INCIDENCE: F > M (2:1), 10-20% of population
AETIOLOGY (Primary vs. Secondary)
1. Primary/Idiopathic – Vast majority

• Main factor: Inherited structural weakness of valves
• Contributing factors: increasing age, female gender, OCP use, occupations requiring long hours of standing,
pregnancy, obesity
2. Secondary
1. Pelvic tumours with venous compression (Eg. malignancy, gravid uterus)
2. Congenital anomalies with absent valves
3. AV fistulae - Pulsatile
4. Tricuspid regurgitation - Pulsatile
HISTORY
• Complaint of unsightly appearance
• Diffuse aching, fullness/tightness
• Nocturnal cramping
• Aggravated by prolonged standing (end of day), premenstrual
NB: MUST ALSO!!:

1. Ask history of past DVT!
2. Ask history of all risk factors for thrombosis/DVT (i.e. Virchow’s triad)!
3. Ask history of complications of varicosities (Esp. features of phlebitis!!!)
EXAMINATION FINDINGS
MUST EXAMINE WITH PATIENT STANDING!!
• Visible long, dilated and tortuous superficial veins along thigh and leg
• Identify the distribution of the varicose veins!!! (MUST COMMENT IN EXAM!!) – Say whether long saphenous (i.e. medial
distribution) vs. short saphenous (lateral distribution)
o NB: 80% of varicosities involve the long saphenous vein!!
• Evidence of deep venous insufficiency: hyperpigmentation, haemosiderosis, stasis eczema, lipodermatosclerosis and
ulceration
• **MUST GENTLY PALPATE ANY VISIBLE VARICOSITIES for evidence of phlebitis

• If associated phlebitis: Hard, tender veins. Inflamed overlying skin (± Systemic: fever, malaise)
• Saphena varix
• Cough test, Tap test and thrill test are unreliable

• **Brodie-Trendelenburg test (valvular competence test)
o With patient supine, raise leg to empty superficial veins and compress saphenous vein at thigh with tourniquet (“high-thigh
tourniquet”), have patient stand – if veins fill quickly from top down then incompetent valves;
o Using multiple tourniquets to localize incompetent veins is the MODIFIED Trendelenburg test (aka. the “Tourniquet test”)
COMPLICATIONS OF VARICOSE VEINS
1. Superficial thrombophlebitis – Manage by bed rest, elevation of leg and pressure bandage on leg. Rarely, antibiotics if
secondary infection
2. Haemorrhage: external or subcutaneous
3. Ulceration, eczema, lipodermatosclerosis, and hyperpigmentation
INVESTIGATIONS
1. Hand-held Doppler probe – Diagnose reflux at SF and SP junction. BUT less sensitive for perforators
2. Duplex sonography (gold standard) – Can MAP venous anatomy in legs. Diagnoses valvular AND perforator incompetence
(reflux) + occlusion
3. Venography – Place a tourniquet around ankle, inject contrast dorsum of foot. Then sequential x-rays and observe for
REFLUX and OCCLUSION (The tourniquet is to force the contrast to drain into the deep rather than the superficial system, so any
reflux from deep to superficial at a higher level can be observed)
4. Intravascular ultrasound (IVUS) - using a specially designed catheter with a miniaturized ultrasound probe attached to the
distal end of the catheter. The proximal end of the catheter is attached to computerized ultrasound equipment. It allows the
application of ultrasound technology to see from inside blood vessels out through the surrounding blood column, visualizing the
endothelium (inner wall) of blood vessels in living individuals.
§ IVUS better identifies obstructive lesions than venography, which can fail to detect even severe obstruction
5. MRVI – Magnetic Resonance Venous Imaging
It is important to determine whether the venous insufficiency is superficial, deep, or both as it affects management
MANAGEMENT
CONSERVATIVE/NON-SURGICAL vs. SURGICAL
Largely a cosmetic problem. Indications for surgery have recently come under scrutiny due to the cosmetic nature AND possible need
for the great saphenous vein for future arterial surgery such as coronary artery bypass
A. CONSERVATIVE (Non-invasive and invasive):

1. Elevation of leg and/or
2. Elastic, graded compression stockings – For MINOR VARICOSITIES. MUST ensure compliance. Much higher
pressure at ankle than thigh.
§ DO NOT USE IF CONCOMITANT ARTERIAL INSUFFICIENCY!!
§ ABPI SHOULD BE MEASURED. If the ABPI is < 0.8, the arterial circulation may be inadequate; it should be assessed and necessary treatment
instigated BEFORE compression therapy as (a) poor arterial supply may be part of the reason for non-healing of an ulcer and (b) compression
bandaging with low arterial pressure will make ulceration worse.
§ IF YOU SEE A PATIENT WITH LARGE VARICOSITIES IN EXAM, NEITHER THIS NOR SCLEROTHERAPY IS LIKELY TO BE SUCCESSFUL SO
REMEMBER TO MAKE THIS POINT IN YOUR ANSWER
Invasive
3. Sclerotherapy – Inject sclerosant + bandage for 2 weeks to allow fibrosis
a. For small-moderate sized BELOW KNEE varices. High recurrence rate
b. Sclerosants: **5% Ethanolamine oleate **0.5% Sodium tetradecyl sulphate **Recently FOAM!! (Mixture of
air/sclerosant) has been shown to be more effective (Different from sclerosants used for haemorrhoids)
c. Complications: Phlebitis, skin staining, ulceration, DVT, recurrence
4. Endovenous laser therapy (EVLT) – REPLACING conventional sclerotherapy and surgery

a. Pass laser fibre into vein under U/S guidance, fire laser to ablate endothelium and thrombose the vein. Gradually
withdraw until entire vein treated. Compress with bandage for 2 weeks
5. Radiofrequency ablation – GOLD STANDARD
B. SURGICAL:
• LSV surgery vs. SSV surgery vs. Perforator surgery
• Some options:
o High saphenous ligation
o Long saphenous vein stripping (and its tributaries)
INDICATIONS FOR SURGERY:

1. Cosmetic
2. Symptomatic varix (pain, bleeding, recurrent thrombophlebitis)
3. Tissue changes (hyperpigmentation, ulceration)
4. Failure of conservative treatment
NOTE WELL: CANNOT ABLATE OR REMOVE THE SUPERFICIAL SYSTEM IF PATIENT HAS CONCOMITANT DEEN VENOUS
DISEASE (ESP. DVT)!!! THERE WOULD BE NOWHERE FOR BLOOD TO FLOW FROM THE LOWER LIMB
WOULD RESULT IN “VENOUS GANGRENE”
SURGICAL TUTOR
LSV SURGERY
§ Trendelenburg position with 20-30° head down
§ Legs abducted 10-15°
§ Saphenofemoral junction (SFJ) found 2 cm below and lateral to pubic tubercle
§ Essential to identify SFJ before performing flush ligation of the LSV
§ Individually divide and ligate all tributaries of the LSV
o Superficial circumflex iliac vein
o Superficial inferior epigastric vein
o Superficial and deep external pudendal vein
§ Check that femoral vein clear of direct branches for 1 cm above and below SFJ
§ Stripping of LSV reduces risk of recurrence
§ Only strip to upper calf. No need to strip below knee!
§ Remove vein from cranial to caudal in order to spare the saphenous nerve
§ Stripping to ankle is associated with increased risk of saphenous neuralgia
§ Post operative care:
o Elevate foot of bed for 12 hours
o Class 2 varix stocking should be worn for at least 2 weeks
SSV SURGERY
§ Patient prone with 20-30° head down
§ Saphenopopliteal junction (SPJ) has very variable position
§ Preoperative localization with duplex ultrasound is strongly recommended
§ Identify and preserve the sural nerve
§ Need to identify the SPJ
§ Stripping associated with risk of sural nerve damage
§ Subfascial ligation inadequate
PERFORATOR SURGERY
§ Significance of perforator disease is unclear
§ Perforator disease may be improved by superficial vein surgery
§ Perforator surgery (e.g. Cockett's and Todd's procedure) associated with high morbidity
§ Subfascial endoscopic perforator surgery (SEPS) recently described
§ Not indicated for uncomplicated primary varicose veins
§ May have a role in addition to saphenous surgery in those with venous ulceration
RADIOFREQUENCY ABLATION
§ Uses high frequency alternating current delivered via a bipolar catheter
§ Placed intraluminally under duplex guidance
§ Performed under general anaesthesia
§ Local heating results in venous spasm and a collagen seal
§ Long saphenous vein accessed at the knee using Seldinger technique
§ 90% vein occlusion achieved in first week after treatment
§ Associated with less pain than open surgery
§ Improved quality of life and earlier return to work
§ Complications include paraesthesia and skin burns
§ Recurrence rates are similar to open surgery
ENDOVASCULAR LASER TREATMENT

§ Laser energy deliver via narrow laser fibre to obliterate the vein
§ Causes heat injury to vessel wall
§ Usually performed under local anaesthesia
§ Clinical and symptomatic improvement seen in 95% patients
§ Patient satisfaction high and early return to work is possible
§ Complications include paraesthesia and skin burns
§ Recanalisation seen in less than 10% patients
SCLEROTHERAPY
§ Only suitable for below knee varicose veins
§ Need to exclude SFJ or SPJ incompetence
§ Main use is for persistent or recurrent varicose veins after adequate saphenous surgery
§ Sclerosants
o 5% Ethanolamine oleate
o 0.5% Sodium tetradecyl sulphate
§ Recently foam (Mixture of air / sclerosant) has been shown to be more effective
§ Different to sclerosants used for haemorrhoids
§ Needle placed in vein when full with patient standing
§ Empty vein by raising legs with needles in situ prior to injection
§ Apply immediate compression and maintain for 4-6 weeks
§ Do not exceed maximum volume
§ Injection about 5 sites possible
REASONS FOR RECURRENCE POST SURGERY

Significant post-operative recurrence, especially with sclerosing agent injection
1. Failure to treat underlying cause if secondary
2. Inaccurate clinical assessment

a. Confusion as to whether varicosities are in LSV or SSV distribution
b. Can be avoided with use of hand held doppler
3. Inadequate primary surgery
a. 10% cases SFJ not correctly identified
b. 20% cases tributaries mistaken for LSV
c. Failure to strip LSV
4. Injudicious use of sclerotherapy
a. 70% of those with SF incompetence treated with sclerotherapy alone will develop recurrence
5. Neovascularization
a. With recurrent varicose vein need to image with duplex or varicography
DEEP VENOUS INSUFFICIENCY

In normal person at rest, pressure in veins at ankle is equivalent to the height of a column of blood from the right atrium to the ankle -
100 cm H2O. On walking, this drops to ~20 cmH2O as the soleal pump drives the blood upwards. In valvular incompetence, venous
pressure remains high.
AETIOLOGY
1. Primary: Congenital syndromes with absent valves
2. Secondary:
• Venous hypertension:
a. DVT IS THE MAJOR CAUSE of deep venous insufficiency
b. AV fistulae
CLINICAL FEATURES
1. Pain - Most common – relieved by elevation
2. Swelling – Ankle and calf oedema – relieved by elevation
o
• Due to transudation of fluid 2 to increased hydrostatic pressure (Disturbed Starling’s forces)
Following changes occur mainly in the “medial gaiter area” (just above the medial malleolus)
3. Hyperpigmentation – brown discolouration due to haemosiderosis (breakdown product of Hb in extravasated RBCs)

4. Venous eczema/stasis dermatitis (and pruritus!)
5. Lipodermatosclerosis – Inflammation and fibrin exudation leads to fibrosis of the normally soft subcutaneous tissues.
When the leg is elevated, prominent venous guttering seen
6. Ulceration – 2 causes: Poor skin nutrition due to stasis and repeated excoriations due to irritation of eczema
INVESTIGATIONS
1. Ambulatory venous pressure measurement (gold standard)

2. Duplex sonography (most commonly used) – Demonstrate REFLUX and OCCLUSION
3. Venography – Detect perforators that may be treated and identify occlusions
4. Photoplethysmography
MANAGEMENT
NO SUCCESSFUL WAY TO REPAIR OR REPLACE THE VALVES OF DEEP VEINS. SEE DR. POWELL NOTES FOR POSSIBLE
SURGICAL OPTIONS
VENOUS ULCERATION
Generally due to incompetence of the DEEP VEINS

See separate notes on leg ulcers

6 M
Wayne Robinson. MBBS Class of 201?
Senior Medicine
DVT (See my separate notes on PE)
Sources: Toronto
January 2015
VENOUS THROMBOEMBOLISM
DEFINITION
• Thrombus formation and subsequent inflammatory response in a superficial or deep vein
o Superficial thrombophlebitis, deep vein thrombosis (DVT) and pulmonary embolism (PE)
• Thrombi propagate in the direction of blood flow (commonly originating in calf veins)
• More common in lower extremity than upper extremity
• Incidence -1 % if age >60 yr
• Most important sequelae are pulmonary embolism (-50% chance with proximal DVT) and chronic venous insufficiency
AETIOLOGY
Always m ention: Virchow's Triad (M ust know well!)
1. Venous stasis
• Immobilization (post-MI, CHF, stroke, post-op, prolonged sitting during travel, immobilization of an extremity after
surgery/fracture)
o Inhibits clearance and dilution of coagulation factors
• Chronic venous insufficiency
• Heart failure (risk of DVT greatest with right heart failure and peripheral edema)
2. Endothelial damage
• Exposes endothelium to prompt hemostasis
• Leads to decreased inhibition of coagulation and local fibrinolysis
• Post-op injury
• Trauma
3. Hypercoagulability
• Inherited coagulopathies
■ Factor V Leiden (most common overall).
■ Prothrombin G20210A variant.
■ Inherited deficiencies of antithrombin III, protein C or protein S
• Acquired
■ Antiphospholipid antibodies (i.e. lupus anticoagulant, anti-cardiolipin antibody and anti-Beta2-glycoc^c?e“ -‘
■ Hyperhomocysteinemia
■ Malignancy (especially adenocarcinomas. Lung, pancreas, colon, rectum, kidney and prostate
■ Cancer/cancer treatment
■ Hormone related:
1. Pregnancy, post-partum
2. Exogenous oestrogen administration: OCP, HRT, SERMs
■ Blood dyscrasias (myeloproliferative neoplasms, especially PRV, ET),
■ PNH, hyperviscosity (multiple myeloma, polycythemia, leukemia, sickle cell disease
■ Nephrotic syndrome
■ Major surgery (especially orthopedic, thoracic, Gl and GU)
■ Major trauma (especially fractures of spine, pelvis, femur or tibia, spinal ccxa injury
4. Personal history of DVT/PE, family history

5. Increasing age
6. Idiopathic (10-20% are later found to have cancer)
C LINICAL FEATURES OF DVT

Absence of physical findings does not rule out disease!!
■ Unilateral leg oedema, erythema, warmth and tenderness
A
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DIFFERENTIAL DIAGNOSIS OF DVT/LEG SW ELLING 0\r CKÂAdSN
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2. Lym phangitis or lym ph obstruction
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3. C ellulitis
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5. Muscle strain o r tear (e.g. Gastrocnemius) iy b la g ^ d i^ c P lo u i't^ H o h c£ £V\x€yy\
$. A rte ria l occlusive disease
d o m n h <5 .S tan—► iHS eps'iK vc,
INVESTIGATIONS FOR DVT v - > pgfo m C&Vf m uSC\ei on
Passive d o y fi H e x io rv of- f o o - v .
1. D-dim er test: Only useful to rule out DVT if negative AND low clinical suspicion of disease and no other acute medical
issues/recent surgery
2. Doppler ultrasound Most useful diagnostic test for DVT

ai Sensitivity and specificity for proximal DVT ~95% (Proximal DVT = Occurring in the popliteal vein and above
(popliteal, femoral or iliac veins)}
b. Sensitivity for calf DVT ~70%
3. Other non-invasive tests include:

a. MRl and
b. Impedence plethysmography
4. Venography is the gold standard, but is expensive, invasive and higher risk
Approach to Treatment of Venous Thromboembolism (VTE)

MUST KNOW: GOALS:
1. Prevent further clot extension

2. Prevent acute pulmonary embolism!!! (occurs in up to 50% o f untreate d patients)
3. Reduce the risk of recurrent thrombosis
4. Treatment of massive ileofemoral thrombosis with acute lower limb ischemia and/or venous gangrene (phlegmasia cerulea
dolens)
5. Limit development of late complications, e.g. Postphiebitic syndrome, chronic venous insufficiency and chronic
thromboembolic pulmonary HTN 0 .
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Absolute Contraindications to Treatment L? c 5ijvripfoyY7T 4 .S’f&nr of-
1. Active bleeding c W r iic v e n o u j -fbllouinvi o v t
2. Severe bleeding diathesis or platelet count <20 x 109/l (<20,000/mm3)
3. Intracranial bleeding L* hefluX du.£ To v e n o u s .fff» <2- 'fo
4. Neurosurgery or ocular surgery within 10 d Y ^ lv u lo J r ^ C -+j
\h(u>VY\pe\^M, g b s h u c - fto n
Relative Contraindications to Treatment
1. Mild-moderate bleeding diathesis or thrombocytopenia V S j MphoPnsjSiCjwS; -
2. Brain metastases
* p a in
3. Recent major trauma
4. Major abdominal surgery within the past 2 d venouj dilation
5. Gl or GU bleeding within 14 d * oedem a
6. Endocarditis 4 5 L ih p i e m e n f red n e ss
7. Severe hypertension (sBP >200 or dBP >120)
4 v e n o m s U.lC£v-?
8. Recent stroke
CLASSIFY: A C U T E T R E A TM E N T vs. LONG -TEE
IN ITIAL TREATMENT
Wayne Robinson. MBBS Class ot zftf?
1. Low molecular weight heparin (LMWH)
■ Administered SC, at least as effective as UFH with a lower bleeding risk
■ Advantages:
a. Predictable dose response and fixed dosing schedule;
b. Lab monitoring not required;
c. <1% HIT;
d. Safe and effective outpatient therapy!!!
■ Disadvantages: Only partially reversible by protamine, long-term use associated with osteoporosis
* Penally cleared - must adjust dose in patients with renal dysfunction
2. Urrfractlonated heparin (UFH)

■ In patient with average risk of bleed;
■ Advantages: Rapidly reversible by protamine!
■ Disadvantages: Must monitor aPTT with adjustment of dose!!! to reach therapeutic level (~2x normal value) ,
monitor platelet counts for development of HIT
Alternatives to LMWH and UFH
3. Heparinoids (Patients with HIT)

4. Direct thrombin inhibitors (Dabigatran)
5. Factor Xa inhibitors (Fondaparinux, rivaroxaban)
6 ~hrqmbolytic drugs (e g streptokinase, tPA) RESERVED FOR ACUTE LIMB/LIFE-THREATENING THROMBOSIS, and
low bleeding risk
LONG-TERM TREATMENT
1. W arfarin:
■ Standard treatment; should be initiated with heparin overlap: Dual therapy for at least 5 days!! due to:
1. Initial prothrombotic state
2. Half life of vitamin K factors and
3. Risk of warfarin-induced skin necrosis
■ Discontinue heparin after INR >2.0 for two consecutive days!!

* Warfarin should be dosed to maintain INR at 2-3 except in select cases
■ Monitor INR twice weekly for 1-2 wk, then weekly until INR stable, then every 2-4 wk!!
• LM W H more effective than warfarin at preventing recurrence of venous thrombosis in cancer patients
MUSTK N O W :■ ftstsattoryofwarfarinT
m ra p ? RequiresOverfap-wtnHejssnn-Therapyfor Saya
t 10 load rsj dom o i wattMn causes s pasajpffeu* decern fct pfstarr C-tewefe (a -f.pamm- fc depended arfftssapântj si feat 36 ft reaiSng in a ' ranaent ftypmcoegattite state
2. Wartatm oscreasm. FacM Vi- fewfe m Hast 46 ft gfff is pies? tm m sm ts Faofor vft ferets; ftowwcr« antiSirerBfKsiic effect a*net astwenaaCmm Factor IX, X and 0 are
auffcemiy isdueaf (occurs after agyresr 40):
MUST KNOW: Duration of anticoagulant treatment (with warfarin unless otherwise noted):
o First episode DVT with transient risk factor: 3 m p
o First episode DVT without identifiable risk factor (idiopathic) or single inherited risk factor (e.g. Factor V Leiden): 6-12 m o
or in d e fin ite th e ra p y (controversial)
o First episode DVT with ongoing risk factor (e.g. cancer, antiphospholipid antibody) or >1 risk factor: consider in d e fin ite
thera p y
o Recurrent DVT (2 or more episodes): in d e fin ite th e ra p y
2 . IVC filters
• Temporary filter indicated MLY I distal acute DVT (<4 wk) with significant contraindications to anticoagulant
therapy (i.e. active bleeding)
■ Must remove once safe to do so as filter is pro-thrombotic in the long-term (anticoagulation if left in)
Special considerations
1. Pregnancy: treat with LMWH during pregnancy, then warfarin for 4-6 wk post-partum (minimum total anticoagulation time of 3-
6 mo) [WARFARIN CROSSES PLACENTA AND TERATOGENIC - causes “chondrodysplasia punctate”]
2. Surgery: avoid elective surgery in the first month after a venous or arterial thromboembolic event
■ Preoperatively: IV heparin may be used up to 6 h pre-operatively
■ Perioperatively: Surgery safe when INR <1.5; warfarin should be discontinued for at least 4 wk pre-operatively to
allow INR to fall
Wayne Robinson, MBBS Class of 201:
■ Postoperative!y: IV heparin or LMWH can be used for anticoagulation (start 12 h after major surgery until therapeutic
INR reached after restarting warfarin)
■ For patients at high risk for thromboembolism (VTE <12 wk, recurrent VTE, lupus anticoagulant, atrial fibrillation with
prior stroke, mechanical heart valve), IV heparin or LMWH (bridging) should be given before and after the procedure
while the INR is below 2.0
Prophylaxis
Consider for those with a moderate to high risk of thrombosis without contraindications
■ Non-pharmacological measures include:
1. Early ambulation
2. Elastic compression stockings (TEDs)
3. Intermittent pneumatic compression (IPC)
■ UFH 5000 IU SC bid for moderate risk

■ UFH 5000 IU SC tid or LMWH as per hospital protocol (i.e. enoxaparin 40 mg SC daily) or
■ UFH 5000 IU SC tid for high risk
Contraindications and Adverse Reactions of Anticoagulant Therapy

■ Absolute: active bleeding, severe bleeding diathesis or platelets <20 x 109/L (<20,000/mm3), intracranial bleeding, neuro or
ocular surgery within <10 d
■ Relative: mild-moderate neurologic diathesis or thrombocytopenia, brain metastases, recent major trauma, major abdominal
surgery within page 2 d, GI/GU bleed within 14 d, endocarditis, severe HTN (sBP >200 or dBP >120), recent stroke
VERY G O O D A D D ITIO N AL INFO
Wells' Score for DVT Criteria (Score) [NB: This is different from the PE Welt’s criteria):
1. Paralysis, paresis or recent orthopedic casting of lower extremity (1)
2. Recently bedridden (>3 d) or major surgery within past 4 wk (1)
3. Localized tenderness in deep vein system (1)
4. Swelling of entire leg (1)
5. Calf swelling >3 cm than other leg (measured 10 cm below the tibial tuberosity) (1)
6. Pitting edema greater in the symptomatic leg (1)
7. Collateral non-varicose superficial veins (1)
8. Active cancer or cancer treated within 6 mo (1)
9. Alternative diagnosis more likely than DVT (e.g. Baker's cyst, cellulitis, muscle damage, superficial venous thrombosis) (-2)
Total Score Interpretation:

3-8: High probability, 1-2: Moderate probability, -2-0: Low Probability
Low-ffctecolar-WetQht Heparin versus a Coum&fin for trie Prevention of Recurrent Venom Th roroboemboiram m Patients with Cancer
NEMJ 2003:349:146-153
Study: RCT comparing the efficacy of LMWH (dalteparin) with an oral anti-coagulant agent (coumarin) in preventing recurrent thrombosis in patients with cancer.
Conclusions: In patients with cancer and acute VTE, dalteparin was more effective than coumadin in decreasing the risk of recurrent thromboembolism without increasing the
risk of bleeding.
Duration of Treatment with Vita mm K Antagonistsin Symptomatic Venous Thromboembolism

Cochrane DB Syst Rev 2009:CD001367
Study: Meta-analysis of 8 RCTs (2994 patients) comparing different durations of treatment with vitamin K antagonists in patients with symptomatic VTE
Conclusion: Prolonged treatment with vitamin K antagonists leads to a consistent reduction in the risk of recurrent VTE for as long as therapy is continued. Therapy should be
discontinued when the risk of harm from major bleeding (which remains constant over time) is of greater concern than the absolute risk of recurrent VTE (which declines over
time). No specific recommendation was made regarding optimal duration of treatment.*1
Common Medications that Interact with Warfarin

1. Acetaminophen (interference with vit K metabolism)
2. NSAIDs (Gl injury)
3. Metronidazole
4. Sulfamethoxazole
5. Fluconazole
6. Allopurino!
7. Tamoxifen
Camest d t Both Venous and Arterial Thrombosis include:

1. Antiphospholipid antibodies
2. Myeloproliferative neoplasms
3. Heparin induced thrombocytopenia
4. Distal venous clot with patent foramen ovale1
Malignancy ta a common cause of acquired hypefcoagtttobtBty

Workup may include (controversial):
1. Complete history and physical
2. Routine bloodwork
3. Urinalysis
4. CXR and abdominal ultrasound
5. Age appropriate screening: mammogram, Pap, PSA, colonoscopy
6. Close follow-up
Surgery Elective
Lower Limb Venous Disease
Class: Dr. Powell
June 19, 2014
Peripheral Vascular Disease refers to disease of:

o Arteries
o Veins
o Lymphatics – Less common surgically and often forgotten
The venous tree in the lower limb is very variable. Though there are some constants.
Essentially, there is a deep system and a superficial system
• Normally, blood always from superficial to deep
• And always from caudal to cephalad. (Don’t like to use “distal to proximal” because of the confusion that can be created when referring to
arteries and veins with direction of flow)
• There should be no reflux of either
Superficial venous system: HAVE VALVES

• Dorsal venous arch in foot gives rise to the greater saphenous vein medially and the lesser saphenous vein laterally. Receives from
dorsal metatarsal veins
• Greater saphenous enters common femoral vein at a constant site (Saphenofemoral [SF] junction) after passing through fossa ovalis
• Lesser saphenous enters popliteal vein at a variable site (Saphenopopliteal [SP] junction)
Deep venous system: DOES NOT HAVE VALVES

• Veins from the deep plantar venous arch drain to à medial and lateral plantar veins - drain to à paired posterior tibial veins
• Join with paired peroneal and anterior tibial veins à then enter popliteal veins
• Also have soleal sinuses and gastrocnemius veins
Perforators:
Mnemonic for perforators
Apply to:
• (Medial side)
• (Distal to proximal)
K CBD H
1. Kuster – Ankle perforators

2. Cockett perforators (I, II, III) – Lower leg perforators – These are actually connected to posterior arch vein which enters long saphenous.
So they aren’t actually directly from saphenous
3. Boyd – Gastrocnemius perforators
4. Dodd – Mid-thigh perforators
5. Hunterian
*** Most venous problems affect the medial side (incl. long saphenous vein distribution)
What can cause problems?
1. DVT is a major risk factor. Its not just the existing DVT that causes problems during the time it is present
1
• Look up post-thrombotic (postphlebitic) limb
2. Pressure from intra-abdominal or pelvic masses
• Eg. ***Pregnancy: acts via 3 main factors:

1) Direct compression of iliac veins à caudal venous hypertension
2) Hormonal: Progesterone surge à Relaxation of venous smooth muscle à Passive venous dilatation à Valvular dysfunction.
Also affects collagen. Same collagens in the ligaments that soften to allow passage of fetus through pelvis are in veins
3) Intravascular volume increase
• Other pelvic masses. Tumours etc.
3. Collagen Vascular Disorders
1 Cause of PTS is not entirely clear. Inflammation is thought to play a role as well as damage to the venous valves from the thrombus itself. This
valvular incompetence combined with persistent venous obstruction from thrombus increases the pressure in veins and capillaries. Venous hypertension
induces a rupture of small superficial veins, subcutaneous hemorrhage and an increase of tissue permeability. That is manifested by pain, swelling,
discoloration, and even ulceration.
Wayne Robinson 1
• This is less common
• In this case failure of maturation of collagen
• Haphazard and disordered. This weakens the annular structure especially at leaflets of valves. Cause leaky valves
** Know what happens when there are leaky valves and reflux à varicosities etc.
*** What defines the clinical transition from varicose veins to chronic venous insufficiency (CVI)?
1. Permanent skin changes
2. Ulceration
Basic explanation:
§ Increased pressure in the veins results in the forcing out of fluid because of increased hydrostatic pressure
§ WBCs and RBCs are forced out into interstitial space
§ Initially there is some oedema, some blood etc.
§ WBCs and inflammatory cells then act on these à Breakdown of these cells, including RBCs
§ Haemoglobin release à This is oxidized by inflammatory cells à This causes the darkness
§ Eventually, inflammation and fibrosis à results in scarring à Dark discolouration. Hard, woody subcutaneous space
§ This closes around on capillaries. An intense inflammatory cuff forms. Called “Perivascular cuffing”. This is an end result of the inflammatory
process
§ The skin becomes relatively ischaemic
§ Therefore any minor trauma or denuding may result in failure of skin to heal à Spreading of ulcer
Varicose veins. Some confusion in the nomenclature:
Varicose veins usually refers to 3 things
1. Axial veins – i.e. the great and small saphenous veins represent the largest caliber veins of the superficial venous system.
2. Telangiectasia - Small dilated blood vessels near the surface of the skin
3. Reticular veins - Tiny subcutaneous lines in skin
(2 and 3 are more cosmetic problems)
Surgically à mostly refer to axial veins
Investigation
Clinical tests:
1. Trendelenburg test: NOTE: This specifically tests SF junction ONLY!!!

• Problem with this is that it can’t tell if there are problems both above and below the tourniquet
2. Tourniquet test - sometimes referred to as Modified Trendelenburg.

• This is an addition to the Trendelenburg test where the tourniquet is moved further to detect the level of incompetence
** But we need to identify specifically which perforator or valve is incompetent.

Can do this by:
1. Venogram: Uses contrast

2
2. Duplex ultrasound: - Better test - study of choice
• Has 2 things:
i. Colour doppler: M-mode
ii. Anatomical study: B-mode
• Duplex checks for structure AND flow
• Doppler mode looks at flow
2 Duplex ultrasonography (more commonly but less correctly known as duplex ultrasound) is a form of medical ultrasonography that incorporates
two elements:
• Grayscale Ultrasound to visualize the structure or architecture of the body part. No motion or bloodflow is assessed. This is the way
plaque is directly imaged in a blood vessel, with the reader typically commenting on crossectional narrowing (greater than 70% is typically
considered worthy of treatment).
• Color-doppler Ultrasound to visualize the flow or movement of a structure, typically used to image blood within an artery. Blood flow
velocities increase through a region of narrowing, like a finger pressing up against the end of a running garden hose. Increased velocities
indicate a region of narrowing or resistance (velocities greater than 250 cm/s typically considered worthy of treatment).
Both displays are presented on the same screen ("duplex") to facilitate interpretation.
Wayne Robinson 2
• *** Normally à Should be no reflux with patient performing valsalva maneuver
• Therefore it is incorrect to say duplex doppler. Just say Duplex U/S
This can now direct decisions about management
MANAGEMENT
Most these patients à can start managing conservatively
Non-pharmacological:
1. Elevate leg as often as possible
2. Graded compression stockings

a. 25-28 mmHg usually the highest
b. *** Must ensure patient does not have a concomitant arterial problem. This can limit flow and precipitate limb ischaemia!!
3. Injection sclerotherapy: Doesn’t work for large perforators. Mainly for cosmetic
Pharmacological:
Some drugs
1. Tribenoside (Glyvenol) - Supposed to increase venous tone à Limited effectiveness. Veins don’t have as much smooth muscles. Also used
in haemorrhoids.
Surgical:
• SF ligation or perforator ligation

o If the problem is only superficial eg at SF junction:
• Vein stripping: Strip the entire system removing the superficial vein
o If multiple levels:
• Other alternatives:
• Endovenous laser ablation - uses heat
• Endovenous radiofrequency ablation

o Both involve passing a probe through vein and pulling
o These 2 are very similar
VERY GOOD TO ALSO NOTE:

*** Can actually operate on the venous system. Invariably the problem is if you cut open the deep venous system, the venous blood will clot. Remember
Virchow’s triad
1. There is fairly sluggish blood flow in these systems
2. Injury to the vessel
3. Surgery can cause a hypercoagulable state. (Mainly major surgeries though)
Can still be done

• But must try to circumvent Virchow’s triad
Involves:
• Anticoagulate patient
• Then create a temporary distal AV fistula that will increase the flow in the deep veins to overcome sluggish blood flow
• Then do a procedure to repair the valves microscopically or by grafting from the upper limb
CEAP CLASSIFICATION FOR CHRONIC VENOUS INSUFFICIENCY - ASKED BY DR. HILARY BROWN. Dr Says she likes to ask this for real -
Anggelos
CEAP Classifies varicose veins in 7 stages. It stands for Clinical, Eitiology, Anatomy, Pathophysiology
Clinical = How the patient presents, Etiology = Aquired or congenital, Anatomy = Which vessels are affected, Pathophysiology = Direction of blood flow
(normal or abnormal)
C0 - No varicose veins
C1 - Telangectasia
C2 - C2A: Varicose veins without symptoms, C2B: Varicose veins with symptoms
C3 - Swollen ankle (edema)
C4 - Skin changes due to varicose veins
C5 - Healed ulcer
C6 - Leg ulcer
Wayne Robinson 3
General Surgery
Peripheral Arterial Disease – MUST ALSO DO ACUTE ARTERIAL OCCLUSION – TORONTO ETC.! SEE STARTING PAGE 6 FOR VERY
IMPORTANT IMAGES
Sources: Toronto Notes, Surgical Tutor, Dr. East, Online Sources, Dr. Hilary Brown Lecture, Essential Surgery
February 2015
Definition of peripheral arterial disease: Atherosclerotic disease of the peripheries, anatomically defined in the upper limb as distal to teres major and
in the lower limb as distal to the inguinal ligament
CHRONIC ARTERIAL OCCLUSION/INSUFFICIENCY

AETIOLOGY
§ Predominantly due to atherosclerosis: primarily lower extremities
**COMMON SITES OF PLAQUE FORMATION

1. Superficial femoral artery, esp. in Hunter’s Canal
2. Aortic bifurcation
3. Carotid bifurcation
4. Tibial Vessels
**Dorsalis pedis and peroneal vessels most commonly spared**
RISK FACTORS
§ Major: Smoking, DM (Uncontrolled)
§ Minor: HTN, hyperlipidemia, *family history, *obesity, *sedentary lifestyle
CLINICAL FEATURES
Spectrum from intermittent claudication à Critical limb ischaemia (Rest pain à Gangrene and Ulceration)
A. Intermittent claudication. 3 main characteristics (MUST KNOW)

1. Pain with exertion: Usually in calves or any exercising muscle group
2. Relieved by short rest: 2 to 5 min, and no postural changes necessary
3. Reproducible: Same distance to elicit pain, same location of pain, same amount of rest to relieve pain
GOOD MUST-KNOW POINTS!:

§ The calf is involved first because the superficial femoral artery is most commonly affected with atherosclerosis
§ 5% of claudicants progress to critical ischaemia each year
§ 75% of patients remain stable or show clinical improvement
§ Only 5-10% with claudication will need endovascular or surgical intervention by 5 years for worsening claudication or severe limb ischaemia
§ Some 10% of claudicants have a non-fatal cardiovascular event (either MI or stroke) within 5 years and the 5-year mortality rate is 30% with ¾
being cardiovascular
B. Critical limb ischemia

1. Includes rest pain, night pain, tissue loss (ulceration or gangrene)
2. Ankle systolic pressure < 40 mmHg, toe systolic pressure < 30 mmHg, ABI < 0.40
Pulses maybe absent or present
MUST KNOW: European consensus definition of critical limb ischaemia: “*Persistently recurring rest pain requiring analgesia for more than 2 weeks, or
*ulceration or gangrene affecting the foot, *plus an ankle systolic pressure of less than 50 mmHg”
Examination signs of poor perfusion (KNOW ALL)

Inspection
1. Trophic skin changes: Hair loss, hyperpigmentation
2. Hypertrophic nails
3. Atrophic muscle
4. Venous guttering (collapse of superficial veins of foot)
5. Skin ulcerations and infections (especially on pressure areas: Tips of toes and dorsum of foot)
Palpation and auscultation
6. Cool limb
7. Positive Buerger’s tests (see page 6) [Prolonged pallor with elevation and rubor on dependency]
8. Slow capillary refill
9. Pulses may be diminished or absent at some locations (NB: Dr. H. Brown: 8% of healthy individuals have absent DP, 2% have absent PT)
10. Thrills and bruits may be present
Other manifestations of atherosclerosis: CVD, CAD, impotence, splanchnic ischemia

Leriche’s syndrome: Bilateral gluteal claudication, absent distal pulses, impotence secondary to atherosclerotic occlusion of the internal & external iliac
arteries
INVESTIGATIONS
NON-INVASIVE vs. INVASIVE
A. ROUTINE BLOODWORK, fasting metabolic profile
B. NON-INVASIVE
1. ABI: take HIGHEST BRACHIAL and HIGHEST ANKLE [dorsalis pedis (DP) or posterior tibial (PT)] pressures for EACH SIDE generally
§
ALL claudication pts should have resting ankle systolic pressures measured in clinic to confirm the diagnosis
§
Use a Doppler ultrasound flow detector
§
ABI <0.90 abnormal, rest pain appears at <0.3
§
Procedure explained on image on page 5!!
2. Duplex sonography: Better information as to the significance of stenoses
§ MUST KNOW: Combines greyscale ultrasound imaging (GSUS) and colour Doppler blood flow estimation (hence duplex)
§ GSUS allows estimation of plaque narrowing and colour Doppler allows estimation of flow velocities, which increase in areas of stenosis.
§ Provides a ‘road map’ of atherosclerosis in the arterial tree and are usually performed in a vascular laboratory by specialist
ultrasonographers.
§ It is non-invasive and rarely requires intravenous contrast media. There is substantial user dependency in the results.
3. CTA and MRA:
§ **Excellent for large arteries (aorta, iliac, femoral, popliteal), may have difficulty with tibial arteries (especially in the presence of
disease).
§ Look for inflow, outflow, intaluminal lesions, collaterals
§ **Both require IV injection of nephrotoxic contrast (Iodinated contrast for CT, gadolinium for MR)
C. INVASIVE
1. Conventional arteriography: superior resolution to CTA/MRA, better for tibial arteries, can be done intraoperatively
a. Dr. East: Don’t perform conventional angiography on a claudicant as it won’t affect management! (Mgmt. is non-surgical)
ABI recording Degree of ischaemia

(Dr. H. Brown)
> 1.2 Suspect wall calcification (most common in diabetics)
> 0.91-1.2 Normal/no ischaemia
0.7-0.9 Mild obstruction (Claudication range)
0.4-0.69 Moderate obstruction (Claudication range)
<0.4 Severe obstruction (Possible critical ischemia)
TREATMENT
(A very useful and more detailed explanation of some of these options is at the end of this document after this summary)
FIRST REVIEW AND REMEMBER THESE PRINCIPLES!!!! (THE OPTIONS AVAILABLE DEPEND ON THE SEVERITY OF THE DISEASE AND ARE
A COMMON QUESTION):
A. Mild to moderate claudication

§ No active treatment except advice to stop smoking, exercise regularly, take statin and aspirin, lose weight
§ Balloon angioplasty
B. Disabling claudication
§ Reconstructive arterial surgery
C. Critical ischaemia
§ Intravenous drug therapies such as prostacyclin
§ Lumbar sympathectomy (surgical or by phenol injection)
§ Reconstructive arterial surgery
§ Amputation (below, through or above knee)
§ Palliative care including appropriate analgesia
CONSERVATIVE vs. INVASIVE & OPERATIVE

Conservative may be non-pharmacological or pharmacological
1. NONINVASIVE (NB: Critical limb ischaemia is NOT managed conservatively!!!)

A. Conservative (Non-pharmacological/Lifestyle modification)
1. Risk factor modification (*smoking cessation, *treatment of HTN, *hyperlipidemia (STATINS), *DM)
a. Good point: Smoking cessation aids: Smoking cessation programmes + pharmacological aids such as nicotine replacement therapy,
bupropion and varenicline
2. ***Diet & Exercise program: ***MOA: Improves collateral circulation, oxygen extraction at the muscle level. Weight loss à less muscle effort
§ NOTE WELL: At least 30 minutes, 4-6 times per week! May be as effective as bypass, and more effective than angioplasty!!!!
3. **Foot care (especially in DM): keep wounds clean/dry, avoid trauma and pressure on wounds
4. Burgers exercise - Patient walks to point of claudication and told to continue walking through pain. This encourages collateralization of vessels.
B. Pharmacotherapy
1. Antiplatelet agents (ECASA, clopidogrel or more rarely ticlopidine)
2. Cilostazol (cAMP-phosphodiesterase inhibitor with antiplatelet and vasodilatory effects) – improves walking distance for some patients with
claudication. Superior to pentoxifylline
3. Pentoxifylline – Unimpressive and doubtful effect
4. Lumbar sympathectomy -
NB: Mild to moderate claudication will often improve over 6-18 months with compliance on conservative management!!!
Dr. East: Who are candidates for surgery?

1. Critical ischemia with a lesion amenable to surgical bypass. The others will usually require amputation eventually.
2. KNOW THIS POINT: Surgery should only be considered for intermittent claudication ONLY IF it seriously impairs quality of life. Even this is in
question because a recent study comparing intervention and conventional therapy for claudication showed no benefit for intervention at 1 year.
2. INVASIVE and OPERATIVE

Indications: *Severe lifestyle impairment, *occupational/vocational impairment, *critical ischemia
Surgical options:
1. Endovascular
a. PTA – Percutaneous Transluminal Angioplasty - Balloon angioplasty – Most useful for short occlusions (< 2-10 cm)
or significant stenoses (> 70%). Increases risk of embolization and vessel perforation
§ Restenosis may be an issue secondary to elastic recoil (Dr. H. Brown):
§ Common iliac angioplasty has a 5 year patency rate of approximately 70%
§ Infrainguinal angioplasty has a lower 5 year patency rate
§ Many authors report app 60% 1 year patency rates with SFA/Popliteal Angioplasty
§ But the technology is improving
§ Complications (< 2%): Wound haematoma, acute thrombosis, distal embolization, arterial wall rupture
b. Endoluminal stenting
2. Bypass graft (Anatomic vs. Extra-anatomic – look up)

§ Sites: Aortounifemoral, aortobifemoral, femoropopliteal (“fempop”), distal arterial. Extra-anatomic: axillofemoral (“Axfem”),
femorofemoral
§ Graft choices: Biological (E.g. autogenous (vein) graft) (reversed or in situ) vs. prosthetic/synthetic – PTFE graft or
Dacron®
a. NB: Biological grafts may be autografts or allografts
b. The reversed autogenous saphenous graft is turned inside out during the reversal process. In situ has valves removed
c. Autografts: (native arteries and veins)
d. Allografts: (human umbilical vein)
e. Xenografts: Gluteraldehyde treated bovine grafts
§ NOTE VERY WELL (Dr. H. Brown & Surgical tutor):

1. Autologous vein is best graft material but not always available Best because they decrease risk of 1. infection 2. rejection
2. Native vein/Autogenous OR Prosthetic material are utilized for ABOVE KNEE bypass grafts (70-80% five year patency
rates in appropriately selected patients) BUT
3. Autogenous material should be utilized for BELOW KNEE vessels secondary to far superior patency rates (see next page)
§ 4 Factors to consider: *Inflow, *Outflow (most important), *Conduit (graft), *Patient

Inflow - where graft begins
Outflow - "Run off" where a. Good inflow, poor outflow not reconstructable by bypass because there are no vessels to receive a bypass, regardless of
graft ends site of origin BUT
Conduit - Material choice b. Poor inflow, good outflow correctable by extra-anatomic bypass (i.e. use a different site of origin for the inflow)
§ Reasons for graft failure

a. < 30 days - Technical failure
b. 30 days - 1 year - Neointimal hyperplasia at distal anastomosis
c. > 1 year - Progression of distal disease
§ Complications: Intimal dissection, distal embolization, graft thrombosis. Dr. H Brown: Grafts require regular follow-up looking for
delayed graft failure. 50% of patients develop contralateral critical limb ischaemia
3. Amputation: If not suitable for revascularization, failed reconstructive surgery, persistent serious/life-threatening infections/gangrene
Others:
1. Endarterectomy: Removal of plaque and repair with patch (usually distal aorta or common/profunda femoris)
2. Chemical lumbar sympathectomy: Sympathetic plexus destroyed with EtOH or phenol injection into nerve plexus, may stimulate vasodilation
(rarely effective)
3. Surgical sympathectomy
PROGNOSIS
§ CLAUDICATION: Conservative therapy: 60-80% improve, 20-30% stay the same, 5-10% deteriorate, 5% will require intervention within 5
yr, <4% will require amputation
§ For patients with critical ischemia (rest pain, night pain, ulceration or gangrene): high risk of limb loss
Differentials of Claudication Venous disease (e.g. DVT, varicose veins) Reflex sympathetic dystrophy
Vascular Popliteal entrapment syndrome (e.g.
Atherosclerotic disease Baker’s cyst, tumour) MSK
Vasculitis (e.g. MUST KNOW ABOUT: Osteoarthritis
Buerger’s disease, Takayasu’s arteritis) Neurologic Rheumatoid arthritis/connective tissue
Diabetic neuropathy Neurospinal disease (e.g. spinal stenosis) disease
Remote traum
à DR EAST RE: INVESTIGATION OF PAD
A. Claudicants
§ Risk factor assay (cholesterol, etc.)
§ May do duplex ultrasound mapping but not mandatory. Classical angiography should never be performed on a claudicant – it will make a few
worse and will make none better since claudicants are not treated surgically.
B. Critical Ischemia
§ Risk factor assay
§ ALL patients with critical ischemia who are otherwise fit for surgery should be investigated with a view to performing corrective
surgery if an amenable lesion is found.
§ Non-invasive duplex, CT or MRI angiography are usually performed initially, followed by classical angiography if necessary for clarification.
Classical angiography is justified in critical ischemia because it cannot make the situation worse (the patient will require amputation if
it is not treatable by bypass anyway) but it has the potential to make the situation better if a lesion amenable to surgical correction is
identified.
Complications of classical angiography include hemorrhage, false aneurysm, AV fistula, dissection, thrombosis, embolus, anaphylaxis, renal failure.
à SURGICAL TUTOR: GRAFT PATENCY RATES
Comparative 3-year patency of vein and synthetic grafts

Overall veins have better perfusion rates.
Vein PTFE Veins are always best to use, however if
Above knee anastomosis 85-90% 75-80% there is need for other bypasses such
as a cardiovascular bypass, prosthetic
material maybe best for either below or
Below knee anastomosis 70-75% <50% above knee as the veins would have to be
used for the cardio bypass.
à MUST KNOW!!!: CONVENTIONAL VS. CT ANGIOGRAM (SEE IMAGING NOTES ON THIS)

Toronto Notes:
Conventional angiogram:
1. Invasive
2. Intraarterial approach (Usual approach via femoral puncture – Also brachial, radial)
3. Catheter used
4. 2D imaging data
5. More complications
6. Allows for concomitant interventional procedures
Flush aortography: catheter injection into abdominal aorta, followed by selective arteriography of individual vessels
CT & MR angiogram:
1. Non-invasive
2. Uses IV contrast (no catheterization required)
3. 3D imaging data
4. CT and MR angiography use lower doses of intravenous contrast media so less renal risk
5. CTA accuracy may be decreased by vascular calcification (not MRA)
Major advantages and disadvantages of the principal diagnostic modalities employed for clinical imaging of peripheral vessels
http://www.nature.com/nrcardio/journal/v4/n12/fig_tab/ncpcardio1035_T1.html
Modality Advantages Disadvantages

Contrast-enhanced MRA 3D imaging data set Not feasible in patients with metallic implants or severe
Accuracy not affected by vascular calcification claustrophobia
Relatively safe Reduced accuracy in vascular segments with stents/clips
Good repeatability
Conventional angiography Possibility for concomitant interventional procedures Need for arterial access
Accuracy not affected by vascular calcification Radiation exposure
2D imaging data set
Potentially nephrotoxic contrast agents
CT angiography 3D imaging data set Radiation exposure
High spatial resolution Potentially nephrotoxic contrast agents
Fast image acquisition Reduced accuracy in calcified segments
Duplex ultrasonography Low cost Highly operator dependent
Completely safe Long imaging sessions
Great repeatability Limited feasibility in obese patients
MRA VERSUS INVASIVE ANGIOGRAPHY

Conventional digital subtraction angiography still is the historic standard in the assessment of lower extremity arteries. This invasive modality exposes
patients to radiation, uses iodinated, potentially nephrotoxic, contrast agents and has a complication rate of approximately 1%. Compared with
conventional angiography, multiple studies have shown that CE-MRA has sensitivity and specificity greater than 95% in the detection of significant
peripheral stenoses. The diagnostic accuracy of CE-MRA is thus at least comparable with and perhaps superior to conventional angiography, when
considering that traditional x-ray angiography is somewhat of a flawed standard. The superiority of CE-MRA is evident, especially for imaging the distal
vessels around the ankle and in the foot; studies have consistently demonstrated that CE-MRA is able to identify more run-off vessels than conventional
invasive angiography in this area. Hence, in a number of centers in which CE-MRA is available, this modality has replaced invasive angiography as the
initial imaging test in PAD evaluation
à VERY GOOD ADDITIONAL MANAGEMENT INFORMATION
TECHNIQUES OF REVASCULARISATION FOR CHRONIC ARTERIAL INSUFFICIENCY
PERCUTANEOUS TRANSLUMINAL ANGIOPLASTY (PTA)

§ PTA involves cannulating an artery (usually the common femoral but occasionally the brachial), introducing a guidewire into this remote artery
and advancing it to lie across the stenosis. A balloon catheter is passed over the wire and into position and the balloon inflated to a high
pressure (5–15 atmospheres), crushing the atheroma into the arterial wall to relieve the obstruction. Success is very operator-dependent and
also depends upon the site, length and nature of the diseased artery
ARTERIAL RECONSTRUCTIVE SURGERY

§ Arterial reconstructive surgery began in the 1950s with open removal of atheromatous plaques and thrombus from the aorta and iliac arteries.
This is known as thromboendarterectomy, and is technically difficult, bloody and time-consuming. It has been replaced by bypass grafting,
except for carotid endarterectomy, which remains the standard operation for stenosis and for isolated common femoral artery occlusions.
§ Arterial bypass grafting was first developed during the Korean War to treat arterial trauma, using homografts from human cadavers. The initial
results were excellent but grafts eventually suffered from aneurysmal dilatation and rupture. This led to the introduction of synthetic graft
materials for large arteries, now available in a variety of shapes, sizes and types of cloth. Knitted polyester (Dacron) is the most popular and is
the standard material for aorto-iliac obstruction.
§ Many grafts are now sealed with gelatin or other proteins to minimize porosity. For smaller arteries, autogenous long saphenous vein from the
leg is the best conduit
§ Vein is also inherently resistant to infection, a useful attribute when treating infected lower limb wounds and ulcers.
§ The most common procedures are synthetic ‘trouser’ grafting for aorto-iliac (supra-inguinal) disease and femoropopliteal grafting using
saphenous vein, for infra-inguinal disease
Aorto-iliac disease
§ GOOD INFO: The usual surgical procedure is a Dacron trouser or ‘Y’ graft, anastomosed to the side of the aorta below the renal arteries
and to both common femorals below the inguinal ligament (aorto-bifemoral graft). This is a major operation, needing a laparotomy to access
and cross-clamp the aorta and carries a mortality risk of about 5%. In patients with critical ischaemia but poor physiological reserve, legs can
be revascularized using extra-anatomic synthetic grafts with a lower operative risk. Examples include a cross-over graft to supply blood from
one femoral artery to the other or an axillo-bifemoral graft, supplying blood from one axillary artery to both femorals, tunnelling the graft
subcutaneously along the lateral chest and abdominal wall.
Femoro-popliteal disease
§ The superficial femoral artery is the most commonly obstructed peripheral artery. If PTA is unsuitable, femoro-popliteal bypass grafting is
employed using an autogenous vein graft. The long (great) saphenous vein (LSV) is dissected from groin to knee, its tributaries ligated and
then reversed proximal to distal so the valves do not obstruct flow. An end-to-side anastomosis is performed at each end. If the LSV is
unsuitable (i.e. diseased, small diameter or previously removed for CABG), the LSV from the other leg or veins from the arm can be used. An
alternative technique leaves the vein in situ and destroys the valves with a valvulotome. As the vein tapers from proximal to distal, this allows
bypasses to tibial, dorsalis pedis artery or smaller foot arteries for distal disease.
§ Synthetic materials (e.g. PTFE or Dacron) are much less satisfactory; these have lower long-term patency, particularly when crossing the knee
joint, and are more prone to infection
OTHER THERAPIES FOR ARTERIAL INSUFFICIENCY
Sympathectomy
§ Blood flow in the skin (but not muscle) is controlled by the sympathetic nervous system. Thus, early rest pain affecting the skin may sometimes
be relieved by sympathetic blockade even if the overall arterial supply is inadequate. It is not beneficial in claudication.
§ Sympathectomy can be performed by excision of part of the lumbar sympathetic chain or, more commonly, by translumbar injection of 6%
aqueous phenol. Chemical sympathectomy is performed under local anaesthesia with radiographic control. Only about 15% of patients obtain
sufficient relief to avoid reconstructive operation or amputation and there is no way of selecting those likely to benefit;
USEFUL IMAGES
ABPI (Harold Ellis + Essential Surgery):
Ankle brachial pressure index (ABPI): The ABPI should be measured IN EACH LEG as part of the routine examination. A Doppler probe is held over the
brachial artery and a blood pressure cuff inflated to occlude the blood flow. As the blood pressure cuff is deflated, a Doppler signal reappears and a
systolic pressure can be recorded. Similar pressure readings are taken from the dorsalis pedis and posterior tibial arteries with a cuff just above the
ankle. The ABPI is the ratio of pressure at the foot pulse to that at the brachial artery. Values less than 0.4 indicate significant (‘critical’) ischaemia.
Heavily calcified vessels, as are common in patients with diabetes, may be incompressible and give false high readings.
All claudication patients should have resting ankle systolic pressures measured in clinic to confirm the diagnosis, plus a full blood count to exclude
polycythaemia and thrombocythaemia. Pressure is measured using a Doppler ultrasound flow detector. Normal pressure is slightly above brachial
systolic whilst patients with claudication usually range between 50 and 120 mmHg.
Values may be spuriously elevated in patients with diabetes owing to calcification in the arterial media which prevents cuff compression.
Buerger's test is used to assess the adequacy of the arterial supply to the leg. It is performed in two stages.
With the patient supine, elevate both legs to an angle of 45 degrees and hold for one to two minutes. Observe the
color of the feet. Pallor indicates ischaemia. It occurs when the peripheral arterial pressure is inadequate to
overcome the effects of gravity. The poorer the arterial supply, the less the angle to which the legs have to be raised
for them to become pale.
Then sit the patient up and ask them to hang their legs down over the side of the bed at an angle of 90 degrees.
Gravity aids blood flow and colour returns in the ischaemic leg. The skin at first becomes blue, as blood is
deoxygenated in its passage through the ischaemic tissue, and then red, due to reactive hyperaemia from post-
hypoxic vasodilatation.
Both legs are examined simultaneously as the changes are most obvious when one leg has a normal circulation.
General Surgery
Leg Ulcers
Sources: BMJ, Harold Ellis, various
February 2015
Major causes of leg ulcers (ALL THESE ARE DIFFERENTIALS FOR THE OSCE): MUST KNOW THIS
1. Arterial (ischaemic) ulcers
2. Venous ulcers (most common!!)
3. Neuropathic ulcers (esp. diabetic foot)
4. Sickle cell disease (get mechanism)
5. Malignant ulcer (SCC often arising in a pre-existing chronic ulcer (e.g. Marjolin’s Ulcer))
6. Ulcer complicating systemic disease (e.g. UC, RA)
FEATURES OF VENOUS AND ARTERIAL ULCERS

