UCD School of MedicineCopyright © 2021 SVUH Surgery

Helen Heneghan, Laoise Coady

1

ISBN: 978-1-8383951-0-0 (eBook)

Surgical Handbook ISBN: 978-1-8383951-1-7 (Paperback)

Edited by Professor Helen Heneghan, Ms Laoise Coady

Contents

1. Principles of Surgery Page 4

• Author: Ms Laoise Coady

2. Upper GI Surgery Page 20

• Author: Mr Paul Cromwell, Ms Laoise Coady, Prof Helen Heneghan

3. Hepatobiliary Surgery Page 54

• Author: Mr Kin Cheung Ng

4. Colorectal Surgery Page 80

• Authors: Ms Helen Mohan, Mr Noel Lynch, Dr Sinéad Ryan,
Dr Odhrán Ryan, Dr Ailbhe O’ Driscoll Collins

5. Inflammatory Bowel Disease Page 114

• Author: Mr Liam Devane

6. Hernias Page 123

• Author: Mr Ian Reynolds

7. Vascular Surgery Page 136

• Authors: Ms Aoife Kiernan, Mr Thomas Aherne,
Mr Nawar Masarani, Mr Ahmed Hassanin

8. Breast Disorders Page 158

• Author: Mr Andrew McGuire

9. Endocrine Disorders Page 165

• Author: Ms Carolyn Cullinane

10. Urology Page 184

• Author: Ms Sorcha O’ Meara

11. Cardiothoracic Surgery Page 204

• Authors: Mr Adam Daly, Joseph McLoughlin, Prof David G Healy

12. Trauma Page 219

• Authors: Dr Micheal Sheehan, Dr Jessica Lynch,
Dr Izabella Kinga Orban, Dr Jeffrey Mulcaire, Dr Enda Hession

13. Plastic Surgery Page 254

• Authors: Ms Laoise Coady, Ms Stephanie Bollard,
Ms Christine Quinlan

14. Orthopaedic Surgery Page 304

• Author: Ms Laoise Coady

Copyright © 2021 SVUH Surgery 2

Helen Heneghan, Laoise Coady
ISBN: 978-1-8383951-0-0 (eBook)
ISBN: 978-1-8383951-1-7 (Paperback)
 15. Transplant Surgery Page 326
• Authors: Ms Laoise Coady, Mr Adam Daly, Joseph McLoughlin,
Prof David G. Healy

16. Radiology Page 338

• Author: Dr Kevin Quinlan

Editors
• Professor Helen Heneghan
• Ms Laoise Coady

Expert Reviewers
• Ms Shirley Potter
• Professor David G Healy
• Ms Mary Barry
• Mr Joseph Dowdall
• Professor John Ryan
• Ms Rachael McBride
• Professor Eric Heffernan

Cover Illustration
• Ms Laoise Coady

Illustrations
• Ms Laoise Coady
• Mr Paul Cromwell
• Ms Sorcha O’ Meara

Radiology Images
• Professor Eric Heffernan
• Dr David Murphy
• Dr Rory O’ Donohoe
• Dr Stephen Skehan
• Dr Ronan Ryan
• Dr Ciaran Redmond

Copyright © 2021 SVUH Surgery 3

Helen Heneghan, Laoise Coady
ISBN: 978-1-8383951-0-0 (eBook)
ISBN: 978-1-8383951-1-7 (Paperback)
1. Principles of Surgery

• Ms Laoise Coady

• History Taking
• Differential Diagnosis of the Acute Abdomen
• Common management principles of the Acute Abdomen
• Incisions
• Surgical Drains
• Nutrition in Surgical Patients

4
History Taking

Pain

SOCRATES

• Site
• Onset
o When and where did the pain start
o Sudden/Gradual onset
o Has it moved since onset
• Character
o Sharp/Burning/Stinging/Dull/Throbbing/Colicky
• Radiation
o Gallbladder Disease: right side of back/shoulder tip
o Pancreatic Disease, AAA: straight through the back
o Renal/Ureteric Colic, Testicular torsion: Loin to groin
o Appendix: Umbilicus to RIF
o Chest: MI
• Associated Symptoms
• Time/Duration
• Exacerbating/Relieving Factors
• Severity
o Out of 10, Recording baseline & maximum pain

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Associated Symptoms

General
• Fever
• Rigors
• Shortness of breath
• Dizziness on standing (e.g. hypovolaemia secondary to haemorrhage)
• Weight loss

Gastrointestinal Symptoms
• Dysphagia – subjective sensation of difficult or abnormal swallowing
• Odynophagia – pain on swallowing
• Dyspepsia – persistent/recurrent upper abdominal discomfort
• Reflux/Heartburn – Sour/bitter tasting fluid in mouth or throat
• Nausea/Vomiting – onset, duration, persistence, how much, frequency, composition – blood/bile/small
bowel contents/coffee-ground
• Haematemesis
o Blood after repeated vomiting – Mallory-Weiss Tear
o Dark blood – variceal or arterial
o Coffee ground vomitus – old/low volume gastric bleeding
• Diarrhoea – Frequency/consistency/blood/mucus/pus
• Constipation
• Tenesmus – sensation of incomplete emptying following a bowel motion
o Suggests low rectal tumour
• Melaena – dark tarry stool - sign of upper GI bleeding
• Steatorrhoea – fatty stool – sign of malabsorption
• Rectal Bleeding
o Dyschezia: painful defecation suggests anal fissure
o Haemorrhoids: bright red blood on wiping
o Rectal bleeding: blood on surface of stool
o Colonic bleeding: dark red blood/mixed up with stool/clots
• Altered Bowel Habit
o Change in frequency/consistency/colour
o May indicate inflammatory bowel disease or underlying cancer
• Features of bowel obstruction – last bowel opening/last time passed flatus/distension/vomiting

Hepatobiliary Symptoms
• Jaundice
o Yellow discolouration of skin and sclera secondary to hyperbilirubinaemia
o Symptoms: Pruritis, dark urine, pale stool

Urology Symptoms
• Dysuria
• Frequency
• Urgency
• Nocturia
• Hesitancy
• Poor stream
• Terminal dribbling
• Haematuria
o Blood at start of urination suggests bladder pathology
o Blood during/at the end of urination suggests prostatic/penile pathology

6
Gynaecology Symptoms
• Menses
• PV Discharge
• PV Bleeding
• Intermenstrual bleeding
• Postcoital bleeding
• Postmenopausal bleeding

Peripheral Arterial Disease Symptoms

• Claudication
o Pain in buttock, calf or thigh precipitated by exercise and relieved by rest secondary to inadequate
arterial flow during exercise
• Rest Pain
o Severe pain in the affected limb due to inadequate arterial flow
o Neuropathic pain secondary to neuronal ischaemia

7
Differential Diagnosis of the Acute Abdomen*

RUQ Pain Epigastric Pain LUQ Pain

• Biliary Colic • Peptic Ulcer • Splenic abscess/infarct
• Cholecystitis Disease/Gastritis • Gastric Ulcer
• Cholangitis • Pancreatitis • Gastritis
• Hepatitis • GORD • Left Lower Lobe
• Right Lower Lobe • Ruptured AAA Pneumonia
Pneumonia • Cardiac – Inferior
MI/Pericarditis
Right Flank Pain Umbilical Pain Left Flank Pain
• Renal Colic • Appendicitis • Renal Colic
• Pyelonephritis • SBO • Pyelonephritis
• MSK: lumbar • UTI • MSK: lumbar
disc/sciatica/bony disc/sciatica/bony
metastases metastases
RIF Pain Suprapubic Pain LIF Pain
• Appendicitis • PID • Diverticulitis
• Ovarian Cyst • UTI/Cystitis • Ovarian Cyst
Rupture/Torsion • Urinary retention Rupture/Torsion
• PID • Prostatitis • PID
• Inguinal Hernia • IBD • Inguinal Hernia
• IBD • Osteitis pubis • IBD
• Renal Colic • Renal Colic
• Psoas Abscess • Psoas Abscess

*NB
• Always consider a ruptured abdominal aortic aneurysm in any adult presenting with abdominal pain
• In a female of child bearing age presenting with abdominal pain, always consider a ruptured ectopic
pregnancy.

8
Causes of Right Upper Quadrant Abdominal Pain
Biliary
Clinical Features
Biliary Colic • Dull discomfort in RUQ/Epigastric Region
• Associated nausea, vomiting
• Lasts for at least 30 minutes and plateaus within an hour
• Patients generally appear well and have a benign abdominal
examination
Acute Cholecystitis • Prolonged RUQ/epigastric pain (>4 Hours)
• Associated fever
• Abdominal examination reveals guarding and positive
Murphy’s sign
Ascending Cholangitis • Charcot’s Triad: Fever/Rigors, Jaundice, RUQ Abdominal Pain
Hepatic
Acute Hepatitis • RUQ pain
• Associated fatigue, malaise, nausea, vomiting and anorexia
• Patients may also be jaundiced with dark urine and pale
stools
• Varying aetiologies: Hepatitis A, Alcohol & Drug Induced
Liver Abscess • Most common symptoms are fever and abdominal pain
• Risk factors: Diabetes; Liver transplant; Underlying
hepatobiliary/pancreatic disease
Budd-Chiari Syndrome • Very rare
• Caused by occlusion of the hepatic veins
• Presents with classical triad: Abdominal pain, ascites,
hepatomegaly
• Associated with fever, jaundice, GI bleeding, hepatic
encephalopathy, lower extremity oedema

Causes of Epigastric Abdominal Pain

Epigastric
Clinical Features
Acute pancreatitis • Acute onset persistent epigastric pain radiating to back
• Associated with vomiting
• Relieved by sitting forward
Chronic pancreatitis • Epigastric pain radiating to back

Peptic Ulcer Disease • Epigastric discomfort

• Can localise to one side/be aggravated by movement
• Duodenal ulcer – wake up with pain; relieved by eating
GORD • Epigastric pain radiating to chest
• Associated with heartburn, dyspepsia, regurgitation
• Relieved with Gaviscon/Cool drinks
Acute MI • Can be associated with shortness of breath and exertional
symptoms
• Always consider in patients with risk factors for coronary
artery disease

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Causes of Left Upper Quadrant Abdominal Pain
Left Upper Quadrant Pain
Clinical Features
Splenic Abscess • Fever and LUQ tenderness
• Uncommon
• May be associated with splenic infarct
Splenic Infarct • Severe LUQ pain
• Associated with underlying conditions including
splenomegaly, hypercoagulable states and atrial
fibrillation
Splenic Rupture • LUQ/Left chest wall/Left Shoulder pain worse on
inspiration
• Most often associated with trauma

Causes of Lower Abdominal Pain

Lower Abdominal Pain
Localisation Clinical Features
Appendicitis RIF • Periumbilical pain initially which radiated to the
RIF
• Associated nausea, vomiting and anorexia
Diverticulitis LIF • Constant pain, usually in LIF
• Associated nausea and vomiting
Nephrolithiasis Left/Right • Pain is most common symptom – occurs as stone
passes from renal pelvis to ureter
• Generally present with flank pain, but may have
back/abdominal pain also
Pyelonephritis Left/Right • Flank pain
• Associated with dysuria, urgency, frequency,
haematuria, fever, costovertebral angle
tenderness
Infectious colitis Left/Right • Diarrhoea with associated abdominal pain
Cystitis Suprapubic • Lower abdominal pain associated with
haematuria, dysuria, frequency and urgency
Acute urinary Suprapubic • Lower abdominal pain and discomfort
retention • Unable to urinate

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Common Management Principles in an Acute Abdomen

Investigations

Bedside Vitals Shock

Urine Dipstick Haematuria, UTI, Bilirubinuria
Urine output Hypovolaemia, Urinary retention
ECG MI
Capillary Glucose DKA

Urine Amylase Pancreatitis

Culture & Sensitivity UTI
b-HCG Pregnancy, Ectopic Pregnancy

Stool/Swab Culture & Sensitivity If there is an abscess/wound infection/diarrhoea

Blood Full Blood Count Hb – Anaemia; WCC - Infection

CRP Infection
Culture & Sensitivity Sepsis
Urea, Electrolytes, AKI
Creatinine Dehydration
Calcium Ureteric stone, Pancreatitis
Albumin Pancreatitis, Malnutrition
Liver Function Tests Hepatobiliary disease, Pancreatitis
Coagulation Screen Liver Dysfunction
Type & Screen If any blood loss; Also useful in pre-op assessment
Amylase Pancreatitis
ABG Ischaemia, Sepsis (Lactate)
Glucose DKA
Troponin MI
b-HCG Pregnancy, Ectopic Pregnancy

Imaging Ultrasound
• Abdominal • Hepatobiliary disease, Appendicitis, AAA,
pancreatitis
• Pelvic • Ectopic Pregnancy
Erect CXR Visceral perforation
PFA Bowel obstruction
• Small Intestine <3cm
• Large Intestine <6cm
• Caecum/Sigmoid <9cm
CT +/- Contrast
• Abdo/Pelvis • Obstruction, Perforation, AAA, Diverticulitis,
Appendicitis etc
• Angio • Mesenteric Ischaemia
• KUB • Renal/Ureteric stone
MRCP Evaluation of pancreaticobiliary ductal system

Invasive OGD/Colonoscopy PUD, Inflammatory Bowel Disease, GI Malignancy

Endoscopic US Investigation of dilated CBD/Biopsy of pancreatic mass
Diagnostic If cause of symptoms unknown after non-invasive
Laparoscopy investigations

11
 Incisions

Carotid Thyroidectomy/
Endarterectomy/ Parathyroidectomy
Neck Dissection

Pacemaker/ICD

Midline Sternotomy
(CABG, Cardiac surgery,
Valve Replacement

Whipple’s

Paramedian
Kocher (Open Cholecystectomy)

Reverse L (Liver Open Nephrectomy

Transplant/ Liver
Resection)

Midline Laparotomy

McBurney
(Appendectomy)
Rutherford Morrison
(Renal Transplant

Lanz (Appendectomy)

Pfannenstiel
(Caesarean Section)

12
Laparoscopic Laparoscopic
Appendicectomy Cholecystectomy

13
Fluids

Water Balance

• Water loss leads to increased serum sodium and serum osmolality, resulting in:
o Increased thirst and increased release of antidiuretic hormone (ADH)
o Increased water intake and reduced water excretion
o Restoration of normal water balance

• Patients who are alert, have access to water and have an intact thirst mechanism will not become
hypernatraemic

• Intravenous fluids should be prescribed for patients whose fluid requirements cannot be met by oral or
enteral routes.
o NPO for medical/surgical reasons e.g. bowel obstruction, pre-op etc.
o Vomiting/Diarrhoea
o Hypovolaemia

Types of Fluids

• Crystalloids
o Solutions of electrolytes and sterile water e.g. NaCl, Hartmann’s Solution
o Can be isotonic, hypotonic or hypertonic with respect to plasma
o Balanced/Buffered electrolyte solutions e.g. Hartmann’s solution have an electrolyte composition
similar to plasma with the addition of a buffer e.g. lactate

Fluid Tonicity Na +(mmol/L) K +(mmol/L) Cl- HCO3- Glucose

(mmol/L) (mmol/L) (mmol/L)
Human N/A 135 - 145 3.5 – 5.0 100 – 110 22 – 26 3.5 – 7.8
Plasma
0.9% NaCl Isotonic 154 154
(Normal (Used for
saline) resuscitation/
maintenance)
Hartmann’s Isotonic 131 5 111 29
Solution (Used for
resuscitation/
maintenance)
0.18% NaCl Hypotonic 30 30 40g/L
/ 4% (Used for
Glucose maintenance)
5% Hypotonic 50g/L
Dextrose (Used for
maintenance)

• Colloids
o Solutions of large organic molecules – bigger molecules stay in blood for longer
§ Human plasma derivatives e.g. albumin, fresh frozen plasma
§ Semisynthetic preparations e.g. Gelofusine

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Prescribing IV Fluids
• 5 R’s
o Resuscitation
o Routine Maintenance
o Replacement
o Redistribution
o Reassessment

• Overall requirements = Replacement + Maintenance

Fluid Therapy
• Resuscitation – patient showing signs suggestive of hypovolaemia
o Initial fluid bolus – 500ml Crystalloid solution (e.g. Hartmann’s) within 15 minutes
o Reassess – ABCDE
o Repeat process up to 2000ml of fluid (goal-directed fluid resuscitation)
o Seek expert help if ongoing persistent hypovolaemia

• Maintenance therapy – replace ongoing losses of water and electrolytes under normal physiological
conditions – sweat, urine, respiration, stool.
o Preserves water and electrolyte balance
o Provides nutrition to patients who are unable to eat or drink
o Instigated when patient is not expected to be able to eat or drink normally for a prolonged period of
time e.g. pre-op or on a ventilator
o Patients who are expected to have insufficient fluid or energy intake for > 7 days should be
considered for parenteral or enteral nutrition.
o Maintenance fluids should be increased if the patient has fever, burns, surgical drains, tachypnoea,
polyuria, sweating or ongoing significant GI losses.