MUST READ PAD AND VENOUS DISEASE NOTES IN CONJUNCTION WITH THIS SUMMARY
• Systematic examination of limb: Inspection, palpation, ± auscultation (for bruits)

• Describe from outside in: Limb itself (quickly). Then wound edge à wound bed à exudate/oedema. Surrounding skin changes
• Palpation: Temperature of surrounding skin, peripheral pulses (from distal to proximal), capillary refill, pitting oedema
ARTERIAL VENOUS
(Most common leg ulcer ~70-90%)
History suggestive of peripheral arterial disease, intermittent claudication, Venous ulceration usually due to DEEP VEIN incompetence and venous
and/or rest pain. HTN. Can also be due to SUPERFICIAL VEIN incompetence!
Major risk factors: HTN, DM, hyperlipidaemia, smoking, obesity History of varicose veins, DVT (or a cause of DVT i.e. Virchow’s triad),
venous insufficiency or venous incompetence. History of thrombophlebitis
ULCER APPEARANCE ULCER APPEARANCE
Classic site: Pressure points. Usually over toes, foot, ankle (lateral Classic site: Medial gaiter region of leg (just above medial malleolus)
Medial = Long Saphenous V. Problem at the Sapheno-Femoral junction
malleolus usually) Lateral = Short Saphenous V. Problem at the Sapheno-Popliteal junction
Edge: Sloping and irregular
Edge: “Punched out” – sometimes very deep
Unhealthy appearance Wound bed: Often covered with slough at the base and healthy
granulation tissue. Depth: Superficial
Wound bed: Often covered with varying degrees of slough and necrotic
tissue. Depth: Deep Exudate level: Usually high
Exudate level: Usually LOW (Unless infected!) Oedema: Common (venous HTN/increased hydrostatic pressure)
Oedema: Uncommon Pain: Moderately painful or no pain at all. More aching. Unless infected
Pain: Extremely painful, even without infection Associated features:

Pain lessens with “dependency” (Eg. hanging foot off bed), increased with § Must describe obvious varicose veins! (DON’T FORGET TO LOOK
leg elevation FOR AND COMMENT ON THES IN EXAM)
Associated features: § Hyperpigmentation: Brown due to haemosiderosis

§ TROPHIC CHANGES!!! Gangrene may be present
§ Skin is PALE, SHINY, TAUT, LITTLE OR NO HAIR, hypertrophic nails § Venous eczema/stasis dermatitis: Erythematous, scaling, itching –
scratching predisposes to ulcer formation
§ Cold skin
§ Atrophie blanche: Previous scarring appearing as a white rim around
§ Distal pulses absent (examine pulses proximal to distal) ulcer edge
§ Capillary refill delayed § Lipodermatosclerosis: Inflammation and fibrin exudation result in thick
fibrous tissue replacing the normal soft subcutaneous tissue
Would like to perform Doppler/ABI as part of your clinical
examination MARJOLIN’S ULCER – Squamous cell carcinoma developing in the edge
of a longstanding ulcer
Others:
§ Buerger’s test: Pallor on elevation, rubor on dependency Treatment summary: Compression is mainstay
§ Venous guttering + delayed venous filling
§ Bed rest with foot of bed elevated (abolishes high venous pressure)
Treatment summary (READ PAD NOTES): à Heals ulcers fairly quickly provided kept clean
1. Rest, no elevation, no compression! However, this simple treatment is often impractical as most patients elderly and many
2. Moist wound dressing +/- topical or systemic antibiotics other complications associated with prolonged recumbency
3. Debridement of necrotic tissue Not economically feasible in younger patients
AND Appropriate REVASCULARIZATION surgery for arterial insufficiency: Other options:

1. Vascular surgical consultation § Elastic graded compression stockings (30 mmHg)
2. Balloon angioplasty § Moist wound dressings
3. Stent § Other zinc-oxide wraps,
4. Bypass Graft (Saphenous vein vs. synthetic (Dacron/PTFE)), § Split-thickness skin grafts
(Anatomic vs. extra-anatomic)
5. Amputation
*Antibiotics only administered if grossly infected with surrounding cellulitis.
Also modify risk factors and treat underlying conditions *Avoid topical!!! (sensitivity reaction is high)
*Debridement if necessary
Surgical
If conservative measures fail, or if recurrent/large ulcers

Surgical ligation of perforators in region of ulcer, (GSV/LSV ligation and
stripping)
All chronic ulcers require vascular studies and a vascular consult.
NEUROPATHIC ULCERS
MUST SEE DR. POWELL NOTES ON DIABETIC FOOT
Cause
Main cause is loss of sensation in tissues allowing unrecognized trauma to occur
Only indirectly caused by ischaemia
Usually: Deep, penetrating

Occur over pressure points
Surrounding tissues usually healthy and have circulation
Features
Painless ulcer
Painless surrounding tissue. Associated paraethesias
Surrounding tissue may have normal blood supply. But decreased pulses likely (DM foot usually associated with arterial disease)
Can easily be mistaken for ischaemic ulcers. Also irregular or “punched out” or deep. Superficial/deep
Therefore neurological exam important
ABI is inaccurately high – due to the arteriolosclerosis associated with diabetes
Causes:
1. Diabetes
2. Leprosy
3. Syringomyelia
NB: Neuropathic ulcers may occur with ischaemic ulcers
§ History – Numbness, paraesthaesias. Loss of sensation in foot. DM

§ Location – Sites of pressure (E.g. metatarsal heads, heals, toes)
§ Edges – Surrounding callus
Treatment:
General principles of management of DM foot
MUST Do 5 things for patient – *** standard answer at UWI:
1. Resuscitation: Control fluid and electrolyte status

2. Control glucose – Glycaemic control
3. Control local sepsis- dressings, amputation, debridement
4. Control systemic sepsis- IV antibiotics
5. Rehabilitate/educate (wound care, foot care etc.)
Complete management must assess and treat peripheral arterial disease as well – revascularization if necessary
General Surgery
Chronic Leg Ulcer
Sources: Power Point by Dr Chris Valentine
Chronic Ulcer
Ulcer is a breakdown of skin and epithelium
Ulcer that is present for >6 weeks or keeps reoccurring
Classification of Leg Ulcers
CHRONIC LEG ULCERS

Vascular Non-Vascular
1. Venous 1. Infectious
a. Venous Insufficiency, a. Bacterial (Syphilis, TB)
Varicose Veins, Post- b. Fungi
sclerosis 2. Traumatic
2. Arterial a. Decubitus
a. PAD, Raynaud’s Syndrome, b. Radiation
Vasculitis, Burger’s Disease 3. Hematological
3. Lymphatic a. Sickle Cell
b. Thalassemia
4. Neoplastic
a. BCC (Basal Cell Carcinoma)
b. SCC (Squamous Cell Carcinoma) e.g
Marjolin’s Ulcer
5. Drugs
a. Steroids
b. Chemotherapy
6. Metabolic
a. DM
b. Gout
7. Systemic
a. SLE
b. Rheumatoid
Chronic Leg Ulcers occur due to an interruption in the INFLAMMATORY AND

PROLIFERATIVE PHASE
There are 3 phases in wound healing:
Inflammatory phase
Vasoconstriction and formation of platelet plug for hemostasis. Release of cytokines
and inflammatory cells such as macrophages and neutrophils. The classic signs of
inflammation occur: Pain, Redness, Swelling, Warm, Loss of Function.
Proliferative phase
Granulation tissue formation using collagen and new blood vessel formation
(angiogenesis). Healthy granulation tissue is pink/red while dark granulation tissue
signifies low perfusion. Epithelial cells resurface for epithelization.
Maturation phase
Occurs once the wound is closed. Remodeling of collagen from type III to type I
and decrease of blood vessels from the area
Inhibitors to ulcer healing are either:

Local
Infection
Tissue hypoxia
Trauma
Necrosis and debris
Systemic
Sickle Cell
Diabetes Mellitus
Nutrition
Immunocompromised
Drugs (Chemo, Steroid)
General Surgery
Lower Limb Amputations
Source: Online, Essential Surgery 5E, Medscape
February 2015
NB: VERY IMPORTANT INFORMATION/EXPLANATION AT THE END OF THIS LIST
The indications for amputation are most easily remembered as the three Ds: dead (or dying), dangerous and damned nuisance.
1. Dead or dying: Peripheral vascular disease accounts for almost 90% of all amputations. Other causes of tissue death are
severe trauma and burns (fourth degree)
2. Dangerous: 'Dangerous' disorders are malignant tumours, potentially lethal sepsis and crush injury. In crush injury, releasing
the compression may result in renal failure (the crush syndrome).
3. Damned nuisance: Retaining the limb may be worse than having no limb at all - because of pain, gross malformation,
recurrent sepsis or severe loss of function.
Types of Lower Extremity Amputation and Considerations

Organized by anatomical location; distal to proximal
1. Toe Amputation:
§ Phalangeal or partial toe amputation involves excision of any part of one or more of the toes.
§ Common, account for 24% of DM amputations.
§ Prosthesis is not usually necessary.
§ Patients’ may have weight-bearing restrictions, the Physical Therapist needs to clarify with surgical team.
§ In dysvascular cases where neither pain nor infection is a concern, auto-amputation can be awaited
2. Toe Disarticulation (Transphalangeal Amputation):

§ Amputation done at the metatarsophalangeal joint
§ May result in biomechanical deficiencies:
§ Amputation of great toe affects push-off during fast gait and running, and may result in a non-propulsive gait pattern.
§ If the base of the proximal phalanx with the insertion of the flexor hallucis brevis is saved, stability is enhanced.
§ Second-digit amputation results in severe hallux valgus.
3. **Ray Amputation Also known as Wedge Amputation

§ Toe and a variable portion of its metatarsal are excised.
4. Transmetatarsal Amputation (TMA):

§ Foot amputation in which a dorsal incision is made through the mid- to proximal metatarsal shafts, and a long, thick
myocutaneous plantar flap including the flexor tendons is used, with closure of this flap onto the dorsum of the foot.
§ There are approximately 10,000 TMA’s performed each year in the U.S.
§ Patients’ may have weight-bearing restrictions. The Physical Therapist needs to clarify these restrictions with the surgical
team.
§ Once incision is healed and the patient is ambulatory, they may require a prosthetic orthosis (rocker-bottom sole and a
polypropylene ankle-foot orthosis (AFO) to offset increased weight-bearing load on remaining tissues.
5. Metatarsal Disarticulation (**Lisfranc Amputation):

§ Performed at the tarsometatarsal joint and involves disarticulation of all five metatarsals and digits.
§ Uncommon
§ Often result in an equinus and varus deformity due to the pull of the plantarflexors and loss of dorsiflexor and peroneal
muscles.
6. Midtarsal Disarticulation (**Chopart Amputation):

§ At the talonavicular and calcaneocuboid joints, it involves disarticulation through the midtarsal joint leaving only the
calcaneus and talus.
§ Uncommon
§ Often result in an equinus and varus deformity due to the pull of the plantarflexors and loss of dorsiflexor and peroneal
muscles.
§ For Lisfrac, Chopart and transphalangeal amputations, orthotic shoe fillers or shoe modifications may be used, such as a
spring-steel shank extending to the metatarsal heads, and a rocker sole or padding to the tongue of the shoe to assist in
holding the hindfoot firmly in the shoe.
7. Ankle disarticulation (**Syme Amputation):

§ Ankle disarticulation in which the heel pad is kept for good weight-bearing.
§ Thick heel pad can allow direct weight-bearing.
§ Post-operative complications may include an unstable heel flap, development of neuroma of the posterior tibial nerve, and
poor cosmesis.
§ Patients are typically kept non-weight-bearing (NWB) immediately post-op.
§ Uncommon
8. Transtibial Amputation (*BKA):

§ Very short transtibial amputation occurs when less than 20% of tibial length is preserved.
§ May result from trauma, and not usually an elective procedure.
§ Results in small-moment arm, making knee extension difficult.
§ Standard Transtibial Amputation occurs when between 20% and 50% of tibial length is preserved.
§ At least 8cm of tibia is required below the knee joint for optimal fitting of a prosthesis.
§ Long Transtibial Amputation occurs when more than 50% of tibial length is preserved.
§ Usually not advised due to poor blood supply to the distal leg.
§ Long posterior flap is normally used because of good vascularization and it provides an excellent weight-bearing surface.
§ Fibula is usually transected 1-2cm shorter than the tibia to avoid distal fibula pain.
§ Transtibial amputations have been reported to account for 27.6% of dysvascular amputations performed in the U.S.2.
9. Knee Disarticulation (Through-Knee Amputation or TKA): (**Gritti-Stokes Amputation)

§ Old and anatomic procedure which does not require surgically cutting through bone or muscular bellies.
§ Offers good weight distribution and retains a long, powerful femoral lever arm.
§ Yields a non-cosmetic socket due to need for an external joint mechanism and resultant difficult swing-phase control.
§ Often performed on patients who will not become a prosthetic walker, or in growing children to maintain femoral length.
10. Supracondylar Amputation:

§ Surgical procedure in which the patella is left for better end weight-bearing.
§ Area between the end of the femur and patella may delay healing.
11. Transfemoral Amputation (AKA):

§ Short transfemoral amputations occur when less than 35% of the femoral length is present.
§ Uncommon
§ Medium transfemoral amputations occur when between 35% and 60% of femoral lengthis preserved.
§ In general, the residual limb must be at least 4 to 6 inches in length from the groin to fit a prosthesis
§ Ideally, amputations should be at least 4 inches (10cm) above the lower end of the femur to allow room for the prosthetic
knee.
§ Normally, anterior and posterior muscular surfaces are well vascularized, so equal flaps are used.
§ Long transfemoral amputations occur when more than 60% of femoral length is present.
§ Transfemoral amputations have been reported to account for 25.8% of dysvascular amputations performed in the U.S
The sciatic nerve is cut shorter than normal so that there is no pain on pressure
12. Hip Disarticulation:
§ Involves loss of all the femur
§ Uncommon
§ Usually done in cases of malignant tumors, extensive gangrene, massive trauma, or advanced infection.
13. Hemipelvectomy:
§ Involves loss of any part of the ilium, ischium, and pubis.
§ Uncommon
§ Can be internal, in which the limb is salvaged, or external, in which the limb is removed.
§ External hemipelvectomy may also be referred to as a transpelvic amputation.
§ Usually done in cases of malignant tumors, extensive gangrene, massive trauma, or advanced infection.
14. LOOK UP “HIND-QUARTER” AMPUTATION

Removal of the leg plus pelvis. It is a type of hemipelvectomy = External Hemipelvectomy
COMPLICATIONS Late
Early
1. Hematomas Hemorrhage Pain
2. Infections Hematoma Ulcers
3. Necrosis Dehiscence Neuroma
4. Neuromas Infection Phantom sensation
5. Phantom sensations Gangrene Unresolved infection
6. Deep venous thrombosis DVT Contractures
7. Terminal overgrowth
8. Bony spurs
9. Contractures
FOLLOWING FROM ESSENTIAL SURGERY, Fifth Edition (Must read):
Strenuous efforts should be made to preserve ischaemic limbs by reconstructive surgery or interventional radiology. This is because the
functional results of successful revascularisation are far better than even the best major amputation
However, amputation cannot be avoided in patients where revascularisation is technically impossible (particularly in diffuse distal
arterial disease), or if there is substantial tissue necrosis and a functionally useless foot, or deep spreading infection.
Two principles guide the level of amputation:
1. The amputation must be made through healthy tissue. If not, there is a high risk of wound breakdown and chronic ulceration,
requiring further amputation at a higher level. When amputation is for (uncorrected) peripheral ischaemia, it is almost always
necessary to amputate at mid-tibial level or above to ensure healing
2. The choice of amputation level must take into account the fitting of a prosthetic limb. For this purpose, the mid-tibia (below-
knee) and lower femoral levels (above-knee) are preferred. If the knee joint can be saved, the functional success of a
prosthesis is much better. With improved prostheses, through-knee amputation is possible but healing rates are poor; most
surgeons and prosthetists prefer above-knee to through-knee amputation as it has a better healing rate and easier prosthetics
The traditional ‘guillotine’ amputation of the battlefield simply sliced off the limb, leaving the wound to heal by secondary intention. This
reduced the risk of fatal gas gangrene or tetanus but the outcome for fitting a prosthetic limb was poor. There have been huge
developments in amputation techniques in recent decades, particularly in the use of myoplastic flaps. For below-knee amputations, a
long posterior flap of muscle and skin is wrapped forward over the amputated bone and sutured in place. This results in more reliable
healing and a suitably shaped and cushioned stump. A variation, the Robinson ‘skew flap’, uses a long posterior muscle flap but equal
skin flaps.
With these techniques and in experienced hands, 70% or more of below-knee amputations for ischaemia will eventually heal even
without revascularization, preserving the knee joint and allowing reasonable walking. Modern below-knee prostheses are modular in
construction and weight is borne mainly on the patellar tendon
DON’T NECESSARILY HAVE TO READ THIS. CAN IF YOU HAVE TIME

MEDSCAPE COMPLICATIONS (CUT THESE DOWN TO POINT FORM AND REMOVE THE UNNECESSARY INFORMATION)
Common complications include wound breakdown and skin problems, swelling, edema, joint contractures, pain, and phantom
limb sensation.
1. Wound healing in the patient with vascular disease can be severely compromised by the patient's underlying disease or
skin closure under tension.
2. Folliculitis of the residual limb can be avoided by not shaving. When folliculitis is present, it can be treated with oral
antibiotics. Similarly, hidradenitis should be managed with appropriate hygiene and occasional oral antibiotics.
3. Postoperative edema may occur and further compromise wound healing. This problem can be minimized by performing
medullary canal closure and myoplasty. Postoperative bulbous swelling of the distal residual extremity is due to tight
proximal dressings. This may lead to congestion and subsequent wound and prosthetic-fitting difficulties.
4. Joint contractures of the hip or knee may occur at the time of surgery or postoperatively from lack of activity and
prolonged sitting or wheelchair ambulation
5. In patients who have undergone transtibial and transfemoral amputations, prolonged sitting with the hip and knee flexed
should be avoided. Patients who have undergone transfemoral amputations should be instructed to lie in the prone
position multiple times during the day to stretch the hip musculature.
6. The sensation that the amputated limb is still present is known as phantom limb sensation, and this occurs in nearly all
patients who undergo amputations. These sensations tend to gradually decrease over time. Phantom limb pain is
described as a painful burning sensation in the amputated limb, and it is more common than previously thought.
Contributing causes of residual limb pain include neuromas at the level of the amputation, which become adherent to
skin, muscle, and bone. This can lead to direct nerve-end stimulation or pain from traction with extremity motion.
Continuous pulsatile arterial stimulation of the nerve occurs when the neurovascular structures are ligated together.
a. Noninvasive treatment modalities may be tried initially and include desensitization therapy, progressive and
continued prosthetic wear, intermittent compression, medications, transcutaneous nerve stimulation, or a trial of
proximal nerve blocks. Reconstructive surgery is often necessary to remove the neuromas and place them in
an area free of scarring and adhesions and to reorganize the tissues to the most anatomic position possible
through osteomyoplasty
Surgery Elective
Diabetic Foot
Class: Dr. L. Powell
June 5, 2014
- Should read more thoroughly -
Very small topic but very important and has specific details to know.
Major cause of non-traumatic amputation in Caribbean is diabetic foot.
MUST know:
3 major contributing factors:
NEUROPATHY (S, M, A) + VASCULOPATHY + IMMUNOPATHY
1. Neuropathy
Pathophysiology of the neurological deficit. 2 causes:
i. Vascular component: Vasa nervorum affected. This Affects all 3 arms of the nervous system
Vasa nervorum are small arteries that provide blood supply to peripheral nerves
ii. Also nerves are directly affected through AGEp buildup and sorbitol pathway
• Sensory neuropathy
o Glove and stocking distribution sensory impairment
o Specifically, patient cannot detect injury
• Motor neuropathy
o Motor impairment à deformities of the feet à
o Abnormal pressure points (Eventually, Charcot’s joints)
o **Also flexor tendons become more active than extensors and thus creates more pressure at toes, etc.
• Autonomic
o Leads to decreased sweating and sebum production à drying and fissuring of skin à Nidus for
bacteria
2. Vasculopathy
• Both atherosclerosis and arteriolosclerosis implicated
• Large and medium-sized vessels: Atherosclerosis is primarily a disease of large and medium sized vessels.
Meaning aorta and iliacs.
• Smaller vessels: For the smaller vessels it is the arteriolosclerosis from diabetes not atherosclerosis that causes
the vasculopathy.
*** Common question at UWI: At Hunter’s canal (in adductor magnus), the turbulence is due to the change in direction
of the vessel. It isn't due to any bifurcation unlike at most sites atherosclerosis affects e.g. popliteal trifurcation.
Eddy currents – Look up

§ Sites of atherosclerosis predilection occur in areas of low shear or eddy currents characterized by slow, oscillating (back-and-forth) flow.
3. Immunopathy
Lazy leucocyte syndrome - Look up – has to do with AGEp deposition and abnormalities in actin or actin-myosin
complex causing impaired chemotaxis. (He described cells as having muscles (actin) and using them to move)
Online sources:
Lazy leukocyte syndrome a syndrome in children, marked by recurrent low-grade infections with a defect in neutrophil chemotaxis and deficient
random mobility of neutrophils.
The lazy leukocyte syndrome was first described by Miller et al. in 1971 in two children with recurrent infection. They had normal humoral and cellular
immunity with a neutropenia, but adequate numbers of neutrophils in the bone marrow. Intracellular killing and phagocytosis were intact, the defect being
in the mobilization of functionally normal neutrophils in response to chemical and inflammatory stimuli.
General principles of management of DM foot
MUST Do 5 things for patient – *** standard answer at UWI:
1. Resuscitation: Control fluid and electrolyte status

2. Control glucose – Glycaemic control
3. Control local sepsis – dressings, debridement, amputation
4. Control systemic sepsis – IV antibiotics
5. Rehabilitate/educate
6. **Complete management must assess and treat peripheral arterial disease as well – revascularization if necessary
MUST READ THIS AS WELL: DIABETIC FOOT (FROM ESSENTIAL SURGERY 5E):
Treatment should be delivered by a multidisciplinary diabetic team (vascular surgeon, diabetologist, podiatrist, orthopaedic surgeon and
orthotist)
RE: CONTROL OF INFECTION

§ After excluding ischaemia, control of infection is the first priority in managing the diabetic foot. EVEN MINOR FOOT LESIONS must always be
taken seriously and treated early with oral antibiotics (including cover for anaerobes) and frequent local cleansing and dressing.
§ If there is any sign of spreading infection or systemic involvement (i.e. pyrexia, tachycardia or loss of diabetic control), the patient
should be admitted to hospital for intensive treatment including parenteral antibiotics, elevation, excision of necrotic tissue and
attention to blood glucose control.
§ Pus in superficial or deep tissues is a medical emergency and requires immediate drainage. This is difficult to diagnose clinically and
foot imaging with MRI is required. Specialist management of blood sugar is often required as it is often grossly elevated.
RE: REMOVAL OF NECROTIC TISSUE

§ Surgery may involve anything from simple desloughing of an ulcer to major amputation. If performed correctly, these result in complete
and rapid healing
§ Before debridement, arterial inflow must be assessed and the foot revascularised if necessary before debridement or digital amputation
to maximise the chances of wound healing.
§ Osteomyelitis occurs in up to 20% with a diabetes-related foot ulcer. Diagnosis is made clinically if an ulcer can be probed down to bone
or else radiologically (plain X-ray or MRI).
o Treatment consists of long-term antibiotics (often parenteral), with a success rate of around 80%, or surgical excision
ADD TO PATHOPHYSIOLOGY OF DIABETIC FOOT IN POWELL NOTES (IMMUNOLOGICAL PART)
§ Impaired intermediary tissue metabolism and a glucose-rich tissue environment. Both of these favour bacterial growth and spreading infection
§ Identifying the causes of diabetic foot problems: Most diabetic foot problems can be identified as primarily neuropathic or primarily
atherosclerotic but some have elements of both. The term ‘neuro-ischaemic’ foot is sometimes used but is not clinically precise.
Typically, the neuropathic foot is painless, red and warm with strong pulses, whereas the atherosclerotic foot without neuropathy is pale,
painful, cold and pulseless. However, when both occur together, the diabetic trap is that the limb can be seriously ischaemic yet
painless, warm and pink.
§ In diabetics with new foot ulcers, 90% have peripheral neuropathy (compared with 20% in a diabetic control group), whereas only 14% have
peripheral arterial disease compared with 10% in controls (Miami 1983–4)
§ Painless, deeply penetrating ulcers. These usually develop in pressure areas caused by distortion of foot morphology, often beneath the first or
fifth metatarsal head. The infecting organism is usually Staphylococcus aureus. Infection and necrosis spread through the plantar spaces
and along tendon sheaths. Infection and local venous thrombosis appear to be the predominant factors causing tissue destruction
§ Extensive spreading skin necrosis originating in an ulcer and caused by superficial or deep infection. This develops very rapidly and
spreads proximally, threatening limb and life
General Surgery WATCH THIS 1st: https://www.youtube.com/watch?v=Hw8OrU9rgfs
Lymphoedema
February 2015
DEFINITION
§ Obstruction of lymphatic drainage resulting in edema with high protein content. Characterized by excessive accumulation of interstitial fluid
AETIOLOGY
Due to 1. inherited abnormalities, 2. obliteration by disease or 3. operative removal
A. Primary (Congenital):
(There are 2 autosomal dominant inherited forms of lymphoedema)
1. Type 1: Milroy’s disease (congenital hereditary lymphedema) – Very uncommon. Mutation in a gene that encodes for VEGF-3, which is
involved in lymphangiogenesis. Characterized by onset soon after birth
2. Type 2: Meige’s syndrome – Characterized by lymphoedema that is particularly severe below the waist. Divided into lymphoedema
praecox (which develops between puberty and age 35) and lymphoedema tarda (which develops later in life)
Meige's Syndrome is a Triad of BAP = Benign ovarian tumor, Ascites, Pleural effusion
§ [There are 3 principal pathologic processes affecting the lymphatic channels in congenital lymphoedema: Aplasia, hypoplasia and varicose
dilatation (megalymphatics)
B. Secondary (Acquired):
1. Infection: Filariasis (#1 cause worldwide). Filaria bancrofti infects lymphatics à Chronic inflammation à lymphatic obstruction à gross
lymphoedema, especially of lower limbs and genitalia (often called elephantiasis)
2. Post-inflammatory: The result of fibrosis obliterating the lymphatics following repeated attacks of streptococcal cellulitis
3. Malignant infiltration: Axillary, groin or intrapelvic. Late oedema of the arm after axillary clearance and radical mastectomy is often
indicative of massive recurrence of tumour in the axilla occluding the residual lymphatic pathway
4. Radiation (“Post-irradiation fibrosis”)/surgery (extensive axillary, groin, neck lymph node removal): #1 cause in North America
CLINICAL FEATURES
§ Classically non-pitting edema (but see below)
§ Impaired limb mobility, discomfort/pain, psychological distress
INVESTIGATIONS
1. Lymphoscintigraphy involves injecting a radiolabelled protein subcutaneously and monitoring its movement through the lymphatics. It will
confirm lymphatic obstruction.
2. MRI may be used to confirm the cause of obstruction in secondary cases.
DDX
The diagnosis of lymphoedema depends first of all on the exclusion of other causes of oedema, for instance venous obstruction, cardiac failure or renal
disease, and, second, on demonstration of one of the causes mentioned above. It was previously taught that lymphoedema could readily be
differentiated from other forms of oedema on the simple physical sign of absence of pitting in the lymphoedematous limb. However, lymphoedema of
acute onset will initially pit on pressure, although it is true that, when it becomes chronic; the subcutaneous tissues become indurated from fibrous tissue
replacement, and pitting will not then occur. However, oedema of any nature, if chronic, will have this characteristic.
SEE MY DIFFERENTIAL LIST FOR LEG SWELLING IN MEDICINE FOLDER
TREATMENT Pathophysiology (Simple)
Blood flows from the heart through arteries --> arterioles --> capillary
1. Avoid limb injury (can precipitate or worsen lymphedema) bed --> venules --> veins and back to the heart.
2. Skin hygiene The pressure in the arterial system is higher than the pressure in the
a. Daily skin care with moisturizers venous system. Because of this, there is forcing of fluid from the vascular
space into the interstitial space that allows for movement of nutrients and
b. Topical treatment of fungal infection; systemic treatment of bacterial infection other agents into cells at the level of the capillaries.
3. External support Given the lower pressure in the venous system, all the fluid in the
interstitial space cannot be absorbed. At the level of the capillaries there
a. Intensive: compression bandages are LYMPHATIC CAPILLARIES, that carry the extra fluid. The lymphatic
b. Maintenance: lymphedema sleeve system has one way valves similar to veins that prevent back flow of
lymph. The lymph capillaries have larger openings than venules, and is
able to accept FLUID, CELLULAR DEBRI, BACTERIA and PROTEIN.
4. Exercise This is known as lymph. The fluid is carried to the lymph nodes where it is
filtered and re-enters the venous circulation via the right and left thoracic
a. Gentle daily exercise of affected limb, gradually increasing ROM duct --> right and left subclavian and internal jugular veins.
(Must wear a compression sleeve/bandages when doing exercises)
Problems arise when the lymphatic system is occluded, preventing the
contents of lymph to re-enter the venous systmem. This leads to
5. Massage and manual lymph drainage therapy accumulation of the content.
Stages of Lymphedema
6. Surgical: THIS IS PALLIATIVE 2 methods. See Harold Ellis. Results are poor. 0 - Latent phase (partial occulusion of lymphatic system NO EDEMA)
1 - Spontaneously reversible (Pitting phase)
2 - Spontaneously irreversible (Non-pitting phase + Fibrosis [limbs harden
PROGNOSIS and increase in size])
3 - Lymphostatic elephantiasis (Limbs become large and hardened by
§ If left untreated becomes resistant to treatment due to subcutaneous fibrosis fibrosis)
§ Cellulitis causes rapid increase in swelling: can lead to sepsis and death
General Surgery
Wound Reconstruction: Skin grafts and Skin flaps
February 2015
Reconstruction Ladder (in the order of increasing complexity of treatment)

1. Dressings
2. Primary closure
3. Delayed closure
4. Split thickness graft
5. Full thickness graft
6. Tissue expansion
7. Random pattern flap
8. Pedicle flap
9. Free flap
--
SKIN GRAFTS
Definition
§ A segment of dermis and epidermis harvested from a donor site and transferred to the recipient site and that does NOT carry
its own blood supply.
o Survival requires the generation of new blood vessels from the recipient site bed.
§ They are classified according to the depth of dermis they contain:

o Full thickness (entire epidermis + dermis) vs. split-thickness (epidermis + partial dermis)
Sabiston: Full-thickness skin grafts (FTSG) include the epidermis and entire dermis, with portions of the sweat glands, sebaceous glands, and hair
follicles
Donor Site Selection
Must consider size, hair pattern, texture, thickness of skin, and colour (facial grafts best if taken from “blush zones” above clavicle e.g. pre/post auricular
or neck)
Partial thickness grafts usually taken from inconspicuous areas (e.g. buttocks, lateral thighs, etc.)
Sabiston: Graftable beds with adequate blood supply include healthy soft tissues, periosteum, perichondrium, paratenon, and bone surface that is
perforated to encourage granulation tissue growth. Poor graft surfaces with inadequate blood supply include exposed bone, cartilage, tendon, and
fibrotic chronic granulation tissue
Partial Thickness Skin Graft Survival
3 phases of skin graft “take”

1. Plasmatic circulation/imbibition: diffusion of nutrition from recipient site which nourishes the graft with plasma exudate from host bed
capillaries (first 48 h)
Revascularization via:
2. Inosculation: vessels in graft connect with those in recipient bed [Graft and host vessels form anastomoses] (day 2-3)
3. Neovascular ingrowth: graft revascularized [blood vessels grow from the recipient bed into the graft] (day 3-5)
Sabiston: Sensibility returns to the graft over time, with reinnervation beginning at approximately 4-5 weeks and completed by 1-2 years. Pain returns
first, with light touch and temperature returning later.
Requirements for survival
1. Bed: Well-vascularized (unsuitable: bone, tendon, heavily irradiated, infected wounds, etc.)
2. Contact between graft and recipient bed: FULLY IMMOBILE (decreased shearing and hematoma formation)
a. Staples, sutures, splinting, and appropriate dressings (pressure) are used to prevent movement of graft and hematoma or seroma
formation
5 3
3. Site: low bacterial count (<10 /cm , to prevent infection)
Sabiston: The most common cause of skin graft failure is hematoma under the graft, where the blood clot is a barrier to contact of the
graft and bed for revascularization. Similarly, shearing or movement of the graft on the bed will preclude revascularization and cause graft loss.
Additional causes are *infection, *poor quality of the recipient bed, and *characteristics of the graft itself, such as thickness or vascularity of the donor
site.
NB: Dressings can prevent some impediments to graft take. A light pressure dressing minimizes the risk of fluid accumulation.
A bolster or tie-over dressing left in place for 4 to 5 days improves survival by maintaining adherence of the graft to the bed, minimizing shearing, and
preventing hematoma or seroma. A vacuum-assisted compression device can be placed on the grafted surface to stabilize the graft in place; this is
especially useful for larger wounds with an irregular three-dimensional surface.
Classification of Skin Grafts

1. By species
§ Autograft: from same individual
§ Isograft: Donor and recipient individuals are genetically identical (monozygotic twins)
§ Allograft (homograft): from same species, different individual
§ Xenograft (heterograft): from different species (e.g. porcine)
2. By thickness: see table below
Full Thickness Skin Graft Split Thickness Skin Graft
1. Definition Epidermis and ALL of dermis Epidermis and PART of dermis
2. Donor Site Limited donor sites (full thickness skin loss, must be closed More sites
primarily or with STSG)
3. Healing of Primary closure (e.g. sutures) Re-epithelialization via dermal appendages in graft and wound
Donor Site edges
4. Re-harvesting N/A ~10 d (faster on scalp)
5. Graft Take Lower rate of survival (thicker, slower vascularization) Easier; shorter nutrient diffusion distance
o o o o
6. Contraction Greater 1 contraction, less 2 contraction Less 1 contraction, greater 2 contraction
(See below) (Less with thicker graft)
7. Aesthetic Good Poor
8. Comments May use on face and fingers Can be meshed for greater area (see below)
Allows for extravasation of blood/serum
9. Advantage Resists contraction, texture/pigment more normal Takes well in less favourable conditions, can cover a larger
area
10. Disadvantage Requires well vascularized bed Contracts significantly, abnormal pigmentation, poor durability
Must remove fat from graft before application if subject to trauma
11. Uses (GET Face (colour match), site where thick skin or decreased Large areas of skin, granulating tissue beds
MORE) contracture is desired (e.g. finger)
Graft Contraction
§ Primary: immediate reduction in size upon harvesting
§ Secondary: reduction in size once graft placed on wound bed
Sabiston:
A STSG can be taken from anywhere on the body; donor site considerations include color, texture, thickness, amount of skin required, and scar visibility.
The STSG takes readily on the recipient site and the donor site reepithelializes quickly. Its disadvantages are contracture over time, abnormal
pigmentation, and poor durability if subject to trauma.
A FTSG is removed with a scalpel and is necessarily small in size because the donor site must be sutured closed. Containing skin appendages, a FTSG
can grow hair and secrete sebum to lubricate the skin, has the color and texture of normal skin, and has the potential for growth. Generally, FTSGs are
taken from areas at which the skin is thin and can be spared without deformity, such as the upper eyelids, postauricular crease, supraclavicular area,
hairless groin, or elbow crease. The greater thickness makes a FTSG more durable than a STSG but this thickness also means that the graft take is not
as predictable because more tissue must be revascularized from the recipient bed.
Mesh graft
Advantages
§ Prevents accumulation of fluids (e.g. Hematoma, seroma)
§ Covers a larger area
§ Best for contaminated recipient site
Disadvantages
§ Poor cosmesis (“alligator hide” appearance)
§ Has significant contractures
Common reasons for graft loss: hematoma/seroma, infection, mechanical force (e.g. shearing, pressure)
OTHER GRAFTS
FLAPS
Definition
Tissue that is moved from one part of the body to another with a vascular pedicle to maintain blood supply (random, pedicled or
named); not dependent on neovascularization, unlike a graft
May consist of: skin, subcutaneous tissue, fascia, muscle, bone, other tissue (e.g. omentum)
Classification: based on blood supply to skin (random, axial) and anatomic location (local, regional, distant)
Sabiston
Skin-bearing flaps are classified according to three basic characteristics—composition, method of movement, and blood supply.
§ Composition refers to the tissue contained within the flap, such as cutaneous, musculocutaneous, fasciocutaneous, osseocutaneous, and sensory
flaps.
§ The method of movement is local transfer, as with advancement or rotation flaps, or distant transfer, as with pedicle flaps from the abdomen to the
perineum or microvascular free flaps.
§ With regard to blood supply, arteries perfusing the surgical flap reach the skin component in two basic ways. Musculocutaneous arteries travel
perpendicularly through muscle to the overlying skin. Septocutaneous arteries arising from segmental or musculocutaneous vessels travel with
intermuscular fascial septae to supply the overlying skin. With either of these patterns, the flap can have a random pattern, which means that it
derives its blood supply from the dermal and subdermal vascular plexus of vessels supplied by perforating arteries. Alternatively, it can be an axial
flap designed to include a named musculocutaneous or septocutaneous vessel running longitudinally along the axis of the flap to penetrate the
overlying cutaneous circulation at multiple points along the course of the flap’s length to provide greater length and reliability.
Local skin flaps contain tissue lying adjacent to the defect that usually matches the skin at the recipient site in color, texture, hair, and thickness. Flaps
should be the same size and thickness as the defect and be designed to avoid distortion of local anatomic landmarks, such as the eyebrow or hairline.
They can be planned so that the donor site can be closed directly and usually are elevated with incision lines placed in relaxed skin tension lines. Local
flaps rely on the inherent elasticity of skin and are most useful in the older patient whose skin is looser. In some cases, the site from which the flap is
raised is closed with a skin graft. Commonly used local skin flaps include the following:
§ Rotation flaps are semicircular flaps of skin and subcutaneous tissue that revolve in an arc around a pivot point to shift tissue in a circle.
§ Transposition flaps are rectangular or square and turn laterally to reach the defect.
§ Advancement flaps move directly forward and rely on skin elasticity to stretch and fill a defect.
§ V-Y advancement flaps advance skin on each side of a V-shaped incision to close the wound with a Y-shaped closure.
§ Rhomboid flaps rely on the looseness of adjacent skin to transfer a rhomboid-shaped flap into a defect that has been converted into a similar
rhomboid shape.
§ Z-plasty transposes two interdigitating triangular flaps without tension to use lateral skin to produce a gain in length along the direction of the
common limb of the Z.
Failure of a skin flap usually involves necrosis of the most distal portion of the transferred tissue. This could be caused by a flap design in which the size
of the flap exceeds its inherent vascular supply, or could be a result of extrinsic mechanical compromise of the flap pedicle by pressure from a
hematoma, compressive dressings, or twisting or kinking of the flap. Measures to optimize viability include proper flap design and avoiding extrinsic
pedicle compression, undue tension with wound closure, and venous congestion caused by excessive flap dependency.
Toronto: Indications for flaps

§ Reconstruction: replaces tissue loss due to trauma or surgery
§ Provides skin and temporary soft tissue coverage through which surgery can be carried out later
§ Improves blood supply to poorly vascularized bed (e.g. bone)
Complications: flap loss due to hematoma, seroma, infection, poor flap design, extrinsic compression (dressing too tight) or vascular failure/thrombosis,
fat necrosis (in free flaps)
RANDOM PATTERN FLAPS

Blood supply by dermal and subdermal plexus to skin and subdermal tissue with random vascular supply
Limited length:width ratio to ensure adequate blood supply (typically 2:1)
Flap choice is often a combination of available tissue, location of reconstruction site with respect to donor site, and surgeon preference
Types:
§ rotation: cover wounds of various sizes; common use: sacral pressure sores
§ transposition: smaller in size compared to rotation flaps and advancement flaps; commonly used on certain areas of the face using adjacent areas
of excess skin laxity
§ Z-plasty: used to reorient a scar, lengthen the line of a scar or to break up a scar
§ advancement flaps (V-Y, Y-V)
o single/bipedicle V-Y flaps: wounds with lax surrounding tissue; the pedicle is the deep tissue underlying the flap
AXIAL PATTERN FLAPS (ARTERIALIZED)

Flap contains a well defined artery and vein
Allows greater length:width ratio (5-6:1)
Types:
§ peninsular flap: skin and vessel intact in pedicle (see Figure 16)
§ island flap: vessel intact, pedicle is better defined (see Figure 17)
§ free flap: vascular supply anastomosed at recipient site by microsurgical techniques
Can be sub-classified according to tissue content of flap:

§ e.g. musculocutaneous/myocutaneous (e.g. transverse rectus abdominal myocutaneous) vs. fasciocutaneous
FREE FLAPS
Transplanting expendable donor tissue from one part of the body to another by isolating and dividing a dominant artery and veins to a flap and
performing a microscopic anastomosis between these and the vessels in the recipient wound
Survival rates >95%
Types: muscle and skin (common), bone, jejunum, omentum
§ e.g. radial forearm, scapular, latissimus dorsi
Wayne Robinson. MBBS Class of 2015
ENT
Dysphagia and Achalasia
Sources: Dr. Forde, Dr. Ashman, Harold Ellis, Toronto Notes
March 2015
Outline of Notes
1. Physiology of swallowing
2. Causes of dysphagia
3. Specific causes:
4. Zenker’s diverticulum, Foreign bodies, Strictures, Webs, Achalasia
5. Table from Toronto Notes comparing achalasia with the other motility disorders
PHYSIOLOGY OF SWALLOWING (DR. FORDE + DR. ASHMAN)

Swallowing Involves:
1. Oral cavity
2. Pharynx
3. Oesophagus*•
Foreign bodies can become lodged at the 4 areas of narrowing: (Cflo o J

Cricopharyngeus
Aortic arch (Most cases on the left side)
Left main stem bronchus (Anterior to the oesophagus)
Oesophageal hiatus in the diaphragm
[See measurements from upper incisors]
Physiology of swallowing
3 Phases:
Oral phase - Voluntary
• Preparatory Phase - formation of a bolus using tongue, teeth, hard palate. Intrinsic muscles shape tongue ad help formation of bolus
• Propulsive Phase - Pushes bolus toward uvula. Extrinsic muscles involved in this tongue movement
Pharyngeal phase
• Most complex phase as it requires the safe transfer of the bolus across a pathway that is also used for respiration. Contents must be
prevented from passing up into nasopharynx and from down into larynx and trachea
• Lasts 1 second
• Totally involuntary
• Mediated centrally at level of brainstem
Pharyngeal phase is based on the reflex arc with afferent and efferent phases
Afferent occurs when bolus makes contact with the uvula.
!t$PSJd>UrM<A w rix..
iN 9,10, 11 -> Pharyngeal plexus 4
CN 9 (Pharyngeal branch)-> Brain stem -> NTS (Has a swallowing centre)-> NA Êfferent output from NA are
Causes
NA also constriction
connected toofcervical
the constrictor
plexus, muscles and elevation
which supplies of soft
suprahyoid palate jso
muscles Prevents nasal
activation regurgitation)
of the cervical plexus causes elevation of the larynx. Helps
prevent food entering larynx
— ^fcso activation of recurrent laryngeal nerve causing the larynx to close. When swallowing larynx closes from inferior to superiorly
• SO true vocal cords close first, then false vocal cords, then epiglottis/laryngeal inlet!
l Primary function of the larynx is protection of the tracheobronchial tree from aspiration. Phonation secondary.
If these mechanisms fail and larynx doesn’t close in time, mechanism causes you to hold your breath at end of inspiration, so you can cough up what
went down. Does not prevent aspiration but if aspiration occurs, you can cough it up.
Respiratory nucleus of the brain stem is th^fPre-Botzinger Complex
^ f CNX (vagus) after receiving input from CN x f (accessory) joins CN IX (glossopharyngeal nerve) to forrr/pharyngeal plexus )— lO
This plexus is located just adjacent to the middle constrictor
Main^notor)herve supply to the pharynx - Accessory nerve [! [

Cranial portion of this joins the vagus nerve.
[All these events happen in 1 second]
Oesophageal phase
■ Primary peristalsis - a continuation of pharyngeal contraction
Secondary peristalsis - similar to stomach, SI and colon

Involves:
—y-o Meissner’s plexus - in submucosa
Auerbach’s plexus (Myenteric plexus)- between inner circular and outer longitudinal muscles -> Causes contraction proximal to
the bolus via release of acetylcholine -> Causes of relaxation distal to bolus by release of NO and VIP -> pushed to LES
LES then opens to allows bolus to enter stomach.
During respiration, cricopharyngeus is closed. (One of the main functions of the muscle is to prevent air from going into oesophagus. Air not normally in
oesophagus)
DYSPHAGIA
Dysphagia = Difficulty in swallowing
Odynophagia = Pain on swallowing
Can occur at any level in the pathway. Usually patient can say what level;
1.*» Oral cavity
2. -> Pharynx
3. -» Oesophagus
For oesophageal dysphagia: Dysphagia for:

* Liquids first: A motility cause
& • ft Solids: Mechanical cause
• Patients with dysphagia for solids: 70-80% Narrowing of the lumen must occur before oesophageal dysphagia occurs. This is why most
oesophageal malignancies present advanced W
Dysphagia
▼
O ropharyngeal Esophageal
(difficulty initiating swallowing -+ choking, (inability to move food down esophagus!
couching, nasal regurgitation}
+ : i - 1 ------------- f I |
Neurological* M us cula r S tructural Solid food only Solid foods and liquids
Cortical Muscular dystrophy Zenkei's diverticulum
Bulbar Polymyositis Thyromegaly T I
Peripteral Myasthenia gravis Cervical spur Mechanical obstruction Neuromuscular disorder
Cricopharyngeal !_
J ------- 1
▼
Progressive intermittent intermittent Progressive
i
i 1 L—
Age > 5 0 Heartburn Lower Diffuse Reflux
fw t loss} esophageal esophageal symptoms
ring* spasm (DESl i
(chest pain) ▼ ▼
Carcinoma* Peptic Scleroderma* Achalasia*
’ Most common stricture*
Figure 4. Approach to dysphagia (eosinophilic esophagitis om itted)
Other classification system
A. ORAL
■ Malignant lesions such as carcinoma of the tongue and floor of the mouth
■ Inadequate salivation e.g. post radiotherapy or Sjogren’s syndrome
B. PHARYNGEAL
Neuromuscular causes
■ Bulbar palsies
■ Tetanus
Structural causes
■ Zenker’s diverticulum
■ Postcricoid webs
■ Malignant lesions of the oropharynx and hypopharynx HI
C. OESOPHAGEAL ---------------------
- >
Oesophageal dysphagia summary (Dr. Forde)
1. Intraluminal
a. Foreign body - ONLY mechanical cause. Eg Fish bones, meat bolus
2. Intramural
^ v u Wayne Robinson. MBBS Class of 2015
- > a. Mechanical - Dysphagia for solids. Eg. Strictures, neoplasms, webs, rings
- > b. Functional - Dysphagia for liquids first. EgT Achalasia, diffuse oesophageal spasm
Extramural Causes ^ t ~~
a. Mediastinal massesOTsn- T-lymphomas, Teratomas, Thymomas, Thyroid (Retrosternal) - Most common extra-mural cause of
dysphagia s,
b. Vascular anomalies - Dysphagia lusorium (aberrant right subclavian artery), Aortic aneurysm, double aortic arch
FULL LIST FOR OESOPHAGUS: ...

LOCAL vs GENERAL p d fJ ^ " .
LOCAL (Dafraluminal, intramural, extrinsic compression)
A. INTRALUMINAL
1. Foreign bodies (most commonly coins in children, bones in adults)
B. INTRAMURAL (MECHANICAL VS. FUNCTIONAL)

1.C ongenital atresia (trachea-oesophageal fistulae) or stenosis
MccLa*\' tAi •.
2.i/Benign strictures
-*■ GERD with reflux oesophagitis + inflammatory stricture formation
-*■ Caustic stricture
Post-irradiation
-j* Post-traumatic
3. ‘-'Tumours (Benign and malignant) n

4. uPlummer-Vinson/Patterson-Kelly syndrome [ UJcbSy
5. i^Schatzki’s ring with hiatus hernia - Circumferential narrowing of lower part of oesophagus caused by a ring of mucosal tissue or muscular
0 tissue ( j i r t )
G.w'Motility disorders
■Achalasia of the cardia .. . » . t*
■^Chagas’ disease [~Tsuf>anos»*0- ^TU'7' 0 ^SCikdoacA'&tO' * * <=-
■ Cricopharyngeal spasrn
■‘"diffuse oesophageal spasm
sm „ rUi U
t C r tf fJ y J J
7. ‘-'Scleroderm a ^
8. •-'Dermatomyositis
9. KTiron’s disease
C. EXTRINSIC COMPRESSION
1.‘-'Mediastinal tumours (e.g. bronchial carcinoma)

2vÊnlarged mediastinal lymph nodes (secondary cancer or lymphoma)
3.-'Retrosternal goiter
4. Para-oesophageal hiatus hernia
5. Pharyngeal pouch (Zenker’s diverticulum) - [THIS IS MORE A PHARYNGEAL CAUSE]
^ E N E R a6. T ^Thoracic
^ ' aortic aneurysm
V O jfT __H ) t h c g & m & z h i-
7. w-Bysphagia losura - difficulty swallowing caused by aberrant right subclavian artery
Neural andTieuromuscular disorders
Myasthenia gravis
2. £ Multiple sclerosis
3. - Bulbar palsy
4. - Tetanus
THE COMMONER CONDITIONS ARE:

■ '^Carcinoma of the oesophagus
■ "R eflux oesophagitis
■ —Achalasia of the cardia
Special investigations
History and examination may suggest underlying pathology
A. Radiography
1. Barium/gastrografin swallow
2. Barium meal - can demonstrate associated gastric disorders e.g. carcinoma of the cardia extending into stomach, hiatus hernia, PUD
3. Videofluoroscopy
4. P1 InI UHU nO cV r/ Wn ^n/IiVr Ui iIlUt r Uo Uo Vr »/ Ui irI I»VHI Tl*Ju»u
5. CT/MRI scan e a s t
'IX
Wayne Rnhinson MBBS Class of 2015
B. Endoscopy
1. Flexible fibreoptic endoscopy +/- biopsy +/- therapeutic dilatation
C. Oesophageal manometry for motility disorders

Tfryropharyngeus
SPECIFIC CONDITIONS Thyroid cartilage
j%n ZENKER’S DIVERTICULUM Criosphjryngeus
CrkokJ c«ftHage
A false (mucosal) diverticulum
A pulsion diverticulum - due to increased intraluminal pressure Pharyngeal pouch
Occurs at Killian’s dehiscence (posteriorly, between ^ricopharyngeus and thyropharyngeus of 'mtenoijpnsbt'cfa r

M > F, Elderly " ==== ~
Reason some persons get Zenker’s diverticulum:

1 theory;
■ Spasms of cricopharyngeus (when it is supposed to relax and it closes instead) buildup of intraluminal pressures Overtime KD gives
way and outpouching forms
■ As the pouch enlarges, it sisplaces the oesophagus laterally
Clinical features
■ Dysphagia, regurgitation of food collected in the pouch
■ Food retained in the pouch leads to a foetor and late regurgitation maylead to aspiration pneumonia and lung abscess
■ Often a palpable swelling in the neck which gurgles
Must investigate and confirm with barium swallow - See the outpouching at the level of the pharynx
Treatment-
j r ^ ___.
^VTraditional surgery is/excision of the pouch)and perform a posterior^ ricopharyngeal
T myotpyrivy1 P? 2-
______„
b -Alternative: Can treat the pouch endoscopically using a stapling device êndoscopic diverticuioiomvT) leaving the pouch in situ and avoiding the risk of
fistula formation and leaks associated with the open operation ^ ------------------
>3 Gr\ Open -O te e c d u K • b_- is sco'pl'-c.
' SWALLOWED FOREIGN BODIES

• Acute onset. Usually after eating
• Patient can usually localize it.
Bone associated with odynophagia (Painful swallowing)

A //
Diagnosis: Need to order a soft-tissue lateral neck x-ray in patients who ingest a foreign body (Different from a c-spine xray which is for trauma)
[X-ray needs to show C7 and T1 junction in order to be adequate]
Know how to identify:

• Atlas - C1
• Tongue base
• Epiglottis
• Hyoid bone
• Trachea
• Pharynx which becomes Oesophagus at C6
MUST KNOW: 4 things to look for on a SOFT-TISSUE lateral neck x-ray (this is different from a lateral c-spine!H)
1. Cervical Lordosis - Normal cervical lordosis is convex anteriorly

• Look for loss of normal cervical lordosis - suggests there is something causing the prevertebral muscles to contract
2. Prevertebral space - Look to see if it is widened. If it is >1/3 of the width of the vertebral body, it is abnormal
• From C4-C6, >2/3 is abnormal
3. Air in the oesphagus - Normally NO AIR in oesophagus. Normally collapsed
4. Radioopaque foreign body
[Ossification of the cricoid cartilage occurs in normal persons in the 20s and sometimes mistaken as a foreign body]
Management
1. Oesophagoscopic removal if stuck in oesophagus

2. Occasionally oesophagotomy is required
3. The treatment of a foreign body that has passed the cardia is initially conservative. The patient is watched and serial X - rays taken to observe
the object’s progress if it is radio - opaque. Operation is performed if a sharp object fails to progress or if abdominal pain or tenderness
develop.
■ The great majority of foreign bodies, once they have passed into the stomach, proceed uneventfully along the alimentary canal and are
passed per rectum. Occasionally, a sharp foreign body penetrates the wall of the bowel (there is a particular tendency for it to lodge in, and
pierce, a Meckel’s diverticulum;
STRICTURES
Histologically, a stricture is fibrous tissue. And fibrosis is a feature of chronic inflammation. So anything causing trauma to the oesophagus either
externally or internally (Radiation, trauma, Acid reflux) can cause inflammation -> Fibrosis -> Strictures
Progressive slow onset for solids

Barium swallow
Treatment is dilatation with a oesophaqoscope

U - a
‘ (Know on x-ray - filling defect)
OESOPHAGEAL W EBS
Harold Ellis: “A syndrome actually described by Paterson and Kelly before Plummer and Vinson, and which sometimes rejoices in all four names,
comprising dysphagia and iron - deficiency anaemia (with its associated smooth tongue and koilonychia - spoon-shaped nails) usually in middle - aged
or elderly women” “ .
_________________ kvu> (0 -VaaS {
• Seen in(middle-aged femaleg- Plummer-Vinson syndrome. Associated with IDA so also Glossitis ' 'n
■ The dysphagia is associated with hvperkeratinization of the oesophagus and often with the formation of sf web jtn the upper part of the
oesophagus. 1 ^
NOTE VERY WELL: The condition i^premalignanând is associated with the development of a carcinoma in the cricopharyngeal
region!!!!
Dysphagia for solids

Barium swallow - Filling defect / A
[u H H C T \ t t w o fl a< l <i oj n aar x
nK ' •
L Treatment is dilatation with a oesophagoscope

E l *3
A C H A L A S iA O F T H E C A R D 1A
A neuromuscular failure of relaxation at the lower end of the oesophagus with progressive dilatation, tortuosity, incoordination of peristalsis and often
hypertrophy of the oesophagus above ~
• Most common motility disorder / W a 5 © - t f Q .

• Seen most commonly in(femafes 30-4Cp
Inactivation of the inhibitory portion of the myenteric plexus. [Recall Mediators are NO and VIP]
■ ■ - —
Vagi show axonal degeneration of the dorsal motor nucleus and nucleus ambiguous
Aetiology is unknown but a neurotropic virus may be important
Similar to Chagas’ disease, which occurs in South America due to Trypanosoma Cruzi. This parasite destroys the ganglion cells of the oesophagus
Clinical features
■ Tends to have progressive dysphagia for liquids first
■ Hx of weight loss as it progresses —'
■ regurgitation, chest^pain
^ c c
% 5% of patients develop squamous carcinoma
F /
< f
3 things associated:
1. Aperistalsis
2. Inability to relax
Increased LES tone
M
Investigations:
1. Gold standard investigation for achalasia is oesophageal manometry - Patient swallows a probe and pressures at LES measured.. Normally
hfermj
pressures are ~ 30 mmHg. In achalasia, ~ 60mmHg. (ST: Absent primary peristaltic wave and non-propulsive tertiary contractions)
If not available: Barium swallow - A smooth filling defect at LES (also known as a rat-tail or bird-beak deformity) with gross dilatation and
tortuosity of proximal oesophagus
CXR - widening of mediastinum due to dilated oesophagus appearing as a mediastinal mass, air/fluid level and absence of gastric fundus gas
bubble, possible pneumonitis from aspitation of oesophageal contents
Endoscopy - essential to exclude ’pseudoachalasia’ due to submucosal îrcinoms). See an enormous sac of oesophagus containing a pond of
stagnant food and fluid
DDx: All the causes of dysphagia, starting with the MOTILITY disorders then the others
ment: p h y la *ris
1. .Balloon dilatation
Filatation of the oesophagogastric junction by means of an endoscopic balloon that is inflated under fluoroscopic (X j~ay) control. Although
this avoids open operation it is accompanied by the risk of rupture of the oesophagus.
Inflated to 300 mmHq for_3 minutes
3% perforation rate
60% dysphagia free at 5 years
May be repeated if necessary
T ’& d If f p t is a x o ix c A U - 'iln
eller’s cardiomyotomy
& (Dividing the muscle of the |ower end of the oesophagus and the upper stomach down to the mucosa. Best performed laparoscopically
85% wiIirr§vearTTmprw ptoms ' ' " ~ " “ --------
■ 10% develop oesophageal reflux
■ 3% will develop and oesophageal stricture
- Some combine cardiomyotomy with an antireflux operation 'JJ
7 3. .A newer alternative involves endoscopic injection of botulinum toxin (Botox) to paralyze the lower oesophageal sphincter, a treatment that
v. y gives relief in many patients and which may last for a year
TUMOURS OF THE OESOPHAGUS

SEE SEPARATE NOTES
PERFORATION OF THE OESOPHAGUS

SEE HAROLD ELLIS
Table 3. Es o p h a fiM M o to r Disorders

Disorder C Achalasia ( .Scleroderma ) (f^ffuse Esophageal Spasm (D E s fN
Definition * Failure of smooth muscle * Seillheumatotoav. RH13 • Normal peristalsis interspersed with
relaxation at LES • Systemic disease characterized frequent, repetitive, spontaneous,
• Progressive loss of peristaltic by vascuiopathy and tissue high pressure, rein-peristaltic waves
function fibrosis (especially skin (tertiary peristalsis)
thickening)
Etiology * Usually idiopathic * Involves autoimmune, genetic, * Idiopathic

* 2s or pseudo-achalasia: e.a hormonal, and environmental
malignancy, Chagas disease factors
f Trypanosoma cruzi) * Dysphagia: caused by reflux,
dysm otijity or both
Pathophysiology * Inflammatory degeneration * Blood vessel damage -» • Potential mechanisms include

of Auerbach's plexus intramural neuronal dysfunction impaired inhibitory innervation to
c9increase in LES pressure, -» distal esophageal muscle esophageal tody, malfunction in
in c o m p le te relaxation of LES weakening aperistalsis and endogenous nitric oxide synttiesis
* w ith swaHowingâperistalsis loss of LES tone -» reflux -»
stricture -* dysphagia
Diagnosis » CXR: no air in stomach, • Clinical features of scleroderma • Barium x-ray: "Corkscrew pattern"
dilated esophagus * Manometry: decreased pressure • Manometry: >30% (but <100%l
* Barium studies; esophagus in LES, decreased peristalsis in of esophageal contractions are
terminates in narrowing at body of esophagus aperistaltic
LES ("bird's beak')
* Endoscopy: r/o malignancy
* Manometry: definitive
diagnosis (signs listed above)
Treatment * Dilatation of LES with balloon, • Medical: agêssive GERD • Reassurance not cardiac pain
± GERD prophylaxis, 50% therapy (PPis bid) • Medical: nitrates, calcium channel
good response, can repeat, ♦ Surgery: anti-reflux surgery • blockers, anticholinergics have
nsk of perforation (5%) (gastroplasty, last resort) variable benefit
* Injection of botulinum toxin • Surgical: long esophageal myotomy
into LES (temporary) if unresponsive to above treatment
* Surgery (myomectomy) (rarely helpful); balloon dilatation
General Surgery
Laryngeal Carcinoma
Sources: Dr. Ashman, Dr. Wiley
February 2015 __________________ ________
EPIDEMIOLOGY
^ 4 5 % of all head and neck cancers

■ In Jamaica, incidence in males is 4 per 100,000 annually
■ Most common in 50s-60s
vfrry~~M >F, a lm o s t 1 0 : t ! 3
Blacks > Whites > Japanese and Chinese to
Higher incidence in urban than rural populations. May be related to urban pollution -> Q ? la e k n o d a > ^ °
RISK FACTORS ~s,

GENETIC vs. ENVIRONMENTAL
Genetic factors: Some families noted to have a higher rate than others
Cfenvironr
nvironmental: Strongly associated with:
' 1 Ci>Cigarette smoking'\Polycyclic aromatic hydrocarbons in cigarettes -> converted to epoxides which bind DNA (the true carcinogens))
2. Alcohol intake
3. (HPV types 16 and l£ (Li et al., 2013) - related to oral sex. Emerging as a more common aetiology . QdMCsrtby If/
Others:
1. Prior radiation to head and neck lb !p
2. Nickel and asbestos exposure
3. Mate tea in Latin America
PATHOLOGY
• 95% = Squamous ce ll ca rc inomas
■ Most are moderate to well differentiated
3 sites:
■ In Jamaica. US & UK:
G lottis ( ) > S uprag lottis (35%) > S ubglo ttis ( ) m !> L—
In cases where the diagnosis has-beeruqreatly delayed -> may be transglottic (extends across all)
Lesion usually arises in thd'anterior 1/3 <bf th e voca l cord s. (May be noted at laryngoscopy)
CLINICAL FEATURES
Depend on location: GLOTTIC vs. SUPRA- OR SUBGLOTTIC
SUMMARY: FEATURES OF VOCAL CORD PALSY + UPPER AIRWAY OBSTRUCTION + SPREAD
Glottip c an ce rs tend to present early wiv \p e rs is ie n t hoa which becomes progressively worse
‘POINT: Any adult who has had persistent hoarseness tor more than2 weeks must be assumed to have malignancy until proven
otherwise!**
Early laryngeal cancer can be treated with minimal morbidity and good preservation of voice
Dyspnoea dnd^strldor ().e. features of UPPER airway obstruction) may be the presenting features in advanced laryngeal cancer.
^ “ "ilprhese symptoms may be present without hoarseness in patients with a supraglottic or subglottic tumor (as the vocal
cSrds are spared -> no hoarseness)!!!
n S t e WELL: Cervical nodal metastases are common in SUPRAglottic cancers (30%) BUT UNCOMMON IN GLOTTIC CANCERS UNTIL
LATE STAGES.
y, Explanation: Reflects the poor lymphatic drainage of the mucosa of the true vocal cords
Others:
Cough ± haemoptysis _
(D ysphagia, odynophagia, globus sensation )
Cervical nodes (POINT: Rare w/ glottic cancer BUT 30% of supraglottic tumors present with this)
o Especially mid deep jugular chain nodes (superior spread), jugulo-omohyoid nodes (inferior spread), prelaryngeal/Delphian node and
pretracheal nodes (anterior spread) ~~~~ -
INVESTIGATIONS
DIAGNOSTIC vs STAGING
DIAGNOSIS (FLEXIBLE FIBREOPTIC LARYNGOSCOPY + BIOPSY)
1. Indirect laryngoscop y (using a mirror in clinic)
2. Flexible fibreoptic nasolaryngoscopy
3. Rigid telescope (70 degree)
4.
With B IO P S Y a t direct laryngoscopy
a. Diagnosis confirmed by biopsies at direct laryngoscopy
b. NB!!! Prior to taking the biopsy, extent of the tumour must be assessed endoscopically!!!
Nj \l 4/
ALSO NOl rformed (laryngoscopy. tracheobronchoscopy, nasopharyngoscopy, oesophagoscopy>
■ Reason : I here is ai cidence of an associated second primary tumour in the head and neck or bronchus\!
STAGING
1 ^ CT or MRI of the NECK and CHEST to assess for mets
2. U/S Of neck + CXR (<r Only if cannot afford above)
3. >FNAC of lymph nodes - should also be performed if nodal enlargement present
TNM STAGING - MUST KNOW

l ■ T1a - 1 vocal cord with normal mobility (as it is still confined to the mucosa)
\ ■ T1b - Both vocal cords with normal vocal cord mobility
J ■ T2 - 1 vocal cord with impaired mobility

■ T3 - Fixation of vocal cords
| ■ T4 - Extends beyond the larynx
TREATMENT
Depends on T-STA GEand may be C U R A T I V t or P A L L I A T I V E
AJRI
AJRE: THE PRIMARY TUMOUR
• T1a, b and T2 - 2 OPTIONS

o+ Option 1: Primary radiotherapy alone -3 95% 5-year survival^ WITH voice preservation
o * Option 2: Surgery: Mucosal stripping + ro ra e ctomy (BUT will be persistently hoarse as it is normally the mucosa that vibrates)
o NOTE WELL: No increase in survival with chemo for T1 or T2
■ T3 - Prim ary chemo-radiation:

o Method: 2 cycles o f primary chemotherapy, THEN ->
■ If 50% reduction, then radiotherapy
■ If not, then (secondary) surgery (total laryngectomy)
• T4 - Primary surgery if possible (total laryngectomy) OR palliative chemoradiation instead
Arty surgery is followed by reconstruction of the pharynx
B. RE: LYMPH NODES
■ lf(oodes > 2.5 Cervical nodal mets treated with neck dissection: Options:
o RADICAL neck dissection ( LNs + sternomastoid + accessory nerve + IJV) vs. FUNCTIONAL neck dissection (LNs only)
CJRE: VOICE REHABILITATION
4 options:
1. Teach patient oesophageal speech
2. Electrolarynx -> Patient will have a mechanical sounding voice
3. Tracheo-oesophageal puncture (most popular):
■ Make a fistula between trachea and oesophagus. Insert a Twgy (Blom-Sinqer or Provox) valve.
■ Allows air from trachea to oesophagus but contents do not pass in reverse (food etc.)
4. Neoglottic techniques
U.fp p e r oLKr\oao V
~ R o cu ?£/i © & U
- c fu s p o . o <Oj
m
^ { r \d o r
C M X ^ l^ y , In G & to p 'h y c tU
ENT
Oesophageal Cancer
Sources: Harold Ellis, Toronto Notes, Dr. Forde
March 2015
TUMOURS OF THE OESOPHAGUS

Classification
A. BENIGN
■ Leiomyoma.
B. MALIGNANT
I. Primary:
- Carcinoma;
1. Squamous Ceil Carcinoma
2. Adenocarcinoma
• Leiomyosarcoma.
II. Secondary: direct invasion from lung or stomach
MALIGNANCIES OF THE OESOPHAGUS

PATHOLOGY
Squamous Cell Carcinoma (Locally this is BY FAR more common)

• MUST KNOW: Frequency (Highest to lowest) .4LU {Middle> Lower> Uppet)
2. A denocarcinom a - Main cause is GERD. (Becoming mo re common as diet chanainalmcLGERD-incidence increases!. Occurs due to
glandular metaplasia related to GERD etc.^Le. Gastric/intestinal metaplasia, a.k.a. BARRETT’S OESOPHAGUS)!
■ (Recall the normal oesophagus Is lined with stratified squamous epithelium)---------- ------------------------
a. This is the most common worldwide *T ' " ~~
b. Most commonly distal (Lower > Middle > Upper): MAKES SENSE as the distal end is the part most exposed to the reflux
THEREFORE: Squamous cell carcinoma is most common in the MIDDLE third of the oesophagus while adenocarcinoma is most common in the DISTAL
oesophagus. SO, since SCO is more common in Jamaica, the middle third is the most common site overall for oesophageal cancer in Jamaica!!! While
worldwide, the most common site is distal as adenocarcinoma is more common.
GROSS: The tumour commences as a nodule, which then develops into an ulcer, a papilliferous mass or an annular constriction.
RISK FACTORS
Pi
, a . see
Cigarette smoking and\ alcohol
Also linked tc/achaiasia\r\6(6oeliac
<6 oeliac disease,
disease) — ^
' B. Adenocarcinom a
■ Cigarette smoking and alcohol, with
■ Barrett’s oesophagus as a consequence of metaplastic change at the gastro-oesophageal junction.
CLINICAL FEATURES
Carcinoma of the oesophagus may present because of the following:
A. Local symptoms - dysphagia ^ +
B. Direct spread - Trachea: dyspnoea, stridor. Left recurrent laryngeal nerve -> Hoarseness and a bovine cough
C. Metastatic deposits: ^
i. Lymphatic: Enlarged neck nodes
ii. Haematogenous: Liver & lungs: Occasionally jaundice and/or hepatomegaly,
D. Constitutional symptoms of malignant disease - loss of weight, anorexia, anaemia.
Dysphagia in an elderly male with a short history is almost invariably due to carcinoma of the oesophagus or the upper end of the stomach.
SPREAD
Local: into the mediastinal structures - the trajêa, a ^ a , mediastinal pi^yra and Iqyg.
Lymphatic: to para-oesophageal, tracheobronchial, supraclavicular and subdiaphragmatic nodes.
Bloodstream: to liver, lungs and peritoneum (relatively late).
INVESTIGATIONS
Classify: DIAGNOSTIC vs. STAGING
INVESTIGATION BASICALLY SIMILAR TO ANY Gl CANCER
A. DIAGNOSTIC
1. B arium csw a llow h Irregular filling defect ! l - c b <c s lio t A d o u x a „
2. Followed by o e s o p h a g o s co p y and b io p s y
M R STAGING V U > tL ^ c o !. S -f C T CAP -ir
t? ♦ ’ 1 # Endoscopic Ultrasound,^to assess depth of penetration through wall of oesophagus

# v 2 jJ* C T ph est^b d o m eiV p elvisA For staging. Detects invasion + spread to surrounding structures in chest + lymph nodes
3. l aparoscopwfrhay be indicated to exclude peritoneal mets prior to resection
TREATMENT
Depends on the stage and may be CURATIVE vs. P ALLIA T IVE
A. E A R LY S T A G E L E S IO N S (***Since high propensity fo r even m icroscopic spread) ->
• NOT PRIMARY RADIATION

SURGERY -^TO TA L oesophaqectomy. Followed by a “stomach pull-up” (-> Anastomose s with hypopharynx)
■ 15% mortality rate from surgery ^ ________
B. LA TE S TA G E
If CURE is plan:
■ Neoadjuvant chemoradiotherapy then surgery
< If PALLIATION is plan (Eg. Mets to lungs)

• Stent
■ Endoscopic laser therapy to vaporize the growth and restore the lumen - may need repeat courses
■ Radiotherapy- Esp. for SCC. Either external beam or Intraluminal
• Open gastrostomy ^ **
■ For incurable cases: Average life expectancy is in the region of 3 months with a maximum survival of about 1 year, but at least the patient is
spared the misery of total dysphagia
The overall prognosis is < 10% at 3 y e a rs\^
POINTERS FROM HAROLD ELLIS LECTURE NOTES
Post-cricoid carcinomajifeually occurs in women and is associated with thevglummer-Vinson syndrome,The remaining oesophageal growths occur
~mare~ofterrirr menTusually elderly men. YKecommonest site has changed in recenfyears, with distal tu mours becoming more common than tumours of
the mid-third, with upper oesophageal tumours being least common.
Carcinoma of the oesophagus is a relatively common tumour in the UK (12 per 100 000 incidence), but is 20 times more common in China, and twice as
common in France. The incidence is rising in the Western world.
Microscopically, the majority are now adenocarcinomas arising at the lower end of the oesophagus, either in gastric metaplasia (Barrett ’ s oesophagus)
or as a result of an invasion of the oesophagus from a tumour developing at the cardiac end of the stomach. Tumours of the upper two-thirds are usually
squamous carcinomas. j /
d u e *)c v a — V
BARRETT’S OESOPHAGUS AND ADENOCARCINOMA
This is an increasingly common condition with an estimated prevalence of about 2% of adults in the UK. The normal oesophagus is lined by
stratified squamous epithelium. In pa tie n ts w ith lo n g -s ta n d in g re flu x o f d u o d e n o g a s tric co n te n ts , th e lo w e r oesop ha g ea l
e p ith e liu m u n d e rg o e s m e ta pla sia to an in te s tin a l-ty p e c o lu m n a r e p ith e liu m . Continued inflammation may lead to dysplasia and
subsequently to malignant change.
Carcinomas in such cases are adenocarcinomas, and most occur in the lower third of the oesophagus or at the gastro-oesophageal junction. They
are commonest in male smokers, with a long history (over 10 years) of Barrett’s metaplasia and frequent symptoms (more than three times a week)
of gastro-oesophageal reflux.
As metaplasia to a Barrett-type oesophagus is premalignant, such patients should undergo regular endoscopic surveillance, with biopsies to look
for dysplasia. Severe dysplasia (carcinoma in situ) is an indication for endoscopic treatment or resection.
- p r tu d iq n a a b / -> • In c n c e frc o u b rA c r/i
(ttk w
OM'
General Surgery
BPH - STARTS ON PAGE 2 (ANATOMY FIRST)
Sources: Toronto Notes, Bailey and Love’s
February 2015
Embryology: Skene’s tubules, which open on either side of the female urethra, are the female homologue of the prostate
Surgical Anatomy of the Prostate

The prostate is divided into the peripheral zone (PZ), which lies mainly posteriorly and from which most carcinomas arise, and a central zone (CZ),
which lies posterior to the urethral lumen and above the ejaculatory ducts as they pass through the prostate; the two zones are rather like an egg in an
egg-cup. There is also a periurethral transitional zone (TZ), from which most benign prostatic hyperplasia (BPH) arises.
Smooth muscle cells are found throughout the prostate BUT, in the upper part of the prostate and bladder neck, there is a separate sphincter muscle
that subserves a sexual function, closing during ejaculation -> Resection of this tissue during prostatectomy Is responsible for retrograde
ejaculation. ,
Benign prostate hypertrophy starts in the periurethral transitional zone and, as it increases in size, it compresses the outer
PZ of the prostate, which becomes the false capsule.
C *
\ There is also the outer trug fibrous anatomical capsule, and external to this lie condensations of endopelvic fascia known as the periprostatic
“5 sheath of endopelvic fascia.
Between the anatomical capsule and the prostatic sheath lies the abundant prostatic venous plexus. The prostatlc sheath Is
contiguous with the fascia of Denonvllllers, which separates the prostate and its coverings from the rectum.
The neurovascular bundles supplying autonomic innervation to the corpora of the penis are in very close relationship to the posterolateral
aspect of the prostatic capsule and are at risk of damage during radical cystoprostatectomy or radical prostatectomy: inadvertent diathermy
in the region of these nerves may be the cause of uncommon erectile impotence after transurethral prostatectomy (TURP).
Antenor Urethral glands

IfblOfflL&CUldf Anterior
Arorrd Submucosal glands fibromuscular area Transition
(adenomatous zone; zone
Capsule Prosfatic urethra
C*nual Tfansitfonaf
zone
Ejaculatory
duct
Distal
P e rip h e ra l spfnchter
zone rm*banfern Prostatlc glands proper
(carcinomatous zone)
Anatomical capsule
Figur© 77.1 Sagittal diagram of ffie prostate just futef&l fc iK© urethra
showing ihe division rnfc the d$ef~r}t zone-s by Me Mebf Figure 77.2 A transverse section of the prostate The petipherol zone
The transitional zone 15 the oteo ftam wkteh most benign pfostatic is the area from which most prostate cancers arise The adenomatous’
hyperplasia (BPHj arises zone comptises the centra! and tramiliono! zones Ejaculatory zone
PHYSIOLOGY
The prostate has a sexual function, but it is unclear how important its secretions are to human fertility.
SYSTEMIC hormonal influences (endocrine) and LOCAL growth factors (paracrine and autocrine)
Many local and system ic hormones govern the grow th o f the prostate.
Main hormone acting on the prostate is y yvhich is secreted by the Leydig cells of the testes under the
controt-oTIutemTzing hormone (LH)
\t ^
Testosterone is converted to 1,5-dihydrotestosterone (C by the e m e 5a-reduciase, which is found in high concentration in the prostate and
—-------- ^ _ E>(i~p— tlle perigehital skin (type II). ' ' -
Also: fed serum oestrogens levels, by acting on the hypothalamus, f the secretion of LHRH (and hence LH) and thereby i serum testosterone levels.
Thus, pharmacological levels of oestrogens cause atrophy of the testes and prostate by means of reductions in testosterone
Summary box
Androgenic horm ones
• Androgenic horm ones, which drive prostate growth, are derived from several sources
• The majority of testosterone (90 per cent) is secreted by the Leydig cells ot the testes under the control of LH, secreted from the anterior pituitary
• Metabolized adrenal androgen accounts for the remaining 5-iO per cent of testosterone
• Testosterone is converted to DHT by the enzyme 5a-reductase type II, which is found in high concentration in the prostate and the perigenital skin
• DHT has five tim es the potency of testosterone
KNOW THIS: Elaboration and secretion of prostate-specific antigen and acid phosphatases
Prostate-specific antigen (PSA) is eT g i y c o p r o t e i n t h a l is a\serine protease, its function may be to facilitate liquefaction of semen, but it is a marker
itatic disease.
for prostatic y —. ■
■— ^ v—
It is measured by an immunoassay, and the normal range can differ a little from laboratory to laboratory. -
The levels increase with age, with prostate cancer and with BPH. There are age-related values but,
it, in
i general, in men aged 50-69 years, a
level of about 3-4 na/mL would prompt a discussion about the need for prostate biopsy.
***(
Men with focajly confined prostate cancer usually have serum PSA levels |c7 0 - /5 ng/mL
■ Its level in men with metastatic prostate cancer is usually increased fo\>30 ng/mL tnd falls to low levels after successful
androgen ablation. —= * V *■* J
NOTE WELL: Although PSA is a reliable marker for the progression of advanced disease, it \£neither specific nor sensitivefri the differential
diagnosis of early prostate cancer and BPH, as both diseases are compatible with PSA in the range of 3- 15 ng/mL
PSA measurement has superseded measurement of serum acid phosphatase.
In summary, only about a quarter of men with a PSA o f 4 - 10 ng/mL have prostate cancer (i.e. it is not very specific in this range), and about 15-20 per
cent of men with a PSA of 1-4 ng/mL have prostate cancer. In general, one would advise men aged 50-69 years to undergo prostate biopsy if the
PSA was more than ~3 ng/mL. The threshold would be lower in younger men with a strong family history.
BPH
DEFINITION
• Periurethral hyperplasia of glandular epithelium and connective tissue stroma in p ro s ta ti
--------------• + . ------------------
INCIDENCE
• Age-related, extremely common
• 50% of 50-60 yr olds, 80% of 80 yr olds
• Most common cause of bladder outflow obstruction in men >70 years of age
AETIOLOGY
• Aetiology unknown. 2 main theories:
1. Serum testosterone levels slowly but significantly ! with age, while oestrogenic steroids are not decreased equally.
o According to this theory, the prostate enlarges because of increased oestrogenic effects
2. Another theory is that DHT and other androgens, which normally stimulate the prostate gland to produce various growth factors, result in the
BPH. Men with BPH have a higher concentration of the type 1 and 2 isoenzymes of 5-alpha reductase in the prostate
• Also, secretion of Intermediate peptide growth factors and Impaired apoptosis play a role
PATHOLOGY * * *\\
Affects both glandular epithelium AND connective tissue stroma (i.e^STRQMOGLANDULAR HYPERPLASIA) to variable degrees
BPH typically affects the submucous group of glands in theffransitional zone / r z p forminq a nodular enlargement.
Eventually, this overgrowth compresses the PZ glands into a false caosule and causes the appearance o f the typical ‘lateral’ lobes
When BPH affects the subcervical CZ glands, a ‘middle’ lobe develops that projects up into the bladder
CLINICAL FEATURES OF BPH

CLASSIFY:
1. Result mainly from symptoms bladder outlet obstruction (BOO) (LUTS) and compensatory changes in detrusor function
2. May also present with complications (See below)
Lower urinary tract symptoms (LUTS) grouped into:
A. STORAGE SYMPTOMS (problem with containing urine)

1. Frequency (+ Nocturia)
2. Urgency
3. Urge incontinence (+ Nocturnal incontinence (enuresis))
B. VOIDING SYMPTOMS (difficulty with releasing urine)

1. Hesitancy, when trying to start
2. After starting -4 Poor flow (unimproved by straining)
3. While going -> Intermittent stream (stops and starts)
4. Towards the end -> Dribbling (including post-micturition)
5. And when finally finished -> Sensation of poor bladder emptying
8. Episodes of near retention
NB: Post-micturition dribbling is now known NOT to be a consequence of BOO and is not usually improved by prostatectomy
*NB: History must assess ALSO LUTS SEVERITY and impact on quality of life (QOL) —USING TH^fpSS j
* * * (INTERNATIONAL PROSTATE SCORING SYSTEM) ^ S
RE: BOO (Causes: SEE^ftrAlKEN~tECCrURE. Some: BPH, prostate cancer, bladder neck stenosis, bladder neck hypertrophy, urethral strictures)
Definition: This is a/Grodynamic concept baêd on the combination of LOW flow rates in the presence of HIGH voiding pressures (MUST HAVE
BOTH!!!!)
-d iagnosed definitively ONLY by p re s su re -flo w s tu d ie s !!! [ This is because symptoms are relatively non-specific and can result from detrusor
instability, neurological dysfunction and weak bladder contraction (these would result in low flow rates and low voiding pressures)]
The primary effects of BOO on the bladder are as follows:
1. Urinary flow rates decrease (use 10 and 15 mL/s)

• > 15 mL/s is normal, 10-15mL/s is equivocal and one < 10 mL/s is low
2. Voiding pressures increase (use 60 and 80 cm H20)

• (pressures > 80 cm HiO are high, pressures between 60-80 cm H2Q are equivocal and pressures < 60 cm H?Q are normal).
EXAMINATION - MUST BE SYSTEMATIC - ALSO HELPS MEMORY

*
1. General physical examination may demonstrate signs of chronic renal Impairment with anaemia and dehydration.
2. Abdominal examination - Usually normal,

o In patients with chronicjetention distended bladdeh w ill be found on paipation, on percussion and sometimes on inspection
with loss of the transverse suprapubic stun crease.
*^ > 'Rectal examination

o in BENIGN ENLARGEMENT, the posterior surface of the prostate i| sm t (convex)and typicallyw lastlc/rubberw, BUT the fibrous
element may give the prostate a firm consistency,
o The rectal mucosa can be maddlomibve over the prostate.
o *** NO T E : i f there is a c on sid erab le a m o u n t o f re s id u a l urine p rese n t, it pu s h e s the p ro s ta te do w n w ard s, m aking it ap p e a r la rg e r than it is
Neurological examination - examined to eliminate a neurological lesion.

a. Diabetes mellitus, tabes dorsalis, disseminated sclerosis, cervical spondylosis. Parkinson’s disease and other neurological states
may mimic prostatic obstruction
b. Anal sphincter tone, active anal sphincter contraction, lower extremity neuromuscular function assessed
MUST KNOW: COMPLICATIONS (MAY ALSO PRESENT WITH THESE)

POINT: Basically these are all the complications of BOO
0 1. v'Acufe urinary retention is sometimes the first symptom of BOO.

o Postponement of micturition is a common precipitating cause; overindulgence in beer and confinement to bed on account of intercurrent
illness or operation are other causes.
2. i/^ h r o n ic urinary retention

o -> Results in functional obstruction o f the UPPER urinary tract -> development o f bilateral hydronephrosis
o As a result,*i/p p e r urinary tract Infection and*renal impairment may develop.
3. vîmpaired bladder emptying - >/stasis UTIs and stones

o * U r in a r v Infection and* calculi are prone tto develop.
4. J s Haematuria
o May be a complication of BPH. Other causes m ust be excluded by carrying out an intravenous urography (IVU). cystoscopy, urine
culture and urine cvtolooical examination.
*NB: Other than pain from retention, pain is not a symptom of BOO
• Presence should prompt the exclusion of acute retention, urinary infection, stones, carcinoma o f the prostate and carcinoma in
situ o f the bladder
INVESTIGATIONS
IMPORTANT: Investigation of men with LUTS:
Essential Investigations
1. ''u r in e analysis by dipstick for blood, glucose and protein^
2. Urine culture for infection
3. Sfi Serum creatinine
4. t / u r i nary flow rate and residual volume measurement
Additional investigations
1. <jhPSA)f indicated
2. Pressure-flow studies
IN V E S TIG A TIO N S S U M M A R Y - W O RK UP FO R LUTS
: A. Blood tests
1. \/C 8 C : Haemoglobin should be measured (Baseline, assesses anaemia secondary to renal impairment)
2. Serum creatinine, electrolytes (goal is to assess renal impairment) - USUALLY PERFORMED
3. i -PSA if indicated
B. Urine investigations
1 .sÔrinalvsis: The urine is examined for glucose, protein, blood, nitrites (DR. AIKEN - THIS AND MICROSCOPY ARE THE ONLY
MANDATORY)
2. vSltflSU: Gramjjain, culture and sensitivity - bacteriological examination, and
3. i^Cytological examination may be carried out if carcinoma in situ is thought possible
( hC. Flow rate measurement and Pressure-flow^jrogynamig^stydies

Prerequisites for use: For this to be meaningful, two or three voids should be recorded, and the voided volume should be in excess of 150-200
mL
• NOTE: Typical history and a flow rate <10 mL/is (for a voided volume of >200 mL) will be sufficient for most urologists to recommend
treatment.
Decreased flow rates and symptoms of prostatism may be seen in:
• BOO;
• Low voided volumes (characteristically in men with detrusor instability);
• Men with weak bladder contractions
‘ D. Upper tract imaging - Optional/specifically indicated
1. mitravenous urogram or Midominopelvic ultrasound scan - Obviously, if infection or haemgjuria is present, then the upper tract
should be imaged by means of the above
QEjp ystourethroscopy - Optional/specifically indicated^

• Inspection of tbeCiJrethrA, th e firostatdiand the Orothelium of the bladder should ALWAYS_be done immediately prior to prostatectomy,
whether it is being done transurethrally OR by the open route to exclude a urethraTstricture\ a bladder carcinoma and the occasional non-
opaque vesical calculus.
• The decision of whether to perform prostatectomy must be made before cystoscopy.
• Direct inspection of the prostate is a poor indicator of BOO and the need for surgery.
Transrectal ultrasound scanning (TRUS)

• No need to carry this out routinely
RE: PSA
Difficulty here is the uncertain benefit of early detection and radicat treatment of prostate cancer - this is dealt with in the section on prostate
cancer.
AFTER SUITABLE COUNSELLING, measurement of serum PSA may be helpful.

• Men in whom a diagnosis of early prostate cancer might influence treatment option (such as those < 70 years or those with a positive family
history who might be offered radical treatment) should be offered a PSA measurement.
o ***lf this is in excess of 2.5-4 nmol/L, then transrectal ultrasound scanning (TRUS) plus multiple transrectal biopsies (10
biopsies) should be considered.
If rectal examination is quite normal with no suspicion of cancer, and if no change in treatment policy would in any case result from the diagnosis of early
prostate cancer, then there is little point in the routine measurement of PSA in men with uncomplicated BOO. However, because of the fear of future
litigation, many find it easier to offer a PSA test.
MANAGEMENT OF BPH p ,
INDICATIONS: Strong indications for treatment (usually prostatectomy) include:
1. Acute retention accounts for 25% of prostatectomies

2. Chronic retention and renal Impairment: (accounts for 15% of prostatectomies).
a. Residual urine of > 200 mL,
b. a raised blood urea.
c. hvdroureter or hydronephrosis or
d. uraemic manifestations
3. Complications of bladder outflow obstruction:
a. — Stone,
b. — Infection and
c. — Diverticulum formation.
4. Haemorrhage: occasionally, v e n o u s bleeding from a ruptured vein overlying the prostate will require prostatectomy
Elective prostatectomy for (severe symptom^ this accounts for abouf 60% of prostatectomies.
a. increasing difficulty in micturition, with considerable frequency aayand night, delay in starting and a poor stream are the usual
symptoms for which prostatectomy is advised.
Exact cut-off for operative or non-operative treatment will depend on careful discussion between the patient and the
urologist
M U S T K N O W : O PTIO NS FO R TR E A TM E NT
A. Conservative
B. Medical
C. Surgical
D. Minimally Invasive Surgical therapies
WHEN TO USE OPTIONS
1. Conservative All patients Watchful wafting: 50% of patients improve spontaneously
Lifestyle modifications (e.q. evening fluid restriction, planned voiding)
2. Medical Moderate to severe symptoms, no 2 main options

improvement after trial of conservative
1. a-adrenergic antagonists: reduce stromal smooth muscle tone
2. 5-a reductase Inhibitor: block conversion of testosterone to DHT; act to reduce
prostate size - These drugs, when taken for a year, result in a 25% shrinkage o f the prostate gland.
Combination is synergistic
Anti-cholinergic agents (for storage LUTS, without elevated PVR)

3. Surgical Moderate to severe symptoms 1. Prostatectomy
The prostate can be approached
The most common reason for TURP 1. Transurethrally (TURP)
is a combination of severe 2. RetropubicaHv (RPP)
symptoms (IPSS) and a low flow 3. Throuah the bladder (transvesical: TVP) or
rate <12 mL/s 4. From the perineum
Absolute Indications NOTE WELL: AFTER TREATMENT ->Most urologists irrigate the bladder with
1. Renal failure with obstructive sterile saline by means of a three-way Foley catheter for 24 hours or so.
uropathy
2. Refractory urinary retention 2. TUIP fprostate <30 g) - Transurethral INCISION of the prostate
3. Laser ablation
Relative Indications
1. Recurrent UTIs
2. Recurrent hematuria refractory
to medical treatment
3. Bladder stones
4. Renal insufficiency (r/o other
causes)
4. Minimally Patients who wish to avoid or may not 1. Microwave therapy

invasive Surgery tolerate surgery 2. TUNA ( Transurethral needle ablation1
3. Prostatic stent
NB: Men with planned cataract surgery should avoid starting a-adrenergic antagonists until after their surgery due to the risk of intraoperative floppy iris syndrome.
More on medical therapy:
1. a-Adrenerqic blocking agents inhibit the contraction of smooth muscle that is found in the prostate.
2. 5a-reductase inhibitors, which inhibit the conversion of testosterone to DHT, the most active form of androgen.
a. These drugs, when taken for a year, result in a 25% shrinkage of the prostate gland.
***IMPORTANT POINT: Both groups of drugs are effective; however, a-blockers work more quickly and, although the 5a-
reductase inhibitors have fewer side effects, they need to be taken for at least six months, and their effect is greatest in
patients with large {>50 g) glands.
W ayne Robinson. MBBS Class of 2015
Drug t herapy results in improvements in maximum flow rates by about 2 mL/s and results in mild (20%)
improvement in symptom scores
TUf4P however, results in improvements in maximum flow rates from 9-18 mL/s and a 75% improve ment
in symptom scores
ALSO: These drugs are expensive in comparison with their effectiveness, and a significant proportion of men who try these
drugs will subsequently undergo TURP. They may be best targeted at men who have failed an initial trial of watchful waiting and who wish to
avoid surgery for a period.
More on surgery (Toronto Notes):
COUNSELLING MEN UNDERGOING PROSTATECTOMY

Men undergoing prostatectomy need to be advised about the following:
Retrograde eiaculatioruThis occurs in abouf65%)of men after prostatectomy.

Erectile impotence.(~5%)of men, usually thoWwhose potency is waning.
The success rate. On the whole, men with acute and chronic retention do well from the symptomatic point of view.
o 90% of men undergoing elective operation for severe symptoms and urodynamically proven BOO do well in terms of symptoms and
flow rates
o Men with unobstructed detrusor instability do not respond well to TURP.
The risk of reoperation. After TURP, this is about 15% after 8-10 years
The morbidity rate:
o — Severe sepsis is found in about 6% and
o — Severe haematurla requiring transfusion of more than two units of blood occurs in about 3%.
o - Death after TURP is infrequent (<0.5%),
o After discharge, about 15-20% of men subsequently require antibiotic treatment for symptoms of urinary infection
'Sf&uZ
COMPLICATIONS OF SURGERY
CLASSIFY: LOCAL vs. GENERAL
A. LOCAL
jr . Haemorrhage is a major risk following prostatectomy whatever the surgical approach. Care should be taken in diathermising arterial bleeding
points after TURP —
o Check that the bladder is draining adequately; if it is not, this may indicate that a clot is blocking the eye of the catheter. Should be
changed by the surgeon
o Secondary haemorrhage tends to occur after the patient has been discharged. All men should be warned about this possibility and
given appropriate advice to rest and to have a high fluid intake
Perforation of the bladder or the prostatic capsule can occur at the time of transurethral surgery.
Jk Sepsis
o Bacteraemia is common even in men with sterile urine and occurs in >50% of men with infected urine, prolonged catheterisation or
chronic retention. Septicaemia can occur in these patients shortly after operation or when the catheter is removed. In men at high
risk, the use of prophylactic antibiotics is recommended
o Broad spectrum antibiotics with Gram-negative activity given parenterally, e g. augmentin and gentamicin
xA. Incontinence t
o Incontinence is inevitable if the external sphincter mechanism is damaged. The bladder neck is rendered incompetent by any
prostatectomy and, therefore, an intact distal sphincter mechanism li'essential for continence.
o If pelvic floor physiotherapy is ineffective, then the only satisfactory treatment is the fitting of an artificial urinary sphincter.
jk Retrograde ejaculation and-tfnpotence

o Impotence in men with good sexual function before surgery is uncommon, but retrograde ejaculation occurs commonly (65%)
because of disruption to the bladder neck mechanism.
-r Urethral stricture t t .
o This may be secondary to prolonged catheterization, the use of an unnecessarily large catheter, clumsy instrumentation or the
presence of the resectoscope in the urethra for too long a period.
o An early stricture can usually be managed by simpllFbouginage but, later on, it may be necessary to cut the densely fibrotic stricture
with the optical urethrotome
Bladder neck contracture

o Occasionally, a dense fibrotic stenosis of the bladder neck occurs following overaggressive resection of a small prostate.
Reoperation p. *-*•
o It is now well known that, after eight years. 15-18 ner rent nf men with BPH will undergo repeat TURP (the rate after open
prostatectomy is about 5 per cent).
S. GENERAL COmPLiCA TiONS

1. ^6eath occurs in about 0.2-0.3%of men undergoing elective prostatectomy. In very elderly men, in men with prostate cancer admitted as an
emergency with acute or chronic retention or in those with very large prostates, the 30-day death rate may be in the order of 1 per cent.
2. 1Cardiovascular + Pulmonary
o Pulmonary atelectasis, pneumonia, myocardial jnfarction. congestive cardiac failure and deep vepous thrombosis are all potentially life-
threatening conditions that can affect this elderly
" 'N 'V - -m u S T K N O v x J !!/
' ' water intoxication (also known aajTUR syndrome) ) ^
o The absorption of water into the circulattorraHho time-ofTransurethral resection can give rise to congestive cardiac failure,
ft hvponatraemia and flaemolysis. Accompanying this, there is frequently confusion and other S&rebral events often mimicking a
stroke (cerebral oedema) **■
The incidence of this condition has been reduced since the introduction oCjsotonic qlycineior performing the resections and the use
of isotonic saline for postoperative irrigation. The/ireatment consists of fluidresTncffSTT
4. ^ Osteitis pubis
This is rare.
Special problems in the management of chronic retention

• For those who are uraemic, urgent catheterization is mandatory to allow renal function to recover and stabilize.
• Haematuria often occurs following catheterization owing to collapse of the distended bladder and upper tract, but settles within a couple of
days
VERY IMPORTANT: POST-OBSTRUCTIVE DIURESIS: 4 j£C\i£X>^ [([
• Uraemic patients with chronic retention are often dehydrated at the time of admission.
Owing to the chro nic backpressure on the d istal tu b u le s w ith in the kidney, the re is loss o f th e a bility to
reabsorb salts and w ater.
* The result, following release of this pressure, may be an enormous outflow of salts and water, which is known as
p o st-o b structive d iu resis
It is for this reason that a <€ nmfuUJuid~charb (laity m easurem en ts o f the p atie n t’s weici'ht and s eria l estim ations o f
creatinine a nd electrolyte s are essential.
• Intravenous flu id replacem ent is required if the patient is unable to keep up with th is flu id loss.
• These patients are often anaemic and may require a blood transfusion once fluid balance is stabilized (if
haemoglobin is <9 g/L)
©
General Surgery
Prostate Cancer
Source: Bailey and Love, Toronto
February 2015
INCIDENCE
■ Most common cancer in males
■ 3 rd leading cause of male cancer deaths (following lung and colon)
■ Throughout the world, rates of microscopic foci of prostate cancer are constant, BUT rates of clinically evident disease are low In men In South-
Central Asia, Japan and China.
■ Mean age at diagnosis i^ 7 2 A75% diagnosed between ages of 60 and 85;
■ Up to 50% risk of CaP at ag£"5t)??????
IN JAMAICA:
• Most common cancer in Jamaican men [Last recorded ASR (2007) of PCa in K&SA: 78.1/100,000 men/yr]
• Most common cause of cancer-related deaths in J’can men: age-adjusted MR: 53.9/100,000 men/yr (30.3% of deaths)
• Lifetime risk is 10% (1 In 10 men)
RISK FACTORS
^ 1 .t/A g e
2. { /A fr ic a n d e s c e n t (2-3x risk compared to Caucasian - PROCESS trial in Britain) (**VERY rare in most Asian populations)
3. ‘/'F a m ily h is to ry
/ o 1 1s' degree relative = 2x risk
J 0 2 1 s1 degree relatives = 5x risk
) 0 3 1s1degree relatives = 11x risk
/ 4. t/ H i g h d ie ta r y fat = 2x risk (Evidence based on clinical, laboratory and transmigration studies)
AETIOLOGY - Unknown
The follo w in g 5 type s o f prostate cancer occur (BAILEY):
1. Microscopic latent cancer found on autopsy OR at cystoprostatectomy,

2. Impalpable tumours found Incidentally during TURPlTla and Titi\ O ff following screening by PSA measurement (T1c )\
3. Early. palpable, localized prostate cancer (72);
4. Locally advanced prostate cancer (73 and T4):
5. Metastatic disease, which may arise from a clinically evident tumour (72, 73 or T4) Off from an apparently benign gland (TO, T1), i.e. occult
prostate cancer.
***lt should be noted that only the last two groups cause symptoms, and such tumours are NOT curable. Only screening or the
treatm en t o f incidentally found tum ou rs can re su lt in cure o f th e disease! i! The problem is that many such tumours would
never progress during the patient’s lifetime; herein lies the problem with prostate cancer***
ANATOMY (PZ > TZ > CZ)

60-70% of nodules arise in the peripheral zone 2 C 2 -
10-20% arise in the transition zone
5-10% arise in the central zone
PATHOLOGY:
HISTOLOGICAL APPEARAN< Gy=ASQN SCORE” TO CLASSIFY GRADE
t/" Adenocarcinom a(> 95%) often multifocal
ALSO
iS Urothelial carcinoma (4.5%)
o Associated with TCC of bladder; does NOT follow TNM staging below; not hormone responsive
Ly / Endometrial (rare)
o Carcinoma of the utricle
- CLINICAL FEATURES
FIRST POINT: ONLY ADVANCED DISEASE GIVES RISE TO SYMPTOMS!!! but even advanced disease may be
asym ptom atic.
CLASSIFY: TUMOUR ITSELF vs. LOCAL SPREAD vs. DISTANT METS
Usually asymptomatic
Wayne Robinson, MBBS Class of 201>
» MAJOR POINT: Most com m only detected by DRE, elevated PSA, o r as an incidental fin ding on TURP
)jr Symptoms of NO E disease include:
Q A. Locally advanced tumour itself, but m ainly direct spread tA ll these sym ptom s are uncommon without spread)
1. **L UTS: BOO (Any storage and voiding symptoms) (all the features of and urinary tract obstruction & its complications)
2. **Pelvic pain
3. **Haematuria
4. **Post-renat renal failure (i.e. secondary to obstruction)
5. Erectile dysfunction
B. Metastasis:
■ Bony metastasis: Bone pain, malaise, ‘arthritis’, features of anaemia or pancytopenia
■ VisceraI mets are less common (liver, lung, and adrenal gland most common sites)
■ Nodal mets obstructing lymphatic and venous drainage: Leg pain and oedema
DRE ~ U la t sa/uSi
Can detect nodules within the prostate arid advanced disease &
In d u ration, characteristically(*sfony harq in part or in the whole of the gland (with Obliteration of the
median sulcus), suggests carcinoma.
Extension beyond the capsule up into the bladder base and vesicles is diagnostic, as is local extension through the
capsule
POSSIBLE FINDINGS: Hard irregular nodule OR diffuse dense induration involving one or both lobes
METHODS OF SPREAD
1. Local spread (Think the tumour growing upwards and downwards)

■ Locally advanced tumours tend to grow upwards to involve the seminal vesicles, the bladder neck and trigone
■ Further upward extension obstructs the lower end o f one or both ureters, obstruction of both resulting in anuria
■ Later, the tumours tend to spread d 1stally to involve the distal sphincter mechanism
■ *The rectum may become stenosed by tumour infiltrating around it, **BUT direct involvement is rare.
2. Haematogenous
Haematogenous dissemination occuraCearly
Particularly to cone: NB: Prostate is me most common site of origin for skeletal metastases!!!, (followed in turn by the breast, the
kidney, the bronchus and thethyroid gland). ^ ^
o Most frequently Vne'pelvicJsopes and the lumbar vertebrae. The 'femoral head, nbcage and skull are other common sites.
Also, liver, lu n g , ad re n als next
3. Lymphatic spread
■ Obturator > iljac > presacral/para-aortic
STAGING - AJCC TNM

T - MOST IMPORTANT N M
T1: clinically undetectable tumour, normal DRE and TRUS NX: regional lymph nodes were not MO: no distant metastasis
Tta: tumour incidental histologic finding in <5% of tissue resected assessed M: distant metastasis
T1 b: tumour incidental histologic finding in >5% of tissue resected NO: no regional lymph node metastasis M1a: nonregional lymph nodes
T1 c: tumour identified by needle biopsy (because of elevated PSA level) N1: spread to regional lymph nodes M1 b: bone(s)
T2: palpable, confined to prostate M1c: other site(s) with or without bone disease
T2a: tumour involving < one half of one lobe
T2b: tumour involving > one half of one lobe, but not both lobes
T2c: tumour involving both lobes
73: tumour extends through prostate capsule
T3a: extracapsular extension (unilateral or bilateral)
T3b: tumour invading seminal vesicle(s)
T4: tumour invades adjacent structures (besides seminal vesicles)
IN V E S T IG A T IO N S — R d f ItT rou > !(/

G E N ER AL vs. S P E C IF IC (Diagnostic & Staging)
A. GENERAL Blood tes ts

1. CBC
a. Anaemia: 3 reasons: 1. Constitutional, 2. Leukoerythroblastic anaemia 2° to bone mets with BM failure 3. 2° to renal failure
b. Thrombocytopaenia and DIC in some pts
2. U & E s : Assess BUN and Cr for renal failure
B. SPECIFIC: (For BOTH DIAGNOSIS and STAGING w orkup!!!)

DRE
P S A - Interpretation:
o Has replaced acid phosphatase measurement!!
o Lacks sensitivity and specificity in diagnosing early prostate cancer
o BUT good at following advanced disease!!
PSA > 1 0 nmol/mL is SUG G ESTIVE o f cancer and
> 3 5 ng/mL is ALMOS T diagnostic o f advanced prostate cancer
IMAGING (-> for detection, staging andMuicUmJliPPsv)

. C r o s s -s e c tio n a l im a g in g : W R I p r e fe rr e d
O MR! with high tesla m a g w T ^ O S T ^ ^ U R A T E METHOD OF STAGING LOCAL DISEASE
May be used to guide biopsy ~ “
TBUS
T ran s re c ta I u ltra s o u n d ( T R U S )
o CAN ALSO BE USED FOR STAGING
fY lftl R■o n GCCUrak
7
o Used for TRUS-quided biopsy
V—7 >—
T ra n s re c ta l b io p s y
o if there is suspicion of prostate cancer, because of local findings, a raised PSA or metastatic disease, then a ransreciai bio / using
an automated gun is recommended._________
o Take ( f temat i c bioosv co7$5s+ as well as biopsy o f any suspicious/hyperechoic areas
o ' “ Routine local anaesthetic is used to decrease pain.
o ■' 'Broati-spccirum antibiotic cover is given to all patients to reduce the incidence of sepsis.
o If there are associated symptoms of BOO, then:

o A TURPcan be performed, which will provide diagnostic material and symptomatic relief
OTHER STAGING INVESTIGATIONS FOR METASTATIC WORKUP:

Bone: ALP, bone scan, bone marrow aspirate, AXR, CXR Osteolytic mets are also very common in prostate ca and may coexist with sclerotic
ones " * ^ —"
a. Once diagnosis made,Qnust perform bone scan if PSA > 1 0 nmol/m). or if biopsy shows high grade cancer
b. If PSA <10 nmol/mL, only perform it there are clinical indications ~~
Liven LFTs, CT abdomen
3. Lung: CT chest, CXR
4. Adrenal: CT abdomen
J r Upper urinary tract: Excretion urography, ultrasound
NOTE WELL: TRUS + DRE + m easurem ent o f PSA w ill detect o nly 30-50% o f cancers th a t are known to be
present on autopsy studies (although it may d ete ct th e larger, m ore sig n ifica n t cancers).
MANAGEMENT MU V c tO '* )
3 KEY PRINCIPLES - MUST UNDERSTAND THESE FIRST
1. Treatment options for prostate cancer depend on stage of disease, grade of disease, life expectancy of the
patient and patient preference
2. Curative treatm ent can only be offered to patients with early disease (T1 and 72)!!!
3. The treatm ent of patients w ith advanced disease (T3, T4 o r any M) is only palliative!!!
A. LOCALIZED CANCER can be treated by (choose one): **1. Radical prosta tectom y (RP - open o r laparoscopic
o r DaVinci robot), **2. Radiation the rapy (a. EBRT o r b. brachytherapy) and **3. A ctive m onito ring
B. ADVANCED DISEASE treatment is palliative, and **androqen ablation remains the first-line therapy___________
SUMMARY OF TREATMENT
CLASSIFY: EA R L Y DISEA SE vs. LO CALLY ADVANCED vs. M ETASTA TIC
A. EARLY DISEASE
1. T1/T2 ( lo c a liz e d . lo w -r i s k - FNB. M ortality risk is based on PSA, Gleason score and stage])
m if adequate life expectancy (younger, fitter <7Ch or no other significant co-morbidities, consider either active surveillance vs. definitive
local treatment (Radical prostatectomy, brachytherapy, or EBRT) AFTER COUNSELLING ABOUT THE RISK VS. BENEFITS
c “ 'POINT: No significant difference in cure rate between definitive treatment modalities (i.e. RP vs. radiotherapy)!!!
■ In older population (> 70): Conservative treatment: Watchful waiting + palliative treatment for symptomatic progression
2. T1/T2 (intermediate o r high-risk)
■ Definitive therapy preferred over active surveillance, unless older
■ NB: Active monitoring is still an option
■ In the elderly patient with outflow obstruction, TURP with or without hormone therapy is indicated
■ 25% risk of progression to metastatic disease in 10 years
B. LOCALLY ADVANCED DISEASE
3. T3. T4
■ Significant risk of progression
Androgen deprivation therapy alone. If sexually active, careful conservative mqmt. until symptoms arise
2* EBRT + androgen deprivation therapy (for 3 yr) (standard treatment for younger men with T3) (OR RP + adjuvant EBRT)
C- METASTATIC DISEASE
4. N >0 or M >0
■ Requires hormonal therapy/palllative radiotherapy for metastases,
* May consider combined androgen blockade - symptomatic relief in > 2/3 of patients
Local irradiation of painful secondaries or half-body irradiation - offers excellent palliation
Hormone-refractory prostate cancer

o Systemic chemotherapy: docetaxel, cabazitaxel, sipuleucel-T
METHODS OF ANDROGEN ABLATION/ANPROGEN DEPRIVATION THERAPY ^
A. SURGICAL
1. Bilateral orchiectomy - removes 90% of testosterone
B. MEDICAL
1. GnRH/LHRH agonists (e.g. leuprolide, goserelin)
2. Oestrogens [e.g. diethylstilbestrol (DES)]
3. Antiandrogens (bicalutamide)
Complete androgen blockade - concept is that of abolishing the testicular secretion of testosterone by means of orchidectomy or the use of
LHRH therapy and then inhibiting the effects of adrenal androgenic steroids by means of androgen receptor blockade with fiutamide,
bicalutamide or the use of cyproterone acetate
SOME DETAILS ON OPTIONS
5 TREATMENT OPTIONS FOR LOCAUZEL PROSTATE CANCER
1. Watchful waiting
■ Population considered: Short life expectancy (<5-10 yr); will likely only receivenon-curative hormonaltherapy if disease progresses
■ Limitations: Disease progression ' —
2. Active surveillance (serial DR E PSA and biopsies)

■ Population considered: Low grade disease, good F/U; is still considering more curative treatment if disease progresses
■ Limitations: Disease progression; decrease in QOL associated with serial testing; risks associated with biopsies; no optimal monitoring
schedule has been defined to date
3. Radical prostatectomy
■ Population considered: Young patients, good life expectancy (<75 yr),high-risk disease,mets excluded bybone scan, CT PSA < 20
■ Limitations: ED (30-50%), Incontinence (10%), ~ — ”
Dr. Aiken: 3 Main side effects of radical prostatectomy
1. v ^ r ectile Dysfunction^ y y
2. vÛrinary Inconti nence<~f°/o
3 VÂnastomotic Strictures 5%
4. External Beam Radiotherapy (EBRT)

■ Population considered: I ocallv advanced disease, older patients
■ Limitations: Local complications: irritation o f the bladder with urinary frequency, urgency and sometimes urge incontinence and similar
problems affecting the rectum with diarrhoea Radiation proctitis (5%), ED (50%), risk of rectal cancer
5. Brachytherapy -____________________________________
■ {Raaioactive seeds are nermariftnfiy imnlantPri into tho pcngtajy) Placed through transperinpal Delivers an intense, confined
radiation dose, which falls off rapidly to spare the surrounding structures
■ Population considered: Low volume, low PSA (<10), low grade. T1 disease mainly
■ Limitations: ED (50%), long term effectiveness not well-established
General Surgery
Urinary Tract Calculi
Sources: Bailey and Love, Harold Ellis, Toronto Notes
February 2015
INCIDENCE
■ Prevalence of 2-10%
■ M > F = 3:1
■ Peak incidence 30-50 yr of age
■ Recurrence rate: 10% at one yr, 50% at 5 yr, 60-80% lifetime
RISK FACTORS/AETIOLOGY/PATHOPHYSIOLOGY
Knowledge of stone formation within the urinary tract is still inadequate and many stones form without apparent explanation. Summary of current
opinion:
Predisposing factors may be classified into 4 main groups:

1. Inadequate drainage;
2. Excess of normal constituents in the urine -> SUPERSATURATION -> Necessary but not sufficient to cause stone formation!!! Hence 3 & 4!!!
3. Presence of abnormal constituents (“STONE PROMOTERS’) in the urine.
4. Lack of STONE INHIBITORS
1. Inadequate drainage;
• Calculi may form whenever urine stagnates, e.g. within a hydronephrosis
2. Excess o f normal constituents in the urine;

■ Increased concentration of solutes in the urine, because of either a low urine volume OR Increased excretion -> precipitation from a
supersaturated solution.
a. Inadequate urine volume: Renal stones are particularly common in people from temperate climates who qo to live in the tropics
DEHYDRATION
b. Increased excretion: (hypercalciuria) may be secondary to hypercalcaemia or, more commonly, idiopathic. COMMON CAUSES
of hypercalcaemia incl hyperparathyroidism and prolonged immobilization
c. Increased a excretion: (hyperoxaluria) results from increased dietary intake, with strawberries, rhubarb, leafy vegetables and tea
being among the culprits. Also a complication of loss of the terminal ileum (e.g. in Crohn’s disease or after surgical resection), which results
in increased oxalate absorption bv the colon.
d. Increased serum ... : may be accompanied by uric acid stone formation. The most common cause is gout, but it may also occur
following chemotherapy for leukaemia, lymphoma or polycythaemia.
e. :: loop diuretics (furosemide, bumetanide), acetazolamide, topiramate, and zonisamide
3. Presence o f abnormal constituents (“STONE PROMOTERS”) in the urine.

a. Urinary infection, particularly in the presence of obstruction, e.g. hydronephrosis or chronic retention, produces epithelial sloughs
upon which calculi may deposit In addition, infection may alter the urine pH, favouring precipitation of certain solutes. A high pH.
brought about bv the presence of urea-splittina organisms such as Proteus, favours calcium phosphate stone formation
b. Foreign bodies, such as non-absorbable sutures inserted at operation, ureteric stents, sloughed necrotic renal papilla
c. , which may occur in primitive communities, results in hyperkeratosis of the urinary epithelium, which again provides
the debris
d. Cystinuria, caused by a mutation in one of two different genes responsible for amino acid transfer in the kidney, may result in cysteine stone
formation.
4. Lack o f “STONE INHIBITORS ”

a. Citrate (forms soluble complex with calcium)
b. Magnesium (forms soluble complex with oxalate)
c. Potassium
d. Pyrophosphate
e. Tamm-Horsfall glycoprotein
ALSO HEREDITARY FACTORS RTA, G6PD, cystinuria, xanthinuria, oxaluria, etc.
COMPOSITION OF STONES: (MORE DETAILS ON LAST PAGE)

The three common stones are oxalate, phosphate and urate.
1. Oxalate stones {calcium oxalate) (60%) = most common - monohydrate, dehydrate, mixed (They are hard with a sharp, spiky
surface, which traumatizes the urinary tract epithelium; the resultant bleeding usually colours the stone a dark brown or black)
2. Phosphate stones (33%) are composed of a mixture of calcium, ammonium and magnesium phosphate ((calcium phosphate often with
ammonium magnesium phosphate (struvite)) ‘triple phosphate stone ). They are hard, white and chalky. They are nearly always found in
an infected urine and produce the large stag-horn calculus deposited within a pyonephrosis.
a. B&L: It grows in alkaline urine, especially when urea-splitting Proteus organisms are present. The calculus may enlarge to fill most
of the collecting system, forming a qtag-horn calculus
3. Uric acid and urate stones (5%) are moderately hard and brown in colour with a smooth surface. Pure uric acid stones are radiolucent
but, fortunately for diagnosis, most contain enough calcium to render them opaque to X-rays (by casting a faint radiologic shadow)
4. Cystine stones account for about 1% of urinary calculi. An uncommon congenital error of metabolism leads to cystinuria.
Note that a stone found in the lower urinary tract may have arisen there primarily or it may have migrated there from a primary source within the kidney.
CLINICAL FEATURES
DR. AIKEN: OVERALL SUMMARY

1. Asymptomatic
2. Silent obstruction
3. Pain (75% of presentations)
4. Haematuria
5. Infection
A. RENAL STONES
■ Silent calculi: Renal failure may be the first indication of bilateral silent calculi, although secondary infection usually produces symptoms first
■ Pain
Pain is the presenting feature of the great majority (75%) of kidney stones (but if the calculus is embedded within the solid substance
of the kidney it may be entirely symptom free) (within the major and minor calyx system, the stone produces a dull loin pain)
o ‘ "Fixed renal pain occurs in the renal angle, the hypochondrium, or in both. It may be worse on movement.
o Impaction of the stone at the UPJ or migration down the ureter itself -> Ureteric colic:
■ Ureteric colic is an agonising pain passing from the loin to the groin.
• Pain resulting from renal stones rarely lasts more than 8 hours in the absence of infection.
■ There is no pyrexia, although the pulse rate rises because of the severe pain. The severity of the colic is NOT related to the
size of the stone.
Points on ureteric colic

- Severe exacerbations on a background of continuing pain (severe waxing and waning pain)
Radiates to the groin, testis, tip of penis, scrotum or labium as the stone progresses down the ureter
Assc with typical restlessness, writhing. Patient unable to He still in bed
Unlike the usual textbook description, the pain is NOT usually intermittent but is continuous, although quite often with sharp
exacerbations on a background of continued pain.
There is often accompanying vomiting and sweating.
- Haematuria Is very common
■ Haematuria - microscopic (90%) or macroscopic

o Common and sometimes is the only symptom of stone disease.
■ Pyuria
o Infection is particularly dangerous when the kidney is obstructed -> Pressure builds in the system, organisms are forced
into the circulation and a septicaemia can Quickly develop.
o Stones may cause pyuria by irritating the urothelium even in the absence of infection.
Abdominal examination
■ During an attack of ureteric colic, rigidity may be present but not prominent. Percussion over the kidney produces a stab of pain and there may
be tenderness on gentle deep palpation.
■ Hydronephrosis or pyonephrosis leading to a palpable loin swelling is rare.
■ General exam in acute ureteric colic: Tachycardia, tachypnoea
B. URETERIC STONES
A stone in the ureter usually comes from the kidney!! Most pass spontaneously.
A stone passing down the ureter often causes intermittent attacks of ureteric colic.
■ Ureteric colic
■ Impaction
o There are FIVE sites of narrowing where the stone may be arrested.
o An impacted stone causes a more consistent dull pain, often in the iliac fossa and increased by exercise and lessened by
rest.
o The stone may become embedded as the adjacent ureteric wall becomes eroded and oedematous as a result of pressure
ischaemia. Perforation of the ureter and extravasation of urine is a rare complication.
o Severe renal pain subsiding after a day or so suggests complete ureteric obstruction. If obstruction persists after 1-2 weeks,
the calculus should be removed to avoid pressure atrophy of the renal parenchyma
■ Haematuria
o Almost ail ureteric colic is associated with transient microscopic haematuria. Serious bleeding is uncommon and
should suggest clot colic.
Abdominal examination
■ There is tenderness and some rigidity over some part of the course of the ureter. The presence ot haematuria does not rule out appendicitis because an inflamed
appendix can give rise to a local ureteritis leaking some red cells into the urine. The patient with acute ureteric colic is usually in greater pain and less ill than
one with appendicitis or acute cholecystitis
C. BLADDER STONES
■ Result in . STORAGE and VOIDING LUTS, terminal haematuria. suprapubic pain Ufeftrfope}vtc
■ If fever, r/o concurrent pyelonephritis and/or obstruction junction
Some points:
Location of Stones
• Calyx: may cause flank discomfort, persistent infection, persistent hematuria, or remain Crossjr*g
tKeilio'
asymptomatic
■ Pelvis: tend to cause obstruction at UPJ, may cause persistent infection J'jxJopcoifton
of vets
■ Ureter: <5 mm diameter will pass spontaneously in 75% of patients
The four narrowest passage points for upper tract stones are:
1. UPJ E ntering the-
2. Pelvic brim (where the ureter crosses the true pelvis/iliac artery) bidder wall
3. Under vas deferens/broad ligament 5
4. UVJ U re te r r<
onltre
Figure 75.28 N orm al onoSomicol ncmowtngs (f-5) c-\ the ureter
Table 11. Differential Diagnosis of Renal Colic
GU A b d om in a l N e u ro log ica l
* Pyelonephritis * AAA * Radiculitis ( L 1 ): herpes zoster.