Normal Daily Fluid and Electrolyte Requirements

25-30 ml/kg/day Water
1mmol/kg/day of sodium, potassium, chloride
50-100g/day glucose

Traditional Regimen = 1 Salty & 2 Sweet

0.9% NaCl + 20mmol KCl over 8 hours
5% Dextrose + 20mmol KCl over 8 hours
5% Dextrose + 20mmol KCl over 8 hours

• Replacement therapy – corrects existing water and electrolyte deficits

o Deficits can result from GI, skin or urinary losses, bleeding and third space sequestration
Existing Fluid or Electrolyte Deficits or Excesses
Dehydration
Fluid Overload
Hyperkalaemia
Hypokalaemia

15
 Ongoing Abnormal Fluid/Electrolyte Losses
Vomiting/NG Tube Loss
Biliary Drainage Loss
Diarrhoea/Excess Colostomy Loss
High/Low Volume Ileal Stoma Loss
Ongoing Blood Loss e.g. Malaena
Urinary Loss e.g. Polyuria, Post AKI
Pancreatic/Jejunal Fistula/Stoma Loss
Sweating/Fever/Dehydration

o Replacement fluids are prescribed by adding to or subtracting from routine maintenance fluids
o Type of fluid replacement depends on the type of fluid lost
o Extracellular Fluid Loss e.g. diarrhoea and vomiting, stomas, burns, pancreatitis, NG aspirates
– should be replaced with a fluid similar to plasma e.g. Hartmann’s
o Classical Dehydration e.g. poor intake, pyrexia should be replaced by normal maintenance
fluids e.g. dextrose-saline
o Blood Loss should be replaced with blood – packed red cells; further blood products such as
fresh frozen plasma, platelets and cryoprecipitate may be needed if ongoing blood loss.
o Adjust for all other sources of fluid and electrolytes (oral, enteral, drug prescriptions)
o Monitor and reassess fluid and biochemical status by clinical and laboratory monitoring

• Redistribution
o Fluid distribution must be considered prior to prescribing fluids.
o Seek senior help as necessary
o IV fluid prescription should be altered to account for abnormal distribution in the following
circumstances

§ Gross oedema
§ Sepsis – causes intravascular depletion due to plasma loss secondary to vasodilation and
leaky capillaries
§ Heart Failure – patients are prone to fluid overload and pulmonary oedema – monitor fluid
balance – do not exceed 2 litres of fluid within 24 hours
• If overload develops
o Give furosemide as necessary
o Fluid restrict (e.g. 1.5L per day)
o Low sodium diet
o Daily weights (1Kg lost – 1 L lost)
§ Liver Failure – excess Na may cause ascites – used 5% Dextrose. If hyponatraemic seek
specialist input
§ Acute Renal Failure – avoid potassium supplementation
§ Chronic Renal Failure – avoid sodium, potassium and excess fluids
§ Post-op fluid retention/redistribution
• Salt and water retention occur to maintain cardiovascular homeostasis and fluid
volume – avoid saline post-operatively – risk of hyperchloraemic acidosis and
increased renal load
• Potassium is intracellular - levels of potassium can increase post-operatively due to
cell lysis during surgery – do not give any potassium supplementation if it is over
4.5mmol/L; small volume potassium e.g. 40mmol in 24 hours can be given if
potassium is normal/low
§ Malnourishment/Refeeding Issues – avoid dextrose which can precipitate re-feeding
syndrome
§ Hyper/Hyponatraemia

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Drains

• Drains are used to remove collections of fluid (e.g. serous fluid/ascitic fluid), pus (e.g. empyema), blood (e.g.
haemothorax) or air (e.g. pneumothorax)
• Drains can be passive (non-suction, rely on gravity) or active (rely on negative pressure/suction)
• Drains are primarily placed at the time of surgery to prevent fluid collection and subsequent infection
around the operative site
o Intra-abdominal procedures which may be associated with large collections of blood and serum
should consider prophylactic drain placement (e.g. liver resection)
o Drains are placed adjacent to an anastomosis at risk of leaking e.g.
pancreaticoenteric/choledochoenteric or adjacent to the injured tissue
o Drains are inserted post mastectomy/harvesting of skin flaps to drain the dead space

• Complications
o Infection
o Haemorrhage
o Hernia formation
o Kinking
o Damage to surrounding structures if migration occurs

• Drains are left in place until drainage has decreased to <25-30mL per day for two consecutive days

• Types of Drains
o Open Drains
§ Allow free drainage of secretions
§ Yates Drain, Penrose Drain
o Closed Passive Drains
§ Allow drainage of secretions using gravity
§ Robinson Drain, Nasogastric tube, chest tube
o Closed Active Drains
§ Generate active suction by use of negative pressure
§ Jackson Pratt Drain, Redivac drain, Minivac drain
o T-Tube
§ Placed in common bile duct following CBD exploration with choledochotomy or post repair
of CBD damage
§ Facilitates external drainage of bile to allow healing
§ Drains ~600ml a day and then reduces
§ Before removing should be clamped for 24 hours and patient monitored for signs of
obstructive jaundice
§ Generally has been superseded by ERCP

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Nutrition in Surgical Patients

• Nutritional support is important in the management of surgical patients

• Stress of surgery results in a catabolic state which can lead to malnutrition within a few days

• Nutritional status assessment must be performed for each patient in order to identify those in need of
nutritional support
o Malnourished patients requiring surgical intervention
o Healthy patients undergoing major surgery with anticipated lengthy recovery times
o Advanced malignancy, sepsis, prolonged vomiting and bowel obstruction can all result in excessive
catabolic states

• Poor nutrition results in:

o Impaired albumin production
o Skeletal muscle weakness
o Impaired wound healing
o Reduced neutrophil, macrophage and lymphocyte function

• Malnutrition in surgical patients is associated with:

o Poor wound healing
o Increased risk of infection
o Increased frequency of decubitus ulcers
o Overgrowth of bacteria in the GI tract
o Abnormal nutrient loss through stool

• Malnutrition is diagnosed if a patient has two or more of the following

o Insufficient energy intake
o Loss of muscle mass
o Weight loss
§ BMI - Weight/Height2
• <18.5 Kg/m2 – Underweight
• 18.5 – 24.9 Kg/m2 – Normal
• >25 Kg/m2 – Overweight
o Loss of subcutaneous fat
o Localised or generalised fluid accumulation
o Diminished functional status (handgrip strength)

• Indications for Nutritional Support

o Pre-existing malnutrition
o Anticipated/Actual inadequate intake by mouth
o Multiple comorbidities
o Early enteral feeding is appropriate following many types of surgery
o Parental feeding is indicated in those who will be unable to receive adequate enteral nutrition by
postoperative days 10-14

• Types of Nutritional Support

o Enteral Nutrition
§ Oral
§ Feeding tube – nasogastric/nasojejunal
§ Gastrostomy/Jejunostomy
• Gastrostomy: for patients who have a functioning gastrointestinal tract but are
unable to swallow
• Jejunostomy: used when stomach needs to be bypassed e.g. due to ulcers, or after
major oesophagogastric surgery

18
o Parenteral Nutrition
• Oral/NG/NJ routes not possible e.g. bowel resection, fistula
• Can be given peripherally or centrally
§ Central most common route
• Peripheral parental nutrition should be given via a large diameter venous catheter

• Parental nutrition should be given via a central venous catheter if indicated for more than a
few days, as high osmotic load is not tolerated by peripheral veins and extravasation can lead
to tissue damage
§ PICC Line (Peripherally inserted central venous catheter)
§ Hickman line (dedicated tunnelled catheter)

§ Complications of TPN
• Hyperglycaemia
• Serum electrolyte abnormalities
• Refeeding syndrome
• Macro/micronutrient excess/deficiency
• Wernicke’s encephalopathy
• Bacteraemia
• Complications secondary to central venous catheterisation: bleeding, vascular injury,
pneumothorax, venous thrombosis, arrhythmia, air embolism
§ Monitoring
• Daily glucose, urea and electrolytes until stabilised
• Twice weekly liver function tests (LFTs)
• Weekly copper, magnesium, phosphate and manganese

19
2. Upper Gastrointestinal Surgery

• Mr Paul Cromwell, Ms Laoise Coady, Professor Helen Heneghan

• Upper Gastrointestinal Bleeding

• Dysphagia and Odynophagia
o Differential Diagnosis
o Upper GI Investigations
• Benign Oesophageal Disorders
o Hiatus Hernia and Paraoesophageal Hernia
o Gastro-Oesophageal Reflux Disease
o Peptic Ulcer Disease
o Barrett’s Oesophagus
• Oesophageal Motility Disorders
o Achalasia
o Diffuse Oesophageal Spasm
• Oesophageal Cancer
• Gastric Cancer
• Consent for Upper GI Endoscopy
• Bariatric Surgery

20
Upper GI Bleeding

Definition
• Bleeding from the upper GI tract (oesophagus, stomach and duodenum)

Epidemiology
• Typically elderly patients with comorbidities, often taking anticoagulants or antiplatelets.
• Mortality is 10%.

Pathophysiology
• Peptic ulcers (36%)
• Oesophagitis (24%)
• Gastritis (22%)
• Varices (11%)
• Others: Malignancy, Duodenitis, Mallory-Weiss tear, Vascular ectasia, Dieulafoy’s lesion

History and Presentation

• Major upper GI bleeds usually present with haematemesis and melaena and occasionally with
haematochezia (15%).
• Look for stigmata of chronic liver disease (jaundice, ascites, spider naevi, hepatomegaly, caput medusa).
• May have signs of low blood volume (tachycardia, low blood pressure, cap refill <2, reduced GCS, cool
peripheries, urine output <0.5ml/kg/hour)

Risk Factors Investigations

Alcohol FBC, U&E, LFTs, Crossmatch 4 units, Coagulation profile, Arterial

blood gas
Smoking
ECG
Liver disease

NSAIDs OGD (diagnostic and therapeutic)

Vomiting CT angiogram
Steroids IR angiogram (diagnostic and therapeutic) can identify 5% more
PUD bleeds over CTA

Treatment
• Initial goal is volume resuscitation:
o Insert large bore IV cannula and take blood samples (as above)
o If low BP give IV crystalloids initially
o Urinary catheter to monitor urine output
o Give IV PPI bolus (some give infusion)
o Give blood transfusion when available

• If the patient is stable they should have upper GI endoscopy within 24 hours
• If unstable they should have endoscopy urgently.
• Upper GI endoscopy can utilise a combination of haemostatic clips, adrenaline injections and haemostatic
powder to stop haemorrhage.

o If massive haemorrhage:
§ Activate hospital’s massive transfusion protocol
§ Use O-negative blood initially
• Available in the fridge in ED until crossmatched blood is available.
§ Then give a balanced transfusion of RCC, platelets and plasma (1:1:1)
21
 § Keep Hb >8 (or >9 if cardiac history)
§ Correct underlying coagulation defects (Fibrinogen)
§ Reverse anticoagulant medications (Vit K, Prothrombin complex)

Tranexamic acid does not reduce mortality in GI bleeding and should not be given.

• If suspected variceal bleeding:

o May require Sengstaken-Blakemore tube
o IV terlipressin and octreotide to reduce portal hypertension
o OGD for variceal banding
o TIPS – Transjugular Intrahepatic Portosystemic Shunt

• Surgery is reserved for those with ongoing bleeding despite OGD and Interventional Radiology.

Scoring system
• The Glasgow Blatchford scoring system can predict the need for intervention.
• If 0 patient can be safely discharged.
• Higher scores indicate higher risk of mortality.

Admission risk marker Score

Blood urea
6.5 - 8.0 2
8.0 - 10.0 3
10.0 - 25.0 4
>25 6
Hb (men)
12 - 13 1
10 - 12 3
<10 6
Hb (women)
10 - 12 1
<10 6
Systolic blood pressure
>110 0
100-109 1
90-99 2
<90 3
Pulse >100 1
Presentation with melaena 1
Presentation with syncope 2
Hepatic disease 2
Cardiac Failure 2

22
Dysphagia and Odynophagia
• Focused differential diagnosis

Intraluminal
• Foreign body
• Food bolus
• Oesophageal webs
Intramural
• Benign neoplasm
• Malignant neoplasm
• GORD
• Oesophagitis
• Dysmotility disorders
• Scleroderma
• Stricture
• Eosinophilic oesophagitis
• Neurological
• Hiatus Hernia
• Volvulus
Extraluminal
• Lymphadenopathy
• Goitre
• Pharyngeal pouch
• Haematoma

Further causes of Odynophagia:

• Oesophageal rupture
• Mallory-Weiss tear
• Oesophageal ulceration

23
Upper GI investigations

OGD Intraluminal visualisation via flexible endoscopy generally under sedation.

Can be used to take biopsies, localise tumours, assess hiatus hernias and
can be used for therapeutic interventions.

Contrast swallow Oral barium or gastrografin is used to assess the functional and
anatomical properties of the oesophagus under X-ray.

High Resolution Evaluates oesophageal motor function. Displayed and interpreted by

Manometry oesophageal pressure tomography. Investigates dysmotility.
pH studies and Measures acid reflux into the lower oesophagus over 24 hours.
impedance DeMeester score generated.

Endoscopic Combines endoscopy with ultrasound to obtain detailed images. Used for
Ultrasound (EUS) staging of oesophageal tumours and biopsies.
CT TAP Diagnostic and staging CT scan (thorax, abdomen, pelvis)

24
Benign Oesophageal Disorders

Hiatus Hernia and Para-Oesophageal Hernia

Definition
• Displacement of part or all of the stomach through the oesophageal hiatus

Epidemiology
• 10% of the population

Pathophysiology
• Widening of the diaphragmatic crura at the oesophageal hiatus and stretching the phrenoesophageal
membrane.

• Type 1: Sliding hiatus hernia

• Type 2-3: Para-oesophageal hernias (includes rolling hiatus hernia)
• Type 4: Intrathoracic herniation of abdominal viscera (e.g. colon, spleen) into hernia sac

Risk Factors Presentation and Clinical Features

Age >50 50% are clinically silent

BMI >25 Epigastric or chest pain Heartburn

Male gender Iron deficiency anaemia Post-prandial fullness

Familial Dysphagia Regurgitation

Pregnancy

Complications Investigations
GORD CXR
Anaemia Contrast swallow
Gastric outlet obstruction CT TAP
Gastric volvulus High Resolution Manometry for oesophageal dysmotility
Gastric ischemia (will guide choice of fundoplication)

25
 • Type 2 typically presents without reflux
• Emergency surgery required in 1.2% of patients with Type 2-4 paraoesophageal hernias
• Mortality rate in these patients is 5.4%

Treatment
• Conservative
o Weight loss, smoking cessation and alcohol reduction.
o PPI
o Motilium
• Surgical:
o If asymptomatic
§ Type 1 (Hiatus Hernia): conservative management
§ Type 2-3: Watchful waiting advised (treat if symptoms occur)
§ Type 4: Consider risks and benefits of surgical repair
o If symptomatic repair all type 2-4 hernias
§ Symptoms include
• GORD
• Gastric outlet obstruction
• Anaemia
• Concern for gastric strangulation (epigastric or chest pain)

• Most common approach is laparoscopic transabdominal repair.

o Remove the hernia sac
o Reduce the stomach
o Repair of the diaphragmatic hiatus.

• If emergency presentation of gastric volvulus attempt NGT (nasogastric tube) decompression, if unsuccessful
may need urgent surgical repair.

26
GORD – Gastro-Oesophageal Reflux Disease

Definition
• A condition that develops when the reflux of stomach contents causes troublesome symptoms and/or
complications.

Epidemiology
• The highest prevalence of typical reflux symptoms is in North America (19.8%) and Europe (15.2%)

Pathophysiology
• A combination of:
o Transient increase in abdominal pressure
• e.g. coughing and straining
o Loss of anti-reflux mechanisms:

Loss of mechanical barriers Physiological and cellular barriers

Lower Oesophageal Sphincter Rapid peristaltic acid clearance
Diaphragmatic sphincter Transient lower oesophageal sphincter
Cardio-oesophageal angle relaxations (TLORS)

Mucosal rosette Cellular buffering

History and Presentation

• Symptoms can be subjective and misleading
o Typical: Heartburn, regurgitation, abdominal pain
o Atypical: Bloating, intermittent dysphagia.
• Extra-oesophageal features:
o Cough, laryngitis, asthma, dental erosions

Risk Factors
Investigations
Obesity Diabetes Mellitus
Breath test for H. pylori
Smoking Hiatus Hernia
Upper GI Endoscopy
Alcohol Oesophageal dysmotility Contrast Swallow
Family history Gastric dysfunction Ambulatory pH and Impedance
monitoring
Pregnancy Medications
Oesophageal manometry

Clinical Features
• The physical exam rarely contributes to the diagnosis of GORD

Sequelae
Oesophagitis and ulceration
Schatzki ring
Barrett’s Oesophagus
Adenocarcinoma

27
Treatment

• Conservative management
o Lifestyle advice: alcohol reduction, smoking cessation and weight loss
o Review medications that can cause dyspepsia (e.g. NSAIDs)
o PPI (e.g. esomeprazole 40mg od for 8 weeks) step down as needed
o Add H2 antagonist if ineffective response
o Metoclopramide PO (prokinetic agent – to increase gastric emptying)
o If H. pylori treat with triple therapy (PPI, amoxicillin and clarithromycin for 14 days)

• Surgical
o Laparoscopic Nissen (360°) fundoplication reserved for cases of severe reflux
§ Suitable patients:
• Patients that have adequate acid control with PPI but do not wish to continue long
term medical therapy
• Patients that have adequate control with PPI but are not tolerant of acid
suppression therapy
• Complicated reflux disease
• Stricture formation
• Chronic cough, laryngitis and sinusitis

o Patients with uncontrolled and persistent symptoms of heartburn and regurgitation should be carefully
investigated for other causes before surgery is offered

o Post-procedural complications:
§ Gas-bloat syndrome (inability to burp or vomit), stricture, dysphagia, splenic injury,
oesophageal perforation, pneumothorax
§ Alternative surgery: Toupet - posterior partial fundoplication, often used for patients with
oesophageal dysmotility.

• Endoscopic therapies
o Partial endoluminal fundoplication procedures are available but have less successful outcomes when
compared with traditional surgical procedures (e.g. EsophyX).

28
Peptic Ulcer Disease

Definition
• Erosions in the gastric or duodenal mucosa that extend through the muscularis mucosae.

Epidemiology
• The incidence has been declining in the last few decades likely due to the identification and eradication of H.
pylori and a better understanding of the risks of long term NSAID use.

Pathophysiology
• Ulcer formation is a result of either aggressive factors, decreased defence or a combination of both
o Aggressive factors: H. pylori infection, NSAIDs, hydrochloric acid secretion, pepsins, ethanol
ingestion, smoking, bile reflux, ischemia, cocaine and hypoxia.
o Protective factors: Mucosal bicarbonate secretion, mucus production, blood flow, growth factors,
cell renewal and endogenous prostaglandins.

H. pylori
Helical gram negative rod with four to six flagella that reside in the gastric type epithelium beneath the mucous
layer. It produces urease which is capable of splitting urea into ammonia and bicarbonate creating a favourable
alkaline microenvironment.

Humans are the only known host. H. pylori can colonise the gastric body and antrum.

80-95% of duodenal ulcers and 75% of gastric ulcers are associated with H. pylori

How H. pylori causes ulcers:

- Production of toxic products
- Induction of local mucosal immune response (proinflammatory cytokines and reactive oxygen
metabolites)
- Increased gastrin levels
- Gastric metaplasia of duodenum

Most patients with gastric cancer have current

or past H. pylori infection.
Strong association with MALT
(mucosa-associated lymphoid tissue)

Marshall and Warren won the Nobel prize in Medicine in 2005 for their discovery.

History and Presentation

• Most commonly epigastric pain and nausea

Risk Factors
• See Pathophysiology

29
Clinical Features
• Comparing gastric to duodenal ulcers:

Gastric Ulcer Duodenal Ulcer

Epigastric pain on eating Relieved initially by food but pain returns 3-4
hours after eating

Reflux, chest discomfort and early satiety more Reflux, chest discomfort and early satiety less
common common

Vomiting common Vomiting less common

Haematemesis more common Melaena

Small percentage associated with cancer

Sequalae
Haemorrhage (hematemesis or melena)
Anaemia
Perforation
Gastric outlet obstruction (chronic scar)

Investigations
CXR: air under the diaphragm suggesting perforation

CT- Abdomen and pelvis if features of perforation

OGD + CLO (Campylobacter-like organism) test + ulcer biopsy
for malignancy

Urea breath test (to assess for eradication)

Serum gastrin (if multiple ulcers)

Treatment
• Medical
o H. pylori eradication: Triple therapy (e.g. PPI, amoxicillin and clarithromycin for 14 days then PPI
alone for 4 more weeks).
o Retest with Urease breath test. If positive, give second line Triple Therapy.
o Consider the addition of ranitidine for symptom control
o Avoid triggers of gastritis
o Consider sucralfate

• Surgical
o Perforation may require an omental patch repair (Figure)
o Haemorrhage may require duodenostomy + oversewing
of ulcer
o If cancer suspected may require distal gastrectomy (
see Gastric Cancer)

30
Barrett’s Oesophagus

Definition
• An oesophagus in which any portion of the normal distal squamous epithelial lining has been replaced by
metaplastic columnar epithelium. This should be clearly visible endoscopically (>1cm) and confirmed on
biopsies.

Epidemiology
• Prevalence 1.6% overall
• 2.3% of patients with reflux

Pathophysiology
• Columnar metaplasia of squamous epithelial cells with goblet cells

History and Presentation

• Symptoms of heartburn.
• However 40% of patients with Barrett’s have no symptoms.

Risk Factors
Smoking
Obesity
>50 years
Male
White

Clinical Features
• At endoscopy Barrett’s epithelium is often described as a velvet-like texture and has a pale pink colour.
• The Prague classification is used to standardise the extent of Barrett’s oesophagus (Figure). C is the proximal
(highest) circumferential margin, M is the proximal Barrett’s tongue, both are measured in cm (e.g. C3M5).

Complications
• Progression to oesophageal adenocarcinoma (0.33% of those with Intestinal metaplasia)
• Men with Barrett’s Oesophagus develop cancer at twice the rate of women.

Treatment
• Medical
o High dose PPI for symptom control
o The addition of aspirin may reduce progression to high grade dysplasia (HGD) and carcinoma

• Endoscopic
o Surveillance endoscopy to identify dysplasia early

• Surgical
o Role of oesophagectomy: T1b tumour or greater
o Anti-reflux surgery in patients with Barrett’s oesophagus does not reduce the risk of developing
adenocarcinoma.

31
 Indications for Barrett’s endoscopic SCREENING
Not currently for the general population

Must have Chronic GORD + 3 of:

>50years

Male

White

High BMI

or

First degree relative with Barrett’s or Oesophageal Adenocarcinoma

Surveillance
• Interval: if no dysplasia and Barrett’s segment length
o <3cm: 3-5 years
o >3cm: 2-3 years
• Low grade dysplasia (LGD)
o Surveillance at 6 monthly intervals until 2 consecutive non-dysplastic biopsies
• High grade dysplasia (HGD)
o MDT discussion and eradication (Endoscopic mucosal resection (EMR) or Radio Frequency Ablation
(RFA).
• Mucosal irregularity
o EMR
• Post eradication
o Continued surveillance

32
Oesophageal Motility Disorders

Achalasia

Definition
• Condition where the lower oesophageal sphincter fails to relax

Epidemiology
• It is the most common primary motility disorder of the oesophagus
• Incidence 2.5/100000

Pathophysiology
• The lower oesophageal sphincter (LOS) fails to relax in response to a peristaltic wave
• This is a result of progressive neuronal loss in the myenteric plexus.

History
• Patients experience progressive oesophageal dilation and wall thickening which leads to worsening
regurgitation.

Presentation Complications
Dysphagia (can be to both solids and liquids) Increased risk of oesophageal cancer
Regurgitation Aspiration
Chest pain Perforation during treatment (dilation or
Weight loss surgery)

Risk Factors
• Increasing age
• Possibly alcohol and smoking

Investigations
• OGD to exclude malignancy. Features of achalasia include subtle tightness of the lower oesophageal
sphincter, oesophageal dilation and often food or debris in the lower oesophagus.
• Barium swallow – “bird beak” appearance
• CT/EUS if malignancy is suspected
• High resolution manometry

Chicago Classification System

Type 1: Very few peristaltic waves, none >30mmHg – good response to treatment

Type 2: Waves >30mmHg throughout the oesophagus in >20% of swallows – good response to
treatment

Type 3: Spastic activity of oesophagus – poor response to treatment

Treatment
• Medical
o Calcium channel blockers and sildenafil – often limited results

• Endoscopic
o Botulinum toxin – response limited to 3-6 months
o Pneumatic dilation to disrupt the muscle at the LOS
33
 o Peroral Endoscopic Myotomy (POEM) – higher rates of reflux after this procedure due to lack of
fundoplication.

• Surgical
o Laparoscopic Heller Myotomy – anterior single incision through longitudinal and circular muscle
fibres to open the tight lower oesophageal sphincter.

34
Diffuse Oesophageal Spasm

History and Presentation

• Dysphagia and chest pain

Investigations
• Classical appearance of a cork screw oesophagus on contrast swallow
• Manometry will show premature contractions but the LOS relaxes appropriately
• pH studies to out rule GORD as an underlying trigger

Treatment
• Most patients can be reassured and managed symptomatically with dietary modifications
• Calcium channel blockers, sildenafil, nitrates or Botox injections may help

35
Oesophageal Cancer

• 6th most common cause of death from cancer in Ireland with 387 deaths per year.

Epithelial Type Carcinoma

• Types: Adenocarcinoma and Squamous cell carcinoma
• Arise from the mucosal layer and are detected as mucosal irregularities

Adenocarcinoma Squamous Cell Carcinoma

Definition Malignant epithelial tumour with Malignant squamous epithelium that
glandular differentiation that has penetrates the epithelial basement
infiltrated the lamina propria membrane

Epidemiology Incidence has doubled in the US and Highest incidence in Iran, China, South
Europe since the 1980s. and America and East Africa. 50-60 is the
continues to increase by 5% yearly. commonest age at presentation

Highest incidence: UK, Australia, Male:Female is 2:1

Netherlands and USA

Male:Female is 5:1

Pathophysiology Progression of columnar metaplasia - Progression of squamous epithelial

> dysplasia -> adenocarcinoma dysplasia -> carcinoma in situ -> invasive
carcinoma

Location Almost exclusively lower oesophagus Ratio of location in oesophagus:

and Oesophagogastric junction Upper (1) : Middle (5) : Lower (2)

Risk Factors Barrett’s oesophagus >3cm Tobacco smoking, Alcohol, Hot

GORD beverages, barbequed meats
Tobacco smoking Also: Achalasia, corrosive substance
Obesity ingestion, ionizing radiation, coeliac
disease.

History and Presentation

• Dysphagia is the most common presentation
• Unexplained weight loss
• Odynophagia
• Dyspepsia
• Persistent cough
• Vomiting
• Haemoptysis

Investigations for Diagnosis and TNM staging

Upper endoscopy (OGD)
CT – TAP
Endoscopic Ultrasound (EUS) +/- biopsy for assessment of tumour invasion
PET-CT
Staging laparoscopy (Identification of peritoneal disease in OG junction tumours)

36
Treatment
• Cancer treatment must take a multidisciplinary approach

MDT Member Indication for Referral

Oncology MDT discussion
Dietician referral
Physiotherapist
Medical social worker
Clinical nurse specialist
Speech and Language
Evidence-based management planning
Patients are often malnourished
Pre-operative inspiratory muscle training
Psychological and other supports
Support and coordination of management
Dysphagia following treatment

• Endoscopy
o Endoscopic resection of visible early oesophageal squamous cell neoplasm (including high grade
dysplasia)
o If extensive disease, palliative stenting of oesophagus

• Radiotherapy and Chemotherapy

o Preoperative (neoadjuvant) chemoradiotherapy is often indicated for resectable or potentially
resectable tumours (CROSS trial)
o Adjuvant chemotherapy is offered but often poorly tolerated
o “Definitive” radiotherapy with or without chemotherapy is often offered to patients unfit for surgery

• Surgery
o Surgery should only be attempted if a cure is thought to be possible
o Enhanced recovery after surgery protocol should be in place
o Minimally invasive surgery preferred

Transthoracic Oesophagectomy Transhiatal Oesophagectomy

Locally advanced tumours Very early tumours (HGD and T1a)

OGJ tumours that are more advanced but patients

are considered higher risk for surgery. e.g.
Respiratory comorbidities

• Surgery for early oesophagogastric junction (OGJ) cancer (Siewert classification)

o Type 1 (distal oesophagus): 5cm Oesophagectomy and Proximal Gastrectomy
o Type 2 (cardia): Transhiatal/transthoracic oesophagectomy or extended total gastrectomy
o Type 3 (proximal stomach): Transhiatal extended total gastrectomy

37
 Complications
Anastomotic leakage
Chylothorax
Recurrent laryngeal palsy
Diaphragmatic herniation
Gastric outlet obstruction
Duodeno-gastro-oesophageal reflux
Benign anastomotic stricture

• Common Procedures
o Ivor Lewis – Transthoracic oesophagectomy – Incisions in abdomen and thorax
o McKeown – Transthoracic oesophagectomy – Incisions in abdomen, thorax and neck
o Transhiatal – incisions in abdomen and neck (avoids thoracotomy)

• Palliative Care
o For incurable disease with a focus on symptom control
§ Stenting can allow ongoing food intake
§ Radiotherapy (e.g. bleeding tumours)
§ Chemotherapy

38
Benign Tumours of Oesophagus
• 1% of all symptomatic oesophageal lesions (usually dysphagia)
• Leiomyoma (>50% of all benign tumours)
• Inclusion cysts/developmental cysts
• Fibrovascular polyps (12%)
• Squamous cell papilloma

39
Gastric Cancer

Gastric Epithelial tumour

• Adenocarcinoma

Gastric Mesenchymal Tumours

• GIST
• Glomus tumour
• Inflammatory myofibroblastic tumours
• Leiomyoma
• Leiomyosarcoma
• Schwannoma
• Synovial sarcoma
• Kaposi sarcoma

GIST (Gastrointestinal Stromal Tumour)

• Can occur in any part of the stomach
• Most show spindle cell morphology
• c-KIT receptor expression
• All have the potential to become malignant
• Imatinib medial therapy in sensitive tumours
• Surgery to resect, with negative margins

Gastric Lymphomas

MALT Lymphoma
• >50 years of age
• Associated with H. pylori infection
• Eradication of H. pylori with antibiotics can induce remission
• Certain subtypes require chemotherapy, radiotherapy and H. pylori eradication
• Surgery if non-responsive to other therapies

40
Gastric Neuroendocrine Tumours

Gastric Neuroendocrine Tumours

• Almost all located in the body of the stomach
• Arise most commonly from enterochromaffin-like (ECL) cells

High Gastrin Levels

s
ECL Hyperplasia Dysplasia Tumour

Achlorhydria
•

• Type 1: Well differentiated. Predominantly affects middle aged females - Autoimmune

chronic atrophic gastritis and pernicious anaemia due to autoantibodies against parietal
cells. Most common. Respond to octreotide. Metastasis in 2-5%.

• Type 2: Tumours associated with Zollinger-Ellison syndrome in patients with MEN type 1.
Associated with loss of Tumour suppressor gene MEN1. Metastasis in <10%.

• Type 3: Sporadic tumours. Larger >2cm and more aggressive. No associated atrophic
gastritis, neuroendocrine hyperplasia or dysplasia. Metastasis in 52%.

Epithelial Tumours
• Gastric adenocarcinoma

Epidemiology
• Steady decline in gastric carcinoma at a rate of 5% per year since the 1950s. However it remains the 5th most
common carcinoma in the world.
• Male:Female 1.6:1
• 75% of all gastric carcinomas are diagnosed in Asia.