• Ureteral obstruction from other cause: UPJ * Bowel ischemia nerve root compression
obstruction, dot colic secondary to gross hematuria, • Pancreatitis
sloughed papillae * Other acute abdominal crisis
* Gynecological; ectopic pregnancy, torsion/rupture ot
ovarian cyst, PiD
INVESTIGATIONS
Classify into CONFIRMING DIAGNOSIS vs. UNDERLYING CAUSE
General blood work

1- CBC
2. Uric acid (+/- serum calcium, serum phosphate, serum albumin)
Urine
3. Urinalysis - haematuria
4. Urine microscopy, C&S
(The above are for everyone!!!! even though they also look for underlying cause)
Radiologic Imaging
1. Plain KUB x-ray (KUB - not “abdominal” not “pelvic”!)

■ 90% of stones are radiopaque
■ An opacity maintaining its position relative to the urinary tract during respiration is likely to be a calculus.
■ NB: Calcified mesenteric nodes and opacities within the gut will be anterior to the vertebral bodies on a lateral x-ray and thus
outside the urinary tract!!! ALSO, do not mistake phleboliths for stones! (see below)
- Good for follow-up
2. Spiral CT scan (non-contrast: reason)

■ CT, preferably spiral, has become the MAINSTAY OF INVESTIGATION OF ACUTE URETERIC COLIC ( as replaced IVU
where available!!!)
■ MUST KNOW ADVANTAGES: Rapid, more sensitive for stone than IVU, can diagnose alternate pathologies (eg. torted ovarian
cyst, ruptured AAA)
■ Disadvantage: More radiation exposure
■ Can distinguish radiolucent stone from soft tissue filling defect
- B&L: If the CT or urogram is normal during an attack, the patient does NOT have renal colic!!!
3. IVU (i.e EXCRETION UROGRAPHY)

■ Establish the presence and position of a calculus and the function of the other kidney.
■ Demonstrate the exact anatomy of the renal system, e.g. the presence of associated hydronephrosis, although a completely
obstructed kidney may show no function whatsoever
W ayne Robinson. MBBS Class of 2015
There is an im p o rta n t ca tc h fo r the unw a ry ; a s m a ll ston e within the k id n ey m a y b e com p le te ly o bs c u re d b y the c o n tras t o f th e py elogram .
N e v e r s tate th a t a kidn e y is free from stories w ith o u t firs t c are fu lly in spe c tin g a plain x -ra y o f th e re na l area.
■ IVU while the patient has pain can confirm the diagnosis. May only demonstrate dilatation of ureter above obstruction after 36
hours
4. KUB ultrasound
- NOT GOOD AT VISUALIZING STONES!!!
■ Use: Paediatric cases or those concerning for obstruction
■ No radiation. Visualize hydronephrosis
■ Ultrasound scanning is of most value in locating stones for treatment by extracorporeal shock wave lithotripsy (ESWL)
5. Retrograde ureterography is performed as an immediate preliminary to an endoscopic operation to remove a calculus
6. MAG 3 renography
7. Cystoscopy
■ ± Those concerning for bladder stone
■ Cystoscopy is not indicated routinely but may reveal oedema around the ureteric orifice when the stone is nearby.
Investigating underlying cause (BLOOD LEVELS OF ALL THE STONE COMPOUNDS AND INHIBITORS):
■ PTH
- Cr, Ca2\ Na+, P 043', Mg2+
■ Oxalate, citrate, ± cysteine
■ 24 h urine x 2 for volume
• Analysis of the stone itself!!
BOX: Opacities on a plain abdominal radiograph that may be confused with renal calculus
■ Calcified mesenteric lymph node
■ Gallstones or concretion in the appendix
■ Tablets or foreign bodies in the alimentary canal (e.g. cyclopenthiazide (Navidrex-K))
- Phleboliths - calcification in the walls of veins, especially in the pelvis
■ Ossified tip of the 12th rib
■ Calcified tuberculous lesion in the kidney
■ Calcified adrenal gland
MUST KNOW: COMPLICATIONS (DR. AIKEN)

1. High Grade Obstruction
2. Obstruction with secondary infection
a. Infected hydronephrosis
b. Pyonephrosis
3. Renal Impairment
4. Anuria due to either impaction of calculi in the ureter on each side, or blockage of the ureter in a remaining solitary kidney. Obstruction of a
solitary kidney
5. Unrelenting Pain
6. Unrelenting vomiting
MANAGEMENT
A. ACUTE MANAGEMENT
MEDICAL vs. INTERVENTIONAL DECOMPRESSION
(know indications)
I. Medical
1. Analgesia ± antiemetics ± IV fluids IF vomiting
* NSAIDs help lower intra-ureteral pressure!!
■ NSAIDS. such as diclofenac and indomethacin, have replaced opiates as the first line of treatment for renal colic. The value of
smooth muscle relaxants, such as propantheline (Pro-Banthine), is debatable.
■ IV fluids If vomiting (note: IV fluids do NOT promote stone passage!!!)

■ ± antibiotics for bacteriuria
**The great majority of small stones within the ureter (up to 5 mm) pass spontaneously. (The lower the stone, the more likely it is to pass
spontaneously.)**
2. Medical expulsion therapy (MET)

a. g-blockers (e.g. tamsulosin): increase rate of spontaneous passage in DISTAL ureteral stones
b. Calcium channel blockers
“ INDICATIONS FOR URGENT DECOMPRESSION (DR. AIKEN)

ABSOLUTE RELATIVE
1. Obstruction with infection 1. High Grade Obstruction
2. Obstruction with renal impairment 2. Airline Pilot
3. Bilateral ureteric obstruction
4. Obstruction of a solitary kidney
5. Unrelenting Vomiting
6. Unrelenting Pain despite adequate analgesia
II. Interventional Decompression (Dr. Aiken):

■ Required if obstruction endangers patient, e.g. sepsis, renal failure
1. First line: Retrograde insertion of a double-J ureteric stent under anaesthesia (via cystoscopy)
2. Second line: Pla cem e nt o f pe rcu ta n e ou s n e p h ro s to m y +/- Antegrade stent placement as part of interventional radiological
procedure usually under local anaesthesia and sedation
o Advantageous in very ill septic patients at high surgical risk
Admit if necessary:
■ See Indications for Admission to Hospital
B. ELECTIVE MANAGEMENT
POINT: O P TIO N S D E P EN D O N THE LO C A TIO N O F THE S TO N E
DR. AIKEN SUMMARY
Majority of stones will pass spontaneously
1. Extracorporeal shock wave lithotripsy (ESWL)
2. Percutaneous nephrolithotomy (PCNL)
3. Retrograde ureteroscopy - flexible and rigid and intracorporeal lithotripsy
4. Cystolitholapaxy
5. Cystolithotripsy
Open Stone surgery (RARE nowadays)

1. Nephrolithotomy
2. Pyelolithotomy
3. Ureterolithotomy
a. Open
b. Laparoscopic
4. Cystolithotomy
MEDICAL
■ Likely conservative if ureteral stone <10 mm or kidney stone <5 mm and no complications/symptoms well controlled
■ Stones <5 mm especially likely to pass spontaneously
■ PO fluids to increase urine volume to >2 L/d (3-4 L if cystine) and MET
■ Specific to stone type
■ Periodic imaging to monitor stone position and assess for hydronephrosis
Although hypercalciuria is a risk factor for stone formation, decreasing dietary calcium is NOT recommended to prevent stone formation. Low dietary
calcium leads to increased Gl oxalate absorption and higher urine levels of calcium oxalate.
RE: SURGERY
Preoperative treatment
Antibiotic treatment starts before surgery and continues afterwards.
Operation for stone

Most stones should be treated by minimal access and minimally invasive techniques. Open operations are still needed when appropriate expertise is not available or newer
techniques have failed
RENAL CALCULI
Toronto: May stent prior to ESWL if stone is 1.5-2.5 cm
• ESWL if stone < 2 cm
■ PCNL if stone > 2 cm
A. Modern methods of stone removal
ExtracorporeaI shock wave lithotripsy

* Crystalline stones disintegrate under the impact of shock waves produced by the ESWL machine.
■ The shocks may be aimed by ultrasound or x-ray imaging.
Ureteric colic is common after ESWL, and the patient needs analgesia, usually in the form o f a non-steroida! anti-inflammatory drug.
Bulky stone fragments may impact in the ureter, causing obstruction. To avoid this, a stent should be placed in the ureter to drain
the kidney while stone fragments pass
■ The principal complication of ESWL is infection. Many calculi contain bacteria, which are released from the broken stone. It is
wise to give prophylactic antibiotics before E^SWL, and an obstructed system should be decompressed by a ureteric stent or percutaneous
nephrostomy before treatment.
Percutaneous nephrolithotomy (PCNL)

■ Endoscopic instruments are passed into the kidney by a percutaneous technique. Small stones may be grasped under
vision and extracted whole. Larger stones are fragmented by an ultrasound, laser or electrohydraulic probe and removed in pieces.
■ A nephrostomy drain is left in the system when the procedure is complete. This decompresses the kidney and
allows repeated access if necessary. Percutaneous nephrolithotomy is sometimes combined with ESWL
■ Complications of percutaneous nephrolithotomy include: (1) haemorrhage from the punctured renal parenchyma; (2) perforation of the
collecting system with extravasation of saline irrigant; (3) perforation of the colon or pleural cavity during placement of the percutaneous track.
B.JDpen surgery for renal calculi - (Ellis: RARELY is it necessary to perform open surgery simply to remove the stone, either through the
kidney substance (nephrolithotomy) or, wherever possible, through Its pelvis (pyelolithotomy). When the kidney Is grossly and Irreparably
damaged, nephrectomy should be performed.)
1. Pyelolithotom y (p elvis)
■ Pyelolithotomy is indicated for stones in the renal pelvis.
■ Incision is made in renal pelvis directly on to the stone. The stone is removed with gallstone forceps
■ If there is sepsis, a nephrostomy is essential to drain the system.
2. Open nephrolithotomy (parenchyma)
3. Nephrectom y
■ A functionless kidney destroyed by stone disease should be removed,particularly when there is xanthogranulomatous
pyelonephritis.
Treatment of bilateral renal stones

Usually the kidney with better function is treated first
URETERIC CALCULI
Ureteral stones >10 mm
■ ESWL and ureteroscopy (URS) are both first line treatment modalities for all locations
- Ureteroscopy has significantly greater success rates for stones at all locations in ureter, but also has higher complication rates (ureter
perforation, stricture formation, etc.)
■ PCNL is second line treatment

■ Laparoscopic or open stone removal (very rare)
Endoscopic stone removal
1. Ureteroscopic stone removal

■ introduced transurethrally across the bladder into the
A u re te ro s c o p e is
ureter to remove stones impacted in the ureter. Stones that cannot be
caught In baskets or endoscopic forceps under direct vision are
fragmented using an electrohydraulic, percussive or laser iithoiripterj!
Figure 75.29 Donnie stone<otcfi!ng bosket in use (a) basket introduced
_ . , . past stone, (b| opened, and |e| enclosing stone, ready lor witkdrcwo!
2. Pormta basket
■ The use of wire baskets under Image intensHier control has been replaced by ureteroscopic techniques BUT th e y maybe
useful when the instrum ents and expertise are nol available. T h e re is a d a n g e r of u re te ric in ju ry e ven w ith sm a ll ston e s.
3. Lithotripsy in situ
■ A s to n e in a p a rt o f th e u re te r th a t ca n be id e n tifie d by th e im a gin g s y s te m o f th e lith o trip te r can be fra g m e n te d in situ. T his fo rm of
tre a tm e n t is n o t a p p ro p ria te if th e re is c o m p le te o b s tru c tio n o r if th e s to n e h a s b ee n im p a c te d fo r a lo n g tim e.
4. Push-bang
■ A s to n e in th e m id d le o r u p p e r p a rt o f th e ure te r c a n o fte n be flushed back into the kidney using a ureteric catheter. A J -s te n t
s e c u re s th e ca lc u lu s in th e k id n e y fo r subsequent treatment with ESWL
5. Ureteric meatotomy
■ E n d o s c o p ic in c is io n w ith a d ia th e rm y k n ife w ill e n la rg e th e o p e n in g a nd fre e a s to n e lo d ge d in th e in tra m u ra l ureter.
Open surgery
1. Ureterolithotomy
■ An x -ra y c o n firm s th e p o s itio n of th e s to n e im m e d ia te ly b e fo re s u rg e ry.
■ T h e o p e ra tio n ca n be p e rfo rm e d la p a ro s c o p ica lly , b u t a lte rn a tiv e m in im a l a c c e s s te c h n iq u e s d e s crib e d a b o ve a re u s u a lly p re fe ra b le .
BLADDER CALC ULI

* Transurethral stone removal or cystolttholapaxy
■ Cystolithotomy
■ R e m o ve o u tflo w o b s tru c tio n (T U R P o r s tric tu re d ila ta tio n )
TRE ATIN G THE U N D ER LY IN G C A U S E
Prevention o f recurrence
The following investigations are appropriate in bilateral and recurrent stone formers:
- Serum calcium, measured fasting on three occasions to exclude hyperparathyroidism;
- Serum uric acid;
■ Urinary urate, calcium and phosphate in a 24-hour collection; the urine should also be screened for cystine;
■ Analysis of any stone passed.
Dietary advice is not usually helpful in avoiding stone recurrence in people who have a balanced diet. Those who consumeexcessive amounts of milk
products (calcium stones), rhubarb, strawberries, plums, spinach and asparagus (calcium oxalate stones) should be advised to be more moderate.
Patients with hyperuricaemia should avoid red meats, offal and fish, which are rich in purines, and should be treated with allopurinol. Eggs, meat and fish
are high in sulphur-containing proteins and should be restricted in cystinuria. Stone sufferers should drink plenty to keep their urine dilute. Drug treatment
is largely ineffective except in those few patients who are shown to have idiopathic hypercalciuria. Bendroflumethiazide (5 mg) and a calcium-restricted
diet reduce urinary calcium
Unless there is a specific biochemical abnormality, highfluid intake is the best prophylactic measure
Toronto: Prevention
Dietary modification;
■ Increase fluid (>2 L/d), K+ intake
■ Reduce animal protein, oxalate, Na+, sucrose, and fructose intake
■ Avoid high-dose vitamin C supplements
M edications:
■ Thiazide diuretics for hypercalciuria
■ Allopurinolfor hyperuricosuria
■ Potassium citrate for hypocitraturia, hyperuricosuria
Consideration must be given to monitoring stone formers with periodic imaging (i.e. at year 1 and then q2-4yrbased on likelihood of recurrence).
In d icatio ns fo r A dm ission to Hosp ital:

1. In tra c ta b le pain
2. In tra c ta b le v o m itin g
3. F ever (s ug g e s ts in fe ctio n)
4. C o m p ro m is e d rena l fu n c tio n (in c lu d in g s in g le k id n e y, b ila te ra l o b s tru ctin g sto n e )
5. P re g n a n c y
Stones and Infection

If se p tic, u rg e n t d e c o m p re s s io n via u re te ric s te n t or p e rc u ta n e o u s n e p h ro s to m y is in d ic a te d . D e fin itiv e tre a tm e n t o f th e s to n e sh o u ld be d e la y e d until th e
s e p s is has cle a re d
In d ication s fo r PCNL
1. S iz e > 2 cm
2. S ta g h o rn
3. U P J o b stru ctio n
4. C a lyc e a l d iv e rtic u lu m
5. C ys tin e sto n e s (p o o rly fra g m e n te d w ith E S W L )
6. A n a to m ic a l a b n o rm a litie s
7. F a ilure o f le ss in v a s iv e m o d a litie s
TYPES OF STONES
Table 13. Stone Classification

Typeof Slone Calcium175-15%) UHcAdd (5-10%) Struwre Cystine (1%)
Etiology HypercaSduria Uricadd precipitates iniow Infectionwith urea-splittmg Autosoma! recessivedefect m
Hyperuricosufia125%of patients volume, acidic urinewith ahigh organisms tPrcteus, smai bowefmucosal absorption
with Ca** stones) uncacidconcentration: Pseudomonas, Provtdenda, andrenal tubular absorptionof
Hyperoxaluria(< 5%of patients) * Hyperuricosunaafone Klebsiette, Mycoplasma, dibasic aminoacidsresults in
Hypocitraturia(12%of patients) * Lowurinary pH, lowurine Senate. S. aureus) results "COLA" inwine (cystine, omrihine,
Other causes: volumefe,g. Glwater less) inalkalineurinarypHand lysine, arginine)
» Hypomagnesemia- associated * Drugs(ASA. thiazides) precipitation of struvite
with hyperoxatfunaand * Diet (purinerichredmeats) (magnesiumammonium
hypoci'ratuna * Hyperuncosuriawith phosphate)
* Highdietary Na^ hyperuricemia
* Decreasedurinary' proteins * Gout
* Highurinary pH, lowurine * Highrateof ceil turnover
volume(e.g. Glwater loss) or cel death(leukemia,
* Hyperparathyroidism, obesity, cytotoxic drugs!
gout, OM
KeyFeatures RadiopaqueonKlfB Radiolucenf on(CUB PerpetuatesDTI becausestone Aggressivestate diseaseseen in
ReducingdietaryCtf* is NOTah RadiopaiêonCT itself harboursorganism childrenandyoungadults
. effectivemethodof prevention! Acidicurine, pH<6.5(NOT Stoneanda!)foreignbodies Recurrent stoneformation,
treatment necessarily elevatedurinary must beclearedtoavoid tartly hx
uric acid) recurrence Oftat staghorncalculi
Associatedwith staghorn FafotkyradiopaqueonKDB
catcti Positiveurinesodiumnitroprusside
Positiveunneip andcultures test, urinechromatographyfor
Note:E. colt infectiondoesnot cystine
causestruvitestones
3:1 (M:F), U71morecommon
infemale
Treatment Fluidsto increaseurinevolume Increasedfluid intake Completestonedearance IncreasedfluidIntake(3-4 Lof
Medical if stone <5mmandno to >2 L'd Akafotizationof urineto pH6.5 ABxfor6wk urhe/d)
complications for calciumstones: cellulose to 7(bicarbonate, potassium Regular F/Uwine citures A&aiinize urine(bicarbonate,
phosphate, orthophosphatefor citrate) potassiumcitrate), Penicllamme/
Procedurai'Siifgreat treatment absorptive causes i aliopuriho) cf-MPGor Captopri (formcomplex
if stone >5n*nor presence Cateiumoxalate: thiazides, with cystine)
of complications(seeU17for * potassiumcitrate, ± aHopurmol ESWLnoi effective
treatment) Calciumstruvite: ABx (stone must
be removed to treat infection)
O s .
Surgery Class Notes
Urology - Strictures and Image Review
Dr. Morrison
M arch 2015
RADIOGRAPH #1: Retrograde URETHROqram. (Was NOT a cystourethroqram - no contrast in bladder)
Finding: Showed urethral dilation
Must comment on:

( - ■ Smoothness of urethra
4 ■ Sfaliber/Anyjnairowing
3 - . ^ fflu s t state(where^he abnormality is. (On this film it was the distal bulbar urethra)
o It was a solitary tight and short stricture. Comment on this' '
<*• ■ IS ightness djanv stricture
S* ■ i S f present,flength.Vvhat level?
■ 6^\ny proximal dilatation?
CATHETER IS PASSED NO FURTHER THAT AT THE^NAVICULAR FOSSAÔ DELIVER THE CONTRAST
Important point: Remember the urethra is normally SMOOTH and fairly wide. A stricture may not always be dramatically clear. It may
actually just be seen as a loss of the normal smoothness of the urethra. In some cases, it may be very “tight” resulting in arTobvious
Jpnc^defgct
Know the parts of the urethra i(20 cm);and where they are on the radiograph
Anterior urethra *(15 cm) 1constituted by:

1. w-Penile urethra
2. i^Sulbar urethra (Where it curves)
Posteriorûrethra |3-4 crn)jtonstituted by:

1. MembranousTJrethra (This is short and where the sphincter is)
2. P'Prostatic urethra
RADIOGRAPH #2: MCUG. (Showed a lucency that was a suprapubic catheter used to instill the contrast)
Question: Why would you want to do this?

1. Stricture. Especially if there is a tight urethral stricture that did not allow contrast to pass on retrograde urethrogram
2. Assessing for VUR. Done on any child with a UTI because of the associated consequences of this abnormality
3. Outline Fistulae. E.g. colovesical Vistula, vesicovaginal fistula (e.g. due to cancer, radiation, hysterectomy)
RADIOGRAPH #3: Retrograde urethrogram
Findings: vV ^ „ * // w //
■ A long, solitary strictureîn the penile urethra, with proximal dilatation
■ And another^shoifTigh/structure in th^proximal bulbar urethrcf'
■ Was a poor image as the catheter was passed wall the way in. Hence missed the entire glans etc.
So sometimes it is useful to perform both retrograde urethrogram and anterograde cystourethrogram together
RE: URETHRAL STRICTURES
Causes of urethral strictures (From both Dr. Morrison and Dr. Aiken)
CLASSIFY: CONGENITAL (RARE) vs ACQUIRED
Acquired:
1. Up to 40% of strictures are idiopathic.
2. Trauma (A big category)

A. Iatrogenic trauma:
Wayne Robinson. MBBS Class of 20 <
■ Due to catheterization, usually with poor technique (e.g naoez-a*.r ~nation, insufflation of bulb in inappropriate
location)
■ Instrumentation with a rigid instrument e.g. Cystoscope or 'esecsosccoe
B. Blunt or penetrating trauma

Blunt trauma:s
■ E.g. Classically: Pelvic rim fracture, commonly from an 7 , - :e=: -sually occurs at the
bulboprostatomembranous junction. (This is more distal than c- : e r : - gr: - at the inferior border of the pelvic
diaphragm. Used to be thought to occur proximally, at the apex c*
o These are called “distracting injuries”
o Side note: Always do a DRE and check prostate in these cases ng for a “high-riding” prostate)
■ Other important blunt trauma: Straddle injuries

■ (Need to be aware of this for OSCE and written.) (Also known as" - j j t , 2 common mechanisms of straddle injury:
1. Falling off a bicycle -> Causes a focal discrete injury to bulbar ir e r 'a
2. The other cause of straddle injury is kick in the balls eg in sports
C. Sexual injury (e.g. penile frx)
3. Inflammation. Divide into infectious and non-infectious

A. Infectious: The 2 STIs associated with urethral strictures are gonorrhea anc chlamydia
■ Most commonly occur in bulbar urethra. Because this is the location o; the highest density of glands of Littre, and these
glands are tropic to the Gonococcal organism
B. Noninfectious: Lichen sclerosus -> When it affects the urethra calledOXO - xerotica oblitetans. Can cause
increased thickness and scarring in the urethra
Other causes:
4. Post radiation strictures e.g. radiotherapy for prostate ca
5. Impacted stone is a rare cause. Know the 2 common sites of stone impaction in utethra
URETHRAL STRICTURES VERY COMMON AND IMPORTANT
NB: Stricturesjyery rare in worrier]. Most commonly in hypoestrogenic women. E.g. post menopausal
HOW MAY THEY PRESENT
( ■ BOO: so LUTS -> Classify: Both STORAGE and VOIDING symptoms know them all
■ Also haenfatuffg
] ■ Or may havesymptoms of a complication
C0MPLICAI1ONSJ3F-BRETHRAL STRICTURES:
1. UThfevstiMovelonephritistiCprostatitisJ^
■ Sometimes~e^n(ep i^ y m o o rc h itI^ Entire lower urinary tract can be affected! - Don’t limit your answer to “UTI”
2. Fistulae are another complication: Secondary to buildup of urine proximal to the stricture, then decompression of urine via another
patTTof less resistance.
■ Know what is: “Watering can perineum” (this film was also shown) - Watering can perineum is a rare complication of
extensive periurethral fibrosis leading to multiple abscesses and fistule in the perineum
INVESTIGATION
■ Investigation of choice i
TREATMENT
Consider the location (E.g. Penile stricture treated differently from bulbar)
May b ^ o p e ^ r ^ doscopic^
A. Endoscopic - Optical Internal Urethrotomy (OIU):

■ Look in endoscopicallv and excise (or was it incise?) the stricture.
■ Usually for short strictures with minimal scarring.
■ If you do it in one with much scarring, after healing patient may develop a worse stricture.
Then place a urethral catheter and leave in for about 3-7 days, the remove see if patient can void
■ Unfortunately, (most strictures are not amenable to Ojlj^lu e to most strictures being long
B. Open surgery - Urethroplasty
Various options.
1. If short fanastomoticl urethroplasty) -> May excise and bring the edges back together
2. If much longer jtsubsf/fuf/on)urethroplasty) -> Can't excise. Can open longitudinally, then graft, then revascularize it
BuccaTmucusa must commonly used as graft
OR can use the foreskin as a flap Aka
RE: Dilation with a bougie/sound:

-
According to Dr. Morrison:

■ NOT a method of treatment. Harmful actually.
■ The only situation where dilators used are called filiform dilators used after OIU optic internal urethrotomy -> To assess the
current size after the procedure is the success of the procedures.
- SO IT IS NOT ACTUALLY FOR DILATION DESPITE THE NAME.
- DILATION IS ONLY FOR HISTORIC SIGNIFICANCE NOT DONE ANYMORE.
i P
J-
NS5 Neurosurgery Intracranial Pressure (ICP) Dynamics Toronto Notes 2014
Table 2. Consequences of Common Brain Lesions

Locationof lesion __________ Consequence
Frontal lobe 1- Disinhibition
2. Concentration deficits
3, Orientation deficits
4. Judgement deficits
5, ± Primitive reflex re-emergence
Riît parietal lobe Spacial neglect syndrome
• Contralateral agnosia
Basal ganglia 1. Rest tremor
2. Chorea
3. Athetosis
Subthalamic nucleus Contralateral hemiballismus
Amygdala (bilateral) Kluver-Bucy syndrome*
1 Hyperorality
2. Hypersexuality
3. Disinhibition
Mammillary bodies (bilateral) Wernicke-Korsakoff syndrome
t Wernicke
• Confusion
• Ataxia
2. Korsakoff
• Memoryloss
• Confabulation
• Personality changes
Hippocampus Anterogradeamnesia
Reticular activating system (midbrain) Reduced levels of arousal and wakefulness
PPRF Eyeslook awayfrom lesion
Frontal eyefields Eyeslooktoward lesion
Cerebeliar hemisphere 1. Intention tremor
2. Limb ataxia
3. Fall towards side of lesion
ICP mmHg
Cerebellar vermis 1. Truncal ataxia
2. Dysarthria too
80
SO
nust know the /
dONROE-KELLIE ICP/Volume Relationship 40
/
^
1/ / f
*
«
ioctrine!! r * ^
V ' 1
f
i
adult skull is rigid with a cnnstantjntracranial volume * 0
contents ((CSF\bkyo<j'ibrai h) arefecompressit fl Volume — ► |
«
increase in one constituent/space-occupying lesion = increase in ICP When a mass expands Eventually, further
however, ICP does not rise initially due to compensatory mechanisms (autoregulation): within the skull. small increments
compensatoty in volume produce
a imm ediate: displacement of CSF to lumbar theca, displacement of blood from venous mechanisms initially larger and larger
sinuses V
maintain a normal ICP. increments in ICP. J
■ delayed: displacement of ECF or ICF; displacement of brain tissue into compartments under
Figure 5. ICP-voluroe curve
less pressure (herniation) ............................ ............................................................... AdaptedfromLindsay KW. Bone l: Neurologyand
once compensation is exhausted, ICP rises exponentially ^ neurosurgery illustrated. ©2004. With permission
fromElsevier.
Cerebral Blood Flow (CBF)

• CBF depends on cerebral perfusion pressure (CPP) and cerebral vascular resistance (CVR)
• normal CPP >50 mmHg in adults
- cerebral autoregulation maintains constant CBF by compensating for changes in CPP, unless: CBF = CPP/CVR
■ high ICP such that CPP <60 mmHg CPP = MAP - ICP
• MAP >150 mmHg or MAP <50 mmHg
■ brain injury: e.g. SAH, severe trauma
ip e P ^ 15 f ir 3 '7 '2 c L ‘ (d t f r •
NS6 Neurosurgery
2
Intracranial Pressure (ICP) Dynamics Toronto Notes 2014
ICP Meas Autoregulation: CBF maintained despite

change in CPP
$
O
normal ICPv^lS mmHg (8 adult,[3-7 mmHg (4-9.5 cm H20 ) for d varies xsz
with patient
TO3
o2
-2
moderate elevation: increase in mean pressure >20 mmHg
■ severe elevation: increase in mean pressure >40 mmHg J5
XV
y S !
waveform; comprised ol respiratory and cardiac pulsations ( lraube-Hering waves); the Oa3 <60 mnjHg ":>150 mmHq
amplitude increases with ICP Low BP or High ICP High BP
■ [5-waves: coarse, variably increased amplitude, frequency %-2/min, often related to Cerehral perfusion pressure (MAP-ICP)
respiration
■ plateau waves: elevation of ICP over 50 mmHg Lasting 5-20 min, precursor of further Figure 6. Cerebral autoregulation
deterioration curve
Adapted ta n Lindsay, el al. Neurology and neurosurgery
illustrated. £2QM. With permission from Elsevier
should know: Acute Monitoring
lumbar puncture (LP) (see sidebar)
intraventricular catheter/ventriculostomy/external ventricular drain (EVP) ("gold standard”
also permits therapeutic drainage of CSF to decrease ICP) —^
Chronic Monitoring Consider M onitoring of ICP in the

• fibre optic monitor (intraventricular intraparenchymal, subdural), subarachnoid bolt fo lio wing Situations
» Patients with an abnormal head
(Richmond screw), and epidural monitor CT and GCS score of 3-8 after
cardiopulmonary resuscitation
Or
Elevated ICP • Patients w ith a normal head CT and
GCS score of 3 to 8 AND the presence
of two or more of the following:
MUST KNOW Etiology • Age over 40 yr
ALL THESE: . irtr< space-occupying • Unilateral or bilateral motor posturing
* tumour • Systolic blood pressure less than
90 mmHg
■ pus • Postoperative monitoring
* blood [trauma hematoma (most common , subarachnoid hemorrhage] • Investigation of normal pressure
* depressed skull fracture hydrocephalus (NPHj
■ foreign body
increased
_uv ■ vasodilatation (increased pC 0 2/decreasedp02/decreased extracellular pH,
^.e.g. hypoventilation)
Lumbar puncture is contraindicated w ith
• venous outflow obstruction (vehous sinus thrombosis, superior vena cava syndrome, space known/suspected intracranial mass.
occupying lesion)
■ cranialjiep«odency
• cerebral(edema/
■ vasogeHTcTvessel damage, e.g. hypertensive encephalopathy, tumour)
■ cytotoxic (tissue/cell death, e.g. hypoxia, brain injury) Blood Brain Barrier
• osmotic (acute hyponatremia, hepatic encephalopathy) Glucose and amino acids cross slowly
Non-polar/lipids cross fast
• impaired autoregulation (hypotension, hypertension, brain injury)
• hydrocephalus (obstructive, non-obstructive)
• tension pneumocephalus (gas within the cranial cavity)
• pseudotumour cerebri (idiopathic intracranial hypertension)
» status epilepticus (chronic seizure resulting in brain edema) Blood Brain Barrier
m
P
Irrfarctioru'neopiasnj^lJestroy tight
Clinical Features ------C / ( sl P&I ^L- junctions - * yasgoenic edema
1. Acute Elevated ICP
* —> headache (H/A): worse in the morning, aggravated by stooping and bending
* —» nausea and vomitingiN/V) __________ .
* — > decreased level of consciousness|(LOC) if ICP = diastolic Blj or midbrain compressed
i Cushing's Triad of Acute Raised
X J ** —>* drop in GCS = best index to monitor progress and predict'outcome of acute intracranial process ffull triad seen in 1/3 of cases)
(see Neurotrauma7~N$3Q) ^ > *~HypertensTt3rr
->■ • papilledema ± retinalJiemprrhages (may tak^ 24-48 hjto develop) Bradycardia (late finding)
abnormal extra-ocular movements (EOM): Irregular respiratory pattern
CN VI palsy])often falsely localizing (causative mass may be remote from nerve)

upward gaze palsy (especially in children with obstructive hydrocephalus)
HT herniation syndromes (see Herniation Syndromes, NS7)
> focal signs/symptoms due to lesion Papilledem a
Elevated optic disc with blurred
margins
2 C hronic Elevated ICP
Larger blind spot
• H/A #
■postural: worsened by coughing, straining, bending over
■ morning/evening H/A vasodilatation due to increased CO, with recumbency
t f
[\fd rt Wclf
NS7 Neurosurgery Intracranial Pressure (ICP) Dynam ics/H erniation Syndromes Toronto Notes 2014
visual changes
■ due to/papilled
eriTargecTblincl spojîf advanced episodic constrictions of visual fields (“grey-outs”)
■ optic atrophy/blindness
■ differentiate from papillitis (usually unilateral with decreased visual acuity)
decreased level of consciousness
Investigations
• patients with suspected elevated ICP r<
• ICP monitoring where appropriate
H e rn ia tio n S yn d ro m e s
Table 3. Herniation Syndromes
Herniation Syndrome Definition Biology Clinical Features
KNOW THIS 1Subfa,cine Cingulategyrus Lateral supratentorial lesion * Usually asymptomatic <-- Dr. Charles keeps mentioning this in his
ONE > ------------ ' herniates under falx Warns of impending transtentorial herniation cerebral haemorrhage images
>4/ * Riskof ACA compression
H O inL ^ ^ 2■Ce«traITentoâl Displacement of Supratentorial midline Small pupils, moderately dilated, fixed (rostra!
(Axial) diencephalon lesion to caudal deterioration), sequential failure of
through tentorial Diffuse cerebral swelling diencephalon, medulla
notch Late uneal herniation Decreased LOC(midbrain compression) FOM/
upward gaze impairment ("sunset eyes"):
compression of pretectum and superior colliculi
Brainstemhemorrhage ("Duret's"- secondary
to shearing of basilar artery perforating vessels)
Diabetes insipidus (traction on pituitary stalk
and hypothalamus), end-stage sign
Lateral supratentorial lesion
MUST KNOW (often rapidly expanding Figure 7. Herniation types - see
most reliable~signf-r^psilateral EOMparalysis,
THIS ONE!!!
h(/rJckiC* traumatic hematoma) ptosis (CNJII compression) eye is "down an< Jaj}/e 4 for description
2. f Decreased LOC(midbrain compression)
Contralateral hemiplegia ± extensor (upgoing)
plantar response ± ipsilateral hemiplegia
("Kemohan's notch” - afalse localizing sign
jf/V u P U l'X
resultingfrompressurefromthe edge of the
tentoriumonthe contralateral cerebral peduncle) ^ j <1 (
4. Upward Cerebellar vermis Large posterior fossa mass Cerebellar infarct [superior cerebellar artery / Un<bi//l^ rr' iC^ o A '~
herniates through (common after VPshunting) (SCA) compression]
tentorial incisura Hydrocephalus (cerebral aqueduct compression)
C O O dU L ,
5. Tonsillar Cerebellar tonsils Infratentorial lesion Neck stiffnessand headtilt (tonsillar impaction)
herniatethrough Following central tentorial Decreased LOC(midbrain compression)
foramenmagnum herniation Flaccid paralysis
Following LPinpresence of Respiratory irregularities, respiratory arrest i> &cv<
intracranial mass lesion (compression of medullary respiratory centres)
Blood pressure instability (compression of
medullary cardiovascular centres)
2
nO~
Treatm ent of Elevated ICP
<• CT or MRI to identify etiology, assess for midline shift/herniation
t# treat primary cause (Le, remove mass lesions, ensure adequate ventilation)
*. if elevated ICP persists following treatment of primary cause, consider therapy when
Treatment of Elevated ICP:
•^ o a ls;keepit^^<20<MunHg, C^P>65 mmHg, >90mmHg ICP HEAD
Intubate
\{ui Conservative Measures

© » elevate head of bed atQO/, maintain neck in neutral position -* increases intracranial venous
Calm (sedate MComa
Place dratn/Paraiysis
outflow with minimal effect on arterial pressure Hyperventilate

@ • prevent hypotension with fluid and vasopressors, dopamine, norepinephrine prn Elevate head
H<~L <£)• ventilate to normocarbia (pCQ^35-4§)mmHgj -» prevents vasodilatation Adequate BP
Diuretic (mannitol)
oxygen to maintain p 0 2 >60pm m g-» prevents hypoxic brain injury'
osmolar diuresis (mannitoVÔ^fl IV solution 1-L5 g/kg, then 0.25 g/kg q6h to serum osmolarits-
o f 315-320) ^ “V - =
, can give rapidh{acts in 15-30 must maintain sBP >90 mmHg
corticosteroids decrease edema over subsequent days around brain tumour, abscess, blood
no proven value in head iniury or stroke
»N
NS8 Neurosurgery H erniation Syndrom es/Hydrocephalus Toronto Notes 2014
-* “heavy” e.g. fentanyl /MgS04)

sympathetic tone, reduces HTN induced by muscl
mmHg
- also results in (decreased cerebral blood flow
assess each situation independently
with pentobarbital to reduce cerebral blood flow and

over 30 min, then 1 mg/kg q lh continuous infusion)
improvement in neurological outcome
injury MoA.
H ydroc eph alu s

• hydrocephalus in children, see Pediatric Neurosurgery>
, NS.36
(------------------------------------ %
Definition
• increased CSF volume
Etiology
* obstruction to CSF flow
» decreased CSF absorption
• increased CSF production (rarely) - e.g. choroid plexus papilloma (0.4-1% of intracranial
tumours)
Epidemiology
* estimated prevalence 1-1.5%; incidence of congenital hydrocephalus -1-2/1000 live births 1. 'Lateral ventricles
2. Choroid plexus
Classification 3. Third ventricle
4. Cerebral aqueduct (of Sylvius)
5. Fourth ventricle
Table 4. Classification of Hydrocephalus 6. Foramina of Luschka and Magendie
Disorder Definition 7. Arachnoid granulations
Etiology Findingson CT/MRI
8. Subarachnoid space
Obstructive Circulation blocked within Acquired • Ventricular enlargement ^ 9. Superior sagittal sinus
(Non-Cornmuiricating) ventricular systemproximal • Aqueducta! stenosis (adhesions to
proximal bloti Figure 8. The flow of CSF
Hydrocephalus to thearachnoid following infection, hemorrhage) • Periventricular hypodensity
granulations • intraventricular lesions (tumours e.g. (transependyma! migration
3rd ventricle colloid cyst, hematoma) of CSFforced into
» Mass causing tentorial herniation, extracellular space)
aqueduc1/4lh ventricle compression • Sulcal effacement
CSF produced by choroid plexus, flows
• Others: neurasarcoidosis, abscess/ to: ventricles - * foramina of Luschka
granulomas, arachnoid cysts (lateral) and Magendie (medial) - *
subarachnoid space - * absorbed by
Congenita!
arachnoid villi/granuiations into venous
» Aqueductal stenosis, Dandy-Walker sinuses.
malformation, Chiari malformation
(seePediatricNeurosurgery, NS37) CSF production = CSF reabsorption =
—500 rriL/d in normal adults
Non-Obstructive CSFabsorption blocked at • Post-infectious (#1 cause) • All ventricles dilated Normal CSF volume —150 mL (50%
(Communicating) extraventricular she - meningitis, cysticercosis spinal, 50% intracranial - * 25 mL
Hydrocephalus arachnoid granulations • Post-hemorrhagic (#2 cause) -* intraventricular, 50 mL subarachnoid)
SAH, Ml, traumatic

» Choroid plexus papilloma (rare,
causes increased CSFproduction)
• Idiopathic normal pressure
hydrocephalus
Normal Pressure Persistent ventricular •• Idiopathic (50%) • Enlarged ventricles without
Hydrocephalus dilatation inthe context of » Others: subarachnoid hemorrhage, increased prominence of
(NPH) normal CSFpressure meningitis, trauma, radiation-induced cerebral sulci
Hydrocephalus Ventricular enlargement • Normal aging • Enlarged ventricles and
Ex Vacuo resulting fromatrophy of » Alzheimer's, Creulzfeldt-Jacob sulci
surroundingbrain tissue Disease • Cerebral atrophy
General Surgery
Urothelial (esp. Bladder) Carcinoma
Sources: Toronto Notes, Essential Surgery
March 2015
EPIDEMIOLOGY AND AETIOLOGY OF UROTHELIAL CARCINOMA (TRANSITIONAL CELL CARCINOMA)

■ Tumours of urothelium are common. Histologically, they are nearly all urothelial carcinomas (UCs); other than rarities, the rest are squamous
cell carcinomas (7%) or adenocarcinomas (1%).
■ Most arise primarily in the bladder but they also occur in the pelvicalyceai system and ureters and rarely in the urethra.
■ Urothelial tumours uncommon below age 50 (and the incidence increases with age)
■ M > F . (3:1)
■ UC is at least four times more common than renal cell carcinoma.
Cigarette smoking is associated with a four-fold increase in incidence of urothelial tumours; this is probably mediated by urinary excretion of inhaled
carcinogens.
Exposure to industrial carcinogens, once widely used in the rubber, cable, dye and printing industries (Strong association)
The likely carcinogens, benzidine, nigrosine and beta naphthylamine, are now banned in most countries but tumours can develop as long as 25 years
after exposure
(Prolonged exposure to carcinogens causes a 20-60 times increased risk of developing urothelial cancer. These carcinogens are excreted in the urine
and the more prolonged presence of urine in the bladder compared with the rest of the tract probably explains why urothelial tumours most often arise in
the bladder)
BLADDER CARCINOMA
EPIDEMIOLOGY
■ 2nd most common urological malignancy
■ Male > female = 3:1, white > black = 4: 1
■ Mean age at diagnosis is 65 yr
AETIOLOGY
Unknown, but environmental risk factors include:
- Smoking (MAIN FACTOR - implicated in 60% of new cases)
■ Aromatic amines: Naphthylamines, benzidine, tryptophan, phenacetin metabolites
■ Cyclophosphamide
■ Prior hx of radiation treatment to the pelvis
For SCC:
■ Schistosoma hematoblum infection (associated with SCC)
■ Chronic irritation: cystitis, chronic catheterization, bladder stones (associated with SCC)
The “field defect” theory helps to explain why TCC has multiple lesions and has a high recurrence rate. The entire urothelium (pelvis to bladder) is
bathed in carcinogens.
PATHOLOGY
Most aetiological factors act on the whole urothelium, predisposing it to malignant transformation. Consequently, urothelial tumours can be
multifocal and there may already be multiple tumours at presentation. When the primary tumour is in the pelvicalyceai system or
ureter, there is a high risk of tumours developing later in the urothelium distal to the primary. About 50% of patients with upper tract Urothelial tumours
will ultimately develop bladder urothelial tumours
Classification:
1. TCC >90%
2. SCC 5-7%
3. Adenocarcinoma 1%
4. Others <1%
Stages and prognoses of urothelial carcinoma at diagnosis:

■ Non-muscle invasive (75%) -> > 80% overall survival
o 15% of these will progress to invasive TCC
o The majority of these patients will have recurrence
■ Invasive (25%) 50-60% 5-yr survival

o 85% have no prior hx of superficial TCC (i.e. de novo)
o 50% have occult metastases at diagnosis, and most of these will develop overt clinical evidence of metastases within 1 yr - lymph nodes,
lung, peritoneum, liver
“Carcinom a-in-situ” -> Flat, non-papillary erythematous lesion characterized by dysplasia confined to urothelium
■ More aggressive, worse prognosis
■ Usually multifocal
■ May progress to invasive TCC
(Essential: A sinister form of urothelial carcinoma is carcinoma-in-situ. This presents with frequency and dysuria, aptly named ‘malignant cystitis’. These
symptoms are often misdiagnosed as bacterial prostatitis in men. The lesions desquamate easily and have a high pick-up rate on urine cytology.
Untreated, they infiltrate rapidly)
CLINICAL FEATURES OF BLADDER CARCINOMA

■ Asymptomatic (20%)
■ Haematuria (key symptom: 85-90% at the time of diagnosis)
■ P a in (50%) location determined by size/extent of tumour (i.e. Flank, suprapubic, perineal, abdominal, etc.)
■ Clot retention (17%)
■ Obstruction of ureters -> hydronephrosis and uraemia -> (nausea, vomiting, and diarrhea)
■ Storage urinary symptoms -> Consider carcinoma in situ
• Recurrent UTI
■ Palpable mass on bimanual exam -> likely muscle invasion
ESSENTIAL: CLINICAL FEATURES OF UROTHELIAL CARCINOMA

■ Urothelial carcinoma usually presents with “painless haematuria”
o Rapid bleeding from a bladder tumour may cause clot retention, i.e. -» (acute retention of urine due to clot obstruction)
o If bleeding is gross, clots may cause ureteric obstruction.
o Very occasionally, an upper tract lesion may cause ureteric colic (cioi colic) and long stringy clots are seen in the urine.
■ Bladder tumours arising near a ureteric orifice can obstruct ONE ureter, causing hydronephrosis.
o Rarely, BILATERAL obstruction causes uraemia.
o Bladder tumours also predispose to infection; unexplained recurrent urinary tract Infections need investigating to exclude UC as a
cause.
■ Tumour invasion near the bladder neck may cause incontinence but this is usually preceded by haematuria or infection.
The ENTIRE urinary tract must be evaluated in patients with hematuria unless there is clear evidence of glomerular bleeding (e.g. red cell casts,
dysmorphic RBCs, etc.).
Some points:
■ Unexplained hematuria in any individual >40 yr old must be investigated to r/o a malignancy.
■ Cystoscopy is the initial procedure of choice for the diagnosis and staging of urothelial malignancy.
■ Tumour grade is the single most important prognostic factor for progression.
INVESTIGATION OF SUSPECTED UROTHELIAL CARCINOMA

G ENER AL & S P E C IFIC
A. GENERAL
Bloodwork
1. CBC - Anaemia?
2. U&Es - May find uraemia, electrolyte disturbances
Urine
1. U/A - Haematuria,
2. Urine C & S - Exclude infection as a cause of symptoms as well as secondary to stasis from obstruction
3. Urine cytology
4. Ultrasound examination may reveal hydronephrosis if there is ureteric involvement by UC
Confirmed haematuria in the absence of infection must be investigated.
B SPECIFIC'
CONFIRM d Ia GNOSIS: IMAGING + CYSTOSCOPY & BIOPSY
1. Contrast CT (C T UROGRAPHY) scanning will outline the upper tract as well as the renal parenchyma.
a. Look for a filling defect
2. IVU can also outline the upper tract, but is BECOMING OBSOLETE
3. Cystoscopy with bladder washings (gold standard)

a. Imaging is followed by cystoscopy, the only reliable method of examining the lining of the bladder and urethra. If there is an upper
tract tumour, cystoscopy may reveal blood emerging from a ureteric orifice.
4. Biopsy to establish diagnosis and to determine depth of penetration
5. Specific bladder tu m o u r m a rk e rs (e.g. NMP-22, BTA, Immunocyt, FDP)

STAGING & METASTATIC WORKUP

■ For invasive disease: CT or MRI, CXR, LFTs, extended electrolytes (metastatic work-up)
Essential: STAG IN G OF U R OTH ELIAL T U M O U R S OF TH E B LA D D ER
■ Staging is achieved mainly by cystoscopic examination and palpation under anaesthesia, combined with histological examination of resected
specimens.
■ For small and superficial lesions, histology shows the extent of bladder wall invasion, degree of tumour differentiation and whether the tumour has
been completely removed.
■ For larger or deeper lesions, palpation of the bladder under general anaesthesia bimanually between a finger in the rectum and a hand on the
anterior abdominal wall should be performed before and after resection of the tumour. This gives an idea of the extent of bladder wall penetration
and spread into the pelvis, but can be misleading, especially in the obese.
■ CT scanning is a more reliable indication of spread into the bladder wall or beyond. Note, however, that CT scanning can also be misleading if
performed soon after resection of a bladder tumour.
■ TNM replaced the previously widely used Jewett-Scgtt-MarshaU staging system
■ The TNM clinical system is widely used in staging bladder tumours (the ‘T’ is the clinical stage of the tumour). In addition, some pathologists grade
bladder tumours according to P and G pathological criteria. The ‘P’ system (small p for the biopsy specimen and capital P for the whole specimen)
classifies the extent of invasion on gross anatomical and histological grounds. The ‘G’ system grades the lesion by degree of histological
differentiation (G1 = well differentiated, G2 = moderately differentiated and G3 = poorly differentiated or undifferentiated)
Grading (: r ig S y s te n ■There is a 2004 WHO grading sytem but the 1973 still most commonly used)
1. Grade 1 (G1): well-differentiated (10% invasive)
2. Grade 2 (G2): moderately differentiated (50% invasive)
3. Grade 3 (G3): poorly differentiated (80% invasive)
TREATMENT
Treatment depends on stage and may be C U R A T I V E or P A L L I A T I V E
The initial management of bladder tumours is usually aimed at complete removal of tumour tissue by cystoscopic transurethral resection of bladder
tumour (TUJRBT), even with large lesions. Further management then depends on the stage of tumour spread determined by examination under
anaesthesia, CT scanning and histological staging
A. SUPERFICIAL (NON-MUSCLE INVASIVE) DISEASE: TIS. TA, T1