Pathophysiology
• The development of adenocarcinoma has a multi-step process:

Progression to Malignancy
1. Chronic pan-gastritis
2. Atrophic gastritis
3. Intestinal metaplasia
4. Malignant Transformation

• P53 gene mutation seen in 60% of gastric cancers

41
 History and Presentation Risk Factors
Weight loss H. pylori infection
Smoking
Early satiety
Dietary influence
Dysphagia
EBV infection
Nausea Poor socio-economic status
Anorexia Familial cancer syndromes
Abdominal pain • HDGC
• HNPCC
GI bleeding • FAP
Anaemia • Peutz-Jeghers syndrome

Investigations
• Patients usually referred for urgent OGD if they have any of the following symptoms:
1. Dysphagia
2. Age >55, weight loss and any of:
a. Upper abdominal pain
b. Reflux
c. Dyspepsia
3. Upper abdominal mass

• If a gastric tumour is diagnosed at OGD the following staging investigations are carried out:
o CT-TAP – to assess for metastatic disease and gastric wall involvement
o EUS – not routine but can clarify stage by targeting specific lymph nodes
o Staging laparoscopy + peritoneal cytology – assess for peritoneal disease

Treatment
• Endoscopy
o Small early gastric cancer can be removed by two methods:
§ EMR (endoscopic mucosal resection)
§ ESD (endoscopic submucosal dissection)
o Complications include perforation, bleeding and recurrence

Signs of Advanced Disease

Virchow’s node (metastatic lymph node in left supraclavicular fossa)
Sister Mary Joseph’s nodule (periumbilical lymph node)
Intra-abdominal mass

• Surgical
o Larger lesions not amenable to endoscopic resection can be removed surgically.
o Choice depends on tumour location
§ Antrum: Distal subtotal gastrectomy
§ Body: Total gastrectomy
§ Proximal: Total gastrectomy
o Total gastrectomy – minimally invasive approach is preferred

42
 Complications of Gastrectomy
Anastomotic leak
Duodenal stump leak
Pancreatic fistula
Haemorrhage
Post-splenectomy infection
Dumping syndrome
Nutritional deficits (B12 and Iron deficiency)

• Medical
o If the tumour invades through the muscularis propria or involves lymph nodes Chemotherapy can be
administered as
§ Neoadjuvant alone (preoperative)
§ Neoadjuvant and adjuvant treatment (perioperative)
o Radiotherapy is usually not administered for gastric cancers.

43
Consent for Oesophagogastroduodenoscopy (OGD)

Describe the procedure to the patient (avoid jargon)

• They will be taken into a darkened room
• There will be two nurses and an endoscopist present
• After sign in and safety checklist they will be asked to lie on their left side
• Vital signs will be monitored throughout the procedure
• Local anaesthetic throat spray will be given (if applicable)
• A mouthguard will be placed in their mouth to protect their teeth and the scope
• Sedation will be given at this point (if applicable)
• The scope will be placed into the mouth and down the food pipe
• The oesophagus, stomach and first part of the small bowel will be examined
• Biopsies are routine
• Pictures will be taken
• The procedure usually takes around 5-10 minutes
• Reassure that its normal to have air escape throughout (burping)
• When finished they will be brought to the post-procedural area for monitoring

Patient preparation
• They must not eat or drink for 6 hours prior to the procedure
• They should not take their anticoagulants prior to the procedure (some exceptions)
• They can eat and drink once sedation has worn off

Discuss IV sedation
• The most common sedation is Midazolam which is a “conscious sedation” they will be able to respond during
the procedure but will be drowsy and may not remember portions of the test.
• The usual dose is 3mg for adults <65 years old, 1-2mg in the elderly.
• Fentanyl 50mcg is often given in conjunction.
• They will not be able to drive, operate machinery, sign legal documents or drink alcohol for 24 hours
following the procedure

Explain risks
• Bleeding – especially after biopsies
• Perforation – trauma to any part of the oesophagus, stomach or duodenum
• Sedation risks
• Damage to teeth
• Aspiration
• Missed lesions
• Need for repeat procedure or further investigations/procedures

Explain benefits
• This will relate to the patients presentation and indications for OGD.

44
Bariatric Surgery

Obesity is defined as body mass index (BMI) of ³ 30 kg/m2

It is a chronic disease which affects children, adolescents and adults.

The WHO estimates that there are approximately 650 million adults and 38 million children under the age of five
living with obesity worldwide.

Surgical procedures performed for obesity are collectively known as bariatric surgery (from Greek words “Baros”
(weight) and iatrikos (medicine))

Obesity is associated with several complications including heart disease, stroke, type 2 diabetes mellitus,
osteoarthritis, cancers, depression, liver disease and obstructive sleep apnoea.

Increased adiposity increases the risk of developing these conditions, however, weight loss will reduce the risk of
developing these conditions, or improve any pre-existing obesity complications such as hypertension or diabetes
mellitus.

Bariatric surgery is being increasingly performed worldwide. Those who undergo bariatric surgery have lower long-
term mortality rates when compared to matched controls who did not undergo bariatric surgery.

Bariatric surgery procedures aim to induce weight loss via two mechanisms – malabsorption, restriction, or a
combination of both.

• Malabsorption
o Decreases absorption of nutrients by shortening the absorptive length of the small intestine, either
by bypassing the small bowel absorptive surface area or diverting biliopancreatic secretions that
facilitate absorption
§ E.g. jejunoileal bypass; biliopancreatic diversion
• Restriction
o Limit caloric intake by reducing the capacity of the stomach via resection, creation of a proximal
gastric outlet or bypass
§ E.g. laparoscopic adjustable gastric banding, sleeve gastrectomy
• Combination of Restrictive and Malabsorptive
o Roux-en-Y Gastric Bypass – small gastric pouch limits oral intake while reconfiguration of the small
bowel results in mild malabsorption, beneficial gut hormonal change and dumping physiology.

Indications
• BMI ³ 40 kg/m2 without comorbid illness
• BMI of 35 – 39.9 kg/m2 with an obesity-related comorbidity e.g. diabetes, hypertension, gastroesophageal
reflux disease, osteoarthritis, obstructive sleep apnoea, hyperlipidaemia, non-alcoholic fatty liver disease
(NAFLD), non-alcoholic steatohepatitis (NASH), asthma
• Must have attempted and failed previous weight loss measures
• Must understand risks of operation
• Must agree to lifelong follow-up

Contraindications
• Inability to comply with nutritional requirements post-operatively
• Patients with active eating disorders
• Severe coagulopathy
• Major depression or psychosis
• Current drug or alcohol abuse
• Severe cardiac disease with prohibitive anaesthetic risks

45
Preoperative Assessment
Prior to surgery consultation with a multidisciplinary bariatric team is necessary.
• Education on nutrition
• Psychological input
• Lifestyle modification
• Medical assessment
• Anaesthetic assessment

Procedures
• Multiple bariatric surgery procedures exist, however, some are now redundant or infrequently performed.
• The American Society of Metabolic and Bariatric Surgery lists procedures which it endorses on its website.
o Roux-en-Y Gastric Bypass
o Sleeve Gastrectomy
o Gastric Banding
o Biliopancreatic Diversion with Duodenal Switch

46
Roux-en-Y Gastric Bypass (RYGB)
• Gold standard
• A small proximal pouch (30ml in volume) is created separating the proximal stomach from the distal stomach
• The small intestine is divided 50-150cm distal to the ligament of Treitz in order to create the Roux limb and
the biliopancreatic limb.
• The biliopancreatic limb is attached to the small intestine and serves to transport secretions from the
remnant stomach, pancreas and liver.
• The small proximal pouch is then attached to the Roux limb which is 75-150cm in length.
• Both restrictive and malabsorptive components contribute to weight loss
o The new pouch is only able to hold a small amount of food ~1 ounce resulting in feeling full after
consuming only a very small amount.
o The anatomy of the gastrojejunostomy (connection between stomach and jejunum) is associated
with dumping physiology leading to nausea, diaphoresis, light-headedness, abdominal pain and
diarrhoea when a high-sugar meal is ingested. This may result in negative conditioning against
consumption of a high-sugar diet post-operatively.
o Increasing the Roux limb length can result in increased malabsorption. A longer Roux limb results in
a shorter common channel limb where major absorption and digestion of nutrients occurs. The Roux
limb is rarely ever created to be longer than 150cm.
o Ghrelin is secreted in the foregut (stomach and duodenum). It is a peptide hormone that stimulates
appetite. In gastric bypass patients the secretion of Ghrelin is inhibited due to the foregut bypass.
o Glucagon-like peptide-1 (GLP-1) and cholecystokinin (CCK) are increased following RYGB and may
promote an anorectic state.
• It is expected that the patient will lose approximately 25-30% of their preop total body weight after two
years.

47
Sleeve Gastrectomy
• Partial gastrectomy – a tubular stomach is created following removal of the majority of the great curvature
of the stomach.
• Technically easier operation in comparison to RYGB as does not require the formation of multiple
anastomoses
• The tubular stomach which is formed has smaller capacity resulting in restriction and early satiety
• The tubular stomach also has a reduced number of remaining ghrelin-producing cells so hunger levels are
decreased.
• Sleeve gastrectomy makes the resulting stomach a higher-pressure organ with a sphincter at both ends
(lower oesophageal sphincter and pylorus). This can contribute to gastroesophageal reflux in up to 20% of
patients and could be a contributing factor to staple line leaks (1% of cases).
• Hormonal changes are also noted post sleeve gastrectomy – GLP-1 and PYY levels increase and ghrelin levels
decrease resulting in decreased appetite.
• Insulin resistance improves post sleeve gastrectomy which aids glycaemic control.
• The patient is expected to have lost approximately 25% of their preoperative total body weight by two years
post-op.

48
Gastric Band
• An inflatable band is placed around the upper portion of the stomach.
• This band can be adjusted to create a smaller opening between the proximal and distal stomach
• Results in restriction, by compartmentalising the upper stomach, creating a smaller capacity, leading to
reduced food intake.
• The gastric band is a soft silicone ring which is connected by tubing to an infusion port which is placed in
subcutaneous tissue.
• Saline is injected into the port resulting in reduction in the diameter of the band and increased restriction.
• The goal of adjusting the band is to restrict the patient to approximately one cup of dried food, and result in
satiety for at least two hours following a meal.
• This procedure is now rarely performed due to rather poor long term efficacy and complications such as
gastric band slip and erosion.
• Expected weight loss is approximately 15-20% at two years (total body weight loss).

49
Biliopancreatic Diversion with Duodenal Switch (BPD/DS)
• A sleeve gastrectomy is created, along with a Roux limb with a short common channel (50-100cm).
• BPD/DS achieves weight loss through a combination of restrictive and malabsorptive mechanisms.
• Ghrelin production post BPD/DS is reduced.
• Expected total body weight loss two years post-op is approximately 35-40%.

50
Outcomes of Bariatric Surgery
• Weight loss
o Bariatric surgery results in greater long-term weight loss than the best available nonsurgical
interventions for obesity – Swedish Obese Subjects (SOS) study.
• Metabolic Effects
o Metabolic Syndrome
§ Metabolic syndrome is the occurrence of metabolic risk factors for both cardiovascular
disease (hypertension, abdominal obesity, hyperglycaemia, dyslipidaemia) and type 2
diabetes mellitus.
§ Bariatric surgery results in the improvement of metabolic syndrome leading to reduced risk
of cardiovascular disease and improved glycaemic control.
o Diabetes Mellitus
§ Obesity and type 2 diabetes mellitus often coexist
§ Bariatric surgery is the most effective treatment for patients with obesity and diabetes who
don’t achieve adequate glycaemic control with lifestyle management and best medical
therapy.
§ Improved glycaemic control is seen within days to weeks postoperatively.
§ The improved glycaemic control in turn leads to reduced incidence of both macro and
microvascular complications associated with diabetes.
o Hypertension
§ 64% of those wishing to have bariatric surgery have hypertension.
§ It has been found that weight loss improves hypertension and in some cases induces
remission of hypertension
o Dyslipidaemia
§ 64% of those wishing to have bariatric surgery have dyslipidaemia.
§ Improved lipid profiles are seen post bariatric surgery
o Cardiovascular Risk
§ As bariatric surgery results in resolved or improved cardiovascular risk factors (hypertension,
dyslipidaemia, diabetes mellitus), it is associated with a lower incidence of cardiovascular
events and reducing the number of cardiovascular deaths in obese adults.
• Cancer Risk
o Multiple studies have found that there is a reduction in cancer risk post bariatric surgery (approx.
40% reduction in risk).
• Long-Term Survival
o Overall all-cause mortality is reduced after bariatric surgery when compared with non-surgical
management of obesity.
• Functional Outcomes
o Improved quality of life.
o Reduction of apnoea hypopnea index in those with obstructive sleep apnoea – improvement or
resolution.
o Improvement or resolution of gastroesophageal reflux disease
o Improved joint pain and physical function
o Improved renal function
o Improved grade of steatosis, fibrosis and hepatic inflammation in patients with NAFLD
• Psychosocial Impact
o Psychopathologic disorders e.g. depression generally improve post operatively
• Health Care Financial Impact
o Long term cost savings due to improved health

51
Complications
• Early
o Anastomotic or staple line leak
o Anastomotic stenosis
o Bleeding
o VTE
• Late
o Ulceration
o Perforation
o Small bowel obstruction
o Gastric band slippage/erosion
o Dumping syndrome
o Gallstones
o Hernia
o Malnutrition/Vitamin deficiency (Iron, Vitamin D, Vitamin B12)

52
Additional Reading

Textbooks

• Townsend, C., Beauchamp, D., Evers, M. & Mattox, K. Sabiston Textbook of Surgery. (Elsevier, 2016).
• Paterson-Brown, S. & Paterson, H. Core Topics in General and Emergency Surgery. (Elsevier Health Sciences,
2018).
• Griffin, M. & Lamb, P. Oesophagogastric Surgery. (Elsevier Health Sciences, 2018).

Guidelines

• Fitzgerald, R. C. et al. British Society of Gastroenterology guidelines on the diagnosis and management of
Barrett’s oesophagus. Gut 63, 7–42 (2014)
• Náisiúnta, O. & Othar, S. National Patient Safety Office Diagnosis, staging and treatment of patients with
oesophageal or oesophagogastric junction cancer. https://health.gov.ie/national-patient-safety-
office/ncec/national-clinical- (2019).

Articles

• Roberts, I. et al. Effects of a high-dose 24-h infusion of tranexamic acid on death and thromboembolic events
in patients with acute gastrointestinal bleeding (HALT-IT): an international randomised, double-blind,
placebo-controlled trial. Lancet 395, 1927–1936 (2020).
• Vakil, N. et al. Ovid: The Montreal Definition and Classification of Gastroesophageal Reflux Disease: A Global
Evidence-Based Consensus. American Journal of Gastroenterology 1900–1920

53
3. Hepatobiliary Surgery

• Mr. Kin Cheung Ng

• Jaundice
• Gallstones
• Acute Pancreatitis
• Chronic Pancreatitis
• Pancreatic Cancer

54
Jaundice

• Definition
o Elevation of the serum bilirubin >15 µmol/L as a result of imbalance between production and
clearance of bilirubin. It is clinically detectable when bilirubin is >35 µmol/L.

• Physiology
o Approximately 80% of bilirubin is produced by the degradation of senescent erythrocytes by the
reticuloendothelial system in the liver, spleen and bone marrow to biliverdin, which is in turn
converted to unconjugated form of bilirubin. The unconjugated bilirubin is water insoluble. It is
bound to albumin before uptake and further processing in the liver to soluble conjugated form by
the enzyme bilirubin uridine-5’-diphospate glycosyltransferase. Conjugated bilirubin is excreted into
the bile canaliculus through hepatocyte membrane transporter together with bile salts,
phospholipids and cholesterol to form bile.

• Types of Hyperbilirubinaemia
o Unconjugated (indirect) hyperbilirubinaemia – due to the overproduction of bilirubin, impaired
uptake by the liver, or abnormalities of bilirubin conjugation
o Conjugated (direct) hyperbilirubinaemia – due to hepatocellular diseases, impaired canalicular
excretion, defective reuptake of conjugated bilirubin and biliary obstruction

• Classification of Jaundice
o Pre-hepatic
§ Increase bilirubin production (unconjugated hyperbilirubinaemia)
• Haemolysis
• Ineffective erythropoiesis
• Resorption of haematoma

o Hepatic
§ Impaired liver uptake (unconjugated hyperbilirubinaemia)
§ Heart failure
§ Portosystemic shunt
§ Impaired conjugation (unconjugated hyperbilirubinaemia)
• Crigler-Najjar syndrome Type I and Type II (gene mutation of bilirubin-uridine-5’-
diphosphate glucuronosyltransferase gene (UGT1A1) resulting in loss or very low
activity of the gene)
• Gilbert syndrome (defect in the promoter of UGT1A1 resulting in reduced expression
of the normal protein)
§ Impaired hepatocyte transport and storage (conjugated hyperbilirubinaemia)
• Dubin-Johnson syndrome (mutation of membrane transporter resulting in reduced
or absent transport activity)
• Rotor syndrome (defect of sinusoidal reuptake of conjugated bilirubin)
• End-stage liver disease

o Post-hepatic
§ Biliary obstruction
• Choledocholithiasis
• Mirizzi syndrome
• Tumour (cholangiocarcinoma, pancreatic cancer)
• Primary sclerosing cholangitis
• Acute and chronic pancreatitis

55
 § Intrahepatic cholestasis
§ Viral hepatitis
§ Alcoholic hepatitis
§ Nonalcoholic steatohepatitis
§ Primary biliary cholangitis
§ Total parenteral nutrition
§ Sepsis
§ Pregnancy
§ Drugs - co-amoxiclav, phenytoin and isoniazid

• Evaluation of Jaundice
o History
§ Jaundice accompanied by pain is frequently caused by gallstone disease, whereas painless
jaundice can result from malignancy especially when associated with weight loss
§ Any associated itch, dark urine, pale stool, fever
§ Nausea and vomiting may be non-specific or an indication of gastric outlet obstruction
secondary to a mass in the pancreatico-duodenal region Steatorrhoea (the passage of foul-
smelling floating stool) is a feature of pancreatic exocrine insufficiency
§ Hematemesis and/or melaena may suggest variceal bleeding secondary to chronic liver
disease
§ The history should include the following:
• Other medical background including known gallstone disease, pancreatitis,
inflammatory bowel disease
• History of blood transfusion, intravenous drug use and sexual history
• Medications including herbal and recreational
• Family history of liver disease
• Foreign travel
• Alcohol intake
• Social circumstances

o Examination
§ Examination begins with general inspection looking for yellow discoloration of skin, and eyes
(scleral icterus)
§ Moving on to the hands, looking for finger clubbing, palmar erythema, koilonychias and
asterixis for features of chronic liver disease
§ Inspection of the chest to look for gynecomastia
§ Abdominal inspection should pay attention to scars from previous abdominal surgery,
abdominal distension, and presence of spider nevi which may indicate chronic liver disease.
Visible veins radiating from the umbilicus (caput medusa) suggests portal venous
obstruction.
§ This is followed by palpation of abdomen to check for area of tenderness and masses.
Murphy’s sign can be tested by asking the patient to inspire deeply while palpating the right
upper quadrant. A positive test is signified by arrest of inspiration in the presence of
localized tenderness at the right upper quadrant.
§ Courvoisier sign/law states that in a patient with painless jaundice and an enlarged or
palpable gallbladder, the cause is unlikely to be gallstones. The presumed cause is an
obstructing pancreatic or biliary neoplasm until proven otherwise.
§ The liver is examined by palpation and percussion to delineate its border and size.
§ Abdominal ascites can be elicited by a fluid thrill and shifting dullness.
§ Ankle swelling may indicate hypoalbuminaemia, which can occur in many chronic
hepatobiliary disorders.

56
o Laboratory Tests
§ Full blood count (FBC) – to check for the presence and the type of anaemia, leukocytosis,
neutrophilia, thrombocytopenia secondary to portal hypertension
§ Renal profile – to assess the degree of renal impairment and derangement of electrolytes
which can occurs in patient with cirrhosis, volume depletion, sepsis and chronic kidney
disease
§ Liver Function Tests
• Bilirubin – total bilirubin is typically measured in most laboratories unless stated
otherwise. The level of total serum bilirubin is seldom of value in determining the
cause of jaundice. It is usually elevated in biliary obstruction. It can be elevated as a
result of hepatocellular disease such as viral hepatitis, drug-induced and alcoholic
hepatitis as well as end-stage cirrhosis from any cause
• Alkaline phosphatase (ALP) – is produced predominately in liver and bones. The
elevation of ALP in conjunction with the elevation of gamma-glutamyl
transpeptidase (GGT) indicate cholestasis from a hepatic source rather than from
bony origin
• GGT – is abundant in hepatocytes and is also present in the kidney, prostate and
pancreas but not in bone. GGT is elevated as a result of excess alcohol intake, drugs
such as phenytoin and barbiturates. It is useful to measure in children when ALP is
not a reliable indicator due to bone growth
• Aspartate transaminase (AST) and alanine transaminase (ALT) – are released into the
blood from damaged hepatocytes. AST is present in the liver and many other
organs, whereas ALT is present primarily in the liver, therefore ALT is a more specific
marker of hepatocellular injury. AST and ALT are highly elevated (>25 times) in
acute hepatitis. Elevation less than eight times the normal limit is non-specific.
AST/ALT ratio of 2:1 or greater, particularly in the setting of an elevated GGT, is
suggestive of alcoholic liver disease.
• Albumin –a measure of synthetic function of the liver. It is reduced in the setting of
sepsis, systemic inflammatory disorders, nephrotic syndrome, malnutrition,
postoperative period
§ Amylase –elevated in patients with acute pancreatitis. Amylase level decreases rapidly and
can become normal 2 or 3 days after the onset of symptoms.
§ Coagulation profile – a prothrombin time (PT) and INR may reflect a reduction in the
synthesis of clotting factors in the setting of acute or chronic liver dysfunction, or vitamin K
deficiency as seen in fat malabsorption and chronic cholestasis
§ Other tests
• Hepatitis screen – Hepatitis A Ig antibodies, Hepatitis B surface antigen (HBsAg),
Hepatitis C antibodies
• Liver autoantibody panel
• Anti-mitochondrial antibodies (AMA) –found in 95% of patient with primary biliary
cholangitis (PBC)
• Antinuclear antibodies (ANA) –found in up to 70% of patients with PBC and are the
most common circulating autoantibodies in autoimmune hepatitis
• Perinuclear anti-neutrophil cytoplasmic antibodies (p-ANCA) –found in up to 80% of
patients with primary sclerosing cholangitis (PSC)
• Anti-smooth muscle antibodies – associated with autoimmune hepatitis
• Anti-liver-kidney microsomal antibodies - associated with autoimmune hepatitis
§ Tumour markers
• CA 19-9 – tumour marker for pancreatic cancer and cholangiocarcinoma. It can be
elevated in benign HPB disorders such as obstructive jaundice. It is useful for
following the effect of treatment, to detect disease recurrence and for

57
 cholangiocarcinoma surveillance in PSC. Highly elevated level is associated with
advanced disease
• CEA – marker for colorectal liver metastases and cholangiocarcinoma
• Alpha-fetoprotein (AFP) – marker for hepatocellular carcinoma

o Imaging
§ Ultrasound –first line investigation in patients with jaundice. It is used to evaluate liver
echotexture and parenchymal echogenicity to look for the presence of steatosis, the
presence of benign or malignant liver masses, the presence of gallstones, features of
cholecystitis, intrahepatic or extrahepatic biliary duct dilatation, stone in common bile duct,
pancreatitis, pancreatic mass, and associated feature of cirrhosis such as ascites, and
splenomegaly
§ Endoscopic ultrasound (EUS) – involves use of an ultrasound probe inserted endoscopically
into the duodenum. It allows characterization of pancreatic and periampullary tumour,
nodal staging, identification of vascular involvement, and to perform fine needle aspirate to
confirm diagnosis
§ Computed tomography (CT) – provides quick and detailed, cross-sectional views of liver and
pancreas. It is useful in detecting benign and malignant liver and pancreatic lesions with the
use of intravenous contrast agent. By acquiring images at different times (phases), it can
show differential enhancement of the lesion relative to the background parenchyma. For
example, the majority of primary liver tumours such as hepatocellular carcinoma (HCC),
receive blood supply from the hepatic arterial system. On a 4-phase CT (unenhanced,
arterial, portal-venous, delayed phases) HCC will show hyperenhancement in arterial phase
and subsequently become hypoattenuating in later phases. CT also allows detection of
lymphadenopathy and metastatic disease. A pancreatic protocol CT, which includes a late
arterial phase acquisition, is best to evaluate a pancreatic lesion. CT can demonstrate liver
cirrhosis by demonstrating nodular liver contour and can show signs of portal hypertension
such as the presence of ascites, splenomegaly and varices. It can detect biliary obstruction
by demonstrating biliary dilatation, but it is inferior to ultrasound for the detection of
gallstones.
§ Magnetic resonance imaging (MRI) – uses magnetic fields and radiofrequency pulses to
generate images with good tissue contrast. It is useful in evaluating focal liver abnormalities
by using different imaging sequences (T1, T2, DWI). Magnetic resonance
cholangiopancreatography (MRCP) uses heavily T2 weighted images to provide an overview
of biliary and pancreatic ductal anatomy. Choledocholithiasis appears as low signal filling
defect within the bile duct on MRCP.

• Intervention
o Endoscopic retrograde cholangiopancreatography (ERCP) – is now considered a therapeutic
intervention rather than a diagnostic technique for a patient with jaundice. Diagnosis is largely by
non-invasive imaging; US and MRCP.
§ Using a side viewing duodenoscope, the bile duct is cannulated, and cholangiogram is
performed to evaluate for biliary obstruction.
§ Endoscopic sphincterotomy and stone extraction can be performed using a variety of
techniques.
§ A plastic or metallic stent can be inserted in the setting of irretrievable stone(s), a benign or
malignant stricture.
o Percutaneous transhepatic cholangiography (PTC) – involves percutaneous puncture of a peripheral
bile duct within the liver to obtain a cholangiogram.
§ Biliary drainage or stent placement can be performed to relieve obstructive jaundice in cases
of high bile duct obstruction at or above cystic duct insertion, or in a situation where ERCP
fails.
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 Gallstones (Cholelithiasis)

• Gallstones are common, affecting 10% to 15% of the adult population.

Liver

Common Bile Duct

Pancreas

Gallbladder

Ampulla of Vater
Duodenum

• Pathogenesis
o Bile is composed of bilirubin, cholesterol, fatty acid and other minerals.
o Stones form when any of the major components of bile get supersaturated.
o Cholesterol supersaturation can result from excessive hepatic secretion of cholesterol or decreased
hepatic secretion of bile salts for cholesterol absorption.
o Gallbladder hypokinesia causing prolonged bile stasis is also associated with gallstone formation.
o An increase in bilirubin load can lead to the development of black and brown gallstones.

• Risk Factors
o Cholesterol stones account for more than 85% of gallstones in the Western population whereas
brown-pigmented stones accounts for 10%.
o Pigmented stones are more prevalent in Asia, as a result of more common haemolytic anaemia,
biliary parasites and Escherichia coli infection.

o Age – The incidence of gallstones increases with age, Risk factors for Cholelithiasis (‘5 Fs’)
becoming 4 to 10 times more likely in individuals older Female
than 40 years Fair (Caucasian)
o Gender – females > males (Ratio 2:1). It can be partly Fat (high cholesterol excretion,
explained by the effect of oestrogen in decreasing bile individuals with obesity)
salts secretion. Oral contraceptives increase the risk of Fertile (gallbladder stasis in
pregnancy)
gallstone formation.
Forties-Fifties
o Pregnancy – is associated with up to 30% risk of
developing biliary sludge/stones
o Obesity – the incidence of gallstone was found to be 25% in patients with severe obesity. Patients
who undergo weight reduction treatments (e.g. bariatric surgery) are also at higher risk of
developing gallstones.

59
 o Genetics – Family members of an affected person are three times more likely to have gallstones.
Monozygotic twins also show a significant higher concordance rate of gallstones than dizygotic
twins.
o Other risk factors – patients who have inflammatory bowel disease, ileal resection and cystic fibrosis
can have problems with bile salt absorption leading to gallstone formation

• Presentation
o Asymptomatic – Gallstones do not cause any symptoms in up to 80% of the individuals.
o Biliary colic –pain characterized by severe right upper quadrant or epigastric pain radiating to the
back or right shoulder blade. The pain is associated with nausea, vomiting, anorexia and may be
triggered by food rich in fat. The pain is often nocturnal. It is self-limiting and does not typically last
more than few hours. The term ‘biliary colic’ is a misnomer because the pain is typically constant
and not colicky in nature.
o Acute cholecystitis – cholecystitis is suspected when right upper quadrant pain persists for more
than a few hours. A positive Murphy’s sign can usually be elicited. It is often accompanied by a rise
in inflammatory markers (WCC and CRP). LFTs can sometimes be deranged due to localized
inflammations of adjacent liver parenchyma or due to compression of common bile duct from the
inflamed/distended gallbladder.

• Differential Diagnosis
o Gastritis
o Peptic ulcer disease
o Pancreatitis
o Pneumonia
o Irritable bowel syndrome

• Laboratory Studies
o Laboratory studies includes FBC, U&E, LFTs, Amylase, CRP and coagulation studies.
o A more extensive panel of bloods may be indicated if there is doubt about the diagnosis of gallstones
and LFTs are deranged e.g. hepatitis screen, HIV screen, anti-mitochondrial antibody, anti-smooth
muscle antibody, antinuclear antibody, serum immunoglobulins.

• Imaging
o Ultrasound abdomen: the initial investigation of choice. Gallstones appear as echogenic foci with
acoustic shadows, gallbladder wall thickening (³3mm), pericholecystic fluid, and positive
sonographic Murphy sign. Patients fast before an US scan so the gallbladder is distended for best
evaluation.
o CT abdomen: useful in diagnosing cholecystitis by demonstrating gallbladder wall thickening,
gallbladder distension, pericholecystic fluid and inflammatory fat stranding. CT is performed when
the diagnosis is unclear or not confirmed on US, or when complications arising from cholecystitis are
suspected.
o MRCP: performed on patients who present with jaundice, or when common bile duct is dilated on
ultrasound, or when there is an obstructive pattern to LFTs.
o EUS: sensitive for the detection of small stones/microlithiasis in the gallbladder and common bile
duct, when transabdominal ultrasound fails to detect them.

• Management
o Conservative
§ Asymptomatic patients with gallstones do not require treatment.
§ Patients with biliary colic, but no evidence of acute cholecystitis, require analgesia and
referral to a Surgeon to discuss cholecystectomy.

60
 § Acute cholecystitis is initially treated with broad spectrum antibiotics (e.g. co-amoxiclav) and
analgesia. Most patients with acute cholecystitis respond to this conservative treatment and
cholecystectomy can be safely performed from 6 weeks after initial presentation, once the
acute inflammation has reduced. However, 20% of patients undergoing delayed surgery will
get recurrent cholecystitis in the interval period.
o Surgery
§ Cholecystectomy is the definitive treatment for symptomatic gallstone disease and is
routinely performed laparoscopically.
§ Elective cholecystectomy is routinely carried out as a day case procedure.
§ For acute cholecystitis, early cholecystectomy (within 72 hours of symptom onset) can be
considered.
§ Evidence suggests that early cholecystectomy is safe and reduces total length of hospital
stay. If symptoms of acute cholecystitis have been present for >72 hours, then the operation
should be delayed for at least 6 weeks.
§ Cholecystectomy procedure
• The laparoscopic technique involves insufflation of the abdominal cavity with carbon
dioxide.
• The camera is introduced through an umbilical port and three additional 5mm ports
are inserted in the right upper quadrant and epigastrium.
• The gallbladder is grasped at the fundus and pushed cephalad to expose the porta
hepatis.
• Dissection of the peritoneum at the hepatocystic triangle exposes the cystic duct
and artery (the hepatocystic triangle is bounded by the cystic duct, the common
hepatic duct, and inferior edge of the liver). It is now commonly referred to as
Calot’s triangle. On the original description by Calot in 1891, the triangle is marked
by the cystic duct, cystic artery and common hepatic duct).
• The critical view of safety is obtained when cystic duct and artery are seen as the
only two tubular structures entering the gallbladder, clear of surrounding fat and
fibrous tissue.
• The two structures are clipped and divided.
• The gallbladder is dissected free from the undersurface of the liver and is removed
from the abdomen in a specimen bag.
§ Complications
• Bleeding - from gallbladder fossa, slipped cystic artery clip, arterial injury, or from
trocar site
• Bile duct injury (0.2-0.3%, can be an occlusive injury by clipping and transecting the
bile duct, or open injury causing leakage of bile into the abdomen)
• Bowel or other visceral injury (0.1-0.4%)
• Bile leak secondary to leakage from cystic duct stump, damage to the liver, injury to
the common bile duct, common hepatic duct, or exposed accessory bile duct (Duct
of Luschka)
• Retained common bile duct stone
• The rate of conversion to open cholecystectomy has been reported to be around 5%
for elective cases. In the acute setting, the conversion rate is higher (20%-30%).
Reasons for conversion include intraoperative complications, unclear anatomy,
dense adhesions, failure to progress laparoscopically, and other pathology
encountered such as choledocholithiasis which is not amenable to laparoscopic
common bile duct exploration.
o Percutaneous cholecystostomy
§ For patients with high perioperative risk who do not respond sufficiently to antibiotics,
percutaneous cholecystostomy tube placement is indicated.