■ TUJRBT± single dose OR 6-w k course o f intravesical chem o/imm uno-therapy (e.g. BCG, mitomycin C) to decrease
recurrence rate
* Maintenance with intravesical chemotherapy with BCG may be continued for 2-3 yr
■ High grade disease: TURBT + maintenance BCG OR cystectomy in select patients
B. INVASIVE DISEASE: T2A. T2B, T3

■ Radical cystectomy + pelvic lymphadenectomy with urinary diversion (e.g. ileal conduit, Indiana pouch. Ileal neobladder)
a. OR TURBT + chemo-radiation for small tumours
■ Neo-adjuvant chemotherapy prior to cystectomy in some cases to downstage tumour
■ Radiotherapy is a good alternative for the unfit or older patient, in those unwilling to undergo cystectomy, or for relapse after initial
cystectomy or initial systemic chemotherapy
■ Use of adjuvant chemotherapy after definitive local treatment is controversial
C. ADVANCED/METASTATIC DISEASE: T4A, T4B, N+, M+

■ Initial combination of systemic chemotherapy ± irradiation ± surgery
■ NB: T4 tumours are usually incurable; even total cystectomy rarely eliminates the entire lesion. Radiotherapy offers palliation and is
valuable for controlling pain and haematuria.
NB: When radical cystectomy is necessary, some method of urinary diversion is required. The classic operation involves isolation of a segment of ileum;
both ureters are then anastomosed onto the ileal segment, creating an ileal conduit, whilst the other end is opened onto the abdominal wall as a
urostomy. An earlier operation in which both ureters were diverted into the sigmoid colon has long been abandoned because of electrolyte disruption and
a high risk of carcinoma at the ureterocolic anastomoses. Nowadays, most urinary diversions are into a continent pouch (a neo-bladder) usually
constructed from a segment of ileum and anastomosed to the urethra.
FOLLOW-UP AND CONTROL OF RECURRENT DISEASE

■ Patients who have had potentially curative treatment for urothelial tumours (i.e. bladder stages T1 to T3 and all upper tract lesions) must be
followed up for life.
■ The goal is to detect recurrence of the original tumour and to diagnose new primary lesions at an early stage, bearing in mind that environmental
factors that induced the initial lesion predispose the remaining urothelium to malignant change.
« It is not always easy to distinguish between small recurrences and new primaries; all tend to be labelled as ‘recurrences’.
■ Follow-up involves regular ‘check’ flexible cystoscopies under local anaesthesia. Initially, these are performed at 3-monthly intervals and the interval
is gradually extended to once a year if no further tumour is discovered.
■ There is currently a vogue for using nuclear protein tumour markers which can pick up 50% of tumour recurrences; however, the reliability needs to
be improved before it can replace existing methods. Urine cytology may also be used for screening normal individuals with a high occupational risk.
Other urinary markers are also currently undergoing investigation.
■ Recurrent lesions are managed in the same way as the initial lesion, i.e. according to the stage of bladder wall invasion.
o The exception is when the initial treatment involved radiotherapy. For these patients, cure of recurrent cancer is improbable and palliative
surgery ranging from TURBT to total cystectomy may be necessary to treat intractable problems such as severe haemorrhage.
Transurethral resection of tumour Residual tumour sWl present
T4 Radiotherapy alone Radiotherapy
Fig. 36.8 Cystoscopic management of bladder

tumours~“ SUmmary
P R O G N O S IS
Depends on stage, grade, size, number of lesions, recurrence and presence of CIS:
1. T1: 90% 5-yr survival
4. T4/N+/M+: <5% 5-yr survival
C P l& -
Paediatric Surgery
Overview of Common Topics
Sources: Essential Surgery 5E, Toronto Notes
March 2015
OUTLINE OF CONTENTS
Abdominal emergencies in the newborn 9. Congenital hypertrophic pyloric stenosis

1. Intestinal atresia 10. Intussusception
2. Malrotation with volvulus
3. Hirschsprung’s disease (congenital aganglionosis) Abdominal emergencies In older children
4. Congenital diaphragmatic hernias 11. Acute appendicitis
5. Others 12. Torsion testis
13. Meckel’s diverticulum
Abdominal emergencies in infants and young children
6. Inguinal hernias Problems with the groin and male genitalia
7. Femoral hernias 14. Hydrocoele
8. Umbilical hernias
ABDOMINAL EMERGENCIES IN THE NEWBORN

The widespread use of antenatal ultrasound means many congenital abnormalities needing surgical correction can be diagnosed before birth
Detectable abnormalities that will need surgical correction soon after birth include diaphragmatic hernia, abdominal wall defects such as aastroschisis
and exomphalos. and congenita! pulmonary airway malformations (CPAM).
Main non-urological abdominal emergencies occurring in the newborn

1. Incarcerated or strangulated inguinal hernia 6. Hirschsprung’s disease
2. Gastrointestinal atresias and stenoses 7. Congenital diaphragmatic hernia
3. Midgut malrotation with volvulus 8. Deficiencies in the abdominal wall (gastroschisis, exomphalos
4. Anorectal abnormalities and ectopia vesicae)
5. Meconium ileus and other problems with meconium 9. Necrotizing enterocolitis
INTESTINAL OBSTRUCTION - GENERAL POINTS

■ Intestinal obstruction is the underlying phenomenon in most neonatal abdominal emergencies
■ Most causes are NOT detectable by antenatal ultrasound
■ Just as in adults, Intestinal obstruction presents with vomiting, constipation and abdominal distension
In a baby, signs pointing to intestinal obstruction include poor feeding, failure to pass meconium and bile-stained vomiting
The important causes of upper intestinal obstruction in babies are and

Causes of low obstruction include and
Small bowel atresia may affect jejunum or ileum, causing high or low obstruction respectively.
Plain abdominal X-rays usually confirm intestinal obstruction. When obstruction is high, there is a lack of distal intestinal gas; when low,
there are dilated loops of bowel.
* If malrotation is suspected, an upper Gl contrast study can determine the **abnormal position of the duodenojejunal flexure. Other causes
such as incarcerated inguinal hernia or imperforate anus can be detected by clinical examination.
INTESTINAL ATRESIA
D E F IN IT IO N
■ Atresia is defined as complete obliteration o f a s e g m ent o f th e Gl tra c t, which is thus totally obstructed.
INCIDENCE
Incidence 2-14%
A E T IO L O G Y /P A T H O P H Y S IO L O G Y
Oesophageal and duodenal atresias and anorectal malformations em bryologicai a bnormalities, often associated with other
congenital abnormalities. For examble, major cardiac, vertebraJj3f-renal~aS3dfmalities are found in 40% of babies with oesophageal
atresia, andrffi% of duodenal atresias are found in infants with trisomy 21
— ------------------------------- — ^ *
In contrast, jejunal and ileal atresias probably result from intrauterine m esenteric vascular accidents and are therefore rarely
associated with other abnormalities. Small bowel atresia is sometimes associated with cystic fibrosis, and pafients should have a genetic
screen and a sweat test to exclude it
" /or. »/ e g
CQ * C— *i I
Good summary: ' '
■ Duodenal atresia - Failure of bowel to recanalize after endodermal epithelium proliferation (wk 8-10)
Je ju n al/ile a - Acquired as result of vascular disruption -> ischaemic necrosis -> resorption of necrotic tissue -> blind distal and proximal
ends
■ C olo n - mechanism unknown, thought to be similar to small bowel atresia
C L IN IC A L F E A T U R E S
Features o f a high or low obstruction respectively
^ ;
■ Gastric distension and vomiting (usually bilious) *. cjtd. m -
■ort* *
— V ■ Duodenal - wljhir
Duodenal atresia 6AU56s obstruction of theQsecond par t j r f th e d u ode num , usually **just below the common b ile duct entry in
85% resulting in .iio u s vom iting. The anomaly is a web across the lumen OR complete separation of the bowel ends
o REMEMBER: May be associated with other anomalies (Tracheoesophageal fistula, cardiac, renal and vertebral anomalies),
24-28% have Down syndrome
Jejunal/ileal -fw ithin 2 q)of birth, may be associated with cystic fibrosis
o Jejunal orle a l atresias are similar to duodenal atresia, with a gap between bowel ends or an intraluminal web. A gap is often the result of a
mesenteric vascular accident in utero
■ Colonic -<1within 3 djp birth
' MUST EXAMINE FOR ASSOCIATED CONGENITAL ABNORMALITIES!!
IN V E S T IG A T IO N S - E S S E N T IA L L Y T H E S A M E O P T IO N S F O R A L L P A E D IA T R IC B .O
General
— 1. May be antenatally diagnosed by dilated bowel loops
j j u f f ' k x D u t- a'cto d/cs'*'
- 2. Plain abdominal x-ray * v
a. Duodenal atresia: sho [a d o u b le b ub ble one air-fluid interface in the stomach and another in the duodenum
- 3. Contrast enema ± UGI with sm all bowel follow through (SBFT) Group and screen INR and PTT if for surgery
KtlST ( MANAGEMENT - INTERVENTION IS IMMEDIATE, BUT SURGERY IS NOT USUALLY EMERGENT

KVtOUJf n Recall this is complete intestinal obstruction by obliteration. So treat as such ->
‘ ^ NPO/NGT/TPN + RESUSCITA TE THEN SURGICAL ANASTOMOSIS
* * * refuseât1on°mPreSSiqa( W ) 7 ^ fi & K fj (v
* - ; f 3. **B ro a d -s p e c trum a n tib io tic s *
4. S u rg e ry
a. Duodenal -^mjodeno-duodenostomy ofauodeno-iejunostomy
b. Jejunal/ileal - primary anastomosis’, or if atresia associated with short bowel then may create end stoma or defer surgery for bowel
lengthening procedures
c. Colonic - primary anastomosis
Re: Duodenal Atresia

■ Provided there is no malrotation or volvulus, surgery can be delayed
■ This involves joining proximal duodenum to duodenum distal to the obstruction as a duodeno-duodenostomy.
■ The ends can easily be brought together without tension so bypass procedure is not necessary.
■ R e c o v e ry a fte r d u o d e n o -d u o d e n o s to m y is o ften s lo w b e c a u s e th e p ro x im a l d u o d e n u m is a to n ic a n d p e ris ta ls is s lo w to
sta rt. A lm o s t a ll p a tie n ts n e e d p e rio p e ra tiv ^ T P N ^
■ (Previously, gastro-Jejunostomy was performed buTofterTied to bacterial colonization of the defunctioned loop causing failure to thrive, stomal
ulceration and gastrointestinal bleeding)
PROGNOSIS III
■
■ Jejunal/ileal - 84%
fM c d ^ r f £ T
• Colonic-100%
MALROTATION WIT
7
Tbe-rmdgtft-deyelops outside the abdomen during early embryological development. By the end o f the 3 month, it norm ally returns, rotatln\g?270°)
anti-clockw ise)giving a norm ally sited duodeno-lejunal (DJ) flexure and the caecum in the right iliac fossa. The midgut mesentery is wide, v — ^
strefchmg"o5iiquely across the posterior abdominal wall, preventing volvulus. If rotation is incomplete, the DJ flexure lies right of the midline rather
than left; the mesenteric fixation to the goste rjo r abdominal wail is narrow and volvulus may occur
INCIDENCE 3? / /
1/3 p re sen t by 1 week o f age, 3/4 by 1 month of age, 90% by 1 year of age
- M = F = 1 :1 try}<fcH c
els. Ifj.
Higher incidence among patients with cardiac anomalies gy r
PATHOPHYSIOLOGY
■ F ailure o f g u t to n o rm a lly ro ta te a ro u m /s u p e rio r m e se n te ric)a rterv w ith a s so c ia te d a b no rm al in te s tin a l a tta chm en ts
and a n a to m ic p o s itio n s N
Represent a spectrum of rotational abnormalities including complete nonrotation (which is actually not at high risk for volvulus)
M AIN PRO BLEM WITH MALROTA TION: C hild re n w ith m a lro ta tion m ay un d ergo a cu te v o lv u lu s at any tim e , in w h ic h th e m ass
% of b ow e l tw is ts on its axis, o c c lu d in g t h ^ u p e r i o r m esenterlcTfrnidgut) vessels, c a u s in g in te s tin a l ischaem ia a nd in fa rc tio n .
T h is is a surgical em ergency p re se n tin g as m g h In te s tin a l o b s tru c tio n w ith b ile -s ta in e d v o m itin g .
CLINICALFEATURES WITH ASSOCIATED VOLVULUS
B ilio u s v o m itin g in in fa n t is a life -th re a te n in g e m e rge ncy s e c o n d a ry to m id g u t v o lv u lu s u n til p rov en oth e rw ise .
Bilious vomiting is THE cardinal signjespecially if abdomen nondistended (as high obstructions cause less distension!)
therfeaTures or n ig h intestinal obstruction
■ Features df^peritoriftis)if strangulated
Rectal bleed (Tate/onririous signs ) ------------ (j2 s t ho.Ve P& b b jL c i l.\l .
■ If bilious emesis in ill child with distend abdomen, consider surgical exploration to rule out volvulus.
M ay also have intermittent sym ptoms

Examination
■ General: Tachycardic, pale, diaphoretic
■ AbdomenXFlat abdomen, tenderness
■ Bilious drainage from NG tube
'd o J > (c Si
INVESTIGATIONS
1. U&Es <itss> J
IMAGING
1P Plain radiographs show features similar to any other high obstruction
^ a. Erect CXR
b. Supine AXR: Obstruction of proximal small bowel{double-bubble ■ 1intestinal wall thickened
Im mediate UGI series: Dilated duodenum, **duodenolelunal segment (Ligament of Treltz) right of midllne and not fixed posteriorly over
spinal column, ‘ corkscrew"sign indicating volvulus *
31 U/S: "whirlpool" sign, abnormal SMA/SMV relationship indicates UGI to rule out rotational anomalies
M A N A G EM E N T - A CU TE V O LV U LU S IS A S U RG ICAL E M E R G ENCY -»
1. Fluid resuscitation 'r O o z A u * -

j (_ L a d d ' s
2. IV antibiotics —-------—'J<T
3. EMERGENT LAPAROTOMY:
^ Ladd procedure: *Untwlsting of midgut volvulus, *Division of Ladd’s bands, *dlvislon of peritoneal attachments between
r cecum and abdominal wall that obstruct duodenum, *Broadening of the mesentery (open folded mesentery like a book and divide
. congenital adhesions)
p b. Resection of any gangrenous bowel
c. ± appendicectomv
d. Positioning the bowel into non-rotation (small bowel in right abdomen, large bowel in left abdomen)
PROGNOSIS
■ Mortality related to length ot bowel loss: 10% necrosis - 100% survival rate, 75% necrosis - 35% survival rate
■ If there is insufficient small bowel remaining, short bowel syndrome (intestinal insufficiency) is likely
■ Recurrence 2-6%
HIRSCHSPRUNG’S DISEASE f “CONGENITAL AGANGLIONQSIS”!

DEFINITION
■ Hirschsprung’s disease (Harald Hirschsprung 1830-1916) is a c o ng en ita l a b n o rm a lity o f d ista l in tes tin e , w h ic h a ffe cts all o f th e
in tra m u ra l a u to n o m ic n e rves artcLsa u s e s function al intestinal o b s tr u c tio n
■ Ganglion cells are absent from thw NTER-M Y E N T E R lC A ntfSUB M U CQ SAL p le x u se ^, and the parasympathetic and sympathetic
nerves are scattered in a disorderly watHhioughout the layers of trte-bowaLwalL "Z
r
Wavne Robinson. MBBS Class of 2015

The aganglionosialaiways in v o lve s th e re c tu fK e x te n d in g in to th e s ig m o id in 80% and reaching the s m all b o w el in 5%. The
pathology is continuous without ‘skip’ lesions <
.h.t /\ £ <-/( kun LitCAsn-tW-r . x o ^
***■ • 2 THINGS HAPPEN:
1 . Hypo or aperistalsis in the affected bowel AND ^
2. the internal anal sphincter does not relax'firrternal anal sphincter achalasia). The baby therefore has a functional obstruction that
usually presents soon after birth with intestinal obstruction;
■ In patients with long-segment disease, it can present in later childhood with constipation and failure to thrive.
— (0°(. f'OUOl\jc
INCIDENCE
s* A •(o
■ 1:5000 births {3 H ~uAczt tjo - j
■ M > F = 4:1 On
■ JtE T mutation
■ Can have aganglionosis of small bowel!! as well Familial Hirschsprung’s in <5% of cases
MUST KNOW: PATHOPHYSIOLOGY

- Defect in m igration o f neural cre st ce lls to intestine resulting in aganglionic bowel tha t fa ils to peristalse
and internal sphincter tha t fails to relay (internal anal sphincter achalasia) causing functional AND partial mechanical
obstruction. respectivelÂLWAYS STARTS IN THE RECTUM^nd variable involvement proximally;
CLINICAL FEATURES ^ 4 $ A AS A jc
( n°f~
• Failure to pass meconium spontaneousl^within 48 h oflife^s the classic history
o (95% of normal children should pass meconium witfvn Z4 nTand the remaining 5% within 48 h)
■ft ■ Symptoms of bowel obstruction:

- o Abdominal distension
- o Bilious vomiting
- o Constipation
■ POSSIBLE COMPLICA TION: Hirschsprung s Enterocolitis/sepsis
■ Failure to thrive " ^ "
Examination
± abdojnmaJdtstension
Tquin/hiast : Rectal examination may cause an explosive release of air and meconium!!
INVESTIGATIONS uM\-
£ .d C tfj w s p c c k d case
^ !■ Rectal biopsy (gold standard). —
Definitive investigation■\ and should h
hee carried out iirÂ
tAALUs
L L c hildren a riiagnosisof Hirschsprun q’s disease is ent
entertained
- 2 FINDINGS: Look for,r^ganglionosi^fin the myenteric plexus) and(neural hypertrophy (an increase in parasympathetic nerves)
2. Supine AXR
3. Contrast enema MUST KNOW: to find narrow rectum and level of the disease - “transition zone"
4. A nal m anom etry unreliable in infants - classic finding is absence ofrectoanal Inhibitory reflex
MANAGEMENT
Principles:
The general goals of care are 3-fold;
(1) To treat the manifestations and complications of untreated Hirschsprung disease,
(2) To institute temporizing measures until definitive reconstructive surgery, and
(3) To manage postoperative bowel function.
1. Medical care: Goals of medical care are to maintain normal fluid and electrolyte balance & to minimize bowel distension and prevent perforation.
IV fluid resuscitation and maintenance, nasogastric decompression, and administration of intravenous antibiotics (as indicated) remain
the cornerstones of initial medical management.
o *** Colonic lavage, consisting of mechanical irrigation with a large-bore rectal tube and large volumes of irrioant. may be required.
2 . Surgery: Either 1-stage or 2-stage procedure: (2 stage involves placing a diverting colostomy first!)
* Suroical-resection
urcpcai-resection o f qganghom
qqanglionic
c intestinal
mtest segm ent AND anastom osis o f rem aining intestine to rectum at
fntate tine^WENSONPROCEDURE)
3. Timing: Either in newborn period Off staged if extensive aganglionosis y yr

o Definitive surgery for Hirschsprung’s may be carried out any time after birth but has traditionally been delayed until the baby
reaches 10 kg.
eg)
■ Staged procedure: Traditionally, a diverting colostomy was created at the time of diagnosis, and definitive repair was delayed until the child
grew to a weight of 10 kilograms. The diverting colostomy would be placed proximal to the transition zone. Although more often nowadays,
conservative management is employed with frequent rectal washouts at home by parents after training. THEN DEFINITIVE SURGERY
■ Definitive surgery involves removing the entire length of aganglionic bowel and joining normal bowel to rectum at the dentate line. After 4-6
weeks, the patient is readmitted electiveiy for a primary pull-though' operation, typically performed with laparoscopic assistance
■ NOTE: For neonates undergoing creation of a diverting colostomy, the transition zone is identified and the colostomy is placed proximal to this
area. The presence of ganglion cells at the colostomy site MUST be unequivocally confirmed by histological evaluation of a FROZEN-
SECTION BIOPSY. Either a loop- or end-colostomy is created at the surgeon’s discretion.
■ IN MODERN DAY, advancements in anesthesia administration and hemodynamic monitoring have led many surgeons to advocate a single-
stage pull-through procedure without initial diversion.
■ DEFINITIVE SURGERY: A number ofêfinitiy^ropedure^deraonstrate excellent results when performed by experienced surgeons. The most
commonly performed repairs are t h ^ ^ .. frQ luham el, a.&<ôavej}focedures. in any elective operation for Hirschsprung disease, a robust
preoperative colon cleansem usibe peifOfmed. intraoperatJvelyTHISTOLOGICAL EXAMINATION OF A FROZEN-SECTION BIOPSY
MUST CONFIRM THE PRESENCE OF GANGLION CELLS AT THE PROXIMAL MARGIN OF BOWEL INTENDED FOR ANASTOMOSIS.
■ The Swenson procedure was the original pull-through procedure used to treat Hirschsprung disease. The
aganglionic segment is resected down to the sigmoid colon and rectum, and an obligue anastomosis is
performed between the normal colon and the low rectum
■ For patients with extremely short-segment Hirschsprung disease, a norecta i is an alternative surgical option.
o The surgeon removes a 1-cm-wide strip of extramucosal rectal wall, beginning immediately proximal to the dentate line and extending to
the normal ganglionic rectum. The mucosa and submucosa are preserved and closed.
Postoperatively, routine colonic irrigation and prophylactic antibiotic therapy may decrease the risk of developing enterocolitis. For patients
who do develop enterocolitis, nasogastric decompression, intravenous fluids, Antibiotics, and colonic lavage may be necessary. Sodium cromoglycate, a
mast cell stabilizer, has also been reported to benefit these patients/V \
COMPLICATIONS \ V
■ MUST KNOW: A severe form of enterocolitis (r ) maty occur in infants where the diagnosis of congenital
aganglionosis has been delayed, and death may result from circulatory collapse^Jhis enterocolitis can also occur after definitive surgery,
o Parents should be warned of the danger of this occurring during aCyfra! ///nessDwhich may result in ana/ sphincter spasm with
acute obstruction. The danger of these episodes diminishes as children get older
■ Post-operative enterocolitis
o (Medical emergency if progresses to sepsis)
■ Faecal incontinence and constipation
PROGNOSIS
■ Most have normal or near-normal anorectal function
CONGENITAL DIAPHRAGMATIC HERNIAS

INCIDENCE
■ 1 in 2000 to 5000 live births
• M= F
j i M 1" P renatal d ia g n o s is c o m m o n - US/MRI
yt 4 - P resents w ith in h o u rs o f life although some cases of delayed presentation
■ >10% are associated with other congenital anomalies
PATHOPHYSIOLOGY
3 types: C O K h O ^ |[
1. Posterolateral (Bochdalek} - MOST COMMON --
a. Left-sided, 85% - MOST COMMON
b. Right-sided, 13%
c. Bilateral, rare, often fatal
2. Anterior (Morgagni)
3. Hiatus
« Failure of the pleuroperitoneal canal to close results in the most common type of diaphragmatic hernia which is postero-lateral. The incidence is
1:3500 live births and 80% are on the left side. Abdominal viscera lie in the chest, displacing the media
<£. -J^ L u n a developm ent is abnorm alju ith fewer branching events during development causing variable^ pulm onary hypoplasia which
may be so severe as to be incompatible with life. ^
■ Left-sided: small bowel, large bowel, stomach and solid viscera (spleen, left lobe of liver) herniate into thorax
■ Right-sided: liver, large bowel herniate into thorax
CLINICAL FEATURES
Jpi Prenatal diagnosis is common
■ ***Soon after birth, the infant develops respiratory distress; survival depends on adequate residual lung volume and function.
CLASSIC SIGNS:
1. ‘Empty’ (scaphoid) abdomen (due to abdominal contents in chest)
2. Mediastinal shift (due to abdominal contents in chest) and
3. Cyanosis
■ Cardiac malformations are commonly associated.
Examination
• Decreased air entry
• ± Bowel sounds In the chest
■ Displaced heart sounds
INVESTIGATIONS
* £ j* Diagnosis is now frequently made at antenatal screening (U/S or MRI)

------^ Diagnosis is confirmed on CHEST X-ray following passage of an orogastric tube
o CXR (bowel loops in hemithorax, displaced heart)
■ Echocardiography
■ General -> ABG
MANAGEMENT
PRINCIPLE: FIRST PRIORITY IS RESPIRA TORY STABILIZA TION!!!. THEN SURGICAL REPAIR
—>-1 . ‘O r ogastric suction - Initial treatment is orogastric decompression to prevent air entering bowel in the chest to minimize pulmonary compression
2 . Period of respiratory stabilization due to associated pulmonary hypoplasia (may require extracorporeal membrane oxygenation)
3. 'Gentle assisted ventilation with permissive hypercapnoea and low airway pressures is the mainstay of treatment to prevent secondary
pulmonary damage +/- Intubation
4. Surgical repair after Stable: by hernia_reductlon and closure of diaphragmatic defect - open vs. thoracoscopic vs. laparoscopic AND
with or without prosthetic or muscular patch depending on size of defect T ^
& P (NOTE: Urgent surgery is usually delayed until the baby is stable and requiring minimal ventilation. At operation, the diaphragmatic
/ defect is closed via an abdominal incision. A complete diaphragm can often be fashioned by suturing diaphragmatic remnants together. Large
j defects may require a prosthetic patch o ra flap of abdominal wall muscle. Midgut malrotation is present in 25% so the position of the DJ flexure
C -' needs to be assessed and corrected if necessary)
PROGNOSIS -----------------^
Despite advances in care, overal/mortality remains HIGhpbetween 60 and 70%, and is 50% for those diagnosed antenatally. Survival for those who
come to operation has improved steadliyover recent years to around 90%.
■ Later presentations have better outcomes

■ Hearing deficit (40%)
■ Associated GERD
■ Need for long term surveillance for potential recurrence
■ Failure to thrive
■ Chronic lung disease if severe hypoplasia
SEE TORONTO/ESSENTIAL P624 FOR THE OTHERS: GASTROSCHISIS. OMPHALOCELE. NECROTIZING ENTEROCOLITIS
ABDOMINAL EMERGENCIES IN INFANTS AND YOUNG CHILDREN

INGUINAL HERNIAS
DEFINITION
■ Inguinal hernias in children arise because the processus vaginalis fails to close after testicular descent; -> they are
^ T R U E CONGENITAL ABNORMALITIES”
• Anatomically, they are the same as Indirect Inguinal hernias in adults BUT WITHOUT A SUBSTANTIAL ABDOMINAL WALL DEFECT. The
incidence in infants
Essential Surqer^.98% are indirect)

But, Toronto and mosTotiTeTsources^^ll infant inguinal hernias are indirect”: Descent of intra-abdominal contents through the internal
inguinal ring through a patent tunica vaginalis
INCIDENCE
» 5% o f all term newborns
• W-30% nf premature infants, and more likely bilateral if pre-term
■Q l > F, 4?T>
■ 1/5 inguinal hernias will become incarcerated if patient is <1 yr old
■ Incarceration is more common in females
RISK FACTORS
1. Prematurity
2. Low birth weight
3. Associated with other conditions: connective tissue diseases androgen insensitivity
CLINICAL FEATURES
■ Most common presentation: Painless, intermittent lump/mass in groin at the external inguinal ring, when the child cries or strains at stool, but
then reduces spontaneously. May also extend into scrotum
o With larger defects, lump is constant
■ If incarcerated (40% of hernias in the neonatal period are discovered because they become irreducible):
o Tender, vomiting, firm mass, erythema then cyanosis of mass may be noted
o Vomiting -> fluid depletion and electrolyte disturbances
■ Strangulation can follow incarceration (but less common in young children than in adults)
o Inguinal hernias may become acutely irreducible and painful, sometimes with obstructive symptoms such as vomiting,
o In these cases, there is a real risk of testicular necrosis and/or strangulation of the hernia contents, e.g. bowel or ovary. (Pressure on
the spermatic cord at the external ring may cause testicular vascular obstruction, and rapid treatment is needed to prevent testicular
infarction and irreversible damage)
(In known hernias, parents should be instructed to bring the child to hospital for urgent herniotomy if it becomes incarcerated to prevent these risks)
Examination
‘Silk sigir When the hernia sac is palpated over the cord structures, the sensation may be similar to that of rubbing 2 layers of silk
fbgether~Jh\s finding is known as the silk sign and is highly suggestive of an inguinal hernia. The silk sign is particularly important in young
children and infants, in whom palpation of the external inguinal ring and inguinal canal is difficult because the patients' small size.
■ Mass palpated at external inguinal ring and reducible through inguinal canal into abdomen
■ Must always try reduction to confirm that hernia is not incarcerated
INVESTIGATIONS AND DIAGNOSIS
■ Physical exam is gold standard

■ U/S only if physical exam uncertain
MANAGEMENT
(The high incidence of incarceration in young children is a strong argument for operating upon any inguinal hernia in this age group soon
after discovery, with the need greatest in the very young)
relieve acute symptoms

X T * *~
■ The standard operation is . (a common general paediatric operation)
■ In babies and children, this involves separating the peritoneal sac from the cord (or round ligament), ligating the sac at the external ring (high
ligation) and removing it. May be laparoscopic or open
■ There is rarely any need to perform a repair (herniorrhaphy);
■ The incidence of an undiagnosed contralateral hernia in boys is ~ 1 in 8 but contralateral groin exploration is NO LONGER PERFORMED in the UK
INCARCERATED INGUINAL HERNIA MANAGEMENT (ESSENTIAL SURGERY)

There is usually a painful, acutely tender groin swelling. The child is not systemically unwell and the hernia is neither tender nor red. At this stage, it is
very unlikely that bowel has become infarcted. Emergency surgery is best avoided if possible, except in the unwell child with signs of intestinal
obstruction, as the friable hernia sac
sacjrjakes..surgery
rriakesuSU.rgery difficult and recurrence likely.
C ]/o k. VCr*) l t/C/M (a \
" T ;atmentTnvolveâctively reducing he hernia and performing lective herniotomy 48 hours j r s j a ^ r when oedema has
resolved.
Active reduction is by gentle manipulation with the child sedated with intravenous opiates: it succeeds in about 80% but competent technique and
experience are needed. The testis and hernia should be drawn towards the opposite, descended testicfeTwitTHheeftemal ring held open with the other
hand. This results in narrowing of hernial contents, allowing them to pass back through the ring with a satisfying gurgling.
It is often said to be impossible to reduce necrotic bowel in a hernia, but this is untrue so it is important to carefully monitor a child for clinical
deterioration after a difficult reduction, including respiratory rate and oxygen saturation. The hernia must be fully reduced; if there is doubt, or If it
. proves irreducible, urgent surgery should be performed. - ---------------------
~*No child is too small to have surgery provided the team has been trained in paediatric surgery and anaesthesia. Note that failed reduction of an
incarcerated hernia is associated with a high rate of testicular atrophy (up to 40%).
PROGNOSIS
■ Risk of recurrence after surgical reduction <3% but higher if repair done in premature infants or if hernia was incarcerated/strangulated at
repair
FEMORAL HERNIA
Femoral hernias are much less common than inguinal hernias in children and are located lower and more medially in the groin. Enlarged lymph nodes
can also occur here
UMBILICAL HERNIAS
Many newborn babies have umbilical hernias, particularly if premature, but the defect usually cicatrizes and resolves during the firs t 2 years of life ;
Common in Afro-Caribbean babies and can run strongly in families.
PATHOPHYSIOLOGY
- Incomplete closure of peritoneal and fascial layers within umbilicus by 5 yr
CLINICAL FEATURES
■ — ■Majority asymptomatic
Majority spontaneously resolve by age 5
■ Incarceration prior to age 5 very rare
■ Most symptoms occur in late adolescence or adulthood
MANAGEMENT
Small umbilical hernias may undergo spontaneous closure up to 4-5 years of age. Rarely, they become incarcerated or strangulate.
“ IN D IC A TIO N S FO R R EPA IR ARE: * * * ]

1. ts' Symptoms
2. ^ Persistence beyond 5 years
3. Social pressure to prevent teasing \
The size of the abdominal wall defect should be determined; large defects (> 1,5-2 cm) are much less likely to close spontaneously
It is important to differentiate umbilical hernias from epigastric hernias, which do not close spontaneously!!!
At operation, a small subumbilical ‘smile’ incision allows emptying and ligation of the peritoneal sac and placement of a few absorbable repair sutures.
The umbilical skin is usually sutured to the repair to restorejts normaUecessed appearance.
CONGENITAL HYPERTROPHIC PYLORIC STENOSIS

INCIDENCE
■ < 1% of live births
■ Can present at 1-20 wk, most commonly at 6-8 wk (or ~ 1-2 months for memory) Q -. I
- M > F, 4:1
AETIOLOGY/RiSK FACTORS
■ Aetiology unknown
4k ■ ^Family history
■frÊarly erythromycin exposure (<13 d old)
PATHOPHYSIOLOGY
■ Acquired hypertrophy of m ainl^^R CU LAR^YLO R IC MUSCLE, progressively occluding the gastric outlet. Presents with a
gradual onset of progressive pyloric obstruction over"days or even a week or two, with projectile vomiting of milk following feeds
• Prolonged vomiting results in hypovolaemla and characteristic electrolyte disturbances:

o The loss of HCI causes hypocMoraemjc hypokalaemic metabolic alkalosis.
o In severe cases hypokalaemia may occur as a result of renal hydrogen/potassium exchange, in which potassium irons are sacrificed to conserve hydrogen ions,
o There is usually a paradoxical aciduria as dehydration causes the kidney to conserve plasma tonicity at the expense of hydrogen ions, the loss of which
compound the metabolic alkalosis.
CLINICAL FEATURES
■ Typically, the infant thrives for the first 3 or 4 weeks and then begins to vomit 30-60 minutes after every feed
■ The vomitus isN O N /B IL IO U S , readily distinguishing it from duodenal stenosis or atresia
■ Characteristically becomes projectile, (i.e. the vomit clears the baby’s chin)
■ "'Initially, the child appears well and is hungry after vomiting!
■ With sustained vomiting, however, the child becomes progressively d e h y d ra te d and e le c tro ly te d e p le te d and loses vigour
and becomes reluctant to feed. Standard examination often reveals no abdominal abnormality
Examination
**# ■ Diagnosis made by carrying out k “te s t f e e d ” (j.e. feeding the baby and palpating the abdomen at the same time)
o If pyloric stenosis is preselitra firm ,‘h a about 2 cm in diameter (described as\P llve-ltke"T]s usually palpable deeply below the
liver and disappears after the feecT ^ "
■ Visible left-to-right gastric contraction “waves” after feeding

■ (It is important to decompress the stomach first by nasogastric tube, as a dilated stomach often displaces the pylorus to lie under the liver edge)
INVESTIGATIONS
1. U&Es
2. Urine analysis
(3 ^ U/S - M A IN S T A y T s ^ q w s pyloric length >14 mm, muscle thickness > 4 mm
4. UGl contrast study: necessary ONLY WHEN U/S UNAVAILABLE or nondiaqnostic will show “string sign"
a. If the diagnosis remains in doubt, an upper gastrointestinal contrast study can reveal the typical narrow pylorus and little contrast in
the duodenum.
MANAGEMENT &
(PRINCIPLES: FIRST FLUID RESUSCiTA TE and CORRECT ELECTROLYTE ABNORMALITIES THEN SURGERY Ram stedt’s
p yloro m yotomy) f
,OCU'^&C5S'p>v<
1. Fluid resuscitate with normal saline
2. Correct electrolyte and acid/ base abnormalities with D5,1/2NS + 20 mEq/L
o KCI at maintenance rate,
o (NG tube decompression unnecessary)
3. Pyloromyotomy (Options: Open vs. laparoscopic and Ramstedt vs. transumbilical)

Alternative therapies such as TPN/wait or atropine impractical due to long time course of effect
Treatment is surgical, by Ramstedt’s pyloromyotomy described in 1912 (Conrad Ramstedt, 1867-1963).

However GA in an unprepared neonate with alkalosis and an immature respiratory drive would often result in prolonged postoperative ventilation
and all its attendant risks.
pperation should be performed only on a stable baby after correcting dehydration responsible for the metabolic alkalosis. The stomach
should be emptied by nasogastric aspiration and washed out with normal saline to prevent further vomiting. ~
■ Ramstedt’s pyloromyotomy: The procedure is carried out via a periumbilical incision or laparoscopically. The hypertrophied pyloric muscle is
incised longitudinally and then split WITHOUT breaching the mucosa
■ Postoperative recovery is rapid, with full-strength milk feeding started immediately afterwards. Babies typically tolerate sufficient feeds to be discharged within 24 h
■ (The natural history without surgery is for the hypertrophy to gradually resolve over several months. However, most children would die from electrolyte disturbances or
malnutrition before this happened!!)
PROGNOSIS
■ Pyloromyotomy curative
INTUSSUSCEPTION
INCIDENCE
■ ) Most common cause of bowel obstruction between the ages of 6 months - 3 years|(Essential Surgery says 6 weeks to 2
years) — )
- M > F, (3:2)
Acquired disorder
Pathologic “lead points”:

—>• 1 . Enlarged Peyer’s (lymphatic) patches due to viral Infections of the Gl tract - most common in children
—V 2 . Polyp or tumour
- > 3. Meckel’s diverticulum
***ALSO HOTEÎenoch-Schonleln purpi^,(gystic f/ibros/^(^m phom ^^gP^nay increase risk
(There appears to be a seasonal increase in the spring and autumn. Up to 40% of children with intussusception have x commoner at
these times of year) ' “
PATHOPHYSIOLOGY
■ Intussusception arises when a proximal segment of bowel becomes telescoped or prolapsed into the bowel immediately
distal to it, possibly leading to obstruction and vascular compromise. The invaginated segment progressively elongates as it is
propelled distally by peristalsis.
o The part that prolapses into the other is called the intussuscept , and the part that receives it is called the htussuscipiens
■ An anatomic lead point (that is, a piece of intestinal tissue that protrudes into the bowel lumen) is present in approximately 10% of intussusceptions
■ The lead point is commonly a thickening of bowel wall caused by non-specific or viral hypertrophy of Peyer’s lymphatic patches.
ll^ o ra p o a j in tu s su s c e p tio n is the u sual va rie t and ft commonly extends well into the transverse colon and sometimes
even prolapsesfromlheanus' —
■ Intussusception presents with severe colicky abdominal pain. If untreated, the affected segment may undergo venous infarction over a period of
hours or days.
■ Pathology other than Peyer’s patch hypertrophy may initiate intussusception, and should be suspected in a child presenting outside the usual age
range or if it recurs after radiological reduction. 10% of patients have an anatomical abnormality termed a pathological lead point (PLP).
■ In older children or adults, the initiating factor may be a bowel wall tumour or polyp.
■ Meckel’s diverticulum or even a lymphoma may also present in this manner.
■ “ Children with Henoch-Schonlein purpura may sometimes develop ileo-ileal intussusception
C L IN IC A L F E A T U R E S ’— H ast h o '* } .. r . rN
O (pipd fCLi ^ +® rta s ! + k 4
* 4 CARDINAL FEATURES:
1. A c u te o n s e t o f abd o m in a l p a in which is classic severe, episodic “colicky” pain - lasts for minutes with child screaming, then resolves
V o m itin g ± b ilio u s - (often begins later with distal SBO, which is most common)
A bdom inal m ass -S au sage-sh aped mass often found in the RUQ with a scaphoid (hollowed) appearance In the RLQ (b a r e& s
Sig: (^(Dance’s sign is an eponymous medical sign consisting of an investigation of the right lower quadrant of the abdomen for retraction, which can be an
indication of intussusception]
R e d c u rra n t-je lly s to p ! - often within the first few hours - almost pathognomonic when the other features are present (suggests
mucosal necrosis and sloughing)
± Features o f peritonitis with vascular com promise an d gangrene/perforation
Examination
General: Features of dehydration. If strangulation and perforation, tachycardia, febrile, toxic appearance
Abdominal exam:
■ Palpate for masses (especially sausage shaped upper abdominal mass) and tenderness
■ Signs of bowel obstruction - distended abdomen
■ Look for features of localized peritonitis which suggests transmural ischaemia (guarding, rebound tenderness, etc.)
■ Rectum is empty but may contain a little blood
INVESTIGATIONS
Generally a clinical diagnosis
1. U&Es
2. U/S if suspect pathology

- ^ 3 . A X R for signs of bowel obstruction or perforation
-* 4 . A irAvater-so lu b te enema
Intussusception is potentially life-threatening so a definitive diagnosis must be made urgently with a view to treatment, even in children who
appear initially well.
MANAGEMENT — £ k jO U / 0 ^ 6 0 - (f f
Principle: F L U ID R E S U S C IT A T IO N , then non-operative R A D IO L O G IC A L R E D U C T IO N (via air contrast enema or water-soluble enema) OR

O P E R A T IV E M A N A G E M E N T I f c h ild u n w e ll/p e rlto n ltls
Fluid resuscitation: is vital even before attempting to diagnose or reduce an intussusception!!!!

a. Intravenous access should be secured early, as deterioration may be imminent.
b. Patients are usually given a fluid bolus of20ml/kg of suitable crystalloid and an empirical broad-spectrum antibiotic t herapy
BEFORE transfer to the radiology department for non-operative management **= ----------—
2. N on-opera tiv e re d u c tio n : involves reduction vla/klrpontrast or hater-soluble enema with carefully controlled pressure, performed under
X-ray screening
" “"a- Reported rates of successful reduction are as high as 90%.
B Radiological reduction is inappropriate if the childjsfljnwejj) in these, rapid resuscitation should be followed by laparotomy
, Operative manage me n tflFPERITONITIS -> OPERATIVE MANAGEMENT^)

a. Can be done open or laparoscopically
b. At operation, the intussusception is reduced by gentle manipulation,
c. Resecljpn with primary bowel anastomosis becomes necessary£jthe intestine is non-viable OR if it proves impossible to completely
reduce without causing major trauma to the bowel
d. Resection of involved colon if failure to reduce or bowel appears compromised
P R O G N O S IS
10% recurrence rate

recurrent = more iiKeiy^non-idiopathic
In successfully reduced by enema in older children allow 2 wk resolution of edema then perform SBFT to rule out pathologic lead points
ABDOMINAL EMERGENCIES IN OLDER CHILDREN

ACUE APPENDICITIS
SEE SEPARATE NOTES
TORSION TESTIS
SEE SEPARATE NOTES IN UROLOGY FOLDER
MECKEL'S DIVERTICULUM
RULE OF 2S FOR MECKEL’S DIVERTICULUM
■ 2% of the population
■ 2:1 male-to-female ratio
■ Often present by 2 yr of age
■ Symptomatic in 2% of cases
■ Found within 2 feet (10-90 cm) of the ileocecal (!C) valve
■ 2 inches in length
■ 2 inches in diameter
■ 2 types of tissue (gastric, pancreatic)
DEFINITION
» Meckel’s diverticulum is the remnant of the^te//o-/ntesf/na/^gtbf the embryo (connects yolk sac (“vitello”) with
primitive midgut (“intestinal”)).
■ It lies on the antlmesenterlc border of the ileum and, as an approximation, occurs in 2% of the population, arises 60 cm (2 feet) from the
ileocaecal valve. and averages 5 cm (2 Inches) in length.
■ It is a TRUE d iv e rtic u lu m (Contains all layers of the wall of the parent organ (typically mucosa, muscular layer and serosa)
' T
INCIDENCE
■ 2 % of the population
■ M > F, 2-3:1
■ Often present by 2 yr of age. But may present later
PATHOPHYSIOLOGY
■ Failure of vitelline duct to regress 5-7 wk in utero; 50% contain heterotopic tissue (e.g. gastric mucosa, ectopic
pancreas); '=r
■ Other associated anomalies include omphalomesenteric fistula, umbilical sinus, umbilical cyst, fibrous band
CLINICAL FEATURES
It may present in numerous ways:

*-« A symptomless finding at operation or autopsy
Acute Inflammation, clinically identical to acute appendicitis
«-■ Perforation by a foreign body, presenting as peritonitis. Abdominal sepsis(Meckel's diverticulitis ± perforation)
w*- Intussusception (iJeoJJeaH often gangrenous by the time the patient comes to operation.
«*"Peptic ulceration due to contained heterotopfc gastric epithelium, which bears HCi-secreting parietal cells. This particularly occurs in children
and characteristically is the cause ol'fnelaena at about the age of 10 years.
Melaena or Bright red blood per rectum {heterotopic gastric mucosa in Meckel’s causing mucosal ulceration and bleeding in adjacent small
bowel mucosa)
■ Small bowel volvulus around fibrous band
■ Patent vitello-intestinal duct, presenting as an umbilical fistula that discharges intestinal contents
Raspberry tumour at the umbilicus due to a persistent umbilical extremity of the duct.
- Vitello-intestinal band stretching from the tip of the diverticulum to the umbilicus, which may snare a loop of intestine to produce obstruction or act
as the apex of a small bowel volvulus.
Examination
■ Tenderness (lower abdomen) near umbilicus
INVESTIGATIONS
Most diverticula are incidental findings. However, the following investigations may be indicated:
# % Cl- Meckel scarwscan for ectopic gastric mucosa with technetium Tc99m pertechnetate IV (sensitivity 85%, specificity 95%)
2~~~AXH
-^•3. Barium follow-through or small bowel enema may show the diverticulum arising from the antimesenteric border.
-*■4. Computed tomography (CT) enterography scan may demonstrate the diverticulum
MANAGEMENT
■ Stabilize, resection of the diverticulum by laparotomy or laparoscopy ± incidental appendectomy
PROBLEMS WITH THE GROIN AND MALE GENITALIA

EMBRYOLOGY
The indifferent gonad (i.e. ovary or testis) begins to develop at the fifth week in the gonadal ridge, part of the mesodermal urogenital ridge that will also
form the kidney, ureter and genital ducts in the male or uterus and uterine tubes in the female. At the lower pole of the putative testis, a strand of
mesenchyme becomes the cord-like gubernaculum. In the eighth week, a prolongation of peritoneum, the processus vaginalis, appears beside the
gubernaculum (or round ligament), and extends into the labioscrotal fold. The testis then migrates distally along the peritoneal canal.
HERNIAS AND ASSOCIATED PROBLEMS

The processus vaginalis normally closes spontaneously soon after birth. Persistence causes three common problems in boys: patent processus
vaginalis (PPV), hydrocoele and inguinal hernia, which may all present as inguinal or scrotal swellings, usually in babies and pre-school children
PATENT PROCESSUS VAGINALIS (PPV)

This term should be reserved for hydrocoeles communicating with the peritoneal cavity via a remnant too narrow to admit bowel. Children with these
communicating hydrocoeles present with scrotal swelling that increases during the day as peritoneal fluid accumulates and subsides at night. They are
seen up to the age of 3 years. Treatment is excision of the peritoneal remnant as in herniotomy after the age of 2 (see below). Before this age, most
settle spontaneously.
HYDROCOELE
Non-communicating hydrocoeles are mostly seen in neonates and young babies. The usual type is a scrotal swelling resulting from incomplete
reabsorption of fluid within the tunica vaginalis after closure of the processus vaginalis. There may be a separate hernia present. These so-called
‘primary hydrocoeles' sometimes appear following a viral illness. Rarely, a secondary hydrocoele results from testicular trauma or torsion, epididymitis or
a testicular tumour.
o
On examination, there is a fluid swelling surrounding a normal testis; the sac transilluminates brightly and the testis can be felt posteriorly (but note that
neonatal bowel is thin and may also transiltuminate brightly in a hernia). If this cannot be achieved, investigation needs to exclude a secondary
hydrocoele. In inguinal hernia the examiner cannot ‘get above’ the swelling, i.e. the swelling originates in the groin; this is the cardinal feature.
Hydrocoeles also occur in the spermatic cord (hydrocoele of the cord) or in the round ligament in girls where they are known as hydrocoeles of the canal
of Nuck. Most hydrocoeles resolve between 18 and 24 months of age. A hydrocoele persisting beyond the age of 2 or appearing later may require
surgery.
Condition Epidemiology and Pathophysiology Clinical Features and Physical investigations Treatment Prognosis
Risk Factors History
Hydrocele(see 1-2%of livebirths Communicating Painlessscrotal mass TransiKumination U/$ if suspect Most resolve <2%recurrence
Urology, U28I Present at Jbrth, hydroceles; processus Communicating suggestshydrocele pathology spontaneouslyby f yr
majority close vaginalisfailstodose hydrocelesmease Si glovesign; gently Sirgical repair if;
spontaneousby 1yr withsmall openingfor insis with standing palpatinghydrocele -Persistence >2 yr
Mf = 6:1 fluidtomovefreely or Valsalva, maybe sacover pubic -Pain
Prematurity betweenperitoneal cavity absent mthemorning tuberclefeels like -Fluctuating insize
throughpatent processus andlargeinthe rubbings i onsil whichsuggests
(if openingprogresses evening communication
toa8owpassageof - Cosmetic reasons
intestine, it isahemal -Infection
Noncommunicating
hydroceles; fluidtrapped
intunicavaginalis; in
olderchildren, maybe
secondarytotesticular
pathology(reactive
hydrocele)
Wav Be Robinses. MBBS Class o f 2015
ANTISEPTIC AGENTS
Contents:
1. Betadine® (Povidone-Iodine)
2. Chlorhexidine (Savlon®, Hibitane®)
BETADINE® SOLUTION (POVIDONE-IODINE)
A chemical complex of povidone and iodine

An antiseptic microbicide
Comes in different concentrations (2.5-10%)
Also have different preparations including spra}
Iodine has been recognized as an effective broad-spectrum bactericide, and it is also effective against yeasts, molds, fungi,
viruses, and protozoans
MOA
■ r Free iodine, stowlv liberated from the povidone-iodine (PVP-t) complex in solution, kills cells by (
l iodination of lipids and oxidation of cytoplasmic and membrane compounds.
■/ This is why it is allowed to dry/oxidized to take effect, as opposed to being wiped off in mosT cases
INDICATIONS
PVP-I has found broad application in medicine as:
O 1. A surgical scrub; for pre- and post-operative skin cleansing;
2. Aseptic preparation of skin for certain procedures, including urinary catheterization, lumbajLpuncture
Other uses:
3. For the treatment and prevention of infections in wounds, ulcers, cuts and burns;
4. For the treatment of infections in decubitus ulcers and stasis ulcers;
5. Used in p[eurodesis (fusion of the pleura because of incessant pleural effusions). For this purpose, povidone-iodine is equally ■
effective and safe as talc, and may be preferred because of easy availability and low cost.
6. In gynecology for vaginitis associated with candidal, trichomonal or mixed infections
A dvant ag es
■ l/lt has been demonstrated that bacteria do not develop resistance to PVP-I, and the sensitization rate to the product is only 0.7%
DISADVANTAGES
■^ Study showed chlorhexidine has better efficacy than Betadine (see below)
'j ■ Iodine is absorbed into the body to various degrees, depending on application area and condition of the skin. As such, it interacts
with diagnostic tests of the thyroid gland such as radioiodine diagnostics, as well as with various diagnostic agents used on the
urine and stool, for example Guaiacum resin
SAVLON® (CHLORHEXIDINE GLUCONATE + CETRIMIPE)
Chlorhexidine is an antibacterial used a \a n antiseptic and for other applications. It is a cationic polybiguanide.
It is used primarily as its salts (eig., chlorhexidine gluconate, chlorhexidine diacetate (Flibitane®)).
It is on the World Health Organization’s List ofEssential Medicines, a list of the most important medication needed in a
basic health system
■^5* Savlon® combineSj^hlorhexidine gluconate wittf cetrimide,1another antiseptic
MOA as an A n tis eptic:

*) At physiologic pH, chlorhexidine salts dissociate and release the positively charged chlorhexidine cation.
The bactericidal effect is a result of the binding of this cationic molecule to negatively charged bacterial cell
wails.
At low concentrations of chlorhexidine, this results in a bacteriostatic effect; at high
concentrations, membrane disruption results in cell death
■ Chlorhexidine is active against Gram-positive and Gram-negative organisms, and yeasts.

■ The effectiveness against herpes viruses has not yet been established unequivocally
■ Chlorhexidine, like other cation-active compounds, remains on the skin. It is frequently combined with alcohols (ethanol and
isopropyl alcohol
Wayne Robinson. MBBS Class o f 2015
INDICATIONS
■ Mostly the same as Betadine
IMPORTANT POINT - Study showed chlorhexidine has better efficacy than Betadine
In a clinical study of approximately 850 patients which compared the efficacy in preventing post-operative infection of pre-operative skin
cleansing using chlorhexidine-alcohoi vs. povidone-iodine, the rate of surgical-site infection was significantly lower in the chlorhexidine-
alcohoi group than in the povidone-iodine group (overall, 9.5% vs. 16.1%). Chlorhexidine-aicoho! was significantly more protective than
povidone-iodine against both superficial incisional infections (4.2% vs. 8.6%) and also deep incisional infections (1 % vs. 3%).
The team performing the study believes that, although both of the antiseptic preparations possess broad-spectrum antimicrobial activity,
the more effective protection provided by chlorhexidine-alcohoi may be due to its more rapid action, its persistent activity (even when
exposed to bodily fluids), and some residual effect
WATER-BASED LUBRICANT
■ Generally biologically inert, and contains no color or perfume additives.