61
 § It decompresses the gallbladder thus reliving pain associated with gallbladder distension.

• Complications of Gallbladder Disease

o Gangrenous cholecystitis and gallbladder perforation
§ Gangrenous cholecystitis occurs more commonly in diabetic patients.
§ Distention of the gallbladder and venous congestion compromises the blood supply to the
gallbladder.
§ Necrosis of the gallbladder wall develops which may lead to perforation.
§ The fundus is usually affected as it is the furthest from the blood supply.
§ Free perforation presents with generalized biliary peritonitis.
§ Percutaneous drainage of bilious collection should be performed urgently.
§ Localized or contained perforation of the gallbladder may lead to the formation of
pericholecystic liver abscess. It is treated by percutaneous drainage.

o Empyema of gallbladder
§ The gallbladder is filled with purulent bile as a result of progression of acute cholecystitis on
the background of an obstructed cystic duct and bile stasis leading to superinfection of bile.
§ The organisms commonly involved are Escherichia coli, Klebsiella, Streptococcus faecalis, and
anaerobes.
§ Patients typically present similar to acute cholecystitis.
§ As disease worsens, systemic signs of infection or sepsis follow.
§ Ultrasound and CT show usual features of cholecystitis.
§ Ultrasound may show added echogenic content within the gallbladder and CT may show
added high-attenuating material within the gallbladder but both features are non-specific
and may be difficult to differentiate from sludge in the gallbladder.
§ Treatment includes antibiotics and drainage of gallbladder with a percutaneous catheter or
urgent cholecystectomy.
o Emphysematous cholecystitis
§ Rare, insidious, and rapidly progressive form of cholecystitis caused by superinfection of
necrotic gallbladder wall by gas-forming bacteria like Clostridium, E. coli and Klebsiella
species.
§ It is more common in elderly males with diabetes.
§ Patient with emphysematous cholecystitis carry a high risk of gallbladder perforation.
§ It can progress rapidly to septic shock.
§ Mortality is high and it is considered a surgical emergency in unstable patients.
§ CT is sensitive in identifying gas within the gallbladder wall and can detect
pneumoperitoneum and fluid collection indicative of perforation.
§ The definitive management is cholecystectomy, or percutaneous drainage for those who are
surgically unfit.

o Bile duct stones and acute cholangitis

§ Common bile duct stone happens in approximately 8-16% of patients with symptomatic
gallbladder stones.
§ Most of the patients with common bile duct stones do not develop symptoms and stones
often pass spontaneously.
§ In those that have stones causing partial or complete obstruction of the common bile duct,
patients can present with biliary pain, jaundice, pale stool and dark urine.
§ Acute cholangitis develops when bacterial infection occurs with biliary obstruction.
§ It is characterized by fever, jaundice, right upper quadrant pain (Charcot’s triad),
hypotension and altered mental status (Reynold’s pentad).
§ It is potentially life-threatening.

62
 § Although acute cholangitis is often associated with biliary calculi, it can occur as a result of
benign or malignant strictures, biliary-enteric anastomosis, and after the placement of a
biliary stent.
§ CBD stones are best visualized by MRCP or EUS.
§ The definitive management of choledocholithiasis is ERCP.
§ PTC is usually reserved for patients whose biliary anatomy precludes ERCP (e.g. prior
gastrectomy) or where cannulation of the ampulla is not possible at ERCP.
§ Patients who do not respond to nonoperative management of CBD stones may require
surgery by means of laparoscopic or open common bile duct exploration.

o Gallstone pancreatitis
§ One of the most frequent causes of pancreatitis in Western world.
§ The mechanism is transient ampullary obstruction caused by impaction or passage of a
stone, thereby damaging the ductal and acinar cells of the pancreas.

o Mirizzi syndrome
§ Uncommon condition in which the common hepatic duct is compressed extrinsically by an
impacted stone in Hartmann’s pouch or the adjacent cystic duct. This is classically referred
as Type I Mirizzi syndrome.
§ Patients typically present with right upper quadrant pain and jaundice, but it can also
present as severe cholangitis.
§ Imaging studies such as ultrasound, CT or MRCP, which demonstrate dilatation of biliary
system above the level of impaction and normal caliber below the level of the stone, can be
helpful for the diagnosis.
§ ERCP can confirm the diagnosis of Mirizzi syndrome and allows biliary decompression by
placement of stent.
§ The definitive treatment for Type I Mirizzi is cholecystectomy.
§ When a stone has eroded into the bile duct resulting a cholecystocholedochal fistula (fistula
to the bile duct), it is classified as Type II to Type IV Mirizzi syndrome depending on the
degree of bile duct involvement, which varies from one-third, two-third circumference or
complete bile duct destruction.

o Cholecystocolic fistula
§ Rare complication of acute cholecystitis.
§ The transverse colon is the most common site of fistulation.
§ Patients can present acutely with cholangitis from the reflux of colonic bacteria into the
biliary tract, or patients can present more insidiously with increased frequency of diarrhoea,
steatorrhea and weight loss due to fat malabsorption and direct bile acid-induced water
secretion in the colon.
§ Pneumobilia (air within the biliary tract) on abdominal pain film or CT without prior
instrumentation of the biliary tract may raise the suspicion of cholecystocolic fistula.
However, it is rarely suspected clinically and is often found incidentally at the time of
cholecystectomy.

o Gallstone ileus
§ The obstruction of the intestinal tract by a gallstone.
§ It is caused by the passage of stone through a cholecystoenteric fistula causing obstruction.
§ The classic finding of small bowel obstruction, pneumobilia and ectopic gallstone on CT is
pathognomonic for gallstone ileus.
§ The terminal ileum is usually the site of obstruction.
§ A patient with gallstone ileus is initially resuscitated with intravenous fluid and nasogastric
tube decompression.
63
§ Laparotomy and enterolithotomy is the standard surgical approach for the treatment of
gallstone ileus.
§ During laparotomy, the obstructing stone can be manipulated proximally to a heathy section
of the bowel where enterotomy and stone removal can be safely performed.
§ Often, a cholecystectomy is deferred.

64
Acute Pancreatitis
• Pancreatitis is defined as inflammation of the pancreas, specifically the glandular parenchyma of the
pancreas.
• The incidence ranges from 5 to 35 per 100,000 population per year.
• The clinical spectrum is diverse, ranging from mild to life-threatening cases with multi-organ failure.
• The mortality varies from 1% in mild pancreatitis to 20% in severe cases.

• Aetiology
o Gallstones and alcohol collectively account for 80% of acute pancreatitis cases
o Causes can be remembered by the popular mnemonic “I GET SMASHED”
§ Idiopathic – The causes of pancreatitis can be unidentifiable despite comprehensive history,
laboratory and radiologic investigation. However, many idiopathic cases may be caused by
previously unrecognized causes such as genetics, drugs or toxins.
§ Gallstones – Gallstones account for more than 40% of the cases. Between 3 to 7% of
patients with gallstones develop acute pancreatitis.
§ Ethanol/alcohol – Alcoholic pancreatitis is more common in men aged between 40-60.
Despite high prevalence of excess alcohol intake, only a minority of heavy drinkers develop
pancreatitis, suggesting additional genetic and environmental factors may be involved. The
mechanism in which alcohol causes pancreatitis is unknown. It has been suggested that
protein plugs, ductal calculi, acinar cell injury by reactive oxygen species may play a role. In
alcohol-induced pancreatitis, necrosis and pseudocyst are more common.
§ Trauma – the pancreas can be injured by both blunt and penetrating traumas with damage
ranging from contusion to transection of the gland. Ductal injuries can lead to scarring and
stricture of the main pancreatic duct, predisposing to the development of recurrent
pancreatitis.
§ Steroids –high-dose steroid use has been associated with pancreatitis.
§ Mumps – paramyxovirus - was the first virus implicated in the development of pancreatitis.
Other viruses reported to cause pancreatitis includes Hepatitis B, HIV, coxsackie virus, and
cytomegalovirus.
§ Autoimmune – autoimmune pancreatitis usually presents with chronic pancreatitis, jaundice
or a pancreatic mass, but acute presentations are also recognized. High serum titer of IgG4
and a sausage-shaped pancreas with ductal strictures are characteristic features. Often the
radiological finding of a pancreatic mass may not be able to differentiate AIP from pancreatic
cancer.
§ Scorpion venom – toxins such as scorpion’s venom, organophosphate anticholinesterase
insecticides, organic solvents, diethyl glycol have been reported to cause pancreatitis.
§ Hyperlipidaemia/hypothermia/hypercalcaemia – Hypertriglyceridaemia accounts for 1%-
10% of acute pancreatitis. Pancreatitis seldomly occurs unless fasting triglyceride level is in
excess of 10 mmol/L. Hypercalcaemia induced pancreatitis has a prevalence of
approximately 1% to 4%. It may cause the formation of pancreatic duct calculi or induce
cellular injury through activation of trypsin-mediated autodigestion.
§ ERCP – is the most common iatrogenic cause of acute pancreatitis, seen in 1% to 5% of
patient undergoing diagnostic and therapeutic ERCP. Post ERCP hyperamylasemia is
common and does not equate to the presence of pancreatitis. The diagnosis of post ERCP
pancreatitis is defined as abdominal pain consistent with acute pancreatitis with associated
amylase elevation requiring hospitalization.
§ Drugs – Common drugs that have previously been shown to be associated with pancreatitis
include statins, 5-aminosalicylic acid derivatives, antibiotics such as metronidazole and
tetracycline, ACE inhibitors, anti-glycaemic agents such as metformin and glucagon-like
pedtide-1(GLP-1) analogues, furosemide, hydrochlorothiazide, valproic acid, estrogen and
azathioprine.

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 o Other causes include
§ Anatomical – pancreatic divisum, in which the dorsal and ventral pancreatic ducts failed to
fuse, has been associated with the development of pancreatitis.
§ Genetic – Mutations in a number of genes have been shown to increase risk of developing
pancreatitis. This includes cationic trypsinogen gene (PRSS1, PRSS2), serine protease
inhibitor Kazal type 1 gene (SPINK1), cystic fibrosis transmembrane conductance regulator
gene (CFTR).

• Definition and Classification of Pancreatitis

o The Atlanta classification was first proposed in 1992 and subsequently revised 10 years later to
define the terminologies used in acute pancreatitis and provide definitions for the associated
complications.
o Acute pancreatitis can be subdivided into two types
§ Interstitial oedematous pancreatitis – acute inflammation of the pancreatic parenchyma and
peripancreatic tissues but without recognizable tissue necrosis
§ Necrotizing pancreatitis – inflammation associated with pancreatic parenchymal necrosis
and/or peripancreatic necrosis
o The severity of acute pancreatitis is also defined by the Atlanta classification as:
§ Mild pancreatitis - is characterized by the absence of organ failure and the absence of local
or systemic complication
§ Moderately severe pancreatitis – is characterized by the presence of transient organ failure
or local systemic complications in the absence of persistent organ failure
§ Severe pancreatitis – is characterized by persistent organ failure

• Local Complications of Acute Pancreatitis

o Acute peripancreatic fluid collection – peripancreatic fluid associated with interstitial oedematous
pancreatitis with no associated peripancreatic necrosis
o Pancreatic pseudocyst – an encapsulated collection of fluid with a well-defined inflammatory wall
usually outside the pancreas with minimal or no necrosis. It usually occurs more than 4 weeks after
the onset of acute pancreatitis
o Acute necrotic collection – a collection containing variable amounts of both fluid and necrosis
associated with necrotizing pancreatitis. The necrosis can involve the pancreatic parenchyma and/or
peripancreatic tissue
o Walled-off necrosis (WON) – a mature, encapsulated collection of pancreatic and/or peripancreatic
necrosis that has developed a well-defined inflammatory wall.

• Presentation
o Patients with acute pancreatitis presents with acute onset of severe constant pain in the epigastrium
or right upper quadrant and it is classically radiating to the back in most patients.
o The pain usually reaches its peak over 30-60 mins and persists for days to weeks.
o It is commonly associated with nausea and vomiting.
o Upper abdomen can be tender to palpation, but diffuse peritoneal signs are unusual and if present
other differentials of acute abdomen should be considered.
o Flank ecchymosis (Grey-Turner’s sign) or periumbilical ecchymosis (Cullen’s sign) are suggestive of
retroperitoneal bleeding due to pancreatic necrosis in severe pancreatitis.
o In severe cases, patient may have fever, tachycardia, hypoxemia and hypotension.

• Laboratory Tests
o The diagnosis of acute pancreatitis is supported by a rise in serum amylase three times the normal
limit.
o Serum amylase rises within a few hours after the onset of symptoms and returns to normal in 3 to 5
days.
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 o The level of serum amylase elevation does not indicate the severity of the disease or prognosis.
o This elevation may not occur in 20% of cases however, probably due to late presentation or the
inability to produce amylase in chronic pancreatitis, or hypertriglyceridemia causing interference of
the assay.
o Conversely amylase may be elevated in renal impairment, salivary gland diseases or other extra-
pancreatic conditions such as perforated peptic ulcer which can present similarly.
o Serum lipase is less commonly available but has an added advantage of remaining elevated for a
longer period of time.
o Other blood tests aim to determine the aetiology and severity of the disease, metabolic
abnormalities, and the presence of organ failure. These include:
§ FBC
§ Urea & electrolytes
§ LFTs including AST & LDH
§ Calcium and albumin
§ Fasting glucose
§ IgG4
§ CRP

• Assessment of Severity
o About 20% of patients with acute pancreatitis will develop severe disease with local or systemic
complications.
o Identifying patients who will likely progress to severe disease is important as they can benefit from
early intervention.
o Several prognostic criteria have been developed to predict the clinical course of pancreatitis.
o Ranson’s Criteria
§ One of the first widely used scoring system based on 11 parameters that are assessed over a
48-hour period.
§ It is most sensitive for assessing the severity of alcoholic pancreatitis, while a modified
Ranson criteria with 10 parameters is used to assess gallstone pancreatitis.
§ The main limitations are that it requires 48 hours to assess all parameters and not all
parameters are routinely measured. It also has a lower sensitivity and specificity than the
other scoring systems.
o Glasgow or Imrie Criteria
§ Widely used in Ireland and United Kingdom.
§ Modified Glasgow/Imrie criteria reduces the number of measured variables to eight and has
an accuracy of ~79% in predicting the severity of pancreatitis. A score of more than 3
predicts severe pancreatitis. It can be remembered with the mnemonic “PANCREAS”.
• PaO2 <8 kPa
• Age >55 years
• Neutrophilia: WBC >15 x 109 /L
• Calcium <2.0 mmol/L
• Renal function: Urea >16 mmol/L
• Enzymes: LDH >600 iµ/L
• Albumin: <32 g/L
• Sugar: blood glucose >10 mmol/L

o Acute Physiology and Chronic Health Evaluation (APACHE II)

§ Originally devised to predict mortality in the intensive care setting but has been used to
predict severity in acute pancreatitis.
§ It has 12 variables including age, vitals, oxygenation and biochemical status.