■ K-Y jelly, as well as other brands, uses glycerin and hydroxyethyl cellulose as the lubricant, with chlorhexidine gluconate,
as antiseptic with other preservative additives.
■ Water-based lubricant has proven popular because it does not stain and is easily cleaned up.
■ Some contain antiseptic agents, such as chlorhexidine gluconate
MEDICAL USES
Surgical lubricants are substances used by health care providers to provide lubrication and lessen discomfort to the patient during
certain medical/surgical procedures, including:
1. Provide lubrication for digital rectal examination, vaginal examination

2. Provide lubrication for insertion medical instruments, including urinary catheters, NG tubes, various endoscopes
NB: It is sometimes used inappropriately as Ultrasound Gel (See below)
The class of lubricants now known as "personal" derives from surgical lubricants; K-Y Jelly was originally introduced in 1904 for this
purpose, before it gained popularity as a personal lubricant
ULTRASOUND GEL
(May possibly come in exam?)
I
Reason for use (http://www.two-views.com/Ultrasound/Gel-Goo.html):

Ultrasound waves don’t travel very well through air. So any little bit of air that would be between the probe and the skin
would be a problem. And dry skin poses a lot of tiny pockets of air.
Ultrasound gel is a type of conductive medium that enables a tight bond between the skin and the probe or transducer,
letting the waves transmit directly to the tissues beneath and to the parts that need to be imaged. It is formulated to act as a
coupling agent and reduce static. In fact, the more gel, the better - thus why many radiologists giving the exam pile it on. Besides
ultrasounds themselves, the gel is also used with a fetal Doppler, which can be employed to allow parents and doctors to listen to the
heart beat of an unborn child. Ultrasonic gel is usually composed of propylene glycol, water and occasionally a dye. The dye is
more for looks than making it work better. It is usually clear and thick, and a little bit sticky. That way, when it is applied to the skin it
doesn’t drip or run off. At the end of the procedure it can be wiped off easily.
— (jL o d c /t s e a s r -
'a C r o n
( C -O iO yko r U C L c -J
n o -f CtS O pod Cor (n frG m G U .i

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DACRON GRAFT - P®(mc s /c t
n
RIEF HISTORY
Arterial bypass grafting was first developed during the Korean War to treat arterial trauma, using homografts from human cadavers. Thp
initial results were excellent but grafts eventually suffered from aneurysmal dilatation ancTrupture. This led to the introduction of
synthetic graft materials for large arteries, now available in a variety of shapes, sizes and types of cloth. Knitted polyester (Dacron) is
the most popular and is the standard material for aorto-iliac obstruction. — ^
Many grafts are now sealed with gelatin or other proteins to minimize porosity.
The most common procedures are synthetic ‘trouser’ grafting for aorto-iliac (supra-inguinal) disease (see image on last page) and
, femoropopliteal grafting using saphenous vein, for infra-inguinal disease
DESCRIPTION
■ 20 mm woven Dacron tube graft
■ Threaded tube with a longitudinal radiopaque line
■ Dacron is just the brand name. The actual compound is Polyethylene terephthalate (PET), a polyester resin
■ Dacron grafts are manufactured in either a woven or knitted form. Woven grafts have smaller pores and do not leak as much
blood. To reduce the blood loss knitted grafts should be pre-clotted prior to insertion. They are less frequently used than woven
grafts.
■ Many modern Dacron grafts are manufactured coated with gelatin or proteins (collagen/albumin) to reduce porosity, and
antibiotics to prevent graft infection. Impregnated grafts are considerably more expensive than their none coated counterparts
INDICATIONS
Used fo vascular disease, particularly suora-inauinal disease
Dacron grafts are frequently used in aortic and aorto-iliac surgery. Beiow the inguinal ligament the results of all synthetic grafts are
inferior to those obtained with the use of vein grafts. Suitable vein is not always available and in this situation PTFE should be used. It
can be used in conjunction with vein as a composite graft. Neointimal hyperplasia at the distal anastomosis can be reduced by the
incorporation of a segment of vein as either a Millar Cuff or Taylor Patch to improve the long-term patency of the grafts.
CONTRAINDICATIONS
1. All the contraindications to grafting, including poor inflow, outflow, etc. Patients with non disabling intermittent claudication who do
not require invasive intervention
2. In patients who are candidates for surgical revascularization with grafts, Dacron is relatively contraindicated fro grafting across the
¥ knee joint. Vein grafts are preferred due to their superior patency rates
PROCEDURE
r t iu s t i ? m o (P
ADVANTAGES AND DISADVANTAGES
Compc ired to vein grafts: (B

For smaller arteries, autogenous long saphenous vein from the leg is the best conduit, Vein is also inherently resistant to
b
infection, a useful attribute when treating infected lower limb wounds and ulcers.
G ) Venous grafts have a superior patency rate for infra-inguinal disease, particular for grafting across the knee joint. In the latter
cases, Dacron grafts are relatively contraindicated
COMPLICATIONS
Distal thrombosis and distal embolisation - minimized by temporarily anticoagulating the patient
Graft infection
Graft kinking and occlusion
True and false aneurysms at the site of anastomosis
Erosion in to adjacent structures - e.g. Aorto-enteric fistulae m
POSSIBLE OSCE DISCUSSIONS
GENERAL DISCUSSION ON GRAFTS
Vascular grafts can be classified as either biological or synthetic. There are two commonly used types of biological grafts. An autograft
is one taken from another site in the patient. In peripheral vascular surgery by far the most commonly used such graft is the long
saphenous vein. This can be used in situ with the valves surgically destroyed with a intraluminal cutting valvutome. Alternatively the
vein can be removed and reversed but this produces a discrepancy between the anastomotic size of the artery and vein. In thoracic
surgery the use of internal mammary artery for coronary artery bypass surgery is another example of an autograft. An allograft is one
taken from another animal of the same species. Externally supported umbilical vein is rarely used but is an example of such a graft.
Synthetic grafts are most commonly made from Dacron or polytetrafluroethylene (PTFE) also called Gortef graft.. Dacron has already
been discussed. PTFE is a velour graft. Its smooth surface is less thrombogenic than Dacron. Its smooth wall is prone to kinking as it
passes around joints necessitating it to be externally supported
BE PREPARED TO DISCUSS AAA AND ARTERIAL DISEASE MANAGEMENT
Aorlo-irtierooraJ
by pas 5 grafting
P tosam al a n asto m o sis—

en d of graft to sode of
ao rta (o ccasio n ag y ao rta
fcranssecSed an d end-to-
end anastom osis
perfem redjr
Distal anastomosis—
end of graft to skie at
common femoral and
profcincte femora junctxm,
opening Ste profunda
orifice to rr*r*n*se future
stenosis
F ig . 4 1 .4 A iM to -b tfm w a i b y p a ss fo e aorto-tKac (fe * a « using a

tro u se r or 'Y' g ra ft
A Dacron bifurcation graft or prosthesis is used to bypass the aorto-iSae
segment whetsit i$ occluded or stenesed, or to replace it when aorta amt
iftacs are aneurysmal, in the latter case, the distal anastomoses areto the
iliac arteries not the femoraSs so as to maintain pelvic perfusion.
Inflation Capacity kfcndficacion
Rccc^scxf Vfcmdi»£ .% od x m c nc
IfeilTooiv f a f h n o a Huh*
BRIEF HISTORY
Dr. Thomas J. Fogarty (surgeon) invented the "medical industry standard" balloon embolectomy catheter. First used in 1961 and
patented in 1963, this inflated balloon extraction technique revolutionized surgical embolectomy procedures. In 1965, Dr. Thomas '
Fogarty published an article describing "a new method for extraction of arterial emboli and thrombi." Today, using only local anesthesia^
the procedure only takes about an hour.
DESCRIPTION
■ It is a tong, flexible and graduated tubular catheter with a distal inflatable bulb
■ The proximal eryd has a fitting for attachment to a syringe, used for inflation of the bulb
■ Depth markings on catheter indicate distance of balloon from arteriotomy
> m u s r ecvscxA -
INDICATIONS
As the name suggests it is used for embolectomy, which is the extraction of vascular thrombi and emboli
Extraction of arterial emboli in acule_arteriglpcc]usioji

Can also used to remove stones from ther^rinaryb-acfiand the(common bile ducO
Less commonly, to occlude a bronchus to protect the lung during surgery (e.g. lobectomy) on the contralateral lung. In this
case the catheter is passed into the bronchus through a double lumen tube
CONTRAINDICATIONS
PROCEDURE
Overview: The catheter is inserted into a vessel (usually an artery) and is inflated once past the embolus. The catheter is then pulled
back while the balloon is still inflated, pulling the clot out of the vessel.
1. * / Attain informed consent

2. (--Gather instruments
3.i-'-'Set up a sterile field ensuring strict aseptic technique
4. ‘'"Clean area with Betadine and allow it to dry
5. ‘'"Infiltrate local anaesthetic
6. ‘'"Incise skin and bluntly dissect down to artery
7. ‘-'Initial approach is via common femoral artery regardless o f anatomic location.
. ‘■'"fl/lake a small transverse incision on4he-art©iy-(careful not to cut the artery in two!)
. (/Introduce the catheter and wit(l1racliological guidance pass it distal to the embolus, as far as possible into the occluded vessel
10i/fnflate the bulb after it has safely-passedihaêefasion
11. Withdraw the catheter while still inflated
12. It may take several attempts before the clot may be removed
13. Repair and suture the artery, soft tissue and skin.
■ For sepsis, cover with gentamicin + amoxicillin or + 3rd generation cephalosporin.

■ N.B. Non- balloon catheter exists.
A D V A N T A G E S A N D D IS A D V A N T A G E S
C O M P L IC A T IO N S
Massive haemorrhage and transection o larterv
^"5? Distal migration of embolus
i^3. Damage to endothelium of vessel (intimal injury) (less likely)
P O S S IB L E O S C E D IS C U S S IO N T O P IC S
KNOW ALL ABOUT ACUTE ARTERIAL OCCLUSION

INSTRUMENTS
CENTRAL VENOUS ACCESS (CVP LINES!
Sources: Long word document on CVP, UHWI lectures
(MUST CREATE A SUMMARIZED VERSION OF THIS (1-2 pages) FOR QUICK REVIEW)
INTRODUCTION - WHAT IS CVP? * C d P s =" P ^ uK Un

_ (J3 b fp s z r fs * * * ">
Blood from systemic veins flows into thej;ight atrium; thepressure in the ri] ht atrium is thp central venous pressure (CVP). CVP is
determined by thejunction of the right heart and the pressure of venous blood in the vena cava. Under normal circumstances, an
increased venous return results in an augmented cardiac output, without significant changes in venous pressure. However with poor
right ventricular function, or an obstructed pulmonary circulation, the right atrial pressure rises. Loss of blood volume or widespread
vasodilation will result in reduced venous return and a fall in right atrial pressure and CVP.
— —-=j ^
CVP is often used to make estimates p f circulatory function, in particular cardiac function and blood volume. CVP does not measure
either of these directly, but taken in the context of the other physical signs useful information can be gainedllThe supply of blood to
the systemic circulation is controlled by the left ventricle. In a normal patient the CVP closely resembles the LEFT atrial pressure
and is usually used to predict it! However In patients with cardiac disease the right a m f^ T v enWicfes may function different!’
- this can orrty be detected climcaffy by measuringth e pulmonary capillary wedge pressure V 'PCWP)«
Normal CVP: In a spontaneously breathing patient is approximately

midaxillary line 22-—
This rises about 3-5cm H?0 during mechanical ventilation
NOTE: The absolute value is not as important as serial measurements and the change in response to therapy
CVP measurement may still be in the normal range even with hypovolaemia due to venoconstriction
------------------------------------------------------------- --------- m u s t tf/v iQ u o
In short:
CVP is a measure of the pressure in the right atrium, which reflects changes in right ventricular end-diastolic pressure
ESTIMATES cardiac fundi and flood ; It does NOT measure either of these directly - it must be interpreted!
• *** In a normal patient, the CVP closely resembles the left atrial pressure and can be used to estimate it
This depends on the assumption that there is no right ventricular disease and normal pulmonary vascular resistance!
O ' d o m m o tJ < 2 u e s - n o u Hi
Online source: NOTE: A common misconception is that CVP consistently reflects pressures found in the left side of the heart. The
measurement that best reflects left ventricular pressure changes and reserve is the left atrial pressure. OR the nearly equivalent
pulmonary capillary wedge pressure (PCWP)
MUST KNOW: THE 8 FACTORS AFFECTING CVP

C J jP Une ln <_e.v<s ^ r' ■)
T f'
Venous Return:
1. */ Total blood volume ■Po>xm o l
K^Venous tone [Veno-capacitance tone] Is G pporohx^ fQrdrd-
* "IX c s
»^Soleal pump
4. i^Posture
5. wÂtrial compliance
— 6 rv U xenons p *® ** - w. -
x i^lntra-pericardial pressure
7. v^lntra-thoracic pressure — cypako
J3. v/tritra-abdominal pressure
prcSS,arc cn nX)Q m f¥' (=,'e o f
DESCRIPTION OF APPARATUS
• “Multiple access lumen” - double, triple, quadruple lumen _ D f S C n 't *

• Introduced directly into a vein OR tunneled subcutaneously
— cobcr-T- C P ^ * T^ )
& < **(< * d f o v P (£>
— eJr.
INDICATIONS next d r <&tCbr
# p o i ’t s
Diagnostic Qty)
1U
Assess intravascular volume especially when urine output is unreliable-and to guide intravascular replacement
e.g. Hypovolaemia secondary to significant blood loss/large fluid shifts, hypotension not responding to basic management
Pulmonary artery catheterization and monitoring
///
1
^ In,
oc] p c r -f o n tt d c h is KiOT ô r -f&ktey ~Hcxn r<sJ<r.
f o is e u illt 's . ta u o / _ Wayne

W ayn< Robinson. MBBS Class of 2015
_ p k oaÂ. a fg pr&perh
Therapeutic
'Y _ ** *_ u OLû . l) wae^ c® £ *k
1. Infusion of tV fluid s - Eg. Hypertonic solutions. ^Peripheral access actually allows more rapid volume replacement. This is due
to the physics of the shorter length needle/catheter that may be wide bore.)
• NB: Flow rate through a 14 gauge peripheral line is twice that of a 20 cm 16 gauge central venous catheter. So
central line NOT for more rapid resuscitation.
2. Infusion of drugs
• ^ Vasoactive drugs (epinephrine, dopamine)
• ^ Inotropic drugs
• v-C hem oth erap y agents
• Agents irritating to peripheral veins
(All can cause tissue irritation or necrosis if extravasated in peripheral line)...
3. Administration of Partfef/Tctat Parenteral Nutrition (PPN/TPN)

4. #- Transvenous cardiac pacing
5. * Haemodialysis
6. * Gaining venous access w ith poo r peripheral veins
7. Frequent plasmapheresis
8. Aspiration of air emboli
PROCEDURE
Equipm ent:
1. Tilting bed, trolley or operating table

2. Sterile pack and antiseptic solution
3. Local anaesthetic - e g. 5 ml lignocaine 1% solution
4. Appropriate CV catheter for age/route/purpose (see below)
5. Syringes and needles
6. Saline or heparinized saline to prime and flush theJine after insertion (Catheter heparinized or 0.9% sodium chloride infused
slowly)
7. Suture material - e.g. 2/0 silk on a straight needle
8 . Sterile dressing
9. Shaving equipment for the area if very hairy (especially the femoral)
10. Facility for chest X-ray
11. Additional equipment required for CV pressure measurement includes: manometer tubing, a 3-way stopcock, sterile saline, a
fluid administration set
C V Catheters: m a S T
(5?
Catheters differ in length, internal diameter ancTnumber of ports
Two useful lengths are 20 cm catheters for subclavian and internal jugular lines, and 60 cm catheters for femoral and basilic
( J f'f f r au S
, U j uOu li i n" sd " t f L t r & d ^ — 9 -0 c .n g o a - t h e io 'S (o r s u W a v ja ^ —
Method: b e c o m in g uAs^
' 4' C o rr’ ~ < b P em & Q ^ o ro L £ M e . ^
GENERAL METHOD (For all site s)
r T. Obtain informed consent!!! - Explain the procedure to the patient
Shave the needle insertion area if very hairy
Aseptic technique - prepare and check all the equipment for use
4. Sterilize the skin and drape the area ^ ('(fam ine .

/
5. Apply local anaesthetic -TnfOtrate the skin and deeper tissues. In cases where difficulty is anticipated use the small local
anaesthetic needle to locate the vein before using the larger needle. This reduces the risk of trauma to other structures.
6. Position the patient - as for the specific route described tre n d s , rn
7. Identify the anatomical landmarks for the chosen route
2
8. First localize the vessel with a small gauge needle at the recommended point
“f r r d
9. Insert an entry needle into the vessel List an re&Alt / U ? ( A [!J
10. After the needle has penetrated the skin, aspirate gently whilst advancing the needle as directed until the vein is
entered. If the vein is not found, slowly withdraw the needle whilst gently aspirating; often the vein has been collapsed and
transfixed by the entry of the needle.
(D u s t tir o L o !!!
See “Methods of Catheter Insertion” below:
11 . If using a guidewire ( linger techns ) - pass this into the vein through the needle, flexible J-shape end first, then
remove the needle. For small catheters (No dilation needed): Thread the catheter over it until the end of the wire protrudes
from the end of the catheter and whilst holding the wire still advance the catheter into the vein with a twisting motion (Do
NOT release wire). TAKE CARE not to allow the wire to be pushed further into the vein whilst advancing the catheter!
12. For large catheters: It may be necessary to(dilate up the hole in the vein) Can enlarge the puncture site with a number 11
scalpel. Make a small incision in the skin ancffascia where the wire enters the patient. Thread the dilator over the wire into
the vein. Remove the dilator taking care not to dislodge the guidewire. Thread the catheter over the wire as described above.
POST CATHETER PLACEMENT
r ^ 1 3 (Âspirate bloodfromteach porty Check that blood can be aspirated freely from all lumens of the catheter
s— Aspiration of venotrsiSiood:
o Confirms vein’s location
o Arterial puncture can be rule ruled out bv/TTpolour of blood,(g)PaQg measurement, or^}transducing the
wave form.
-)> 14. Flush with saline/sterile water
T 15 Secure the catheter with the suture - and cover with a sterile dressing (Tega-Derm). Tape any redundant tubing carefully
avoiding any kinking or loops, which may snag and pull out the catheter.
_^16. Connect catheter to a bag of intravenous fluid
17. Write a procedure note
Checks before using the line
1. *** Chest X-ray!!! (ideally erect). Reasons:

^ Check the position of the catheter tip and to
( i L j Exclude a pneumo, hydro or haemothorax
NOTE: Early radiograph may not show up abnormalities and it may be best to
develop. Tip should lie at junction of SVC and right atrium!
2. Ensure fluid runs in freely and that blood flows freely back.
n
; Methods
M< of Catheter Insertion a t s
n n a io
1.
2.
Catheter over needle (similar to peripheral cannutation).
Catheter through a needle (requiring large bore needle stick)
7
3. Catheter over guide wire (Seldinger technique) - (Needle, guidewire, (dilator), catheter)
n • tÛse introducing needle (18G) to locate vein
J S 'iD * is threaded through the needle on obtaining free blood flow
• [^Needle is removed
i^Skin and vessel are dilated, if necessary V /< rS S e _
c^Catheter is advanced over the wire
^-"Wire is removed be dt< (o k e d [I .
^-"Catheter is secured in place
SPECIFIC METHOD (See tab le w ith Pros and Cons o f each)
3
With the exception of the external jugular, central veins are often deep and have to be located blindly. This is associated with risk to
nearby structures, especially in the hands of the inexperienced operator. Veins commonly lie close to arteries and nerves, both of which
can potentially be damaged by a misplaced needle. The subclavian vein also lies close to the dome of the pleura, damage to which can
cause a pneumothorax. The choice of route will therefore depend on a number of factors. (See Appendix)
SUBCLAVIAN APPROACH
In conscious patients the subclavian route is often preferred (since head movement does not affect it) and also in trauma patients with
suspected cervical spine injury P«Len<d <3& h e a d ^ o o v fe r^ e r^ « df°* S IOOT
• Positioning $ J J j^ ‘
*
o inflight side preferred - to avoid thoracic duct orvthe left ^
* * 3 L - ^ u''T rendelenburg position (10-1,5 degrees) - to afstend the central veins and prevent air embolism
o impatient supine' head turned away from side to be cannulated (unless c-spine injury), arm abducted - flattens
deltoid bulge
o Shoulders neutral with mild retraction - as the shoulder falls backward, the space between the clavicle and first rib
narrows, making the subclavian vein less accessible
• Needle placement yo
_____________ ^ ________________/^Vff5V397
— yA ^CiLinHToiTorfnfgdTe and mediafthirds of clavicle1
]- here the vein in just posterior to the clavicle and just above the first
rib which acts as a barrier to the pieura.
o At the small tubercle in the medial deltopectoral groove
o Needle should be parallel to skin
— ^ Aim towards the supraclavicular nntnh and just under the clavicle
INTERNAL JUGULAR APPROACH
• Positioning
o Right side preferred - left IJ is more circuitous, thoracic duct on left

o Patient supine, Trendelenburg position - IJ distensible
o Head turned slightly away from side of venipuncture
• Needle placement: Central approach (most common) (Can have high, middle or low level approaches)
Locate th^triangl^formed by the clavicle and the sternal and clavicular heads of the SCM muscle
Gently placethreefingers of left hand on carotid artery
Place needle at 30 to 40 degrees to the skin, lateral to the carotid artery
Aim toward the ipsilateral nipple under the medial border of the lateral head of the SCM muscle
Vein should be 1-1.5 cm deep, avoid deep probing in the neck
FEMORAL APPROACH
• Positioning
o Supine
o Abduct and externally rotate thigh
• Needle placement
1 cm medial to femoral artery - identified by pulsation, 1-2 cm below the inguinal ligament
o Needle held at 45 degree angle
o Aim toward umbilicus
*** Catheter tip reaches junction of Superior vena cava and right atrium ***
*** NOTE: ULTRASOUND GUIDED CENTRAL VENOUS ACCESS ***

• Becom ing standard o f care
• Vein is accessed under direct visualization
• Helpful in patients with difficult anatomy
• \ / < a ir * i o / " * r \ K r » r v r z i c > o i K I ^
W i l l I O V y V I l i p i 'S O O I K / I ^
4
Vein is not always larger
Other tips:
Get chest x-rav after unsuccessful attempt
If attempt at one site fails, try new site onreame sictt to avoid bilateral complications
Use the vein on the same side of a pneumothorax*
CARE OF THE CATHETER / OCX csPCJfcr ]\)
1. Strict asepsis whenever handling (even after placement) - Wear sterile gloves
2. Dressing - keep entry site covered with a dry sterile dressing - changed daily!
a. The dressing should provide an effective barrier to bacteria, allow the catheter to be securely fixed, be sterile, and
easy to apply and remove. Transparent dressings
3. Ensure the line is well secured to prevent movement (this can increase risks of infection and clot formation)
4. Regularly inspect site for inflammation/discharge - soreness, unexplained pyrexia and damaged, wet or soiled dressing -
immediate inspection
5. Skin cleaning chlorhexidine in 70% alcohol and sutures at the entry site and some suggest should be changed every 7
days to reduce risk of sepsis and thrombosis. May not be necessary if cared for very well and patient assessed regularly for
complications. Repeated cannulations may increased risk
CONTRAINDICATIONS
Absolute:
f 1. v ' f ’atient refusal
L 2 .1'lo cal sepsis at potential cannulation site.
3. 'Renal-cell tumour extension into right atrium. (Absolute?)
4. *^ Fungating tricuspid valve vegetation. (Absolute?)
Relative:
1. 'Bleeding diatheses
2. <"'Anticoagulation or thrombolytic therapy
3. ^Combative patients
4. *^ elju !itis, burns, severe dermatitis at site
5. <s Vasculitis
6. ^-Distorted local anatomy
7. Patients with ipsilateral carotid endarterectomy because of possibility of carotid artery puncture
COMPLICATIONS
EARLY:
TV-Arterial Puncture
2. »"Haemorrhage/Bleeding
3. ‘"•Trauma to neighbouring structures
r' 1. ‘""Artery (depends on site - see below) - Haematoma, AV fistula
2. '-''"Nerve (depends on site - see below)
3. ‘-'Lung (pneumothorax, haemothorax)
d 4. ‘-"Cardiac perforation and tamponade
5. '"'Thoracic duct (chylothorax)
**6. ‘’"Diaphragmatic paralysis (Phrenic nerve injury)
4. *" Thrombosis
5. ‘-"Embolism of
f 1. Catheter tip
) 2. *"Air
3. ^-Thrombus
6. 'Cardiac arrhythmias/dysrhythmias (catheter tip is in right atrium or ventricle)
7. "Hydrothorax, hydromediastinum - from infusion of fluid in malplacement
LATE:
5
1. w^lnfections (Sepsis, cellulitis, osteomyelitis, septoarthritis)
2. '"''Venous thrombosis
3. »—Cardiac perforation and tamponade
4. t^ O f the catheter itself: Obstruction of CVP (from poor care), Displacement
Some specific complications:
Specific for Subclavian Puncture:

■ w'gubclavian artery puncture
■ in te rn a l mammary artery laceration
■ ‘■'-'Brachial plexus injury
■ ‘•'''Pneumothorax
■ ‘•'"Pulmonary emboli
Specific to Internal Jugular:

& C ■ C a ro tid artery puncture -> haematoma, tracheal compression and respiratory embarrassment; or dislodging of an
atheromatous plaque -> CVA
L ■ ^'Damage to the trachea or esophagus
INDICATIONS FOR REMOVAL <T\ogrr
1. Confirmation of any infection

a. Blood cultures from the catheter indicate the presence of microorganisms
b. A positive wound swab from the entry site
c. Generalized septicemia
2. A leaking or damaged catheter

3. Blockage
4. Termination of therapy
SPECIAL DETAILS
Seldinqer Technique:
This is the preferred method of insertion. A small diameter needle (18 or 20 gauge) is used to find the vein. A guidewire is passed down
the needle into the vein and the needle removed. The guidewire commonly has a flexible J-shaped tip to reduce the risk of vessel
perforation and to help negotiate valves in the vein e.g the external jugular vein (EJV). Once the wire is placed in the vein, the catheter
is passed over it until positioned in the vein. The wire should not be over-inserted as it may kink, perforate the vessel wall or cause
cardiac arrhythmias. This technique allows larger catheters to be placed in the vein after the passage of appropriate dilators along the
wire and a small incision in the skin at the point of entry.
CVP waveform:
• Three Peaks (a, c, v)

• Two Descents (x, y)
APPENDIX
Table 1. Factors which determine the choice of central vein

How long will the catheter be required? le. Long term / intermediate /
short term Suitability of the vein for technique chosen e.g. for CVP
Patient:
measurement the tip of the catheter must be within the thorax. A femoral
route therefore needs a long catheter
Knowledge and practical experience of the technique - it is be better to
Operator: have a few clinicians in each area who perform all the central venous
cannulations and gain experience (a “central venous access team”)
Success rate for vein cannulation
Success rate of central placement
Technique
Complication rate.
characteristics:
Applicability to patients of different ages
Ease of learning
6
Puncture of a visible and/or palpable vein or ‘blind’ 7enipuncture based
on knowledge of anatomy
Availability of suitable apparatus
Equipment available: Cost
Suitability of material for long term cannulation
Table 2. Problems during CV cannulation

Usually obvious but may be missed in a patient who is hypoxic or hypotensive.
If unsure, connect a length of manometer tubing to the needle / catheter and
look for blood flow which goes higher than 30cm vertically or is strongly
Arterial puncture
pulsatile. Withdraw the needle and apply firm direct pressure to the site for at
least 10 minutes or longer if there is continuing bleeding. If there is minimal
swelling then retry or change to a different route.
If air is easily aspirated into the syringe (note that this may also occur if the
needle is not firmly attached to the syringe) or the patient starts to become
breathless. Abandon the procedure at that site. Obtain a chest radiograph and
Suspected pneumothorax insert an intercostal drain if confirmed. If central access is absolutely necessary
then try another route ON THE SAME SIDE or either femoral vein. DO NOT
attempt either the subclavian or jugular on the other side in case bilateral
pneumothoraces are produced.
Usually from the catheter or wire being inserted too far (into the right ventricle).
Arrhythmias during the
The average length of catheter needed for an adult internal jugular or
procedure
subclavian approach is 15cm. Withdraw the wire or catheter if further than this.
This can occur, especially in the hypovolaemic patient, if the needle or cannula
is left in the vein whilst open to the air. It is easily prevented by ensuring that
Air embolus
the patient is positioned head down (for jugular and subclavian routes) and that
the guidewire or catheter is passed down the needle promptly.
Check that the needle is still in the vein. Flush it with saline. Try angling the
needle so the end of it lies more along the plane of the vessel. Carefully rotate
the needle in case the end lies against the vessel wall. Reattach the syringe
The wire will not thread and aspirate to check that you are still in the vein. If the wire has gone through
down the needle the needle but will not pass down the vein it should be very gently pulled back.
If any resistance is felt then the needle should be pulled out with the wire still
inside, and the procedure repeated. This reduces the risk of the end of the wire
being cut off by the needle tip.
Apply firm direct pressure with a sterile dressing. Bleeding should usually stop
Persistent bleeding at the of
unless there is a coagulation abnormality. Persistent severe bleeding may
entry
require surgical exploration if there is an arterial or venous tear
Table 3
Problem Effect on CVP
High pulmonary vascular resistance - left sided pressure and function may be
Pulmonary embolus
normal. A higher than normal CVP may be needed to ensure adequate return
High intrathoracic pressure
of blood to the left side of the heart.
Resulting rise in pulmonary venous pressure and right sided heart strain.
Left heart failure Initially CVP may be normal but will increase with significant failure.
Paradoxical rise in CVP on inspiration and fall on expiration (opposite of
Constrictive pericardial
normal in a spontaneously breathing patient). The absolute level will be higher
disease
due to impeded filling of the heart
Blocked cotton wool at top
Fluid will not move in the tube to give a correct reading
of manometer
'Cannon waves' on CVP reading the reading will have a strong pulsatile
Complete heart block element when the atrium contracts against a closed tricuspid valve sending the
pressure wave back into the SVC
Tricuspid
Mean CVP will be higher
stenosis/regurgitation
7
rfiosl -111 b e 2 r c \a d t P v / C
(J (ju d e - !(!
Wayne Robinson. MBBS Gass of 2015
ENDOTRACHEAL TUBE
Sources: Wikipedia, UHWI Lectures, Online
DESCRIPTION AND DESIGN
©
A tracheal tube is a catheter that is inserted into the trachea for the primary purpose of establishing and maintaining a patent airway
and to ensure the adequate oxygenation and ventilation (exchange of oxygen and carbon dioxide!
& P ~
Many different types of tracheal tubes are available, suited for different specific applications:
* An endotracheal tube is a specific type of tracheal tube that is nearly always inserted through the mouth (orotracheal) or nose
(nasotracheal).
Tracheal tubes can also be used to deliver:

* •'•"Oxygen in higher concentrations than found in air
* •""Volatile anesthetic agents such as desfluorane, isofluorane, or sevofluorane.
* ^M e d ica tio n s such as salbutamol, atropine, epinephrine, ipratropium, and lidocaine.
* m o th e r gases such as helium' nitric oxide, nitrous oxide, xenon
Commonly used for airway management in the settings of general anesthesia, critical care, mechanical ventilation, and emergency
medicine.
DESIGN MATERIALS
* Most endotracheal tubes today are constructed of polyvinyl chloride (PVC)
• Specialty tubes constructed of silicone rubber; latex rubber or stainless steel are also widely available.
*** Plastic is NOT radio opaque and therefore plastic tubes have a radio-opaque line that makes them more visible on a chest X Ray.
STRUCTURE
Diameter
Have an inne r diameter and an o u te r diam eter — -------------- —

The “size* of art endotracheal lube refers to its/jntem al diameter!?) -4— Kl^>
• For human use, tubes range to size from 2 to 10,5 mm in internal diameter (ID).
_^_j»J>-Note: Narrower tubes increase the resistance to gas flow. This can be relevant in the spontaneously breathing patient who will
have to work harder to overcome the increased resistance. POINT: Thus one should choose the largest diameter
endotracheal tube that is suitable for a given patient
• Paediatric endotracheal tubes have a much smaller internal diameter.
Length
1
• Measured from the end that goes into the trachea and is marked in centimeters.
• Too long prone to kinking and become obstructed. Can be cut to a more appropriate length if necessary.
Bevel
To make it easier to pass through the vocal cords and to give you a betterj/ision ahead of the tip"
As the endotracheal tube is advanced near the cords, th e'le ftfa cinq tevelg lves a better vrew
Murphy's Eye
If the main opening of the endotracheal tube gets blocked by, for example, abutting against the tracheal wall, gas flow can still occur via
the Murphy Eye. Without the Murphy Eye, the endotracheal tube would have been completely obstructed.
Cuff
An inflatable region at the “patient end” of an endotracheal tube
Inflated portion forms a seal against the tracheal wall. This seal s e rv e ^ fp u rp o se e )
i; prevents matter (e.g. pulmonary aspiration^'gastric contents) entering trachea
past the cuff
pressure verrtHatfcw
*** Important Notes:

Un-cuffed mainly for paediatric usage. Reason:
—o Glottis is na rro w e st p o in t in adult
—a Cricoid na rro w e st in child. C ircu la r; th e re fo re un-cuffed fits w e ll
• Some tubes have 2 cuffs to ensure a seal in the event the upper is damaged
Cuffs are designed to have either a high volum e OR a low volum e

• High volume low-pressure cuffs Because of their large volume, jfaey have a larger surface area in contact with the trachea This means that
they apply a lower pressure against the trachea! wall and have auower incidence of tracheal wall ischemia and necrosis. Theseal is not as .
flood as the sea! in high pressure cuffs because of the lower pressures and because the large cuff may develop wrinkles that allow material to
pass by the cuff.
* Low volume high-pressure ûffs: These cuffs have a lower volume and the surface area in contact with the trachea is small This results in a
high-pressure seal that is more effective than the one caused by high volume low-pressure curfs. Howevei, this high pressure is more likely
to cause tracheal ischaemia and necrosis if used for a prolonged period of time
Pilot Balloon
After intubation, the cuff is inflated with air. Done by attaching a syringe to the pilot balloon
• The pilot balloon is connected to the cuff by a thin tube. As the syringe supplies pressurized air, the pilot balloon and cuff
inflate. Once the cuff is inflated the syringe is removed. Air does not leak out as there is a one-way v&hse at the pilot balloon.
• By feeling the pilot balloon, one can estimate the amount of pressure in the cuff. If the cuff is leaking, e.g. due to damage by
the surgeon during a thyroidectomy, the pilot balloon will collapse.
Radio-opaque line
Connectors ^ CT)fT\ —
• Connect the endotracheal tube to the breathing system.
• One end of the connector connects to the endotracheal tube and this end has a diameter that depends on the endotracheal
tube size.
• The other end connects to the breathing system and has a 15 mm outer diameter (British Standard)
SPECIAL TYPES
2
1. vOral or nasai
2. ‘'Cuffed or uncuffed
3. (^Preformed (e.g. RAE (Ring, Adair, and Elwyn) tube),
4. v'Beinforced/Armoured tubes,
5. HDoubie-iumen endobronchial tubes
6. Microiaryngea! tubes
7. Laser-resistant
P R E F O R M E D (“ P O L A R ” ! E N D O T R A C H E A L T U B E S
Preformed endotracheal tubes are molded into special shapes that permit good surgical access in the oronasai area.
how equipm ent w orks com
R E IN F O R C E D /A R M O U R E D E N D O T R A C H E A L T U B E S
Armoured endotracheal tubes are

Cuffed,
2. Wire-reinforced,
3. Silicone rubber tubes
4. Quite flexible
5. MAINLY: Difficult to compress or kinkiH This can make them useful for situations in which the trachea is anticipated to
remain prolonged duration, OR iftfw n e c k 'is to rema in flexed
Achieve this property by having a spiral o f wire em bedded into the w all of the endotracheal tube to give it strength and flexibility at
the sam e time.
Particularly useful for head and neck surgery where the endotracheal tube may be sharply bent and also compressed by the
surgeons. Improve surgical access.
3
Wayne Robinson. MBBS Class of2Gf5
how equipm ent works .com
ENDO TR AC HEAL TUBES

Various types of double-lumen endotracheal (actually, endobronchial) tubes have been developed (Carlens, White, Robertshaw, etc.)
for ventilating each iung independently
• Useful during pulmonary and other thoracic operations (eg. Qesophagectomy to improve access)
s in a ie4um s v e n tila tio n white the o th e r tu rn t& collapsed to m ake surgery easier. The deflated lung is re-
inflated as surgery finishes to check for fistulas (tears).
o One tube is shorter and ends in the trachea and there is cuff at this level called the frache&t cuff
o Other tube extends further an d enters a main bronchus and has its own cuff - bronchial cuff
o Using a special connector and clamp, one can avoid ventilating one lung and let it collapse to provide good surgical
access.
Right Lung left Lang

how equipment works .com
Right sided Left sided

how equipm ent works .com
4
INDICATIONS M a o
3 big headings with some overlap among them,• v.— '
( m VENTILATI
(Often goes hand in hand with protection]
For Depressed levels o f consciousness:!Either INDUCED OR PATHOLOGIC
Induced:
-s^ ^ /ia in ta in s a patent airway in GA
o (Most common indication is administration of volatile anaesthetics to induce or maintain anaesthesia)
o Provides reliable means of ventilation and oxygenation while protecting airway against regurgitation and
pulmonary aspiration
Pathologic:
<2 — Brain Injury (e g. Stroke, head injury, poisoning -> Decreased LOC)
O Severe -> Coma/Stupor.ljgf e
■ *“ Collapse of airway muscles -> Airway Obstruction
-— Loss of protective reflexes (Eg. Swallowing, coughing)
o ETT restores patency and protects from pulmonary aspiration of gastric contents
<s>
[Respiratory failure/hypoxaem ta)
JZo Considered especially in respiratory failure: [when PaO? < 60 mmHg and/or PaCO?> 45 mmHg]
o Due to hypoventilation, aonoea
E.g. in Critically /V^lQlultiple severe trauma e.g. C-spine injury, nb fractures. Severe pneumonia. % R D S
T Airway Obstruction
o Common indication
o u-'-fo reig n body (esp in infants/toddlers) ^ -
— » o ^ - Severe blunt/penetratinq face/neck injury +/- swelling or expanding haematoma +/- larynx, trachea, bronchi
injury ^ ^
o^nhalationaK burns
^ o ^ Sustained qeneralized'êizure,activity
AIRWAY PROTECTION
Tsâbove
f x ) DRUG ADMINISTRATION ,
1. iSOxygen in higher concentrations than found in air
2. Volatile anesthetic agents such as desfluorane. isofluorane, or sevofluorane.
3. ^ Medications such as salbutamol, ipratropium, atropine, epinephrine, and lidocaine.
A n o th e r gases such as helium, nitric oxide, nitrous oxide, xenon
TECHNIQUE
Equipm ent Required
1. Êndotracheal tube
• *** CHOOSING SIZE:
• MALE:
o Internal Diameter 0D% 8.5 - 9 1
o Length: 20 - 23 cm
• FEMALE:
© fDcP . 5 - 8
o LenqtFTi i T - 20 cm
• CHILD:
& fD:({Age/4) + 4;
o LengtlTtAgS® + 12 cm
Ask for a size above a n d sge below as w elt, just in case
2. </£aryngoscopes
5
• Used to sw eep tongue away and push jaw up to s e e vocal cords
• Must have functioning light on the scope
3 . 1 0 - 2 0 ml Syringe: To inflate cuff

• The cuffed tube helps to prevent aspiration
4. ^^Lubricating Gel/Spray
5. t/Suction device (Eg. Yankauer suction tip and suction catheter)
6. (X Magill Forceps
7.inflexible introducer (Malleable stylet +/- gum-elastic bougie)
8 n ia p e or adhesive plaster: Something to tie or anchor the tube in place
9.inQropharyngeal airways: All sizes
10 i/Confirmatory device
• S tethoscope to confirm tube is in right place. When you start to ventilate, listen for air over stomach/epigastrium first,
then apices of both lungs and both bases in axillae. {5 p o in t a u sc u lta tio n )
• Can also use an end tidal resp calorimeter to monitor
11 .M ^rugs
a. ^ Sedative first!!!
m u S T
b.^ P a ra ly z in g agent after!!!
PROCEDURE (Currently from EMED lecture - should edit) R \J I D f o )

fifa LQ U lP fPeM T rS UJOPntN&l'X to * C rfr & ktyoctosof*'- ^ o r
*
Position the patient supine, open the airway with a head-tilt chin-lift maneuver
Open mouth by separating the lips and pulling on upper jaw with the index finger.
Ensure “sniffing position”: **Flexion at lower cervical spine + Extension at atlanto-occipital joint
Hold laryngoscope in left hand, insert scope into mouth with blade directed to right tonsil (see an image of how to hold
laryngoscope!) w ' ~
Once right tonsil is reached, sw eep the blade to the midline keeping the tongue on the left.
This brings the epiglottis into view - DO NOT LOSE SIGHT OF IT!
Advance the blade until it reaches the angle between the base of the tongue and epiglottis (Vallecular space)
Lift the laryngoscope upwards and away from the nose - towards the chest. This should bring the vocal cords into view. It may
be necessary for a colleague to press on the trachea to improve the view of the larynx.
Cricoid pressure
Place the ETT in the right hand. Keep the concavity of the tube facing the right side of the mouth.
Insert the tube, w atcfifffglTenter through the cords
Insert the tube just so the cuff has passed the cords and then inflate the cuff.
3. Confirm placement
//
(^JMUSTKNOVfo CONFIRMING PLACEMENT/5WAYS: 'i --------- V 6 V -* -
j* j^ L _ 1 . GOLD STANDARD: Waveform capnography

2. Direct visualization a s the tube p a sse s through the glottis (Or indirectly with a bronchoscope)
3. 5 point auscultation - Auscultate both lung apices and both axillae (lung bases) - Should hear breath sounds bilaterally.
Final point is over e pigastrium (stomach) - Should hear no sounds.
4. “Misting” o f the tube: Water vapour evident in lumen of tube on each exhalation and NO gastric contents in tube
5. Colorimetric encPtidal CO? detector ^
NASOTRACHEAL INTUBATION
l!
Advantages:
1) Comfortable for prolonged intubation in postoperative period
2) Suitable for oral surgery: tonsillectomy, mandible surgery
3) For blind nasal intubation
6
4) Can take oral feeding
5) Resist for kinking and difficult to accidental extubation
Disadvantages
1) Trauma to nasal mucosa
2) Risk for sinusitis in prolong intubation
3) Risk for bacteremia
4) Smaller diameter than oral route -> difficult for suction
Contraindications
1) Fracture base of skull
2) Coagulopathy
3) Nasal cavity obstruction
4) Retropharyngeal abscess
CONTRAINDICATIONS
(EMED lecture)
£1l ) Patients with intact gag reflex
• Patients likely to react with laryngospasm to an intubation attempt
( jp Basilar skull fracture - avoid NASOtrachea! intubation and nasogastric tube.

J
COMPLICATIONS
urinq laryngoscopy and intubation
T~ Airway trauma
1. i^Tooth damage or dislocation
2. ►'"Lip or»t6ngue laceration
3. d o r e throat
4. d islocated mandible (especially if TMJ is unstable)
Malpositioning
1. ''"'Oesophageal intubation
2. ►'"'Endobronchial intubation
’3. Physiologic reflexes ^Hypertension, tachycardia, intracranial and infraocular hypertension)

4. iDraryngospasm
_5M^Bronchospasm
6. du lm on ary Aspiration
7. Arytenoid dislocation -> Hoarseness
^f)/V hile tube is in situ

1. Pulm onary aspiration
2. Obstruction (from kinking or secretions)
3. t'T.ip or nasaLulcer in cases with proloned period of intubation
(4. ‘'"'Sinusitis or otitis in cases with prolonged nasoendotracheal intubation)
5. ^Disconnection from breathing circuit
6. ^/Unintentional extubation
7. Ignition (only if close to fire source)
^ F o l .lpwing exlubation ^ )d c f-
1. vAirway trauma
2. v"Aspiration
3. Oaryngospasm
4. •'Oedema and stenosis (glottic, sublglottic or tracheal)
5. hoarseness (vocal cord granuloma, paralysis)
6. Laryngeal granuloma
7. t/Sore throat
7
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£ 3 ^ Wayne Robinson. MBBS Class of 201
LARYNGEAL MASK AIRWAY (LMA^
Sources: Medscape, UHWI Lectures
DESCRIPTIO N iCfilOlQIl) — P \r c h < e -B r 6 ifl

H7UST )^ w & S
'he laryngeal mask airway (LMA ) is developed by British Anesthesiologist Dr.
Archie Brain. It has been in use since
Initially designed for use in the operating room as a method of elective ventilation, it is a good alternative to bag-valve-mask
ventilation, freeing the hands of the provider with the benefit of less gastric distention.
LMA has more recently come into use in the emergency setting as an important accessory device for management of the
difficult airway
DESIGN
The LMA is shaped like a large endotracheal tube on the proximal end that connects to an(e i . ;: Ion the distal end.
Designed to sit in the patient’s hypopharynx and cover the supraqiottic structures, thereBylillowing relative isolation of the
trachea.
Success rate of nearly 100% in the operating room -> may be lower in the emergency setting.
Its use results in less gastric distention than with baq-valve-mask ventilation, which REDUCES BUT DOES NOT
ELIMINATE the risk of aspiration. This may be particularly pertinent in patients who have not fasted before being ventilated.
S P EC IA L TY P ES (M ANY M ORE EXIST):
1. l^LMA Classic is the original reusable design. ^

2.1'Tptubati-ng LMA (ILMA) (aka LMA Fastrach) designed to serve as a conduit for intubation. Although most LMA designs
can serve this purpose, the LMA Fastrach has special features that increase the rate of successful intubation. Features:
Insertion handle, a rigid shaft with anatomical curvature, and an epiglottic elevating bar designed to lift the epiglottis as the
ETT passes.
3. L < M A ProSeal: Addition of a channel for the suctioning of gastric contents.
4. LMA Supreme: which is a newer design, is similar to the ProSeal and has a built-in bite block.
5. Newer: LMA CTrach: built-in fiberoptics with a video screen that affords a direct view of the larynx.
IN DICATIO NS
1. Elective ventilation y
• Acafptabtealternative
Ac 5 § 3tatats^!rttemati to mask anesthesia in the operating room.
It is often used for short
.. procedures
- .— ..... when endotracheal intubation is —
not necessary
4V * 2.
^ Diffi
Difficult airway!!
After failed intubation, the LMA can be used as a rescue device as aftemporizincfe measure to a surgical airway
• in the case of the patient who cannot be intubated or ventilated, a surgical airway is indicated and should not be
delayed. However, if the LMA is at hand, it can easily be attempted quickly, while an assistant simultaneously prepares
for cricothyroidotomy
([Prehospital airway Via nagement

• The LMA is useful in the prehospital setting not only for patients in cardiac arrest but also for managing a difficult
airway.
4. Conduit for intubation
5. Cardiac arrest (Approved by AHA)
TECHNIQ UE
Equipment
1. Syringe for cuff inflation (included in LMA kit)

2. Water-soluble lubricant (included in LMA kit)
3. Bag-valve mask
4. Oxygen source
5. Yankauer suction device
6. End-tidal carbon dioxide (ET C 02) detector
7. Intubation equipment and a cricothyroidotomy kit (These items should be close at hand.)
POSITIONING
• Optimal head position
PREPARATION
t--Preoxygenate the patient with 100% oxygen via a nonrebreather mask, as time allows.
• ‘"Choose the appropriate size of laryngeal mask airway (LMA).
• ‘"Check the LMA cuff for leaks.
• -"Deflate the cuff of the LMA completely against a flat surface.
• ••"Apply a water-soluble lubricant generously to the posterior surface of the mask.
• ‘"Administer sedation when indicated.
• '^Position the patient. .
CRICOID PRESSURE
• Cricoid pressure is intended to reduce the risk of aspiration and should be maintained, especially in patients who have not
fasted, until the airway is secured.
• Decreased rates of successful insertion, however, have been seen with application of cricoid pressure
INSERTION
^■4. f Hold the Lfi/IA like a pen} with the index finger of the dominant hand at the junction of the mask and the tube
*£.*L_> 2. ^ lid e the LMA along the' nard palate, pushing it back against the palate as it is advanced toward the hypopharynx, as in the
image below. This prevents the tip from folding over on itself and reduces interference from the tongue.
3. Advance with gentle pressure until resistance is met.
4. If necessary, continue pressure on the tube with the nondominant hand to fully advance the LMA to its proper position.
5. Once in place, inflate the cuff without holding the LMA to allow it to acquire its natural position.
6. Approximately 8 cm of the tube protrudes from the patient’s mouth.
2
CO NTRA IN DICATIO N S
Absolute contraindications (in all settings, including emergent)

i. Cannot open mouth
ii. Complete upper airway obstruction
Relative contraindications (in the elective setting)

i. Increased risk of aspiration
1. Prolonged bag-valve-mask ventilation
— 2. f o r b id obesity
3. '-"'Second or third trimester pregnancy
4. ‘"'Patients who have not fasted before ventilation C-fuU -ZV'&rncacC)
5. Upper gastrointestinal bleed
ii. Suspected or known abnormalities in supragfottic anatomy
iii. Need for high airway pressures (in all but the LMA ProSeal, pressure cannot exceed 20 mm H2O for
effective ventilation.)
R Q e iz U R F \Q t .
C O M P LICA TIO N S
Rare complications due to laryngeal mask airway (LMA) insertion occur in the operating room. The rate of complications was 0.15% in a
large study, but the rate is likely to be higher in the emergency setting. Aspiration of gastric contents
1. Local irritation
2. Upper airway trauma
a. Pressure-induced lesions
b. Nerve palsies
3. Mild sympathetic response
4. Complications associated with improper placement
a. Obstruction
b. Laryngospasm
5. Complications associated with positive pressure ventilation
a. Pulmonary edema
b. Bronchoconstriction
k w o Q
SPE C IAL CO NS ID ER ATIO NS
• Does NOT protect against aspiration
• Approximately 10% of pts develop obstruction despite slits
• Rotation of the tube can occur
MUST KNOW: From an instruments lecture:
ADVANTAGES
1. -Less invasive
2. wtless laryngospasm & bronchospasm
3. Kflo risk of oesophageal or endobronchial intubation
4. wVery useful in difficult intubations
5. Neck mobility not required
6. Less tooth and laryngeal trauma
DISADVANTAGES
1. i^Tncreased risk of gastric aspiration!!!
2 . £""Less secure airway!!!
3.i^Rotation can occur
4.KT_ess safe in prone position
3
OXYGEN ADMINISTRATION SYSTEMS
Sources: Online, Also see Dr. Metalor 0 2therapy notes!
Oxygen Administration Devices. Table from EMED lecture:
Device Liters Per Minute (LPM) 0 2 Percentage (Fi02)
- Mouth to Mouth Outside Air Only 16%

- Pocket Mask
- Face Shield
1. Nasal Cannula 2-6 24-44%
2. Simple oxygen face mask 6-10 35-60%
3. Face Mask with reservoir 10-15 60-90%
4. Bag-Valve-Mask 15 10 0 %
------------------- -----
CLASSIFICATION OF SYSTEMS
1, Variable Performance
a. Nasal Cannula ( - pg. 2)
b. S im p le /V a ria b le p e rfo rm a n c e Face Mask ( - pg. 3)
2, Fixed Performance
a. Venturi Mask ( - pg. 5-6)
b. ETTube
Also look up low flow vs. high flow systems **
Low flow systems:

• Do not meet the patients inspiratory flow demands.
• Normal inspiratory flow rate is 25 to 30 L/min
• Additional flow comes from RA
• *** The percentage of 0 2delivered by a low flow device is variable because RA is entrained.
• Fi0 2will vary depending on the patients RR, pattern and VT
• Patients who have variable ventilatory patterns, RR >25 and VT that vary outside of 300-
770mL, should not use a low flow system
• (High flow 0 2 systems provide all of the inspiratory flow required by the patient at consistent Fi0 2s)
High flow Q? systems: provide all of the inspiratory flow required by the patient at consistent Fi02s
1
NASAL CANNULA
• The standard nasal cannula delivers an inspiratory oxygen fraction (P i0 2) of 24-44% at supply flows ranging from /m in.
• The formula is FiO? - 20% + (4% x oxygen lite r f lo w ) . (i.e. 1 = 24, 2 = 28, 3 = 32, 4 = 36, 5 = 40, 6 = 44)
• *** The RQ2 is influenced by breath rate, tidal volume and pathophysiology. The slower the inspiratory flow the higher the F\02
DESIGN
• Length of plastic tubing, usually 7-14 feet long

• Two small prongs to insert into one of the patient’s nares
• Some have a plastic piece at the neck that slides up under the patient’s chin to tighten the tubing and keep it in place
• Available in a range of sizes
INDICATIONS
• Documentation of need with arterial blood gases or oximetry, or as indicated by respiratory distress or other acute or chronic
indicators.
• *** Used to deliver oxygen when a low flow, low or medium concentration is reguired, and the patient is in a stable state.
CONTRAINDICATIONS
Absolute:
• Patients with nasal obstruction
Relative:
• Patients with facial injuries that would preclude the use of a cannula
• Uncooperative patient who will not leave the nasal cannula in place
COMPLICATIONS
1. Obstruction
2. Irritation of nasal mucosa
3. Epistaxis (due to drying out of nasal mucosa, especially at flow rates above the recommended 6 L/min maximum)
4. Displacement
ADVANTAGES:
1. Simple, reliable and generally well tolerated
DISADVANTAGES:
1. PI02 is influenced by respiratory rate, tidal volume and pathophysiology. The slower the inspiratory flow the higher
the P102 (Fi02 also inversely related to RR)
2. If the flow rate exceeds those as recommended above this may result in nasal discomfort and irritation of the mucous
membranes due to drying out. Therefore, humidification of nasal prong oxygen therapy is recommended
o Can minimize drying out by warmed and humidified nasal oxygen achieved by special devices (Humidifiers)
o When the oxygen is warmed to body temperature and saturated to full humidity, it is comfortable.
2
Wayne Robinson. MBBS Gass of 2015
SIMPLEA/ARIABLE PERFORMANCE FACE MASK
• The volume of the facemask is 100-300 mL.
• It delivers an F102of 35-60% at 7.-10 L m jn" ' .
• *** About 75% of the inspired volume is room air that the patient breathes through the holes in the side of the mask.
Thus an accurate Fi02 is difficult to estimate.
• *** The Fl0 2 is influenced by respiratory rate, tidal volume and pathology.
*** NOTE WELL: The m inim um flo w rate throug h any face mask s hould be 5 LPM to avoid C 0 2 accum ulation,
CO? re-breathing and d row siness ***
DESIGN
1. Plastic mask with rim contoured and conformed to facial features (e.g. mouth and nose)
2. The body
a. Black ones are pliable and adapt to facial structures vs.
b. Transparent ones that allow observation of exhaled humidified pas and immediate recognition of vomitus
3. Has holes on each side that are used for exhalation and for air entrainment if the flow rate is too low
4. Adjustable elastic strap that fits over the patient’s head holds the mask in place.
5. The 22 mm orifice attaches to a breathing circuit through a right angle (90 degree) connector.
6. The retaining hooks attach to a head strap so that it does not have to be continually held in place by anesthesiologist.
INDICATIONS
1. Usually used for patients who reguire a moderate flow rate for a short period of time
CONTRAINDICATIONS
COMPLICATIONS
COMPARED TO NASAL CANNULAE AND FIXED PERFORMANCE MASKS

ADVANTAGES:
1. Indicated in patients with nasal irritation or epistaxis.

2. It is also useful for patients who are strictly mouth breathers.
DISADVANTAGES:
1. Obtrusive, uncomfortable
2. Obstructs coughing
3. Impedes eating
4. Muffles communication
5. Variable FI02: Influenced by respiratory rate, tidal volume and pathology. Accurate Fi02 is difficult to estimate
6. Because COz can accumulate in the mask at low flow rates, do not use a flow rate lower than 5-6 L/min with this type of
mask
SPECIAL NOTES:
**Must NEVER be used at flows less than 5 L/min to prevent rebreathing of C02**
3
NONREBREATHING FACE MASK WITH RESERVOIR AND ONE-WAY VALVE
The non-rebreathing facemask is indicated when an R O? >40-60% is required. USE: It may deliver RO? up to 90% at high flow
settings. Oxygen flows into the reservoir at o L-rnjn , washing the patient with a high concentration of oxygen.
Its major drawback is that the mask must be tightly sealed on the face, which is uncomfortable. There is also a risk of C 0 2 retention
DESIGN
• Similar basic structure to simple facemask

• Non-rebreather masks consist of a facemask, w ith flutter valves on the side of the mask to allow exhaled air to escape freely
AND prevent entrainment of room air on inspiration. This ensures high concentration of 0 2 is delivered
• Attached oxygen reservoir bag and a one-way valve, which prevents expired air entering the bag or RA entrainment into
reservoir bag. Contains 100% 02. As the patient breathes, he or she inhales oxygen from the bag. Thus patient inhales
ALMOST 100% oxygen (60-90%)
• The reservoir bag allows a higher Fi02 to be administered.
• The reservoir bag should be sufficiently inflated (about two-thirds full) by covering the one-way valve with your thumb before
placing it on the patient’s face. Flow rate must be sufficient to keep bag 1/3 to 1/2 inflated at all times.
• *** If it does deflate, the patient is likely to breathe in large amounts of exhaled carbon dioxide. Remember the valves
on the mask prevent room air from entering to replace expired air ***
• If it begins to deflate when the patient inhales, increase the flow rate of the oxygen to refill the reservoir bag.
INDICATIONS
COMPLICATIONS
1. C 0 2 retention (see above)
ADVANTAGES
1. Can provide higher concentration of Fi02 (> 60%) than is able to be provided with a standard face mask
DISADVANTAGES
1. Must be tightly sealed on the face, which is uncomfortable

2. There is also a risk of C 0 2 retention
4
VENTURI MASK/AIR-ENTRAINMENT MASK
Dr. Metalor: Appropriate terminology of the venturi mask is the - - FOE system [High Air Flow Oxygen Entrainment System]
• Fixed performance system: Provides an accurate and constant F\Q2

• A Venturi mask mixes oxygen with room air, creating high-flow enriched oxygen of a settable concentration.
• Uses different size “entrainment ports” to deliver a fixed FiO?
• The Fi0 2 delivered depends on the entrainment port size (larger port = lower Fi02)
• Venturi systems deliver 25% - 60%

• Typical F102 delivery settings are 24, 28, 31, 35 and 40% oxygen.
• The Venturi mask is often employed when the clinician has a concern about C02 retention
• Increasing flow w ill NOT after RO^

• **The size o f the e ntrainmen t port determines FtQ?
o **The larger the port*the more room atr entrained, the lower the FiQ?
I.E, THE LESS ROOM AIR ENTRAINED, THE HIGHER THE FI02
DESIGN
1. Consists of a mask with holes on each side that allow exhaled air to escape
2. At the base of the mask are c olor-coded entrainm ent ports that are adjustable to allow regulation of the concentration of
oxygen administered.
INDICATIONS
1. For critically ill patients who require administration of a specific concentration of oxygen.
2. Used for patients who have CQPD when an accurate FiCU is essential and carbon dioxide buildup must be kept to a minimum.
RE: High flow devices in general:

o **A restriction, such as a kink, or water in the tubing, causes back-pressure into the nebulizer. This decreases the
amount of RA entrained and INCREASES the delivered Fi02.
o Încreasing flow on a high flow device will NOT increase Fi02> only total flow
V E N T U R I-B E R N O U L L I E F F E C T /P R IN C IP L E :
Considering the 2nd Law of Thermodynamics: “Energy can neither be created nor destroyed but converted into one form or the other.”
Using an apparatus as shown below:
£rt 5a
2. m + K t
I =2-3
At the point 2, there is a decrease in potential energy (PE) and an increase in kinetic energy (KE), but energy is neither created nor
destroyed in this apparatus.
This apparatus basically describes Bernoulli’s Law which states:

“For an inviscid flow (basically a fluid that is considered to have no viscosity such as air), an increase in the speed of the
fluid occurs simultaneously with a decrease in pressure, i.e. a decrease in the fluid’s potential energy.”
Consider the same apparatus as before with a hole made to allow atmospheric air in. Due to the decrease in potential energy at point 2
as described by Bernoulli’s law, air entrainment occurs as air rushes in due to the pressure difference between the atmosphere and in
the apparatus.
5
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This is known as the venturi effect. A venturi device entrains air from the atmosphere allowing the oxygen saturation (Fi02) provided to
a patient to be manipulated and controlled. The air entrained can be controlled based on the size of the opening or aperture resulting in
a mixture of atmospheric air and the oxygen provided. This results in alteration to the saturation of oxygen. The venturi device is
attached to the oxygen tube providing air to the patient in a closed system. The oxygen flow rate through the device is set which then
allows a fix amount of air to enter the system mixing with the oxygen lowering the concentration of oxygen provided to the patient.
Added benefit of this device is that attached in a closed system, the flow rate provided exceeds the patient’s peak inspiration rate
preventing the patient from rebreathing expired air at any given time. This device is useful in patients with respiratory pathology
where their hypercarbic drive is abated resulting in the patient being dependent mainly on their hypoxic drive. Too much oxygen in
these patients results in respiratory arrest. Lowering the saturation of oxygen provided gives the ability to properly maintain a patient’s
ventilation.
DR. METALOR COMMENTS:

• Bemoulli-Venturi principle:
• When gas is flowing through a tubing its pressure is kept constant, as it flows and you narrow the tubing there is a change
in energy in the tubing from 1 form to another. The gas molecules come closer together and KE increases and PE
decreases. When tube opens again the reverse occurs.
• Venturi system is an air driven system unlike the variable performance mask. OXYGEN is what is entrained into the
venturi mask NOT air as in the variable performance. You determine the oxygen entrained.
• 02 delivered depends on size of the opening and the flow rate of the oxygen.
• NB: Purpose of venture mask is NOT to give MORE oxygen but to give a PRECISE percentage of
oxygen.
• Therefore one indication for use of a venture mask is COPD. They need a precise percentage of oxygen
• Venturi systems deliver 25% - 60%
H A Z A R D S A S S O C IA T E D W IT H U S E O F O X Y G E N
1. A b s o rp tio n atetecta&fs Occurs when you give 100% oxygen to pt. Nitrogen normally keeps alveoli open as body does not
utilize nitrogen. It acts as a splinting gas keeping alveoli open. Denitrogenating the lungs means replacing with oxygen. If there
is a blockage, all the oxygen will be absorbed and end result is atelectasis as no nitrogen remains to keep alveoli patent. A
large segment collapsing will result in large amount of pulmonary blood shunting.
2. COPD p a tie n ts may lose their hypoxic drive
3. Pulmonary Oxygen Toxicity (POT): Can lead to a r ds
aka retinopathy of prematurity
6
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With adrenaline: " irrtralhecally
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SURGICAL DRAINS
Source: Surgical Tutor, other online
Drains are inserted to:
1. Evacuate established collections of pu.s, blood or other fluids (e.g. lymph) which would otherwise remain in the operative
area
2. Drain(foofenf/a/collections
Line of minimal resistance so that potentially harmful fluids can drain away from a particular site (e.g. drain placed into an intra-
abdominal abscess cavity).
Their use is contentious: A /^ a m e ^ T s
Arguments FOR their use include:

^1 . Drainage of fluid removes potential sources of infection
2. May allow the early detection of anastomotic leaks or haemorrhage
.3. Drains guard against further fluid collections
Leave a tract for potential collections to drain following removal
Arguments AGAINST their use include:

1. Presence of a drain increases the risk of infection - Most drains abdominal drains infective within 24 hours
2. Damage may be caused by mechanica[ pressure or suction
3. Drains may induce an anastomotic leak
L
TYPES OF DRAINS
• Drains can be:

- o->* Open or closed
Active or passive
• ** Drains are often made from inert, silastic material (silicone and plastic)
• They induce minimal tissue reaction
• **Red rubber drains induce an intense tissue reaction allowing a tract to form
o In some situations this may be useful (e.g. biliary t-tube)
Open drains
• Include corrugated rubber or plastic sheets
• Drain fluid collects in gauze pad or stoma bag
• ** They Increase the risk of infection
Closed drains
• Consist of tubes draining into a bag or bottle
• They include chest and abdominal drains
• ** The risk of infection is reduced
Active drains
• ** Active drains are maintained under suction/vacuum
• They can be under low or high pressure
Passive drains
• ** Passive drains have no suction
• Function by the differential pressure between body cavities and the exterior
*** ASSESSING SURGICAL DRAINS: p^ — J^Tv/OLO "T H IS iU

Systematic approach to drain care:
1. Label each drain with a number for easy identification, and consistency in documentation. Note the location and type of fluid
that ought to be draining from each.
4- * * •*
2. Monitor drainage for color, consistency, type, and quantity of drainage.
1
• During the initial postop period, drainage tends to be sanguinous, which is dark-red and thick from leftover blood
around the operative site.
• As the wound heals, and in a day or two the color turns serosanguinous, or pink. The consistency is thinner
because there's less blood in the drainage.
• Once blood is gone, the drainage turns thin and serous, or pale yellow, and slows to a trickle
Sudden change in color, consistency, or amount may indicate complications.

Examples:
f l T ) Serous drainage that suddenly turns bloody and profuse may be a sign of hemorrhage from erosion of an
adjacent vessel
Change from thin and pink to thick and brown could mean fecal material is leaking into the wound from a
failed bowl resection. *
fnC ) Increase in volume coupled with a color change to purulent green can indicate infection, which could
lead to sepsis -> May need culture and sensitivity testing
*** Sudden cessation of drainage, or leaking around the drain,

May signify:
;^ T ) Blockage in the system
(fk) Dislodgement
Important to promptly report and document these changes. Excess drainage warrants appropriate volume
replacement
3. Patient education on drain care: (***Look up instructions for home, and when to contact doctor)
REMOVAL M
• Drain tubes are removed when they are no longer required, for example when there is minimal fluid being drained, or when
a cavity being drained has contracted and is small.
• Drains are removed simply by cutting the suture (which anchors them to the skin) and withdrawing the tube from the
patient.
Steps:
1. Don gloves and other personal protective equipment, such as a gown, mask and goggles. Place a disposable drape next to
the site
2. Remove any sutures first
3. Carefully loosen the drain as it may have a buildup of granulation tissue surrounding it.
4. Using gauze pad, firmly grasp the drain close to its exit site. Stabilize the skin around the drain with your other hand.
5. Ask patient to take a deep breath, as it can ease the discomfort by reducing anxiety (is this appropriate??).
6. On inhalation??, steadily and swiftly withdraw the drain and place it on the drape. You should not feel any resistance.
7. If you do, the drain may need to be surgically removed.
8. If successful, cover the site with a dry, sterile dressing and document the outcome. Continue to record the type and amount of
any ongoing drainage, which should be minimal and stop within 24 hours
2
es
Wavne Robinson, MBBS Class o f 2015
SURGICAL DRAINS
OPEN PASSIVE DRAINS (WORK BY CAPILLARY ACTION)
1. Penrose " -(t-ls Ilf
2. Corrugated penrose (has a radio-opaque line to confirm location) * 3
3. Cigarette (penrose with a piece of gauze inside)
4. T-Tube
P )fl# e .£ \ £U C )r u se d ro G T C
P E N R O S E D R A IN
Open, passive drain
Is a floppy cylinder o f latex rubber^ is flat
Evacuates fluid by capillary action
Uses
o -—Breast flap
o —Foot flap
go (Âbdominal abscess cavities
o — Post thyroidectomy
Advantages: Simple, inexpensive, and promotes the development of a well-established tract within 7-10 days
Disadvantages: requires a relatively large skin incision, there is increased risk of infection with use, and is not very
effective in emptying a cavity
C IG A R E T T E D R A IN - P E N R O S E W IT H G A U Z E IN S ID E
C O R R U G A T E D P E N R O S E D R A IN
• Open, passive drain

• Is made of rubber; is corrugatedjn_staap£---------- —
• May be used when draining anj^ntra-abdominal abscess":
Used to drain abscesses (works by capillary action - the fluid moves out along the ridges)
Cut it to the size of the abscess cavity (AFTER incision and drainage of the abscess)
e **-L You put aûffedgau ze dressing” on it and it drains into that from the exterior end (need to frequently change the
dressing) -'Hence OPEN and passive as no suction attached
CLOSED ACTIVE DRAINS

1. Hemovac
2. Jackson-Pratt
3. J-Vac
Indications for closed active drains:
1
O flU S T k ’N O O
M T " Thyroidectomy -
^ 1 . Mastectomy — ~V“ c t t m n r v c ir v .
^""3. Other neck surgery
Lymphatic surgery
Groin surgery qv
&>. abscess
HEMOVAC
Closed, active drain

o Thus has less likelihood of secondary infection (due to closed nature)
Clear, collapsible drum-type reservoir therefore there is the advantage that the fluid collection can be directly observed
Springs inside that must be compressed to establish proper suction. (To establish suction, squeeze the drain on both sides
until the drain appears to be flat)7 "
■M
Gradations on the side so that volume can easily be measured.
Used for drainage of abdominal abscess cavities, breast abscess cavities, pelvic and others.
J -V A C
• Basically the same as the Hemovac
J A C K S O N -P R A T T
Closed, active drain.

o Thus has less likelihood of secondary infection (due to closed nature)
o Attached to a suction bulb (“grenade”)
To establish suction, squeeze the drain in the palm of your hand with your fingers until the inside walls of the drain touch.
then slowly release your grip
* The drain should remain concave or somewhat flat. It should not be fully inflated. If the drain is not flat, the suction is not
working.
2
Author: Davi t C ( 'hung m.d ( hot Drain \
Chest Drain; FAQ
What are the indication* for die*! drain Idlest tube) insertion?
* Chest drain is inserted into tire pleural space for drainage of:
° CD o hr pneumothorax.
(2) o M B J p o d in h e m o th o ra x .
1 o ' Thud in pleural effusion. particularly m'tmlmmffi effusion.

A @ o bPw* in empyema,
I Q r) : UPostoperarively in ihoracoflcmy or cardiac surgery/.. -— £!>orA
2, What qualification and experience should one acquire before attempting to

insert a chest drain m a patient?
* According to the Cartfiofborack Surgery Student Handbook. T c edition. Chinese
University of Hong Kong.. May 2001: Hmisemen (interns) should never attempt
insertion unless supervised by an experienced senior?* "Students should be familiar
with the drain suction systems?"
* According to die British Thoracic Society Guidelines: "All personnel involved with
insertion of chest drains should be adequately trained and supervised.** "This is pan of
tin Senior House Officer (called MO or resident in Hong Kong) core cusricuhnn
training., ?*
* According to the American College of Chest Physicians' Gtiidelines: ‘"Dedicated
operators performing this procedure Should have ample experience, excellent
knowledge of pleural and thoracic anatomy, mature judgment in interpreting
radiographic images related to pleura! disease, and sufficient surgical skill?' "Trainees
should perform at least JO procedures in a supervised setting to establish basic
competence. To maintain competency, dedicated operators should perform at least five
procedures per year ?*
* In inexperienced hands this procedure can cause serious, even fatal, complications
As a student. houseman, or intern, you should not allow yourself to be coerced into
doing it unsupervised But knowledge of tire perioperative management of chest drain
insertion can make you a more competent assistant.
3. What fo do if you are the only doctor at the scene of a patient who has
collapsed with a tension pneumothorax and yet you are not qualified to
insert a chest drain tinstipervised?
* In such a dire emergency the safest approach is to inset a J4G JY cannula into the
pleural space of the affected side via the 2s6 intercostal space at the mid-clavicular line.
A hissing sound can be heard once the pleural space is entered. Advance the plastic
cannula further into rise space at that point and remove the mner metal cannula. Ask for
experienced help to insert a formal drain after rise emergency is o-ver
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4, What to watch out for in the assessment of a patient requiring a formal

chest drain?
* Obtain a medical history and perform a physical examination to mle out bleeding
diathesis on clinical grounds A coagulation screen is not necessary' unless it is
clinically indicated. Risk ofbeinonhage is not a contraindication to chest drain insertion
bn? increased vigilance should be practised in such a patient,
* Be vigilant in differentiating a giant lung bulla from pneumothorax (both will appear as
an aU'filkd space) and lung collapse from pleural effusion (both will appear as a
unilateral "whiteoni").
* Lung adhesion to the chest wall throughout the entire hemithorax is an absolute
contraindication to chest drain insertion
* Be alert to the dilated heart adjacent to the chest wall.
* Chest drain insertion into a posf-pneiimonectomy space requires expert opinion from a
chest physician or chest surgeon.
5, Is consent required for chest drain insertion?

* Full explanation of the procedure to the patient together with reason for doing it and
risk of complications is always warranted Such encounter should be documented in the
patient's records, Whether a written consent signed by' the patient is required or not
varies among institutions You should check into local practice.
* If chest dram msertion is life-saving and yet the patient is nof in a position to give
informed consent, the procedure may be carried out with the sanction of a second
opinion.
6. Is it acceptable to insert chest drain in the wards?

* Chest drain insertion need not be restricted to the operating room suite: it can tie
performed safely in A&E as well as the general wards so long experienced staff is
available to give assistance and strict aseptic technique is followed.
7. Should prophylactic antibiotics be given for chest dram insertion?

* Infection is not a common complication of chest drain insertion. There is no indication
that prophylactic antibiotic is required in clsest tube drainage of spontaneous
pneumothorax or pleural effusion.
* There is weak evidence that prophylactic antibiotics can reduce the risk of empyema
following chest drain insertion for chest trauma A cephalosporin or clindamycin may
be considered in these cases
8, Is H necessary to sedate the patient?

• Chest drain insertion is painful: administration of a benzodiazepine sedative (e,g..
midazolam) together with a narcotic analgesic (e.g.. morphine) to the patient is
advisable. Be aware that many patients who require chest tube inseition have chronic
lung disease that makes than more sensitive to the respiratory depressant effect of both
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Yutlioi. David (' l luma md iF.cn Chest Q Page 3 I a
benzodiazepines mid narcotic analgesics. Giving these drags in small increments by the
IV mute and titrate the dose to effect is more effective and safer than giving a relatively
large dose of these drugs by the IM route. If necessary fhunazenil can be given to
counteract the side-effect of midazolam and naloxone to counteract that of motphine.
9, Is it necessary' to give the patient a vagolytic drug as premeditation?

* There are case reports of vasovagal reactions resulting m death during chest drain
insertion Some practitioners advocate atropine prophylactically as a preniedication
What is a safe drain insertion site?

The British Thoracic Society
Guidelines recommends that a chain
inserted through a closed dies-! he sited
through the safe fnaugk defined by the
anterior border of theîalissiintis dcash
die lateral border of fheC3pgcforalis
major and a horizontal line through the
anatomical position of tfae^psilateral
nipple.
» The most common insertion site is die
mid-axillary line within this triangle A
more anterior site increases the risk of
going through breast tissue in a female
patient and increases the discomfort
associated with arm movement. A more
posterior site increases patient
discomfort and risks kinking the drain
tube associated with the supine position.
A common mistake is choosing a drain
site that is too low. A low drain
insertion site risks damaging the
diaphragm, entering the abdomen, and
injuring the hver or spleen
Low thoracic drains may be placed
under image guidance by radiologists. Do not use these sites if drain insertion is
performed blindly.
i 1, How should the patient be m onitored during the procedure?

* Patient should be monitored according to his physical condition and concurrent illness.
As a minimum the patient should be monitored by mike oximetry and nomnvasrve
blood pressure tXfBP) monitor. ’
Oxygen supplement by nasal cannula or facemask should be given to file patient, A
—v patent IV should be in situ.
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A uthor D avid C ( hiuis md v r c pc lic-T D ram FA
f iT ) Is local anesthesia necessary?

* The drain sire should be infiltrated with local anesthetic through the entire thickness of
the chest wall. Attempt to aspirate for air or fluid (whatever the case may be that
culflrinafes in the decision to insert a chest drain) from the pleura! space with ibe same
needle is recommended practice. The decision to insert a chest drain should be reviewed
if free ah or fluid casino? be aspirated through the needle.
$ 3 ^ ) What size drain tube should be used?

* Conventionally 28 to 32 F tubes are used This still applies if the fluid to be drained is
blood or pus. Smaller dram tithes cause less discomfort to the patient. Nowadays most
physicians advocate 10 to 14 F tubes if the content to be drained is air.
How is a drain lube inserted0

* Review' the section on who is qualified to perform chest drain insertion.
* Introducing a drain into the dosed chest mine a trocar can bayonet organs within the
chest or abdomen Such practice is dangerous and is disgsatraged ^
* The safest method of introducing a chest drain is bvQdunt dfesedm )A step by step
approach is described on pages 195 to 201 in Roberts; Clerical Procedure hi Emergency
Medicine, 4a' edition;. 2004,. Elsevier; This book is available electronically at
<mdconsuIfcoiB> via the Li Ping Library.
( \ 5 ) How should the drainage system of a chest tube be managed?

After insertion, the chest tube should be
connected to an underwater sea! drainage
system Three types of underwater seal
drainage systems are available; the Mxntle,
the2«boftIe, and- the 3-frottle system
o in the 1-bottle system the chest drain is
connected by collecting tubing to a tube
approximately!;? cinjunder water (the seal)
in the underwater-seal bottle while another
vent tube is open to atmosphere, hi this
system pleural pressure greater than 3 cm
water will force air or fluid from the
pleura! space into the bottle while negative
pressure is the pleural space will suck fluid
up the tube As long as die imderwater-seal
bottle is well below the patient (e g., on the
floor beside the paueni;/the hydrostatic
pressure of the fluid column is the tube
will counterbalance the negative pleural Underwater
pressure and prevent water from being seal bottle
sucked into the pleural space. If should be
remembered that hydrostatic pressure is proportional to the height of the fluid
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column As the level of the underwater-seal bottle ts raised, it will become easier for
fluid to be sucked info the pleural space Therefore it is mandatory that the bottle be
kept well below the patient at all times. A disadvantage of tins single bottle system
is that, as liquid. contents thfootl vas* eflraion fluid) is expelled from file pleural
space and collects in flier underwater-seal bonk, the seal tube becomes immersed
deeper under wafer and the pressure required to force more contents into the bottle
increases. A 2"bonk system can alleviate this problem
From To atmosphere
The working principle of the 2- or suction
patient
bottle system is the same as the
1-bottle system except a 'trap
pottle s interposed between Hie
chain tube and the underwater-
seal bottle.
In both the I-bottle and the 2-
bottle system the vent tube may
be competed to a high-
vohmielow-pressttte suction
system (e.eu the Veraon-
Thompson pomp) set al a level
of -I© to -2© cm TbO. A low-
volume pump fe,g., die Roberts
pump) is inappropriate
Trap Underwater
bottle seal bottle
o In a 3-botfle system a third bonk., called fee^nanomeier bottle1" is added after the
underwater-seal bottle. This manometer bottle has a vent rube under water to
regulate the negative pressure generated by suction.. The maximum negative
pressure (hi an H :0) generated by suction equals to the distance (in cm) this vent
tube is below the wafer line.
Adjustable
From
vent tube
patient To suction
Distance below
water is equal to
L
negative pressure
generated when
suction is applied
Trap Underwater Manometer

bottle seal bottle bottle
http: medicine-oij-line com Chill* l - K0112
■
To suction From patient
Atmosphere
A*
* Many single-use eontposife 5-
bottle drainage systems made of
plastic are available
commercially The Pkiiravac and
flic- Aqua-Seal Dual Drainage
systems are just 2 examples A
diagram of the Ptenravac appears
on the right You should consult
the users' manual of these
systems before use.
Manometer Underwater Trap

chamber seal chamber chamber
• Tile Heimlich Flutter Valve is a one-way valve that can be used in place of the
underwater seal bottle to chain ah from a pneimiojfrorax Its use allows the patient to
ambulate and be managed even at home as ail outpatient Care should be exercised fo
identify tire end to be connected to the chest drain. The other end can be connected to a
drainage bag fo collect pleural fluid (usually only a small amount) tiiaf comes with
pneumothorax. When in operation the Valve honks and makes duck-like quacks with
respiration. This is normal.
To drsairspgo bag From potter#
16/ How should a patient be managed after insertion of a dies! drain?

All connections should be sectored with adhesive tapes to prevent inadvertent
disconnection.
A eliest %-rav should be obtained alter insertion of a chest dram to ascertain its position.
Ideally the tip of the drain should point toward the apex of the pleural space when
•draining air from a pneumothorax and toward the bas ^ fre n chaining liquid contents
from the pleural space Previous concern of a dranTTodged in a pulmonary fissure is
unfounded.
Patient should be managed in a ward with nursing staff familiar with management of
chest chains.
Regular assessment of the amount of bubbling (when if is gas) and drainage (when it is
liquid) should be made ____________
There have been repeats ofêxpansioii milmonaiy edemajalter rapid drainage of large
pleural wfojgfr e « n b g fetgl P a r t y s ig n s fit T e -e x p a n s io n pulmonary edema
http, 'medicine-on-line com kong

Author David C Chuns 1 Iic-.t Dram !■AO t'-ra'-'
include onset oflcmailT^ndKtiWtn i^ of breafhj i? is suggested that no more titan I liter

of effusion fluid should be drained at any oiie rime or continuous drainage should he
limited to about half a liter per hour
J 7.. Is it acceptable to clamp a chest drain?

• In general a bubbling chest drain should not be clamped, hi rare occasions this may be
necessary as when the drainage bottles have to be changed. In this instance the damps
should be released as soon as possible,
* If the- dies? tube is inserted to drain liquid contents and is not bubbling, it is no!
unreasonable to clamp the drain during procedures related to care of die patient Again,
the damps should be released as soon as possible.
* After successful drainage of a pneumothorax confirmed by chest x-ray, some physicians
will damp a non-bubbling chain for several hours before obtaining another chest x-ray
to check for small leaks. In this instance the patient should be confined tor observance
in the ward. Development of shortness of breath or subcutaneous emphysema: demands
immediate uudamping of the drain. (Opinion is equally divided among experts on
whether or not ebesf chain should be clamped to check for small leaks after successful
drainage of pneumothorax.)
18. What to do if the drain mbe is suspected to be blocked and fails to perform
its function?
» Dies? dram inserted to chain fluid contents (effusion, blood, pus) has a tendency to
become blocked by dots. The cardinal sign of a blocked drain is failure of water within
the tube in the underwater-seal bonk to fluctuate with the respiratory' cycle or with
coughing.
• This block may simply be due to kinking of rise drain tube at the site of insertion or the
collecting tubings. Un-kink if if that is the case.
♦ If the drain tube or collecting tubing is blocked by semi-solid contents (e g„ blood dot)
within the lumen, if can be unblocked by 'milking ' or “stripping".
o “Milking" is an attempt to undo a block within the pleural space It is done by
clamping the distal collecting tubing and pumping the proximal segment with one's
fingers like milking a cow to create positiv e pressure to dislodge the block.
o "Stripping" is an attempt to undo a Hock m the collecting tubing. If is done by
clamping The collecting tubing well proximal to The suspected block and pumping
the distal segment wrilr erne's fingers to create positive pressure to dislodge the
block.
19. What to do when the underwater-seal bottle under suction suddenly

bubbles furiously ?
♦ There are 2 possible causes for this massive "leakage" of air;(|T)) disconnection of
collecting tubings or dislodgement of the dram mbe and(0)) increased amount of air
entering the patient's pleural space from within the thorax. You should turn your
attention first to the patient and check if his vital signs are stable and act accordingly.
hup. u icd ic m e -o n -ln ie com iic * Innese I mversirv ■t i loim Kona

V.uli )avidC ( ( licst Drat
* If the patient is not in respiratory distress and his vital signs are stable, you haw tmte in
your hand to troubleshoot the problem. If the patient shows signs of respiratory distress,
subcutaneous emphysema, and his vital signs are unstable, you have an emergency in
your hand and you should:
o Call for experienced help.
o Offer the client 100% oxygen and be prepared to give respiratory support (positive
pressure ventilation) if necessary.
O' Support the circulation as required,
o Monitor his oxygenation by pulse oximetry and his blood pressure by NIBP
o' Examine the patient's chest for telltale signs of a worsening pneumothorax or
tension pneumorhorax.
o Check the drainage system to see if there has been a disconnection or if the drain
tube lias been partially dislodged with dram hole! s) exposed.
o Send for the radiographer to (to a chest x-ray a? the bedside.
* If the cause is due to disconnection in die collecting tubings, air is sucked through tire
underwriter-seal bottle from the atmosphere leading to tire furious bubbling; air is also
sucked into the pleural space dtaing the negative phase o f the respiratory" cycle,
enlarging the pneuntKrtborax You should:
o Ensure the patient is stable and continue to monitor him appropriately,
o Re-connect the1disconnected tubings and tape them together securely,
o Ask the patient to cough to expel any air that may have entered the pleural space
cfetriug disconnection.
o Perform a chest x-ray with the patient in the sitting position to check tine size of the
residual pneumothorax.
o Continue to monitor the patient and the bubbling of air in the underwater-seal bottle
'until you are confident the crisis is corrected
* If the drain tube is partially dislodged with drain hole! s) exposed the situation is similar
to the disconnection of collecting tubings. In this instance the drain tube should be re-
introduced with aseptic precautions:
o Ensure the patient is stable and continue to monitor him appropriately'.
o Send for an experienced assistant and prep the drain site, including a generous
portios of the exposed drain tube, with Betadine and square drape the area,
c Stop the suction, ait the stay suture, and re-introduce -the sham tube until the
exposed holds) is well inside the pleural space. *NB: You must stop the suction
before re-inffoducing the chain tube. If you do not. the negative pressure from
station will stick the surrounding tissue into the drain hole as soon as it disappears
beneath the skin, preventing it from being sued properly in the pleural space.)
o Have your assistant holding the chain tube in place and re-insert a new stay suture
under local anesthesia.
o Secure the re-inserted drain tube m place with the stay suture and tapes,
o Ask the patient to cough to expel any air that may have entered the pleural space
when the chain hole was exposed.
o Order a bedside chest x-ray to confirm the position of the drain tube and the size of
the residual pneumothorax.
o Consider ordering prophylactic amibjotic (Although antisepsis is practised by
sponging the exposed drain mbe with Betaduie. this is not the equivalent of
inserting a sterile tube.)
n
Author David t Chung md f r <?' 4 Draw AO Pass
Continue to monitor the patient and the kibbling in the underwater >eni bottle uniil
you are confident the crisis, is corrected,
* If the problem is due to increased air leak within tlte patient's thorax, definitive
treatment depends on the nature of lire problem Surgical closure of the leak may be
necessary
^5o~)Wliat to do if a sudden asisli ofblood appears in ?5ie drain bottle?

♦ Hie all important factor here is the patient's vital signs. If he is tacjiypneic, tachycardia
and hypotensive, these are signs the bleeding as fresh arid large an amount and demands
immediate action
P G>: •''Call for experienced help it7.
^ C£9o ‘'"Offer the patient 100% oxygen..
(5A ‘-^Support the osculation: replace voltime with crystalloid. colloid. m hjzml-
administration of vasopressor may be indicated.
Order a bedside chest x-ray if tune permits.
E mergency thoracotomy to locate and stop the bleeding na y be indicated
If the patient s vital signs are stable, there is time to look into the matter Hie bleeding
may still be new Inn just not large enough to cause any change in vital signs. In fins
instance it is reasonable to treat the incidence expectantly:
^ O fki rite patient IOC% oxygen and immim ins vital signs frequently
3 ^ heck the drain bottle for new bleeding as frequently as you would check vital signs.
>"1feplace volume loss as necessary.
u-Order a chest x-ray to check if there is accumulation ofblood within the hemitliorax.
o prepared to act accordingly if fresh bleeding is continuous and is affecting the
patient s vital signs.
* In some instances a gush of blood appears after' a period of low drainage from a
partially blocked tube. The gush appears when the mbe becomes unblocked by itself. If
this is suspected, check the patency of the chain rube and unblock flic tube as described
in tire answer to Question 18.
(^5p What are the criteria for chest drain removal?

' * Hie criteria for chest drain removal vary according to the reason why the chest drain
was inserted in the fust place:
* f°o air leak in the last 24 hours in pneumothorax.
rfto fresh bleeding in the last 24 hours in hemothorax
‘"Fluid loss is < 200 mPday in effusion.
^'Clinical and rash©logicaTevidence of resolution of the infection in
22. How to rem ove chest drain safely?

* Always have an assistant skillful in tying surgical knots present
« Prepare and drape the insertion site and follow aseptic technique. •
* Put a purse string suture arotind the drain mbe if it has not been done during insertion.
litfp: median n_I i com ic C hmese t iiiverurv of Hone Kong

Author: David C Chung md f r c pc Chest Drain FAQ: Page 10 10
* Infiltrate the area with local anesthetic only if yon have to put in the suture Otherwise
—> drain removal itself docs not require local anesthesia.
* Unwound and cut rite stiftire holding the drain to flic skm.
->» Have your gloved assisian? form a knot with the purse suing suture without pulling it
tight.
Ask the parent to take a deep breath and perform a mild Valsalva maneuver .
—> * Pull the drain tube our m one quick motion while tire patient is still holding his breath.
Your asp&pil should pull the muse siring knot tight as soon as the lube is out.
-> 9 Cover the site with an occlusive dressing.
Continue to observe the patient and order a chest x-ray ic@ to ffiienrs
* Any deterioration in the patient's condition in the meantime demands immediate
assessment and possible reinsertion of the chest drain.
btrp: mediciite-cm-line com The Chinese I riiversity of Hong Kong

Wayae Robinson. MBBS Class of 2015
URETHRAL CATHETERIZATION
Sources: Medscape, Wikipedia, Prof. Crandon lecture, Dr. Aiken Review
DEFINITION
Placement of a latex, polyurethane, or silicone rubber tube (urinary catheter) into a patient's bladder via the urethra. Most commonly
silicone or natural rubber.
May be used for diagnostic purposes or therapeutically
Catheterization may be long-term (indwelling catheter Eg. Foley catheter), or an intermittent catheter removed after each
catheterization.
BRIEF HISTORY: The name comes from the designer, Frederic Foley, a surgeon working in Boston, Massachusetts in the 1930s. His
original design was adopted by C. R. Bard, Inc. of Murray Hill, New Jersey, who manufactured the first prototypes and named them in
honor of the surgeon.'
DESCRIPTION
• Closed, passive drain

• "^Flexible tube, most commonly silicone or natural rubber.
• The catheter itself may have 1,2 or 3 separate lumens within it
TYPES
Non-self-retaininq
1. Single lumen (Jake’s “in and out” Catheter): Consists of a latex tube with an atraumatic tip and single port for collection of urine.
These catheters have no balloon
Indications: Used for “in and out” catheterization
• Diagnostic:
£t?)To obtain a catheter specimen of urine (e.a. in a patient who is menstruating or
in females in whom you keep getting commensals contaminating)
(2 ) Any and many types of x-rays that require contrast. We don't use self-retaining
catch to instill contrast!!! That's a waste of a catheter!!
( ) To measure post-void residual urine volume before the days of ultrasound (or
where U/S unavailable)
• Therapeutic:
To instill dings, *3 ^
■ Types incl intravesical chemo for superficial bladder cancer
• Anticholinergics for an overactive bladder refractory to less invasive
forms of therapy
2. In refractory haematuria can instill "patash"?? E.g. For cases radiation cystitis with refractory haematuria
1
(*3) To empty bladder stat. Eg. To decompress the urinary bladder during laparoscopic surgery prior to insertion of the
n m h jjical port (reducing likelihood of complications), or
For self catheterization in persons with sginaMnjury and neurogenic bladder with urinary retention
Never do an in and out catheterization in a patient with acute urinary retention and send home. They will come back in a few
hours again in acute urinary retention again, as you have not addressed the underlying problem
• Unique complications: Made of red rubber which can cause severe tissue reaction if left in place for long periods of time
Self-retaining (Indwelling)
1. Double lumen
* 1 for syringe (to inflate bulb to retain in bladder) - This lumen has a valve on the outside end
• 1 for urine drainage - this lumen has no valve (open at both ends) ^
2. Triple lumen
• 1 for syringe (to inflate)
1 for urine_drainage .
1 foiGmgatiorvfe.q. post-prostatectomy or bladder surgery to remove blood/clots)întroduction of medication, and
introduction of sterile crystalloids
Other features:
* Bladder opening/Fenestration
• Bulb/Balloon {1 0 -1 5 ml)
The relative size of a Foley catheter is described using French units (F) - this is a measure of EXTERNAL DIAMETER (NOT
circumference, or internal drainage channel). The most common sizes are 10 F to 28 F. French units are calculated as 3 x external
diameter (in mm). Therefore, divide the French unit by 3 to obtain the external diameter in mm. I F is equivalent to 0.33 mm = .013" =
1/77" of diameter. * —
• Adults - Foley (straight tip) catheter (16-18F)

• Adult males with obstruction at the prostate - “Coude tip” (18 F)
• Children - Foley; to determine size, divide child's age by 2 and then add 8
Diagnostic
1. t/'Monitoring urine output

• Urine output is a reflection of intravascular volume and renal perfusion.
• Adult urine output 0.5 -1.0 cc/ kg/ hr.
• Children urine output s: 1.0 cc/ kg/ hr.
Facilitates:
2. v^lnstill contrast for radiologic investigations: MCUG: Uxetarogram, Cystogram
3. '/'Measurement of post-void residual volume (u s u a llfu m norm al healthy adult - but mis acceptable).
4. ^"Obtaining catheter-specimen urine for microscopy, culture & sensitivity
Therapeutic
1. v/Relieve acute/chronic urinary retention - Know a list of causes (eg, BPFI, neurogenic bladder, spinal cord injury)
2. N/fnstillation of drugs esp. Bladder Cancer i.e. Immunotherapy via intravesical BCG or chemotherapy
3. v^Bladder irrigation
4. To protect anastomoses in extensive post-pelvic surgery
5. Divert the urine stream in patients who have had an incision & drainage of an abscess of the perineum.
6. Prevent strictures?
Extra-Urinary
1. '^Tnstill barium contrast in barium enema

2. ^ "Cervical dilatation in mechanical induction of labour
3. Y'Severe epistaxis, in order to block blood from freely flowing down the nasal passage into the mouth
4. K fla s been used as chest tube in paediatric population
2
5.{^Substitute for a nephrostomy tube, cholecystostomy tube
BE ; Tr ip le lum en s e lf-re ta in in g F oley catheter

Used when you anticipate that there will be haematuria (when you are concerned patient may develop clot retention)
OR in a patient who already has this
Examples;
PostTURP, Post TURBT
Or post any procedure on the bladder where you expect continued bleeding
CONTRAINDICATIONS
Signs/suspicion of possible urethral injury:
Severe pelvic fracture

Blood at urethral meatus rn u s r \m o u O
Scrotal/perineal injury/ecchymosis.
High riding/boggy prostate on rectal examination
4
When any of these findings are present in the setting of possible trauma, a retrograde cystourethrogram should be performed to rule
out a urethral tear prior to placing a catheter into the bladder
(Urethral tears can be investigated by placing the Foley catheter partly in the urethra and instilling 50cc of Urograffin dye as a pelvic x-
ray is shot. A retrograde cystourethrogram is created. If there is rupture, then dye will be seen leaking into the surrounding tissues.)
COMPLICATIONS
Patient complications:
1. t/Bleeding/Haematuria
2. ‘Înfections (Entire spectrum, including urethritis, cystitis, pyelonephritis, and transient bacteremia and sepsis)
• Catheter-associated urinary tract infection is the most common type of hospital-acquired infection
•
To combat this, the industry is moving to antiseptic coated catheters. This has been helpful, but it has not completely
solved this major problem.
3. ^ Paraphimosis*, caused by failure to reduce the foreskin after catheterization
4. v/'~Jrethral strictures
5. •''Ûrethral perforation
Of the catheter itself:
1. v /Catheter obstruction
2. Âccidental removal
3. ^D ifficult removal (Eg. Nondeflating urinary catheter most commonly due to crystallization of normal saline if these is used to
inflate balloon or valve failure) DO NOT USE N/S
4. ^ Breakage of balloon
5. ^ Urine leakage
TECHNIQUE
Equipment:
The contents of the catheterization tray are as follows:

• Urethral catheter
• Povidone-iodine
• Sterile gauze/cotton balls
• Water-soluble lubricant
• Sterile drapes
• Sterile gloves
• Prefilled 10-mL sterile water syringe
• Collection bag
Procedure:
1. Gain consent (Explain the procedure, benefits, risks, complications, and alternatives to the patient)
2. Position the patient supine, in bed, and uncover the genitalia.

3
3. Open the catheter tray and place it on the gurney in between the patient’s legs; use the sterile package as an extended sterile field
4. Don the sterile gloves and use the nondominant hand to hold the penis and retract the foreskin (if present). This hand is the nonsterile hand
and holds the penis throughout the procedure
5. Use the sterile hand to prep the urethra and glans in circular motions with at least 3 different pieces of gauze
6. Using a syringe with no needle, instill 5-10 ml. of lidocaine gel 2% or KY Jelly into the urethra.
a. *SlZE: Choose the smallest catheter that will allow adequate urinary drainage. Size 12-14F is usually adequate for males and
females. Use size 16-20F if the patient has urine with debris, mucous, blood clots or haematuria, which may occlude smaller
lumens. A 22F triple lumen is the standard size for bladder irrigation and ‘washout’. Smaller sizes (6-1 OF) are available for children.
7. Hold the catheter with the sterile hand or leave it in the sterile field to remove the cover.
8. Apply a generous amount of the lubricant
9. While holding the penis at approximately 90° to the gurney and stretching it upward to straighten out the penile urethra, slowly and gently
introduce the catheter into the urethra.
10. Advance the catheter until the proximal Y-shaped ports are at the meatus.
11. Wait for urine to drain from the larger port to ensure that the distal end of the catheter is in the bladder
12. If no spontaneous return of urine occurs, try attaching a 50-mL syringe to aspirate urine. If urine return is still not visible, withdraw the catheter
and reattempt the procedure (preferably after using ultrasonography to verify the presence of urine in the bladder)
13. AFTER visualization Of urine return (and while the proximal ports are at the level of the meatus), inflate the distal balloon by injecting
10-15 ml_ of sterile water through the cuff inflation port.
a. Inflation of the balloon inside the urethra results in severe pain, gross hematuria, and, possibly, urethral tears
14. Gently withdraw the catheter from the urethra until resistance is met.
15. Secure the catheter to the patient's thigh with a wide tape.
16. If the patient is uncircumcised, make sure to reduce the foreskin, as failure to do so can cause paraphimosis
Urethral Catheter Removal

• Use a syringe to empty the balloon, and then apply gentle traction. Pain, severe discomfort, resistance to withdrawal of the catheter, or failure
to aspirate normal saline through the inflation valve should alert the practitioner to the possibility of a nondeflatinq urethral catheter.
• The most common cause of a nondeflating urethral catheter is obstruction of the inflation channel, caused by a failed inflation valve or
crystallization of the inflation fluid.
• The first step in managing the nondeflating Foley balloon is to advance the catheter to ensure that it is actually in the bladder.
• If this does not work, cut the balloon port proximal to the inflation valve. This removes the valve and should allow the water to spontaneously
drain.
• If this does not work, run a lubricated fine-gauge guidewire through the inflation channel. The guidewire or stylet should allow fluid to drain
along the wire itself.
• If this does not work, a 22-gauge central venous catheter can be passed over the guidewire. When the catheter tip is in the balloon, the wire
can be removed, and the balloon should drain.
• If the above techniques are unsuccessful, 10 mL of mineral oil may be injected through the inflation port and will dissolve the balloon within 15
minutes. If this does not occur, an additional 10 mL can be instilled.
• If none of the above techniques are successful, a urologist should be consulted to rupture the Foley balloon with a sharp instrument.
OTHER USEFUL POINTS:
• In female adults the normal position of the urethra is 2.5cm inferior to the glans clitoris. It may be difficult to find in infants or
postmenopausal elderly females. Occasionally the urethral opening recedes superiorly into the vagina and can be found by
palpation.
• Female urethra is 4cm long. The male urethra is 20 cm long - always advance the catheter to the hilt prior to balloon inflation.
• Do not over- or underfill the catheter balloon, as this will lead to balloon distortion, causing the catheter tip to deviate within the
bladder, and can potentially result in bladder wall necrosis.
• Urine must flow from an inserted catheter before the balloon can be inflated. Urine may not flow initially because of obstruction
by lubricating gel. You may be able to expedite flow by gently suctioning the catheter with a syringe, or applying suprapubic
pressure to the patient.
• If the patient is immunosuppressed, or has prosthetic heart valves, catheter insertion may cause a serious bacteraemia and
bacterial seeding. Senior advice should be sought with regard to prophylactic antibiotics prior to catheter insertion
4
From document by Ramarno Forrester:
r f l Uit k fv o ijD !U
t
patient with a very distended bladder is catheterized and then afterwards they become diaphoretic, tachycardic and
tachypnoeic how would ypujuanage this patient? \
a. They patient is in(urosepsi§^The long stasis caused more bacterial proliferation and subsequent catheterization inevitably
caused some amount of epithelial damage leading to systemic liberation of bacteria and thus sepsis. Threat this with
gentamycin antibiotics and fluid resuscitation because of risk of shock.
2. What do you do if the catheter fails to pass in a BPH patient?

a. If there is failure to pass a catheter then use a larger one ie if you are using an (18
ffrench use 20 next). If that fails do a suprapubic catheterization.
3. Would you dilate this patient with a urethral dilator,

a. Do not attempt a urethral dilation.
4. What if a stricture is present? What is the management?

a. If stricture is present then do an optical internal urethrotomy OIU (cystostope done with
blade to cut the strictures)
b. Definitive management is urethroplasty using buccal mucosa or vaginal epithelium.
h
Triple-lumen catheter
Describe: This is a 24 french triple lumen foley catheter (24 F is the external diameter).
Classify: It is a closed passive drain
Describe: It consists of a latex tube with an atraumatic tip, a distal inflatable bulb and 3 proximal ports: one port is for the collection of
urine, one for irrigation and another for inflating the bulb.
Indications
1. Irrigation of the bladder in cases of haematuria and clots
2. Administer medication such as chemotherapy for bladder cancer
3. Patients requiring long-term catheterization
4. Patients undergoing TURP or an other procedure in which significant hemorrhage is expected (a 30cc balloon is required for
TURP surgery)
Complications
1. Complications of Placement:
a. Inadequate lubrication of catheter ->friction trauma -> hemorrhage, and eventually stricture formation after healing.
b. Use of an introducer during placement can -> false passage
c. If the balloon is inflated while in the urethra, this can -> rupture of the urethra and hemorrhage.
2. Complications of the Catheter insitu:

a. Infection
b. Dislodgement
c. Obstruction -> stasis -> Stone Formation
3. Complications of things put thru the Catheter:

a. TURP Syndrome - Instillation of hypotonic fluids for too long a duration -> hyponatremia -> seizures
A triple Lumen Urinary catheter can be kept insitu for a maximum of 3 months before requiring replacement.
5
NASOGASTRIC TUBE (NG TUBEt
Sources: Medscape, Wikipedia, Prof. Crandon ppt.
DEFINITION
• For gastric intubation via the nasal passage (i.e., nasogastric route)
• Provides access to the stomach for diagnostic and therapeutic purposes
STRUCTURE
1. Closed, active OR passive drain
2. Long, narrow, flexible plastic tube -> Facilitates capillary action
3. Multiple fenestrations -> Minimize problems assc. with clogging
4. Radio-opaque line for proper positioning
5. Horizontal markings for correct positioning:
•
Oesophago-gastric junction
•
Antrum
•
Pylorus
6. Rubber stopper -> Admits syringe for feeding, medication, aspiration
INDICATIONS
Diagnostic
1. Evaluation of upper gastrointestinal (Gl) bleed

• Presence of bleed
• Volume of blood
2. Identification of the oesophagus and stomach on a chest radiograph
3. Administration of radiographic contrast to the Gl tract
4. Evaluate/determine quality of gastric fluid content
5. Facilitate Pentagastrin MAO/BAO test*
Therapeutic
1. Gastric decompression:
a. Bowel obstruction: Relief of symptoms and bowel rest in the setting of small-bowel obstruction,
b. Preop/lntraop: maintain decompressed state after ET intubation,
c. Post op: Paralytic ileus
d. Gastric dilatation: Secondary to burns
2. Administration of medications
3. Nutrition: Enteral Feeding
4. Bowel irrigation
5. Aspiration of gastric content from recent ingestion of toxic material
6. Removal of activated charcoal given to children in acute poisoning
CONTRAINDICATIONS
Absolute
1. Basal skull fracture: as evidenced by
1. CSF otorrhoea or rhinorrhea
2. Battle’s sign** (mastoid ecchymosis)
3. Raccoon eyes** (periorbital ecchymosis).
4. Note: CSF is confirmed by the ring sign. Placing a drop of the bloody drainage on a piece of filter paper, and looking
for the Ring Sign. This is the appearance of a yellow ring around the periphery of the drop of blood.
2. Maxillofacial fractures
• The alternative to the nasogastric tube is the orogastric tube, which is placed orally using the McGill’s forceps.
• Complication includes malplacement into the trachea which may result in pulmonary aspiration and abscess
3. Cribriform Plate fractures
Relative
1
1. Oesophageal stricture
2. Coagulopathies
3. Recent banding or cautery of oesophageal varices
4. Alkaline ingestion
COMPLICATIONS
Early:
1. Epistaxis
Malplacement:
2. Respiratory tree intubation
a. Pulmonary aspiration
b. Lung collapse
3. Duodenal intubation - If the N G ’s output appears to be excessive (> 3L/24 hours), consider the possibility that it may have been placed in the duodenum!
4. In tra cra n ia l placement
5. Oesophageal perforation
Late:
1. Erosion of the nose (where the tube is anchored)
2. Sinusitis
3. Sore throat
***ALSO, complication of excess suctioning: Hypokalemic hypochloremic metabolic aikaiosjs (Reason: Loss in gastric fluid—loss
of HCI causes alkalosis, driving K+ into cells)
If the NG tube's output appears to be excessive (> 3L/24 hours), consider the possibility that it may have been placed in the duodenum!
TECHNIQUE
Equipment
• Nasogastric tube
o A d u lt-16-18F
o Pediatric - In pediatric patients, the correct tube size varies with the patient's age. To find the correct size, add 16 to
the patient's age in years and then divide by 2 (e.g., [8 y + 16]/2 = 12F)
• Viscous lidocaine 2%
• Oral anaesthetic spray (Benzocaine spray or other)
• Syringe, 10 mL
• Toomey syringe, 60 mL
• Water-based lubricant
• Tape
• Emesis basin or plastic bag
• Wall suction, set to low intermittent suction
• Suction tubing and container
Anaesthesia
Various methods of topical anesthesia:
1. Viscous lidocaine (ie, the sniff and swallow method) was found to significantly reduce the pain and gagging sensation
2. Nebulization of lidocaine 1% or 4% through a face mask (=s4 mg/kg; not to exceed 200 mg per dose in adults) is an option.
3. An anesthetic spray that contains benzocaine
Placement
Gain consent (Explain procedure, reason, risks, complications etc.)
1. Examine the patient's nostril for patency (Eg. septal deviation). To determine which nostril is more patent, ask the patient to
occlude each nostril and breathe through the other.
2
2. Measure from the tip of the patient's nose, loop around th e ir ear and then down to rou ghly 5 cm below the
xip h oid p rocess.
3. Mark at this level to ensure that the tube has been inserted far enough into the patient's stomach.
4. Apply anaesthetic
5. Position the patient seated upright with the neck partially flexed
6. Lubricate the distal end of the tube
7. Insert the nasogastric tube along the floor of the nose and advance it parallel to the nasal floor (ie, directly perpendicular to
the patient's head, not angled up into the nose) until it reaches the back of the nasopharynx, where resistance will be met
8. When the tube enters the oropharynx, patient may gag; Patient asked to swallow or is given some water to sip through a
straw, and the tube continues to be inserted as the patient swallows
9. Continue to advance the nasogastric tube until the distance of the previously estimated length is reached
10. Secure tube in place to prevent it from moving.
Stop advancing and completely withdraw the nasogastric tube if, at any time, the patient experiences respiratory distress, is unable to
speak, has significant nasal hemorrhage, or if the tube meets significant resistance.
CONFIRMING PLACEMENT
1. Injection of air into the tube performed with the (Toomey) syringe; if the air is heard in t he stomach with a stethoscope
(“swish”), then the tube is in the correct position.
2. Aspirating gastric content: Next most reliable. Fluid is then tested with pH paper (note not litmus paper) to determine the
acidity of the fluid. If the pH is 5.5 or below then the tube is in the correct position
3. Gold standard: Recommend always obtaining a chest radiograph in order to verify correct placement. Most reliable
Surgical recall:
What MUST you obtain and examine before using an NGT for feeding?
• LOWER chest/upper abdominal x-ray to absolutely verify placement into the stomach and NOT the LUNG—patients have died from pulmonary
tube feeding
3
.1
sou. MBBS Class of 2015
RIGID PROCTQSIGMOIDQSCOPE
SOURCE: MEDSCAPE
PLASTIC RIGID SIGMOIDOSCOPES:
METALLIC RIGID SIGMOIDOSCOPES:
Identify: This is a rigid sigmoidoscope

* *
Describe: It is a metallic (or plastic) hollow instrument with a graduated shaft, and three ports for insufflation air,
light source and for visualization. The latter port has a trap door. 25 cm long
o b -h tT o k r t is ir o u m o ^ c - .u s iW i
£
Indications
Rigid sigmoidoscopy is usually performed in an outpatient or theater setting in conjunction with a digital rectal examination to help
facilitate the diagnosis and the management of rectal and anal pathology
Diagnostic
a. Evaluation of rectum (E g. Symptoms that suggest anorectal pathology, e.g. colorectal neoplasia)
'jfc -k y To assess the tme height (distance from anal verge) of rectal cancers
4* c. During anterior resection of rectum to gauge the lower resection margin
d. Prior to anal procedures in clinic or OT
e. Biopsy of any bowel lesion within reach of the instrument
2. Therapeutic: '/
a. '"Foreign body removal
&3CQS iC
Jtf——^ b. Conservative treatment of sigmoid volvulus U l ■—
c.^Sclerotherapy/rubber band ligation for haemorrhoids
Complications
Low incidence of serious complications when performed by a trained clinician:
1. ^Perforation
2. ^^Significant bleeding (especially associated with biopsy)
3. i^Bacteraemia in 5%
Minor complications (60% of individuals)

• 3ain (33%)
• *^Discomfort from rectal preparation (13%)
• Uncomfortable desire to defecate (8%)
• Discomfort associated with patient positioning (4%
Equipment for Rigid Sigmoidoscopy (SEE IMAGE AT END)

The equipment required to perform rigid sigmoidoscopy includes the following items:
^Scope
^ Stylet (obturator)
Eyepiece / )
Bellows ) t ffjU (r e S O U D tU I tf e P
Light source
Air filter
•'"Water-based lubnpafit
Protective clothing as indicated (eg, gloves, apron, face mask, goggles)
Procedure /H fY jS T H b f l G T lA l
1. Obtain informed consent '
2. Rigid sigmoidoscopy is most often performed without sedation
3. The bowel must be properly prepared by giving an enema and ensuring an empty stomach.
4. Gather instruments. Check that the light source is functioning
a. Connect the light source, bellows/air filter, and scope to the eyepiece. Open the eyepiece window and insert the stylet
through the eyepiece into the scope, ensuring that the tip of the stylet protrudes through the tip of the scope.
5. Place the patient in the left lateral position with the knees and hips flexed
a. An alternate position is the prone knee-elbow or jackknife position, in which the patient lays prone in an inverted
position on a specialized table. These positions are particularly helpful to permit a considerable degree of
maneuverability of the scope. When this position is desired but only a normal examination bed is available, a
cooperative patient can still be placed in the knee-chest position
Inspect the anus and surrounding areas for any abnormalities. ALWAYS Perform a digital rectal examination looking for skin
Tags and feeling the anal mucosal for any masses. ~— ' ~'
On rectal examination, special note is made of the general anatomy of the distal rectum, any palpable lesions, and
the contents of the rectum. If the rectum is found to be loaded with feces, an attempt should be made to empty the
rectum with the aid of a laxative suppository or enema prior to performing rigid sigmoidoscopy
7. Lubricate the shaft of the instrument
8 . Hold the scope with the thumb pushing on the base of the stylet to hold it in place. Insert the scop&4 cmjinto the anus in
the direction of the patient’s umbilicus. At this point, remove the stylet and seal the eyepiece witnfPflTglass window.
2
f h u e fc J^ L - Wayne Robinson. MBBS Class of 20! 5
—- ^ ~ a T (Anatomy: At 4 cm from the anus, the rectum anqulates posteriorly over the puborectalis sling into the hollow of
the sacrum. Therefore, when the scope reaches this point 4 cm from the anus, its general direction should
from pqintfnq-anterlorlv to pointing posteriorly)^ -------------
***< 'Turn 90° posterioriand/now visualizeW you advance. You caKjnsufflate with air)o help visualization.
tOriceTFie stylehsn^fnT(Wg97^vance the scope under direcTvislon, using tne bellows to gently insufflate air into the
rectum intermittently as the scope advances)
# 10. Gently insufflate air into the rectum to expand the rectum in front of the scope. Under direct vision, advance the scope into the
middle of the expanded segment. Repeat the insufflate-advance steps as the scope moves along. Note any abnormalities. A
slight lateral angulation of the scope is used to maneuver through the rectal valves
At th^ 1 2 cmhevel, the sacral promontory produces a ^harp angulation of the rectum anteriorly. At this point, the
directi^rnjffne scope is changed to point anterosuperiorly.
12. The usual distance that can be examined comfortably is(j5-20 c m jAnv significant pain is an indication to terminate the
examination. Further examination may be performed using a flexible scope.
-7
DO NOT PASS THE RECTOSIGMOID JUNCTION because it is highly likely that you will perforate the bowel
14. Remove the instrument while you continue to visualize the rectal mucosa.
* ^15. As the scope is withdrawn, follow the above steps backward. Insufflate air and change directions while maintaining direct
vision of the lumen of the rectum
16. Upon complete removal of the scope, wipe off the perianal area and return the patient to a more comfortable position
Contraindications T jU ^ 5
A b s o lu te contraindications include the following: iP C r r N