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 § The APACHE II system is not only limited to disease severity on admission, but it can be
performed daily to assess disease progression.
o CRP
§ Easily applicable in the clinical setting as a single biochemical marker to provide risk
stratification of acute pancreatitis.
§ At a cutoff level of 150 mg/L, it has been shown to have a diagnostic accuracy comparable to
the Ranson/Glasgow criteria and the APACHE II scores.

o CT Severity Index
§ Radiological assessment of severity of pancreatitis devised by Balthazar.
§ A score is given based on the degree of pancreatitis and another score is given for the
degree of pancreatic necrosis.
§ The summation of 2 scores become the CT severity index.
§ A high score is correlated with increased mortality.

• Imaging
o Ultrasound
§ Performed early in patients with suspected acute pancreatitis mainly to identify gallstone or
dilatation of common bile duct secondary to choledocholithiasis.
§ It is less sensitive in diagnosing acute pancreatitis due to overlying bowel gas.
§ In certain cases, in patients with acute pancreatitis it shows diffusely enlarged and
hypoechoic gland on ultrasound.
§ It can demonstrate an anechoic peripancreatic fluid collection, but it is not accurate at
identifying necrosis of the gland or in assessing the severity of peripancreatic fluid and
inflammation.

o CT
§ Not needed for all patients with suspected pancreatitis.
§ It is usually performed 3 or more days after the onset of symptoms, to identify complications
of pancreatitis and to determine the severity of the disease because pancreatic necrosis may
not be apparent early in the course of the disease and early CT may underestimate the
severity of pancreatitis.
§ Performed early if there is any diagnostic uncertainty or alternate pathology is a possibility,
especially in a profoundly unwell patient.
§ Acute pancreatitis on CT can be seen as focal or diffuse enlargement of the gland with
peripancreatic stranding.
§ Lack of parenchymal enhancement indicates the presence of necrosis.
§ CT can demonstrate local complication such as peripancreatic collection, pseudocyst,
necrotic or wall off collection.
o MRI
§ Equivalent to CT in the assessment of pancreatitis.
§ Useful in patients with renal failure.
§ It is limited by its availability and it is not appropriate in critically ill patients due to the long
scanning time.

• Treatment
o Initial management of the patient with acute pancreatitis consists of supportive measures including
fluid resuscitation, pain control and provisional of nutritional support regardless of the severity.
o Regular measurement of vital signs and urine output is imperative.
o Clinically mild pancreatitis can be managed in ward environment.

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o High dependency or intensive care may be need in patients with organ failure due to uncontrolled
systemic inflammatory response.
o Respiratory, cardiovascular renal and gastrointestinal systems are the most commonly affected.
o Fluid resuscitation
§ Aggressive fluid resuscitation is crucial in the management.
§ Fluid loss can be significant even in mild pancreatitis.
§ Hypovolemia develops due to substantial third-space loss secondary to systemic
inflammatory response, vomiting and poor oral intake.
§ Crystalloid fluid such as Hartmann solution at a rate of 5 to 10 ml/kg/hr is recommended.
§ Further resuscitation should be guided by the urine output (>0.5 ml/kg/hr), heart rate (<120
bpm) and mean arterial pressure (between 65 to 85 mmHg).
§ The physiological significance of fluid loss in the severity of pancreatitis is evident by the fact
that a high hematocrit of >44% on admission has been associated with high risk of
pancreatic necrosis.
o Supplemental oxygen
§ Hypoxia is common in acute pancreatitis due to atelectasis, pleural effusion and impaired
gas exchange secondary to pulmonary oedema.
§ Acute respiratory distress syndrome can occur in up to 20% of patients with severe
pancreatitis.
§ ICU admission and mechanical ventilation may be needed.
o Pain control
§ Pain is a predominant symptom, and the management is similar to other intraabdominal
emergencies.
§ Multimodal analgesia with paracetamol and opioids, given via parenteral route is indicated.
o Nutrition
§ Prolonged fasting and the use of total parenteral nutrition (TPN) to reduce pancreatic
stimulation is no longer indicated.
§ In mild pancreatitis, early oral intake can be initiated within 24 hours as tolerated.
§ Early feeding has been shown to reduce the length of stay without an increase in adverse
events.
§ In patients with predicted moderately severe or severe pancreatitis or those who cannot
tolerate oral feeding, enteral feeding via naso-jejunal (NJ) or naso-gastric (NG) route should
be initiated.
§ There is no difference in outcomes between NJ or NG feeding.
§ NJ feeding has a theoretical advantage in reducing pancreatic stimulation. Bedside
placement of NJ tube is feasible and safe.
§ NG feeding can be a viable alternative if the placement of a NJ tube is not possible.
§ Enteral nutrition helps to maintain the intestinal barrier thereby preventing bacterial
translocation from the gut. This may prevent the development of infective complications
associated with necrotizing pancreatitis.
§ TPN should only be started in patients who do not tolerate enteral feeding.
o Antibiotics
§ Patients with severe pancreatitis can exhibit recurrent pyrexia related to the systemic
inflammatory response.
§ The use of prophylactic antibiotics has been discouraged as newer evidence did not show
any benefit in reducing mortality, infected pancreatic necrosis and non-pancreatic infection.
§ Indiscriminate use has been associated with the development of superinfection with
Candida.
§ If antibiotics are indicated, the choice should be one with adequate penetration into
pancreatic necrosis such as meropenem, imipenem or a combination of quinolone and
metronidazole.

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• Complications of Acute Pancreatitis
o Acute peripancreatic fluid collection
§ Common radiological finding.
§ Approximately 50% of these fluid collections will resolve within 6 weeks and usually do not
require intervention.
o Pseudocyst
§ Up to 15% of acute peripancreatic fluid collections will persist as encapsulated pseudocysts.
§ Many pseudocysts can be managed conservatively.
§ Symptomatic pseudocysts that cause abdominal pain, haemorrhage, or obstruction of
nearby stomach, duodenum or bile duct will require intervention.
§ Drainage can be done radiologically via percutaneous drainage catheter, or by a
cystogastrostomy using an endoscopic or surgical approach.
§ The choice of approach depends on the location, size, and available expertise.
o Acute necrotic collection
§ The presence of necrosis in itself is not an indication for intervention.
§ Intervention to necrotic collection may cause sterile necrosis to become infected.
§ Intervention should be limited to patients with infected necrosis.
§ The finding of gas pockets is highly suggestive of infected necrosis.
§ Historically the approach to infected necrosis was aggressive open surgical debridement
(necrosectomy). However, mortality in this setting was high. A step-up approach is
generally advocated. The majority of infected necrosis can be managed by percutaneous
drainage and upsizing of drains.
o Walled-off necrosis
§ Indications for intervention in WON are 1) infection; 2) persistent symptoms; 3) nutritional
failure.
§ Given sufficient time, organization of necrosis happens, in which the solid components
within the collection gradually become liquefied and wall maturation occurs.
§ The delay allows non-surgical intervention to be considered.

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Chronic Pancreatitis
• Definition
o Chronic pancreatitis is characterized by chronic progressive pancreatic inflammation and scarring,
irreversibly damaging the pancreas and resulting in loss of exocrine and endocrine function

• Epidemiology
o The incidence of chronic pancreatitis is approximately 4 per 100,00 population per year in the United
States.
o The prevalence is approximately 40-50 per 100,000 persons.
o Chronic pancreatitis related to alcohol is more common in the West and Japan, and accounts for half
of all cases in the United States.

• Classification
o Chronic pancreatitis can be classified based on etiologic factors and mechanisms.
o The two most commonly used classification systems are TIGAR-O and M-ANNHEIM.
§ TIGAR-O stands for: toxic, idiopathic, genetic, autoimmune, recurrent, and obstructive.
§ M-ANNHEIM stands for: (multiple) alcohol, nicotine, nutritional, hereditary, efferent duct,
immunologic, and miscellaneous.
o Toxic
§ 5-10% of patients with alcohol dependency develop chronic pancreatitis.
§ The quantity and duration of alcohol consumption varies among patients but in general a
large quantity of alcohol over years is needed to develop chronic pancreatitis.
§ Smoking is an independent risk factor for chronic pancreatitis in a dose-dependent manner,
but it can also be a co-factor to potentiate the toxic effect of alcohol.
o Idiopathic
§ Up to 30% of the patients with chronic pancreatitis are idiopathic.
§ Many chronic pancreatitis patients who were previously categorized as idiopathic were
subsequently found to have genetic mutations known to be associated with chronic
pancreatitis.
o Genetics
§ Genetic variations of several genes including PRSS1, SPINK1, and CFTR have been implicated
in the development of chronic pancreatitis.
§ The mutation of cationic trypsinogen PRSS1 gene leads to premature activation of
trypsinogen.
§ The SPINK1 gene encodes a trypsin inhibitor; variation of the gene leads to unchecked
trypsin activity.
§ The CFTR gene mutation can lead to abnormalities in mucin production and secretion.
o Autoimmune
§ Autoimmune pancreatitis is characterized by a raised serum level of IgG4 and is associated
with other autoimmune diseases such as Sjögren’s syndrome, primary sclerosing cholangitis
and inflammatory bowel disease.
§ It is clinically characterized by minimal abdominal pain and diffuse enlargement of the gland
without calcifications or pseudocyst which is often difficult to distinguish from pancreatic
malignancy.
§ Patients have hypergammaglobulinemia, raised titers of antinuclear and anti-smooth muscle
antibodies.
o Recurrent
§ Recurrent acute pancreatitis episodes precipitated the development of chronic pancreatitis
due to scarring and fibrosis of the pancreas.

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 o Obstructive
§ Obstruction of the main pancreatic duct caused by a tumour of the head of pancreas or
ampulla, trauma, or an inflammatory stricture can lead to the development of chronic
pancreatitis.

• Presentation
o Abdominal pain is the most common symptom in chronic pancreatitis.
§ The pain occurs in the epigastric area, radiates to the back and may be worse after food
intake.
§ The pattern of pain varies ranging from constant relentless pain to periodic episodes of pain
with pain free periods in between.
§ In some patients, pain may diminish after years of disease (“burnout of the pancreas”).
§ The severity of pain does not correlate with imaging findings.
§ The cause of pain varies but the most important mechanism is probably the alternation in
pain signaling.
o Patients with pancreatic exocrine insufficiency report steatorrhea (oily or floating malodorous stool)
due to fat malabsorption.
o Steatorrhoea develops later in the course of chronic pancreatitis, when more than 90% of pancreatic
exocrine function is lost.
o Weight loss results from malabsorption and reduced oral intake due to pain.
o The loss of pancreatic islet cells due to progressive fibrosis leads to the development of type 3c
(pancreatogenic) diabetes.
o Deficiency of both insulin and hormones such as glucagon, pancreatic polypeptide occurs due to the
loss of all types of islet cells.
o Patients with type 3c diabetes share a similar risk for micro/macro-vascular complications of
diabetes.

• Diagnosis
o Accurate history is important to diagnose and to determine the aetiology of chronic pancreatitis with
particular attention to alcohol, smoking and family history.
o Baseline laboratory tests includes full blood count, urea & electrolytes, liver function test, blood
glucose, HbA1c, and CRP.
o Serum amylase is often normal or marginally raised in patients with chronic pancreatitis.
o There is a substantial overlap in the presentation of acute and chronic pancreatitis.
o Patients with recurrent attacks of abdominal pain and hyperamylasaemia three times the normal
limit should be treated as acute pancreatitis to ensure adequate initial resuscitation.
o For patients in whom the aetiology of chronic pancreatitis is unknown or imaging findings are
suggestive of autoimmune pancreatitis, serum IgG4 level should be tested.
o Pancreatic exocrine dysfunction can be assessed indirectly by measurement of faecal elastase.
o Direct pancreatic stimulation with secretin and subsequent collection of fluid in the duodenum to
measure the bicarbonate concentration is rarely performed as it is invasive requiring duodenal
intubation, although it is a highly sensitive test of pancreatic exocrine function.

• Imaging
o Ultrasound
§ Not as useful as the other imaging modalities in diagnosing chronic pancreatitis.
§ It is often used to screen for gallstone and can also be used to monitor the size of a
pseudocyst.
o CT
§ The most frequently used test for diagnosis of chronic pancreatitis.
§ The main CT features includes pancreatic gland atrophy, intraductal calcification, and
pancreatic duct dilatation.
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 § It is also useful to detect and evaluate complications of chronic pancreatitis (see below).
o MRI pancreas and MRCP
§ Useful in diagnosing chronic pancreatitis by evaluating both parenchymal and ductal
changes.
§ MRCP has high sensitivity for identifying strictures and dilations in the pancreatic duct,
which are characteristics of chronic pancreatitis.
§ Fibrosis of the pancreas restricts the diffusion of water molecules and can be evaluated in
diffusion-weight MRI.
o ERCP
§ Previously gold standard for the diagnosis and staging of chronic pancreatitis owing to its
superior ability to detect ductal abnormalities. It is now replaced by other high-quality
image modalities such as MRI.
o EUS
§ Can examine the pancreatic parenchyma and duct in high details.
§ EUS features of chronic pancreatitis are not specific and can also be seen in old age.
§ There is also significant inter-observer variability. It complements other cross-sectional
imaging for the diagnosis of chronic pancreatitis. Its distinct advantage is the ability to
obtain biopsy of pancreatic tissue to rule out suspected malignancy

• Management
o The aim of treatment is to control pain, correct the exocrine and endocrine insufficiency, and to deal
with complications.
o Lifestyle changes including abstinence from alcohol and smoking cessation may reduce the risk of
recurrent attacks.

o Pain
§ Pain control should follow the WHO analgesic ladder starting with simple analgesics such as
paracetamol and anti-inflammatories.
§ Opioids often are necessary.
§ Adjuvant therapy with pregabalin or amitriptyline may work synergistically with
conventional analgesics in controlling pain.
§ Resistant intractable pain may benefit from coeliac plexus nerve block.

o Pancreatic enzyme supplements and nutritional support

§ Fat malabsorption is managed by pancreatic enzyme supplement such as CREON, which
contains lipase, amylase and protease.
§ The dosage is measured in lipase units.
§ The starting dose is 50,000 lipase units per meal and 25,000 lipase units per snack.
§ The dosage is titrated according to the frequency of steatorrhea and weight.
§ Patients benefit from dietetics input.
§ Diets rich in soluble fibre and low in fat are advised.
§ Fat-soluble vitamin (A, D, E, and K) deficiencies are common due to fat malabsorption.
§ Vitamin D supplementation is essential to prevent osteoporosis.
o Diabetes treatment
§ Insulin therapy is usually required in patients with type 3c diabetes.
§ Good glycaemic control is essential to minimize the risk of complications of diabetes.
o Endoscopic therapy
§ Endoscopic cystogastrostomy is an effective treatment for symptomatic pancreatic
pseudocyst that is causing pain, jaundice or gastric outlet obstruction, provided that the
pseudocyst is mature and in a favorable position for endoscopic drainage.

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 § Common bile duct stricture or obstruction due to obstructing inflammatory mass can be
treated by endoscopic stenting with plastic or self-expandable metal stents once malignancy
has been excluded.
§ For patients who have pancreatic duct stricture or calculi with upstream pancreatic ductal
dilatation, pancreatic duct drainage or stenting via endoscopic approach is not as effective
as surgery in terms of pain resolution and may require repeat endoscopic procedures.
o Surgery
§ Surgery, while rarely indicated, can be performed in the following circumstances:
• Intractable pain
• Unsuccessful endoscopic management
• Complications of chronic pancreatitis e.g. bile duct stricture in a young patient,
where long-term stenting is not optimal, gastric outlet obstruction
• Pancreatic mass where malignancy cannot be excluded

§ Surgical procedures for chronic pancreatitis can be divided into 3 main categories
• Drainage or decompression procedure (e.g. Puestow procedure)
• Resection in cases of suspected malignancy (e.g. Whipple procedure, distal
pancreatectomy)
• Combination (e.g. Frey procedure, Beger procedure)
• Total pancreatectomy with autologous islet cell transplantation can be performed in
selected patients who have diffuse involvement of the pancreas not amenable to
other drainage procedures.