• t^lauspected or known bowe l perforation
• Anal stenosis (technical consideration)
^ f t * 7000 &&
Relative surgical contraindications include the following (BASICALLY A N Y SEVERE ABDO MINAL INFLAM M ATO RY
CONDITION WITH PERITONITIS):
• Acute peritonitis "
• S Colonic necrosis
• v^Fulminant colitis
• »^toxic meaacolon
• i/Acute severe diverticulitis
• ''Diverticular abscess
• Recent colonic surgery
• wÂcute anal fissure (due to excruciating pain - may wait until it resolves)
May also be contraindicated in patients who are highly uncooperative, agitated, or particularly anxious
NB: If sigmoidoscopy following colonic surgery is judged necessary for evaluation of bleeding or obstruction, it should be
postponed until at least 1 week after the operation
Questions
1. How long are the anus and rectum?
a. 4-5 cm and 15 cm respectively.
2. How long is the rigid sigmoidoscope?

a. It is 25 cm long.
3. What are the advantages and disadvantages o f the rigid over the flexible sigmoidoscope?
a. It is straight so it allows measurement of depth but it does not visualize the sigmoid colon.
4. How far can the flexible sigmoidoscope go?

a. It is 65 cm long and can go up to the splenic flexure.
5. What is the difference between the plastic and metal sigmoidoscope?

a. One is reusable and the other is not
6. What important thing should you tell the patient before they leave
a. That if they feel unwell, experience pain, abdominal distension, fever or see severe bleed per rectum they should come
the hospital as soon as possible as these may be symptoms of a perforation.
3
Wayne Robinson MBBS Class o f 2015
4
Wav Be Robinson. MBBS Class of 2015
^ -T-TUBE
Procedure namt^pT-tube chojedochotomvy^
Must also read up on T-tube chollrigiogram. (5'ee br. Powelinotes as well)
DEFINITION
A T-tube choledochotomy is a procedure indicated mainly to allow t-tube cholangiography. This is s(fluoroscopic procedure)in which
contrast medium is injected through a T-tube into the patient's biliary tree. The T-tube is most commonlyTrfserted duringa
cholecystectomy operation when there is a possibility of “retained” gallstones within the biliary tree.
DESCRIPTION/ DESIGN
n passive drain C lo s e d { a
// // r \
Ascending limb and descending iimb (2 short/transverse arms) AInserted into CBD)via a longitudinal incision made at
and'CBD sutured after placeTnent. To extend proximally and distally. Would be very difficult to insert via cystic duct (as
surgery and
commonly believed by medical students)
* ,r /
1 long/vertical arm -i Drains oercutaneously.)Passed from duct through skin to the external bag (sutured to skin).
Made of very flexible plastic - or rubber?. The flexibility of the plastic facilitates the percutaneous remove of the T-tube
without surgical intervention
Usually sized between 10 French (10F) and 16 French (16F). to & c. u
INDICATIONS (MUST See Dr. Powell notes for explanations and exception)
*** Rarely performed nowadays (see reason in notes)
^ 0t
2J Facilitate T-tube cholangiogram. usually at day 10 post-cholecystectomy.
' Allows biliary drainage after exploration of CBD ^ ^ ^
INDICATIONS FOR REMOVAL R ^
1. Usually removed after 3 weeks

2. w-"After normal T-tube cholangiogram (Usually at Day 10 post-op)
3. ^N orm al LFTs/Bilirubin level
4. *-"No symptoms/signs of cholangitis after clamping
*** After removal of a T-tube the bile duct does not leak bile because a fibrous tract forms around the T-tube prior to removal. The
fibrous tract then scleroses down after removal of the T-tube, resulting in a patent and closed bile duct.
*** See Dr. Powell notes for what is done if stone is detected
CONTRAINDICATIONS
To tube cholangiogram:
1. Non-consent by patient to procedure
w K
2. Contrast or iodine allergy
3. Barium study within last 3 days "tu b < r c J h d c d o ih & iB
COMPLICATIONS a
1. Bile peritonitis
2. \Âscendina cholangitis
3. Persistent biliary fistula (rare)
4. O bstruction of the tube
5. Displacement of the tube
PROCEDURE: http://www.wikiradiography.com/page/T-tube+Cholangiogram
IMAGES
AP/PA supine T-tube cholangiogram image. The biliary tree is outlined with contrast medium. There appears to be extravasation of
contrast medium outside the biliary tree and minimal contrast in the deuodenum.
common bile duct
T-tube
RIGID BRONCHOSCOPE. MEDIASTINOSCOPE. OESOPHAGOSCOPE
SOURCES:
RIGID BRONCHOSCOPE
Identify: This is a rigid bronchoscope 5 ^ - I f-O c v r N 'X t t e m a l -
Describe: It is metallic with a handle and two ports for air introduction/suction and visualization. Some have a port for light too. The
shaft is relatively short compared to an oesophagoscope and is fenestrated at the end to facilitate ventilation.
In d ic a tio n s ^ ^ m o& TTn dau< 4W. <T>03»f y o A hcS b e e r * k

1. Diagnostic
C * - b io p s y of lung tumour K?
4 b. t^Suspicion of foreign body o r Tur*\Q<lc
I—c. t^Wfassive Haemoptysis >600 mL of bloocTTn 24 hours
d. Unexplained + ve sputum. _ __
e. Pulmonary mass on CXR esp. children. (B *'
f. Recurrent/ Unresolved pneumonia
Persistent atelectasis - (remove mucus plug) j . y
h. Diffuse lung disease KJdu--
i. Malignant pleural effusion J
j- Brochioalveolar lavage
Therapei
sutic
a. f o r e ig n body removal
b. Difficult intubation
c. Laser resection of tumors or benign tracheal and bronchial stric
d. Stent insertion to palliate extrinsic compression of the tracheobronchial lumen from either malignant or benign disease
processes
e. Lobar atelectasis
f. Stricture dilation d
Lung abscess
er<'< z l G n o e S 'v L e B G - $
Contraindications:
a.
b.
Small airways.
Severe medical problems contraindicating anaesthesia.
F
Procedure
Bronchoscopy can be performed in a special room designated for such procedures, operating room, intensive care unit, or other
location with resources for the management of airway emergencies. The patient will often be given antianxiety and antisecretory
medications (to prevent oral secretions from obstructing the view), generally atropine, and sometimes an analgesic such as morphine.
During the procedure, sedatives such as midazolam or propofol may be used. A local anesthetic is often given to anesthetise
the mucous membranes of thepharynx, larynx, and trachea. The patient is monitored during the procedure with periodic blood
pressure checks, continuous ECG monitoring of the heart, and pulse oximetry.
A flexible bronchoscope is inserted with the patient in a sitting or supine position. Once the bronchoscope is inserted into the
upper airway, the vocal cords are inspected. The instrument is advanced to the trachea and further down into the bronchial system and
each area is inspected as the bronchoscope passes. If an abnormality is discovered, it may be sampled, using a brush, a needle, or
forceps. Specimen of lung tissue (transbronchial biopsy) may be sampled using a real-time x-ray (fluoroscopy). Flexible bronchoscopy
can also be performed on intubated patients, such as patients in intensive care. In this case, the instrument is inserted through an
adapter connected to the tracheal tube.
R ig id bronchoscopy is perform ed under general anesthesia . Rigid bronchoscopes are too large to allow parallel placement
of other devices in the trachea; therefore the anesthesia apparatus is connected to the bronchoscope and the patient is ventilated
through the bronchoscope. J(f
Complications
1. Anaesthesia and premedication
a. ^Respiratory depressionTArrest
b. Transient hypotension
c. Seizures
d. Syncope r r lu
i
jf
r
f f lc c P
e. i^4_arygospasm
0l
'• R a & o rrjy *S f'
9. H o O io r r i^ '
4r-
avne Robinson. MBBS Class of 2015
Identify: This is a mediastinoscope
Describe
The mediastinoscope has a light and a lens for viewing and may also have a tool to remove tissue.
Indications
Mediastinoscopy is often used for obtaining biopsy samples of lymph nodes for staging of lung .cancer or for diagnosing other conditions
affecting structures in the mediastinum such as sarcoidosis or lymphoma^
Contraindications
1. Absolute
a. Aneurysm
b. Superior vena cava obstruction
2. Relative
a. Previous mediastinum surgery (because of scarring that eliminates the plane of
disection)
b. Precious thoracostomy
Procedure
1. Ôbtain informed consent
2. ‘■'-It is done under general anaesthesia.
3. ^"An incision approximately 1 cm is made above the suprasternal notch of the
sternum.
4. ‘-'Dissection is carried out down to the pretracheal space and down to the carina.
5. ^ A scope (mediastinoscope) is then advanced into the created tunnel which provides a view of the mediastinum.
6. ‘''''The scope may provide direct visualization or may be attached to a video monitor.
7. '^Mediastinoscopy provides access to mediastinal lymph node levels 2, 4, and 7.
8. ‘■'''''Biopsy specinmens are taken (aspirate before you biopsys)
Complications
1. Complications related to general anesthesia
2. Bleeding - On occasion further surgery may be required to control bleeding
3. A pneumothorax
4. Persistent hoarseness if the nerve to the vocal cords is damaged during the procedure
5. Infections fttu n z n ^ (arcjnêrxl nenre .
Serious complications are uncommon following a mediastinoscopy \J 0
Questions
1. What are the contents of the mediastinum?
a. The contents of the mediastinum include the heart and its large blood vessels, trachea, esophagus, and bronchi.
2. How do you classify lung cancers?
3. How does each present?
4. What is the management of a patient with positive lymph nodes?
RIGID OESOPHAGOSCOPE
Identify: This is a rigid oesophagoscope
3
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X ft g o d c d ^ <3. 1
^ ( iH r u C X ^ ,
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f^ ^ (d (s z d { j i* . (± je x iS ~iL- u
ln^ j |^ A \ Xly^ y r
<^ d Y a d u O i . S ^ C ^ fg c p as
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r \ < i KCs€\ r^ * W
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MQUSSEAU-BARBIN TUBE
BRIEF HISTORY AND DESCRIPTION

Source article: Self-Expandable Stents in the Gastrointestinal Tract, By Richard Kozarek, Todd Baron, Ho-Young Song ____
In 1956|Mousseau and~BarMl 2 French surgeons, reported a new method of permanent intubation/stenting of the oesophagus using
the! pusnand puIIkechnloue. Prior to this, oesophageal prostheses were placed by a push technique alone, initially blindly, and then
under endoscopic visualization. Their stent consisted o fa circular, neoplex tube with a catheter-like portion a t the distal end and a
funnel a t the proxim al end. After passing the caXUeXeffransoraTfa blindly into the proximal stomach, a high gastrostomy,was
performed and the lowerr end of the catheter portion was grasped and pulled distally until the proximal stent funnet*enqaqmgaqed the
stricture. The excess lower end of the catheter was then cut in the stomach and the prosthesis remained in place. The authors claimed
that this method had a lower false passage and perforation rate, given the guidance provided by the pull from the stomach, ensuring its
luminal placement
DESCRIPTION * *
A tapering, non-collapsible orange tube with a distal catheter/rat-tail end that has fenestrations and a relatively thick funnel-
shaped proximal end
■ Patients are allowed to consume only liquids/ / if

■ No solid food because the cone and the distal end of the tube are narrow. _
■ Non-compliance -> blockage of tube.
■ Life span of device: It becomes occluded in 6-12 months.
INDICATIONS
1. Palliative management for dysphagia in patients with non-resectable, obstructing oesophageal cancer of th
2. Tracheo oesophagealTistulaertTP1^ - McFarlane)?
CONTRAINDICATIONS
■ f l i p p e r 1/3 oesophageal cancer because it will compress airway
PROCEDURE * trxOCO
1. Informed consent
2. Inserted under general anaesthesia, via a “push and pull” method
3. Laparotomy and gastrostomy performed
4. Pass the MBT transorally, (thin end first) blindly into the proximal stomach
5. Via the high gastrostomy, attach silk strings to Mosseau-Barbin tube distally and anaesthetist pulls back up NGT
6. Surgeon while holding its string, pulls tube until the proximal stent funnel has engaged the obstruction*
7. In-situ, the funnel shaped proximal end is secured above cancer. Tube distally is cut off.
Anchor to anterior stomach wall with 2-0 (secondary) knots of non-abs., synthetic suture.
COMPLICATIONS - (MOSTLY OF THE SURGERY ITSELF)
Immediate: ^Haemorrhage and damage to viscus
Earlv^Wound infection, ischaemia ,^ sk of aspiration since non-collapsible y j
Late Prolapse, herniation, stomal stenosis,*rfiigration of tube
POSSIBLE OSCE DISCUSSION TOPICS

Oesophageal cancer
Wavae Robinson. MBBS Class of 2015
SENGSTAKEN-BLAKEMORE TUBE
gastric festoon port
—gaslrsc asfika&oti port
esophageal balloon part
gastric aspiratson openings

esophageal ba&aom
gastric ba toon
BRIEF HISTORY
fc / '
A ible-baifoon tamponade system originally developed by Senqstaken and Blakemore in 1950 has undergone relatively few
changes to the current day
Also have a Minnesota tube, which has an additional port for oesophageal suction. Another nasogastric (NG) device with a single
— gastric balloon is most effective at terminating bleeding from gastric varices and is known as the Linton-Nachlas tube
The advent o f endoscopy has reduced the use o f balloon tamponade, BUT the use of such devices can still be temporizing or
lifesaving, despite their potential for serious complications
DESCRIPTION
0 Si?
■ The 3 major components of a^Sengstaken-Blakemore tube are a gastric balloon, an oesophageal balloon, and a gastric suction port
J - It also consists of a ^flexible, plastic, graduated tube with radiopague markings
1 ■ The i?proximal ports that inflate the two distal balloons
- INDICATIONS
1. MAJO^JMUQATION FOR WHICH IT WAS DESIGNED: Mechanical tamponade of life-threatening oesophageal or
gastric^ variceahhemorrhage ~ ~ ----------------
■ 'TlDWTârticularly when medical and endoscopic therapy/haemostasis has failed
■ NOT definitive management, but rather a temporizing one: 50% of patients re-bleed after balloon deflation.
2. ALSO employed in obstetrics as a means of tamponade of postpartum uterine haemorrhage
CONTRAINDICATIONS
1. Recent surgery that involved the oesophagogastric junction
2. Known oesophageal stricture
PROCEDURE
1b ^ fDontrol of the patient is essential. Routine use of soft restraints and medications for sedation should be considered in most
patients.
2. Elevate the head of thgbed to 45°^nd position the patient on the bed. The left lateral decubitus position is an acceptable
alternative position. ------
3. The threshold to perform endotracheal intubation should be low, as the risk of regurgitatio n and aspiration is extrem ely
high. To minimize this risk, perform nasogastric (NG) lavage and maximal stomach evacuation prior to the placement of an
oesophageal tamponade tube.
W ayne Robinson. MBRS Class of 2015
4. Ensure that all the appropriate equipment is present. Ensure that the balloons on the tamponade tube are free of leaks
(optimally, test this while balloons are submerged under water).
INSERTION STARTS HERE

5. Deflate both balloons and lubricate generously with water-soluble lubricating jelly. Placed transnasallv oarapsorallv into the
stomach with both balloons deflated, +/- topic anaesthetic coverage of nostrils and posterior pharvnx(t)ra l routers preferred,
especially if patient is intubated. ^
6. Check proper placement by irrigating the gastric aspiration port with water while auscultating over the stomach. If
correct tube placement is at all uncertain or if time permits, obtain a portable chest radiograph. Its position in the stomach has
been confirmed
7. The distal gastric balloon is then inflated with 250-500 ml of air, drawn tight against the GE junction, an
(manually or using a pulley device - A 500-mL bag of intravenous fluid can serve as a convenient initial weight)
8. If the gastric balloon alone does not control the haemorrhage, the proximal oesophageal balloon is inflated to a pressure of 20-40
mmHg or the lowest pressure needed to stop bleeding. May increase traction of bleeding continues to the gastric aspiration port
9. Check the pressures periodically
10. After bleeding has been controlled, reduce the pressure in the oesophageal balloon by 5 mm Hq every 3 hours until 25 mm Hg is
reached without bleeding; this pressure is generallyThamtained ToHITe riexfT2-24 TtOUTS^ If bleeding is controlled, deflate the
oesophageal balloon for 5 minutes every 6 hoursJo help preverrToisophaqeal necrosis.
11. Once satisfactorily positioned, the tube is<generallv left in place for 24liqun»Nf bleeding recurs, the gastric balloon and, if
necessary, the oesophageal balloon may be reinflatedlorâdBitiohar^TTTonrsTRowever, given the high mortality among
patients who rebleed, consider alternatives such as sclerotherapy and transjugular intrahepatic portacaval shunt (TIPS).
Balloon tam ponade is a tem porary measure to co ntrol bleeding and can be applied fo r 12-24 hours. 50% of
patients re-bleed after balloon deflation.
COMPLICATIONS
Major risks include:

i n s piration: Very high risk! - most frequent major complication. Risk greatest during insertion. Minimized by evacuating
stomach via NGT prior and by keeping a low threshold for ET intubation!!
— 2. Asphyxiation: Caused by proximal migration of tube. May be prevented by ET intubation
3 . Oesophageal perforation or rupture: May occur due to inflating the gastric balloon in the oesophagus
" 4.v^Pressure necrosis of oesophageal mucosa from overinflation of the balloon.
Minor complications include: Pain, discomfort, pressure necrosis of nose, lips, tongue
PREPARE TO QUICKLY AND FULLY DISCUSS THE MANAGEMENT OF VARICEAL BLEEDING

FLATUS TUBE
DESCRIPTION
Long, rubber tube. Length ~30”?? With terminal and one lateral eye. Available in different thicknesses.
A long, soft flatus tube is inserted-witbjhe patient in the left lateral position.
The obstruction is usually a f15 cm )
INDICATION
1. ^Cfntwisting a siamoid volvulus
2. ^ôlonic pseudoobstruclion
{o r
3..^ ru n u nv^(Dnline
o e source source - Intussusception?)
- m iussuscepnon' ) -------- v _ ' • /
4. ^ ^ n lin e source - Some places use it for barium enema) J
REQUIREMENTS
1. Protective covering Leave UP
2. Disposable flatus tube and connection tubing
3. Bowl of tepid water (into which the non-lubricated end goes)
4. Lubricant D f d m ere- iU n T -2
5. Disposable wipes
6. Disposable gloves
PROCEDURE
Place the patient in the left lateral position
Lubricate the tube about 15 cm
Insert the tube with the help of a riqid/flexible sigmoidoscope.
4. Hold the sigmoidoscope at the twist. Pass the flatus tube along it. With a gentle rotatory movement, ease the tube past the twist
into the high-pressure area of the dilated sigmoid.
Successful insertion of flatus tube is rewarded by much flatus and some loose faeces. Withdraw the sigmoidoscope, taking care
to avoid displacing the tube.
Tape the flatus tube to the buttock to prevent its proximal migration.
7. Connect the tube to a collection bag. The flatus tube allows for rapid decompression of the distended colon, with the immediate
relief of symptoms.
The tube may be left in situ for 48 hours to allow for complete emptying of the loop and for the resolution of mural oedema. The tube
should not be left for more than 72 hours as it may cause pressure necrosis.
COMPLICATIONS cjo s«^. / H e ''
1. Pressure necrosis if left for > 72 hours

2. Perforation of bowel in patient’s with impaired sensation e.g. spinally injured patients
U dS C g n iv a l^ s h a rj? n e e d le *
— <gu.vT © u ^ c L e i A cl Ji
Q j i C ^ ^ z k .'r C Cjj(L~> / n a t k ,
7
CORE-NEEDLE BIOPSY
Source: http://www.cancer.orq/treatment/understandinqvourdiaqnosis/examsandtestdescriptions/forwomenfacinqabreastbiopsy/breast-
biopsy-biopsy-types
Core needle biopsy uses a hollow needle to withdraw small cylinders for cores) of tissue samples from the breast. It can be used
to biopsy a palpable lump or other masses In the breast. It can be used for non-palpable masses with ultrasound guidance
A CNB is most often done in the doctor’s office with local anesthesia. The needle is put ir{3Jto 16 times j b get the samples, or cores.
This takes longer than an FNAB, but it is more likely to give a clear result because more tissue is taken to be checked. A CNB can
cause some bruising, but usually does not leave scars inside or outside the breast.
The doctor doing the CNB usually places the needle in the abnormal area, sometimes using ultrasound to guide the needle into the right
place. If the area is easily felt, the biopsy needle may be guided into the tumor while feeling (palpating) the lump.
Core needle biopsy is often the preferred biopsy method because it is accurate and does not involve surgery.
DESCRIBE ^ ^ # sfecJ, A©!(o»*

■ It has a plastic handle with a graduated sliding bar and an innerîeedle
Tru-Cut biopsy needle is just a manufacturer trade name. According to their website, the design is as follows:
• 20 mm sample notch
• Scalpel-sharp steel cutting edge retrieves cleanly cut, high quality specimens
• Removable stylet allows multiple sampling capability
• Thin-wall cannula for large core sample
A
• Centimetre depth markings assist in needle placement
S 0& C & -fO

c in
T ^ b J -ro n J S T r e A T c
PROCEDURE o r\u < S T VCcstCXO /S *
‘1. Informed consent
2. Strict aseptic technigue!!
3. Clean the area and apply local anaesthesia
.je f o ; ll 6 fa d *)
Use a blade to nick the area above the mass
Insert the metal tubing with the needle covered
'JH t % 5
-6^- With the handle stable pull the sliding bar backwards to expose the needle then push it forward to obtain the biopsy
specimen.
7. Withdraw the metal tubing and remove the tissue you collected. You may repeat twice.
Core needle biopsy for NONPALPABLE masses

o Abnormal area is located with the help of ultrasound or a special type of three-dimensional mammography, called stereotactic
mammography. The accuracy is similar using either types of imaging
Advantages of core needle biopsy

o Core needle biopsy is accurate when done by an experienced radiologist. It is quick and does not involve surgery. There is
only a small chance of infection or bruising.
Information gained: If breast cancer is found, the tissue removed during a core needle biopsy gives important information including:
/ l . Tumortype ' ^
2. Tumor grade
3. Lymphovascular Invasion ------------- m ii-S f ^
\ 4. Hormone receptor status /
If the tissue sample is benign, surgery may be avoided. In some cases, however, even if the tissue sample is benign, an excisional
biopsy (a surgical biopsy) may be needed to confirm the diagnosis.
DRAWBACKS OF CORE NEEDLE BIOPSY

1. One drawback of core needle biopsy is that the needle can miss a tumor and take a sample of normal tissue instead. This is most
likely to occur when the biopsy is done without the help of stereotactic mammography or ultrasound. This is called a false
negative result and can delay diagnosis.
a. For nonpalpable masses, false negative results occur in up to 8% of stereotactic mammography- or ultrasound-
guided core needle biopsies. For palpable masses, false negative results are more rare.
2. Another drawback of core needle biopsy is that it may not give full information about the tumor. For example, it can't tell the size of
a tumor.
a. Taking multiple tissue samples can help limit this problem. However, in some cases, a surgical biopsy is needed to
get complete information on the tumor.
Core needle biopsy with stereotactic mammography

During a needle biopsy with stereotactic mammography, you lie on your stomach on a special table and your breast fits through a hole
in the table
Before the procedure, the health care provider will use a local anesthetic to numb the area. Your breast will be compressed like it is for
a mammogram, and several images will be taken. These images help the provider guide the biopsy device to the suspicious area in the
breast. A needle in the device removes tissue samples. In some centers, the needle removes tissue with a vacuum assisted probe. The
needle is inserted and removed quickly. You may feel a pushing and pulling sensation on your breast, which can cause some
discomfort.
Needle
w it h
tissue
sample
Breast
tissue
©rieaflnwt&e tncorpofared
OTHER TYPES OF BIOPSY

U/S or mammography guided core needle biopsy (most common). Other types:
^0'' Stereotactic (mammotome) core biopsy: A stereotactic core needle biopsy uses x-ray equipment and a computer to
analyze pictures ot the Breast. The computer then pinpoints exactly where in the abnormal area the needle tip needs to
go. This is often done to biopsy suspicious microcalcifications (tiny calcium deposits) when a tumor cannot be felt or
seen on ultrasound.
£03" Vacuum-assisted core biopsy: Done with systems like the Mammotome® or ATEC® (Automated Tissue Excision and
Collection). For these procedures, the skin is numbed and a small cut (less than !4 inch) is made. A hollow probe is put in
through the cut and guided into the abnormal area of breast tissue using x-rays, ultrasound, or MRI. A cylinder of tissue
is then pulled into the probe through a hole in its side, and a rotating knife inside the probe cuts the tissue sample from
the rest of the breast.
Magnetic resonance imaging (MRO guided core biopsy
Hookwire localization biopsy: GO TO DR. ROBERTS NOTES FOR DETAILS. REMEMBER: Removed breast tissue
must be checked by mammogram to ensure all of the suspicious lesion has been excised
Excisional biopsy: only performed as second choice to core needle biopsy; should not be done for diagnosis if possible
. W ayne Robinson. MRBS Class o f 2015
THROMBOEMBOLIC DETERRENT (TED) STOCKINGS"
USE
& DVT prophylaxis in immobile patients
■ KNOW ABOUT METHODS OF PREVENTING DVT INTRAOP - INCLUDING PNEUMATIC COMPRESSION DEVICES
DESCRIPTION
Below knee or thigh length l ~~ Q o m r r \ t-l
Closed or open toe design
Provide graduated compression to promote venous return
Various sizes - sizing is based on calf circumference and limb length
Washable
CONTRA-INDICATIONS nej2_
(K
Ws
vere peripheral vascular disease (PVD)
Peripheral neuropathy
■'^Severe peripheral oedema
■ i^ttoft tissue diseases including dermatitis, cellulitis or a recent skin graft h (a be
■‘■'''Major lower limb injuries u
COMPLICATIONS
■v^re ssure areas and ulcers if poorly fitted
■Înadequate function if incorrectly sized or too loose —^ / r a ilu t c
■ Falls risk if the patient mobilizes on a slippery surface
■ DVT if inappropriately used alone in high risk patients ?—/
OTHER INFORMATION
■ Thigh length may be superior for DVT prophylaxis
Other measures used to prevent DVT include:

( 3 ■ Sequential compression devices - may be used INTRAOP
( £ ) a Early Stir-up Mechanism (early ambulation)^ ~T?
( £ ) • Anticoagulant therapy (Heparin, Clexane)

■ Be prepared to discuss DVT, Virchow’s triad, anticoagulation
I n t e r m it t e n t p n e u m a t ic c o M P R is s io fo a n D/S e q u e n t ia l c o m p r e s s io n d e v ic
intermittent pneumatic compression is a therapeutic technique used in medical devices that include an air pump and inflatable
auxiliary sleeves, gloves or boots in a system designed to improve venous circulation in the limbs of patients who suffer edema or the
risk of deep vein thrombosis (DVT) or pulmonary embolism (PE)
In use, an inflatable jacket (sleeve, glove or boot) encloses the limb requiring treatment, and pressure lines are connected between the
jacket and the air pump. When activated, the pump fills the air chambers of the jacket in order to pressurize the tissues in the limb,
thereby forcing fluids, such as blood and lymph, out of the pressurized area. A short time later, the pressure is reduced, allowing
increased blood flow back into the limb.
/ ^ r - p u * jO -f- S l- c j2 \jc ^ f 6ot>-f )
^ S ===,
, Wayne Robinson. MBBS Class of 2015
The primary functional aim of the device “is to squeeze blood from the underlying deep veins, which, assuming that the valves are
competent, will be displaced proximally.” When the inflatable sleeves deflate, the veins will replenish with blood. The intermittent
compressions of the sleeves will ensure the movement of venous blood.
Sequential compression devices (SCD) utilize sleeves with separated areas or pockets of inflation, which works to squeeze on the
appendage in a “milking action.” The most distal areas will initially inflate, and the subsequent pockets will follow in the same manner.
Sequential calf compression and graduated compression stockings are currently the preferred prophylaxis in neurosurgery for the
Intraoperative SCD-therapy is recommended during prolonged laparoscopic surgery to counter altered venous blood return from the
lower extremities and consequent cardiac depression caused by pneumoperitoneum (inflation of the abdomen with carbon dioxide)
Wayne Robinson, MBRS Class of 2015
VACUUM-ASSISTED CLOSURE (VAC)
ALSO GET AN IMAGE FROM UWI
DESCRIPTION AND INDICATIONS
Negative-pressure wound therapy (NPWT) is a therapeutic technique using a vacuum dressing to promote healing in acute or
chronic wounds and enhance healing of first and second degree burns. The therapy involves the controlled application of sub-
atmospheric pressure to the local wound environment, using a sealed wound dressing connected to a vacuum pump. NPWT appears
to be useful for diabetic ulcers and management of the open abdomen (laparotomy).
MECHANISM OF ACTION
VAC dressing: This is one form of NPWT. Has 3 main mechanisms:
1. Helps to remove and reduce oedema/exudate/effluent from the wound

• Online source: This results in increased blood flow to the wound (by causing the blood vessels to dilate) and
greater cell proliferation. Another important benefit of fluid removal is the reduction in bacterial colonization of the
wound, which decreases the risk of wound infections.
2. The negative pressure is thought to increase granulation tissue formation
3. And then the physical effect of closing
NPWT promotes wound healing by applying a vacuum through a special sealed dressing. The continued vacuum draws out fluid from
the wound and increases blood flow to the area. The vacuum may be applied continuously or intermittently.
The dressings used for the technique include open-cell foam dressings and gauze, sealed with an occlusive dressing intended to
contain the vacuum at the wound site.
Once the dressing is sealed the vacuum pump can be set to deliver continuous or intermittent pressures, with levels of pressure
depending on the device used, varying between -125 and -75 mmHq depending on the material used and patient tolerance.
POSSIBLE OSCE DISCUSSION
Wound healing and skin grafts

Abdominal wound failure/dehiscence
—. Socltanr) Ph&$pha£c„
FLEET ENEMA
Source. Medscape. Be prepared for this to take you into a discussion about other methods o f bowel prep
DESCRIPTION
(Rectal Sodium Phosphate^® ver the counter) Fleet Enema is a saline laxative.
INDICATIONS
1. Constipation relief
2. Bowel preparation (for surgery??, x-ray or colonoscopic exam)
a NOT USED IN OBSTRUCTED CASES!!
Indicated as laxative in the relief of occasional constipation and as part of a bowel cleansing regimen in preparing the colon for surgery,
x-ray or colonoscopic examination
MECHANISM OF ACTION
Saline cathartic effect
Saline laxatives work by drawing water into the colon/fosmotic effect 1which helps produce a bowel movement. This
provides a soft stool mass and increased bowel a^
A bowel movement should be stimulated iryito 5 minutes>,without pain or spasm.
DOSE
■ 1 bottle PR; not to exceed 1 administration/24 hr
ADMINISTRATION
PO SITIO NS FOR USING THIS ENEMA

• Left-lateral position: Lie on left side with knee bent, and arms resting comfortably
• Knee-chest position: Kneel, and then lower head and chest forward until left side of face is resting on surface with left arm
folded comfortably
1. Remove orange protective shield from enema tip before inserting;

2. With steady pressure, gently insert enema tip into rectum with a slight side-to-side movement, with tip pointing toward navel
■ Insertion may be easier if person receiving enema bears down, as if having a bowel movement; this helps relax the
muscles around the anus
■ Do not force enema tip into rectum as this can cause injury
3. Squeeze bottle until nearly all liquid is gone; it is not necessary to empty the bottle completely, as it contains more liquid than
needed
4. Remove enema tip from rectum and maintain position until urge to evacuate is strong (usually 1-5 minutes)
■ Do not retain enema solution for more than 10 minutes
■ Enema should be at room temperature before use
CONTRAINDICATIONS
Hypersensitivity ^ @ <T) Q
ADVERSE EFFECTS - (MAINLY FLUID, ELECTROLYTE AND ACID-BASE DISTURBANCES. THEN ABDOMINAL
SYMPTOMS) r3SS=* — '
1. -'''Hypersensitivity 11 •'•'Abdominal pain

2. Pruritus S dilUr<
it
12iÂbdominal distension
?.d e h y d r a tio n --------- 13*< Diarrhea
4. ^Hyperphosphatemia 14. Gastrointestinal pain
5. •'•'Hypocalcemia
T P O Hr
6. w^Hypokalemia 15. Chills
7. •''Hypernatremia Co. 16. Blistering
17. Stinging
J3. ^Metabolic acidosis
9.v"'NauseV g rr h y 4L m*&S d 18. Anal discomfort
lO^Vomiting 19. Proctalgia
CAUTIONS
■ Do not use laxatives when nausea, vomiting, or severe abdominal pain is present
■ Caution with renal impairment or ascites
■ Caution in patients with a colostomy
Wayne Robinson, MBBS Class o f 2015
■ Caution in children aged 2-11 years or elderly patients with comorbidities
■ Caution if coadministered with medications known to affect renal perfusion, function, or hydration
■ Caution with pre-existing electrolyte disturbances or patients taking diuretics or other medications that may alter electrolytes
■ Because of risk electrolyte disturbances, caution with medications known to prolong QT interval
■ Additional liquids by mouth are recommended to prevent dehydration
■ Exceeding daily dose, no return of enema solution, retention time >10 minutes, or failure to have a bowel movement within 30
minutes of enema use may lead to electrolyte disturbances, including hypernatremia, hyperphosphatemia, hypocalcemia, and
hypokalemia
■ Severe dehydration and electrolyte abnormalities associated with serious complications (eg, acute kidney injury,
arrhythmias, and death) have occurred in adults and children who overdosed using oral or rectal over-the-counter
(OTC) sodium phosphate solutions to treat constipation
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LAPAROSCOPIC INSTRUMENTS
Sources: http://www.laparoscopic.md/instruments, Wikipedia
Powerpoint presentation from: Jane P Bradley Hendricks [RGN, BSE(hons), MCS, Independent Nurse Prescriber, Surgical Care
Practitioner, Laparoscopic Surgery]
LIST
A VISUALIZATION/OPTICS
■ Light source (halogen or xenon 0 cold light (but can still burn)),
■ Lens and video imaging system with monitor
B. ABDOMINAL ACCESS INSTRUMENTS
C. LAPROSCOPIC INSTRUMENTS (DISCUSSED HERE - THESE ARE IN THE OSCE!)

■ Laparoscopic instruments in general 15 - 1 8 ” in length with an articulated connecting rod between handles and scissor blades, jaws etc.
■ Laparoscope
■ Needle driver
■ Trocar
■ Bowel grasper
DISPOSABLE LAPAROSCOPIC TROCAR (OBTURATOR AND PORT/CANNULAt
'^ ( jr o G Z r —
■ n n u lc .
Q iL r a ib * '
CL ^ crfo»-
LAPAROSCOPIC TROCAR ASSEMBLED (2 ANGLES!
H;yri flow STOPCOCK-----------T Funnel-ihepstf

Ir»5flrum®nrGu»d»
A trocar (variant: trochar, from French: via troquard, i.e., 'three-quarters',) is a medical device that is made up of an o btura tor (which
may be a metal or plastic sharpened or non-bladed tip), a cannula (basically a hollow tube), and a s e a l . Trocars are placed through
the abdomen during laparoscopic surgery. The tro car fu n ctio ns as a portal fo r the subsequent placem ent of othe r
instrum ents, such as graspers, sd s so rs, staplers, etc.
1
Along with the probe, scalpel, and cannula the trocar is one of the oldest implements used by medical practitioners. A trocar is shaped
like a pen and has a sharp triangular point. Trocars are typically placed inside hollow cannulas and introduced inside body cavities to
assist in draining fluids. ^ ^ f^~>\
IKY)Tfj w e /k v SiT*-*-
W | rocars'are"now referred to as both thejjnitial entry devicejas well as the(hollow cannula used during the operation.\These instruments
play an important role in laparoscopic surgery. Instruments such as scissors and graspers are introduced using surgical trocars.
Modern surgical laparoscopes used for minimally invasive procedures are a far cry from the simple hollow tubes that gradually
developed to include lenses for magnified vision. Today, scopes are more like an apparatus with multiple parts that include a CCD
camera, viewing device, lens cleaner, and an energy-supply device.
Come in varying sizes, laparoscopes usually

Diagnostic 3mm scope available
Made up of a rod and lens system.
Bundles of fibres, incoherent carry light and coherent carry image.
Wide range of angles available 0 and 30 degree are fairly standard.
NEEDLE DRIVER
used by laparoscopic surgeons to hold suturing needles when closing wounds. Forming slip-knots to close wounds and surgical
incisions requires precise skills. Suturing can often be tricky to use owing to the property of “memory” which causes tissue to resist
deformation. Needle holders have three parts - the jaws, joints, and handles. The instrument is classified as straight or curved
depending upon the shape of the jaws.
LAPAROSCOPIC GRASPERS
A bowel grasper is used during minimally invasive bowel surgery. The graspers are maneuvered through incisions that are usually no
larger than 5 mm. The advantage with using laparoscopic graspers is that they enable the surgeon to grasp and manipulate
abdomen tissue with precision without having to cut open the abdomen. The graspers facilitate observation, excision, and biopsy
procedures.
2
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WavRe Robinson. MBBS Class of 2015
f ill
LAPAROSCOPY POINT-FORM OVERVIEW
Sources:
Slideshare.com: Anil Haripriya, Colo-Rectal Surgeon at Medical College
HISTORY
laparoscopic examination of abdominal cavity ju ra ts called it CELIOSCOPY

■1j)11 Jacobeus - 1st hum an laparoscopy — i1Hons C io n â -
■ 1938
i » o o Veress
v t J i t J b b oSpring
p i l l i y loaded
l U c i u t s u uobturator
u i u i c u u i nneedle
e e u i c for
i u i [pneumoperitoneum
ji ic u m u fje iiiu iic u m
■ 1966 Hopkins - ***Developed Rod Lens Optical system - , i / / / \

1960-70 Sem m - Developed automatic insufflator & instruments. (j i nCr t ^ lOr^ ~r v lU r t o e ro n r^ J
Perform ed 1 lap ap p en d isectom y in 1983. Father of m odern laparoscopic surgery
1987 Philip M ouret - 1! Lap cho lecystectom y -
GENERAL DIFFERENCES BETWEEN LAPAROSCOPIC AND OPEN SURGERY

fc/VKD J C U ic . c \rc ja c L *
( 3 OR TH E PATIENT
1. Post operative pain related to size of incision - smatter incisions = less pain.
2. Less handling of intestines results in little or no disturbance of normal function.
3. Avoidance of the trauma of abdominal wall injury by the incision allows rapid return to normal activity
4. No incision allows early return to more strenuous activities: driving, lifting, sport etc.
THE SU RGEON
Magnified view often better than obtained via an incision allows precise dissection.
Altered (but not absent) tactile response l i b Jrr^=>
Two-dimensional (flat screen) view. (0S2 cA td&fTlM-> O &d ZP
Usually (but not always) longer operating time L ‘
Need to develop entirely different operating technique
Adaptation of principles of open surgery to laparoscopic surgery.
OR THE HOS P ITAL

1. Initial capital costs to establish laparoscopic surgery in the order of £30,000 - £40,000
2. Reduced overall costs by shortening of hospital stay e.g. cholecystectomy reduced from 5 to 1 day, hiatus hernia repair reduced from 7 to 3
days.
IN GENERAL. LAPAROSCOPIC METHODS ->

■ Result in attenu ated neuroendocrine & cytokine re sponse compared with open technique
■ Reduced surgical injury reduces the impairment of post op immune function specifically related to CM I
EQUIPMENT & INSTRUMENTATION

SEE SEPARATE NOTES FOR IMAGES AND MORE DETAILS
V ISU ALIZATIO N/O PTIC S - Light source (halogen or xenon 0 cqld light but can still burn), lens and video imaging system with monitor
( b ) A BD O M IN A L ACC ESS INSTRUM ENTS — \jS ^ n £ e d //e e rr ^
\ c ) LAPR O SC O PIC INSTRUM ENTS

• Laparoscopic instruments in general 15 - 18” in length with an articulated connecting rod between handles and scissor blades, jaws
etc.
ABDOMINAL ACCESS INSTRUMENTS
A. Open Technique
■ Hasson cannula
B. Closed technique
• Veress needle
VE R ESS NEEDLE
■ Obtains pneumoperitoneum by closed technique
■ Spring loaded obturator needle
■ Drawbacks:
—&■ Preperitoneal placements
—^ Injury to vessels \
Injury to bowel J
H A SS ON ’S CA NNU LA - obtains pneumoperitoneum by open technique
IN SU FFLATO RS
Automatic
Wayae Robinson. MRBS Class o f 2015
■ Pressure regulated high flow
■ Monitor intrabdominal pressure which is usually set at 12-15 mmHq
■ Alarm sound or pressure release valves when pressure limit is exceeded
■ Flow rate of 8-10 L/min
LAPROSCOPIC INSTRUMENTS
(See separate notes for more images and details)
1. Laparoscopes
2. Trocars
3. Laparoscopic graspers
LAPROSCOPES
■ Rigid & Flexible
• Based on Hopkins rod lens system
■ Sizes - 3-10 mm (up to 18 mm)
■ Some angled
o To look around corners
o Difficult to use
o Especially useful in advanced lap procedures
PHYSIOLOGIC CHANGES AND CONSEQUENCES
e/pneum
Physiologic changes are due to theroneumoperitoneum
Required to create working space
P ^ --------
Gases used:
o Air
o
C 02
( /r N2O
y6 Helium, Argon (newer)
C 02 n 2o
Advantaaes: Advantaaes: Qyti Qb-V
oriHHas same refractive index as air so it doesn’t distort the image 0 Readily available
c D o e s not support combustion or explosion 0 Better analgesia
o it Rapidly absorbed, 0 Physiologically inert
orf Rapidly soluble - 4 chance of gas, embolism 0 Hypercarbia not a problem
0 Non explosive
Disadvantaaes: f \ 0 Decreased intraop entitled C02 & minute ventilation required to
0 NgUeadilyavailable maintain homeostasis
CHvoercarbia'i--------- ^ ‘ Disadvantaaes:
0 Causes peritoneal discomfort when used with LA 0 Supports combustion
0 Absorbed slower than C02
/ PHYSIOLOGIC EFFECTS OF THE PNEUMOPERITONEUM

GAS ITSELF
(%. PRESSURE EFFECTS
J3.; RENAL EFFECTS
GAS EFFECTS
• With C02 respiratory acidosis
« Hypercarbia - Tachycardia, f in vascular resistance, t BP, & myocardial O 2 demand
■ Cardiac arrhythmias - Bradycardia (MC)
■ Gas embolism - Sudden hypotension, Mill wheel murmur | end tidal CO 2
B. PRESSURE EFFECTS
■ Vasovagal attack - due to streching of peritoneum
- CVS:
o 4 VR, CO - due to pressure on IVC
o Venous engorgement with endothelial damage of lower limb veins
. pvt ' -
4 lung compliance
■ t PIP, t risk of barotrauma
■ Mild V/Q mismatch
■— Atelectasis
Hypoxia
C. RENAL EFFECTS
Wayne Robinson. MBBS Class o f 2D15
■ | RBF, GFR, Urine output
■ Stimulation of ADH axis
CURRENT APPLICATIONS - SEE A LIST
CONTRAINDICATIONS
ABSOLUTE
1. '-■''Severe cardiac dysfunction (class IV)
2. •"'Haemorrhagic shock
3. ^Concomitant disease requiring laparotomy
4. Întestinal obstruction with massive abdominal distension
5. w'Uncorrectable coagulopathy
6. Frozen abdomen
RELATIVE
1. Severe CO PD
2. *''' Abdominal sepsis/peritonitis
3. ^ Multiple previous abdominal operations
4. Morbid obesity
5. Inability to tolerate GA
6. 'Pregnancy
7. Diaphragmatic hernia
COMPLICATIONS
/ ^ I n s e r t io n r e l a t e d
1. Major vascular injury (0.25%)
2. Gl injury (0.14%)
3. Bladder injury
4. C02 embolism
5. Abdominal wall haemorrhage
/k>OST-INSERTION COMPLICATIONS
1. Gl perforations (acute or delayed)
2. Laceration & bleeding from solid organs
3. Abdominal wall hernia
/ ^ PNEUMOPERITONEAL RELATIVE COMPLICATIONS

v- ^ 1. C02 embolism
2. Hypercarbia
3. Respiratory acidosis
4. Renal failure
5. Venous thrombosis
6. Pneumothorax
7. Subcutaneous emphysema
SOME CLOSING POINTS
Laparoscopy has been used since a century but in last two decades there has been an explosion in these field
But laparoscopy does not change indications of any operation & should be done only when it is indicated
The principles of diatherm y: eie ctr o s o rg er y 47
cavity as the tube is removed Once the drain is out, a

previously inserted purse-string suture should be tied.
THE PRINCIPLES OF DIATHERMY:

ELECTROSUROERY ___________________________
For many years, short wave diathermy has proved a most valu-
able and versatile aid to surgical technique. Its most common
use is in securing haemostasis by means of coagulation, but by
varying the strength or wave form of the current produced, it can
also result in a cutting effect. Both these effects have been used
in open surgery, as well as in laparoscopic surgery or down intra-
luminal endoscopes as in transurethral resection of the prostate.
However, although diathermy is a valuable surgical tool, many
accidents have occurred due to surgeons being unaware of, or not.
fully understanding, the principles of its use. Most accidents are
avoidable if the diathermy or electrocautery is used with care.
It is therefore vital for a surgeon to have a sound understanding
of the principles and practice of diathermy, and how to avoid
complications.
The principle of diathermy

When an electrical current passes through a conductor, some of
its energy appears as heat. The heat produced depends on:
• the intensity of the current;
• the wave form of the current;
• the electrical property of the tissues through which the
current passes;
• the relative sizes of the two electrodes.
There are two basic types of diathermy system in use, monopolar
diathermy and bipolar diathermy (Figure 4-19). In monopolar
diathermy, which is the most commonly used form, an alternat-
ing current is produced by a suitable generator and passed to the (b) Bipolar diathermy
patient via an active electrode which has a very small surface
area. The current then passes through the tissues and returns via
a very large surface plate (the indifferent electrode) back to the
earth pole of the generator. As the surface area of contact of the T h e in te r c o lle g ia te b a s ic s u rg ica l sk ills c o u r s e
active electrode is small in comparison to the indifferent elec- p a rticip a n ts h a n d b o o k ,
trode, the concentrated powerful current produces heat at the
operative site. However, the large surface area electrode of the
patient plate spreads the returning current over a wide surface coagulation of the plasma proteins, dried and shrunken dead
area, so it is less concentrated and produces little heat. tissue and stimulation of the clotting mechanism. In an ideal
In bipolar diathermy, the two active electrodes are usually situation, intracellular temperatures should not reach boiling
represented by the limbs of a pair of diathermy forceps. Both during coagulation, because if it does an unwanted cutting effect
forceps ends are therefore active and current flows between them may be experienced.
and only the tissue held between tire limbs of the forceps heats Cutting occurs when sufficient heat is applied to the tissue
up. This form of diathermy is used when it is essential that the to cause cell water to explode into steam. The cut current is
surrounding tissue should be free from either the risk of being a continuous wave form and the monopolar diathermy is most
burned or having current passed through them. effective when the active electrode is held a very short distance
from the tissues. This allows an electrical discharge to arc across
The effects of diathermy the gap creating a series of sparks which produce the high tem-
Diathermy can be used for three purposes: peratures needed for cutting.
In fulguration, the diathermy matching is set to coagulation
1 Coagulation: the sealing of blood vessels. and a higher effective voltage is used to make larger sparks jump
2 Fulguration: the destructive coagulation of tissues with char- an air gap thus fulgurating the tissues. This can continue until
ring. carbonisation or charring occurs. The voltage and power output
3 Cutting: used to divide tissues during bloodless surgery. can be varied by adjusting the duration of bursts of current, as
In coagulation, a heating effect leads to cell death by dehydra- well as its intensity to give a combination of both cutting and
tion and protein denaturation. Bleeding is therefore stopped by coagulation. This is known as blended current and provides both
a combination of the distortion of the walls of the blood vessel, forms of diathermy activity.
48 BASIC SURGICAL SKILLS AND ANASTOMOSES
Complications of diathermy available so that these can be reset if necessary. In most cases, it
is therefore wise to undertake precautions and to use bipolar dia-
Electrocution thermy wherever possible. If monopolar diathermy is required,
Today, diathermy machines are manufactured to very high safety then the patient plate should be sited as far away from the pace-
standards which minimise the risk of any part of the machine maker as possible so that the path of the current does not pass
becoming live with mains current. However, as with any such through the heart or the vicinity of the pacemaker. Monitoring
instrument, there must be regular and expert servicing. of the heart rate should be undertaken throughout the operation
and a defibrillator should always be available in case a dysrhyth-
Explosion mia develops at any time.
Sparks from the diathermy can ignite any volatile or inflam-
mable gas or fluid within the theatre. Alcohol-based skin prepa- Laparoscopic surgery
rations can catch fire if they are allowed to pool on or around Diathermy bums are a particular hazard of laparoscopic surgery
the patient. Furthennore, diathermy should not be used in the due to the nature of the visibility of the instrumentation and
presence of explosive gases, including those which may occur the actual structure of the instruments used. Such bums may
naturally in the colon, especially after certain forms of bowel occur by:
preparation, such as mannitol, which has now been banned for
this use for this very reason. • Diathermy of the wrong structure because of lack of clarity7of
vision or misidentification.
Bums • Faulty insulation of any of the laparoscopic instruments or
equipment.
These are the most common type of diathermy accidents in both
• Intraperitoneal contact of the diathermy with another metal
open and endoscopic surgery. They occur when the current flows
instrument while activating the pedal.
in some way other than that in which the surgeon intended and
are far more common in monopolar than bipolar diathermy. • Inadvertent activation of the pedal while the diathermy tip is
out of vision of the camera.
These may occur as a result of:
• Retained heat in the diathermy tip touching susceptible
• Faulty application of the indifferent electrode with inadequate structures, such as bowel.
contact area. • Capacitance coupling (Figure 4.20). This is a phenomenon
• The patient being earthed by touching any metal object, e.g. in which a capacitor is created by having an insulator
the Mayo table, the bar of an anaesthetic screen, an exposed sandwiched between two metal electrodes. This can be
metal arm rest or a leg touching the metal stirrups used in created in situations where there is a metal laparoscopic port
maintaining the lithotomy position. and the diathermy hook is passed through it. The insulation
• Faulty insulation of the diathermy leads, either due to cracked of the diathermy hook acts as the sandwiched insulator
insulation or instruments such as towel clips pinching the and by means of electromagnetic induction, die diathermy
cable. current flowing through the hook can induce a current in
• Inadvertent activity such as the accidental activation of the the metal port, which can potentially damage intraperitoneal
foot pedal, or accidental contact of the active electrode with structures. In most cases, this current is dissipated from die
other metal instruments, such as retractors, instruments or metal port through the abdominal wall, but if a plastic cuff is
towel clips. used, this dissipation of current does not occur and the danger
of capacitance coupling is significandy increased. Therefore,
Channelling metal ports should never be used with a plastic cuff. The
Heat is produced wherever the current intensity is greatest. danger of capacitance coupling can be prevented by using
Normally, this would be at the tip of the active electrode, but entirely plastic ports.
if current passes up a narrow channel or pedicle to the active
electrode, enough heat may be generated within this channel
or pedicle to coagulate the tissues. This can prove disastrous, for
example,
• coagulation of the penis in a child undergoing circumcision;
• coagulation of the spermatic cord when the electrode is
applied to the testis.
In such situations, diathermy should not be used, or if it is neces-
sary, then bipolar diathermy should be employed.
Pacemakers
Diathermy currents can interfere with the working of a pace-
maker with its obvious potential danger to the patient’s health.
Modem pacemakers are designed to be inhibited by high fre-
quency interference, so that the patient may receive no pacing
stimulation at all while the diathermy is in use. Certain demand
pacemakers may revert to the fixed rate of pacing and therefore Th e in te rc o lle g ia te b a s ic s u r g ica l skills c o u r s e p a rticip a n ts
it would be important for the anaesthetist to have a magnet handbook,

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ATLS ALGORITHM STARTS ON PAGE 3

TRIMODAL DEATH DISTRIBUTION

1. First peak of death = within seconds to minutes from injury =

Mnemonic "ABCDE" should be followed in all injured patients:

A. Airway maintenance with cervical-spine protection + adjuncts

C. Circulation with control of haemorrhage +adjunts

D. Disability or neurologic status with intracranial mass lesion recognition

Assessment and Management Sequence

ABCDE frequently accomplished simultaneously

§ Re: Elderly: Aging diminishes physiologic reserve.

REMEMBER THIS PRINCIPLE FOR THE ABCDEs OF THE PRIMARY SURVEY:

EACH STEP CONSISTS OF AN ASSESSMENT AND AN ACTION/INTERVENTION

A. AIRWAY AND C-SPINE PROTECTION

NOTE: Hypovolemic shock should NOT be treated by vasopressors, steroids, or sodium

Basic neurological assessment is made using the AVPU score:

X-rays and diagnostic studies:

Other investigations. Re: CT SCAN;

RE: “PERMISSIVE HYPOTENSION”

** Intracellular fluid has a low sodium and high potassium concentration

** Therefore the maintenance requirement is defined by weight of the patient

** In 1L of normal saline there is 154 mEq of sodium

** All NG losses are added to the maintenance as normal saline

BODY FLUID COMPARTMENTS

The electrolyte composition of each compartment differs.

SOURCES: LECTURE NOTES IN CLINICAL ANAESTHESIA + TORONTO NOTES

§ TOTAL FLUID REQUIREMENT = Deficit + Maintenance + Ongoing loss

WHAT ARE THE ONGOING LOSSES?

3. Third spacing (other than ECF, ICF)

§ If a hypotonic solution is given, for example 5%

RECENT CONSENSUS GUIDELINES RECOMMEND:

Toronto Notes: Crystalloid Infusion

Approach to Crystalloid Fluids -

§ 50 g dextrose per L in normal saline

5% DEXTROSE 0.2% SALINE (& 7.5% DEXTROSE 0.2% SALINE)

§ 1 ml of 8.5% NaHCO3 = 1 mmol of bicarb!!!!, or 1 ml of 4.2% = 0.5 mmol.

MUST KNOW: PROF. MCFARLANE LIKES TO ASK THE EQUATION!!

MANNITOL – 10 & 20% SOLUTION – CAN COME IN OSCE – MUST KNOW

§ ? mg/ml OR per Litre

§ CLASSIFY: NATURAL vs. SYNTHETIC

DEXTRAN – 40, 70, 110

COMPLICATIONS OF FLUID THERAPY

GET STARLING FORCES INFO FROM MY PLEURAL EFFUSION NOTES

FLUID AND ELECTROLYTE LOSSES

MUST KNOW: INSENSIBLE LOSSES = SKIN + RESPIRATORY TRACT LOSSES

POTASSIUM – MUST KNOW – CAN COME IN OSCE!!!

– Mild hypokalemia – oral (tablet or mist potassium citrate) OR IV KCL.

Too much crystalloid cause fluid overload

Colloids: Large molecular weight solutions.

Normal fluid losses of an adult - look up

Calculating daily fluid requirement:

Dextrose water gives very small amount of calories.

Maintenance of 80 kg man, day 2 post-op:

Maintenance fluid requirement: 1000 + 500 + 20*60 = 2700 ml

Maintenance fluids: 1500 + (50*20) = 2500 ml

CALCULATE NG LOSSES REPLACEMENT:

*** HOW TO GIVE THIS FLUID:

*** Usually write on fluid balance chart starting from 8 am:

So how the chart would look:

8:00 am – 11:30 am 500 ml 0.9% N/S + 20 meq K+

80 kg pt day 1 post op. Normal urine ouput and u and es no ng losses.

Aims of Surgical Nutrition

o Simple, cheaper o Less aspiration so better for comatose pts

4. Renal failure secondary to under-resuscitation, drugs, *myoglobin, etc.