• Complications
o Pseudocyst
§ Mature fluid collection with a well-defined wall, occur in 10% of patients with chronic
pancreatitis.
§ Caused by the disruption of pancreatic duct.
§ Asymptomatic pseudocysts do not require intervention.
o Pancreatic ascites/pleural effusion
§ Result of pancreatic duct disruption leading to fistula formation to the abdominal cavity or
pleural space, or due to a rupture of pseudocyst.
§ High amylase in the fluid is diagnostic.
§ Patients are managed with octreotide, a somatostatin analogue, to decrease pancreatic
secretions and often require endoscopic stenting to occlude the disrupted pancreatic duct.
§ Surgery is reserved if endoscopic management fails or is technically not possible.
o Biliary obstruction
§ Can result secondary to compression from an inflammatory mass or from a pseudocyst.
§ Endoscopic biliary stenting, pseudocyst drainage, or surgical biliary bypass are the treatment
options.
o Thrombosis of splenic/mesenteric/portal veins
§ Thrombosis may lead to portal hypertension and the development of gastric varices.
o Pseudoaneurysm
§ Splenic artery is most commonly involved, followed by the gastroduodenal and
pancreaticoduodenal arteries.
§ Caused by erosion of the affected artery due to surrounding inflammation.
§ Can be complicated by bleeding.
§ Embolisation of the affected artery is the treatment.

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Pancreatic Cancer
• Neoplasms of the pancreas can arise from ductal cells, acinar cells, or islet cells.
• Pancreatic cancer usually refers to ductal adenocarcinoma, which accounts for 85% to 90% of all pancreatic
neoplasms.

• Epidemiology
o In Ireland, more than 600 people are diagnosed with pancreatic cancer each year, ranking it as the
9th most common cancer.
o Pancreatic cancer is the 4th leading cause of cancer-related death in Ireland and has the worst 5-year
survival of all cancers (only 11%).
o The incidence is greater in males (12.1/100,000) than females (9.1/100,000).
o Pancreatic cancer occurs mostly in the seventh and eighth decades of life with more than 60% of
new cases occurring between the age 65 and 85 years.
o It is a disease affecting mainly the Western population.
o The incidence is higher in black people than in white people.

• Aetiology
o Tobacco smoking
§ The most consistent risk factor for the development of pancreatic cancer.
§ A dose-response relationship between pancreatic cancer and the number of cigarettes
consumed has been found.
§ Stopping smoking decrease the risk.
o Pancreatitis
§ The cumulative risk of developing pancreatic cancer in a patient who has chronic
pancreatitis has been found to be 4% at 20 years.
o Obesity
§ Higher risk of pancreatic cancer is found in individuals with a BMI of >30 kg/m2.
o Diabetes
§ Present in 50% - 80% of patients with pancreatic cancer.
§ Multiple studies have demonstrated an association between diabetes and the risk of
developing pancreatic cancer.
§ The risk of pancreatic cancer is higher in patients who have short history of diabetes and the
risk decreases the longer the diagnosis of diabetes.
§ It has been suggested that recent onset diabetes may also be a consequence of pancreatic
cancer.
o Diet
§ Saturated fat intake, consumption of processed meats and red meat have been associated
with an increased susceptibility to the development of pancreatic cancer.
o Occupation
§ Exposure to chlorinated hydrocarbons, organochlorines, asbestos, insecticides have been
linked to the development of pancreatic cancer.
o Familial
§ 5-10% of patients with pancreatic cancer have a positive family history.
§ The risk of pancreatic cancer is nine times higher in individuals who have at least one first-
degree relatives with pancreatic cancer.
§ Pancreatic cancer has been linked to certain genetic alterations known to cause genetic
hereditary syndromes, such as mismatch repair genes in causing hereditary nonpolyposis
colorectal cancer, BRCA1/BRCA2 gene in causing hereditary breast and ovarian cancer,
STK11/LKB1 gene in causing Peutz-Jeghers syndrome, ATM gene in causing Ataxia-
telangiectasia, CDKN2A gene in causing familial atypical multiple mole melanoma syndrome
and PRSS1 gene in causing hereditary pancreatitis.

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• Pancreatic Carcinogenesis
o Three precursor lesions to pancreatic ductal adenocarcinoma have been recognized.
§ Pancreatic Intraepithelial Neoplasm (PanIN)
• Found in more than 80% of pancreatic cancers
§ Intraductal Papillary Mucinous Neoplasm (IPMN)
• Cystic neoplasm derived from pancreatic ducts
§ Mucinous Cystic Neoplasm (MCN)
• Well demarcated cystic masses typically located in body or tail of the pancreas with
a thick fibrous wall

• Presentation
o Initial presentation varies according to the tumour location.
o About 60- 70% of pancreatic cancers are localized to the head of the pancreas.
o Jaundice is a common presenting complaint in cancer arising from the pancreatic head, due to
obstruction of the common bile duct.
o It may be accompanied by pruritus, dark urine and pale stool.
o Abdominal pain is frequently reported and can indicate poor prognosis due to neural invasion of
coeliac plexus.
o The pain is typically located at epigastrium, radiating to the back.
o Painless jaundice is less common, but if present it is considered a hallmark of pancreatic cancer.
o Other nonspecific symptoms are weight loss, anorexia, recent onset diabetes, nausea or vomiting,
and steatorrhea.
o Jaundice rarely occurs in patients with tumour arising from the body or tail of the pancreas.
o Pain is the most common presenting symptom.
o Patients usually present late, when tumours may be locally advanced or have metastasized.
o On examination, Courvoisier’s sign (palpable gallbladder in jaundiced patient) may be present due to
distal obstruction of the biliary system.
o Hepatomegaly or ascites may be identified in patients with metastatic disease.
o The classic physical findings of Trousseau’s sign (superficial thrombophlebitis indicative of a
hypercoagulable state), Virchow’s node (left supraclavicular node indicative of upper GI malignancy),
and Sister Mary Joseph nodule (periumbilical mass associated with peritoneal metastasis) are found
in disseminated disease.

• Investigations
o Laboratory Tests
§ FBC
§ U&Es
§ LFTs
§ Tumour markers
• CA 19-9: Diagnostic usefulness is limited because CA 19-9 is also elevated in patients
with benign conditions other than pancreatic cancer, such as those that cause
obstructive jaundice. Its low positive predictive value limits its use as a screening
test for pancreatic cancer. It is best used as a marker of treatment response and
recurrence
§ Coagulation profile

o Imaging
§ Ultrasound
• Usually the first line radiological investigation for evaluation of patient presenting
with jaundice.
• It may demonstrate dilation of both pancreatic duct and common bile duct (double
duct sign) which is highly suggestive of a peri-pancreatic head or ampullary lesion.
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 • In some cases, a hypoechoic mass can be detected.
• Further evaluation of the pancreas and assessment of other organs will require CT.
§ CT
• Modality of choice for the detection of pancreatic mass, to determine resectability
and to identify metastatic disease.
§ MRI
• Does not provide additional diagnostic information over CT and it is usually not
needed if the CT is adequate.
• Generally reserved to further assess indeterminate liver lesions or to identify small
liver metastases.
• It is also used in patients who have renal impairment or sensitivity to CT contrast.
• MRCP is useful in evaluating cystic lesions of the pancreas and is sensitive for
detecting a periampullary lesion.
§ EUS
• Useful in patients suspicious for pancreatic cancer but where no mass is
demonstrated on cross-sectional imaging.
• Superior to CT for detection of lesion smaller than 2 cm.
• EUS offers additional benefit of the ability to obtain tissue sample via fine needle
aspiration (FNA) for histological diagnosis
§ ERCP
• Evolved into a therapeutic modality for patients who need biliary decompression by
placement of a metal or plastic stent.
• Not all patients will need perioperative stenting
• Usually for patients who develop cholangitis, those who have locally advanced
disease who are for neoadjuvant chemotherapy and those with unresectable or
metastatic disease.
§ Positron emission tomography (PET)-CT
• May enhance the detection of small volume metastatic disease.
• False positive results can be seen with benign inflammation such as chronic
pancreatitis.
• Not routinely used for staging of pancreatic cancer.
§ Laparoscopy
• Can detect small occult sub-centimeter metastatic deposits on the surface of the
liver or peritoneum that are otherwise not visualized on CT.
• Up to one-third of the patients who were deemed to be resectable on imaging were
found to have metastatic disease on laparoscopy and therefore avoided unnecessary
laparotomy.
• Staging laparoscopy can be used selectively for patients with high risk of occult
metastases including those with large tumours (>3 cm), tumour in the body and tail
of the pancreas, and those with high CA 19-9 level (>100 units/ml).

• Staging
o The staging of pancreatic cancer follows the tumour, node, metastasis (TNM) system of the
American Joint Committee on Cancer (AJCC).
o The primary lesion can be classified as resectable, borderline resectable and unresectable.
o Resectability is determined by the presence/absence of distant metastases and the degree of
vascular involvement.
o The lesion is considered borderline resectable when there is limited tumor contact with the superior
mesenteric artery (SMA) or when venous reconstruction is feasible if there is venous vascular
involvement.
o Management should be discussed at multidisciplinary team meeting.
77
 T stage
T1 Tumour ≤ 2 cm
T2 Tumour > 2 and ≤ 4 cm
T3 Tumour > 4 cm
T4 Tumour involves the coeliac axis, SMA, or common hepatic
artery
N stage
N0 No regional lymph node metastasis
N1 1 – 3 regional nodes
N2 4 or more regional nodes
M stage
M0 No distant metastases
M1 Distant metastasis

Clinical Stage TNM stage Description

Stage IA T1 N0 M0 ≤ 2 cm, node negative
Stage IB T2 N0 M0 > 2 cm, node negative
Stage IIA T3 N0 M0 Tumour beyond pancreas, no involvement of
coeliac axis or superior mesenteric artery
Stage IIB T1 to T3 N1 M0 Positive regional lymph nodes
Stage III T4 Any N M0 Unresectable primary tumour
Stage IV Any T Any N M1 Distant metastasis

• Surgery
o Only potentially curative treatment for pancreatic cancer
o Only 15% to 20% patients of cases are resectable at presentation due to advanced disease at
presentation.
o Pancreaticoduodenectomy (Whipple procedure) is the standard surgical approach for tumours in the
head of the pancreas.
§ It is a complex, high risk procedure with perioperative morbidity up to 50% and mortality
rate of 5% in high volume centres.
§ Can be performed by open, laparoscopic or robotic approach.
§ A conventional Whipple involves the resection of gallbladder, bile duct, the head and neck of
the pancreas, antrum of the stomach and the entire duodenum.
§ Reconstruction involves three anastomoses including a pancreatico-jejunostomy (or
pancreatico-gastrostomy), hepatico-jejunostomy and gastrojejunostomy to establish
continuity for drainage of pancreatic juice, bile and food content respectively.

78
 o A modification of the conventional Whipple procedure, called the pylorus-preserving
pancreaticoduodenectomy (PPPD), has gained popularity.
§ The procedure preserves the gastric antrum, pylorus and proximal 2 to 3 cm of duodenum to
decrease the incidence of postoperative dumping and bile reflux.
o If the tumour is located in the body and tail of the pancreas, distal pancreatectomy is the operation
of choice.
§ Splenectomy is carried out en-bloc with the body and tail of the pancreas along with the
lymph node package.
§ Patients post-surgery will require vaccination against encapsulated organisms such as
Haemophilus influenza B, Neisseria meningitidis and Streptococcus pneumoniae.

• Neoadjuvant therapy
o Neoadjuvant therapy has become standard for patients with borderline resectable pancreatic cancer
with an aim to downstage the tumour to become surgically resectable.
o FOLFIRINOX (5-flourouracil, leucovorin, irinotecan, and oxaliplatin) and gemcitabine/nab-paclitaxel
are the two most common chemotherapy regimen used.
o The benefit of neoadjuvant therapy in resectable pancreatic cancer is under evaluation.

• Adjuvant therapy
o Despite tumour free (R0) resection, the survival after surgery remains low.
o Adjuvant chemotherapy has been shown to improve median and 5-year overall survival compared to
surgery alone.
o Currently the National Comprehensive Cancer Network (NCCN) supports the use of FOLFIRINOX,
gemcitabine, or 5-flourourcil based chemotherapies.
o The use of chemoradiotherapy is uncertain and its use varies depending on geographic regions.

• Unresectable/metastatic disease
o Patients with jaundice can suffer from debilitating pruritis, potentially life-threatening cholangitis
and hepatic failure.
§ Relief of obstructive jaundice can dramatically increase the quality of life and nutritional
status.
§ Biliary drainage can be achieved by endoscopic placement of a self-expandable metal stent
via ERCP.
§ Percutaneous drainage (PTC) with subsequent internalization is an alternative if endoscopic
biliary decompression fails.
o Mechanical obstruction of the duodenum by the tumour causing gastric outlet obstruction can be
relieved by performing a surgical bypass with a gastrojejunostomy, either open or laparoscopically.
§ Endoscopic duodenal stenting is an option for patients who are surgically unfit or for those
with an expected short life expectancy.
o Pain is often severe and is managed by opioid analgesics.
§ A coeliac plexus nerve block can be considered in intractable pain.
o Palliative chemotherapy can be given in unresectable or metastatic setting with the intention of
prolonging life while preserving the quality of life.
o Patients with good performance status can be given FOLFIRINOX or gemcitabine/nab-paclitaxel.
o Both have been demonstrated to give an improvement in overall survival.

79
4. Colorectal Surgery

• Ms Helen Mohan, Mr Noel Lynch, Dr Sinéad Ryan, Dr Odhrán Ryan, Dr Ailbhe O’ Driscoll Collins

• Acute Appendicitis
• Diverticular Disease
• Colorectal Cancer
• Bowel Obstruction
• Perianal Disorders
• Anal Cancer
• Stomas

80
Acute Appendicitis

Definition

• Acute appendicitis is acute inflammation of the appendix. The appendix is traditionally described as
“vermiform” as it is shaped like a worm.

Epidemiology
• Appendicitis is one of the most common surgical presentations to an Emergency Department and
appendicectomy is the commonest emergency operation performed.
• The incidence of appendicitis worldwide is ~100/100,000, with a rising incidence seen in newly industrialised
countries.
• The incidence is slightly higher in males with a lifetime risk in males of 8.6% and 6.7% in females.
• Peak incidence occurs in teens and early 20s.

Pathophysiology
• Acute appendicitis is believed to be initiated by luminal obstruction.
• This is usually due to lymphoid hyperplasia or a faecolith.
• Rarer causes include a stricture, tumour or parasitic infection.
• Obstruction leads to increased luminal pressure, and reduced lymphatic and venous drainage. This can
progress to result in necrosis of the appendix with venous congestion.
• Bacterial proliferation due to stasis within the appendix and ischaemia due to reduced venous drainage
allows bacterial invasion to the submucosa and muscularis propria, causing acute appendicitis.
• Further ischaemia can lead to a gangrenous appendix and bacterial spread to the serosa, and in cases of
perforation spread to the peritoneal cavity.
• Spread within the peritoneum can be walled off by the omentum and in such cases can lead to development
of a phlegmonous mass or peri-appendiceal abscess.

History and Presentation

• The classical history given is usually of colicky periumbilical pain which then migrates to and becomes
localised in the RIF, exacerbated by coughing or movement.
• Associated nausea and anorexia is common, with one to two episodes of vomiting following the onset of
pain.
• Other signs include low grade fever and slight tachycardia.
• As the position (tip) of the appendix can vary, the clinical presentation can also vary. For example, patients
can get urinary symptoms if the appendix is sitting on the bladder.
• The presentation will be different depending on the severity of inflammation also.

Risk Factors
• Extremes of age
• immunocompromised states such as diabetes mellitus
• Presence of a faecolith.

Clinical Features
• On palpation of the abdomen, McBurney’s point is classically the point of maximal tenderness, with
associated guarding and rebound tenderness.
• McBurney’s point is 1/3 along a line drawn from the Anterior Superior Iliac Spine (ASIS) to the umbilicus.
• Clinical signs seen in acute appendicitis:
o Rovsing’s sign, pain in the RIF greater than pain in the LIF on palpation of the LIF.
o Psoas sign, pain on passive extension on the right hip.

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Differential Diagnoses
• Gynaecological causes
o Ectopic pregnancy
o Ovarian cyst rupture/haemorrhage
o Ovarian torsion
• Terminal ileitis
• Meckel’s diverticulum
• Mesenteric lymphadenitis
• Diverticulitis
• Functional bowel disorder
• Caecal tumour
• UTI
• Renal colic

Complications
• Perforation with local peritonitis
• Perforation with diffuse peritonitis
• Septic shock
• An appendiceal mass
• Appendiceal abscess

Investigations
• Bloods
o Elevated white cell count with neutrophil predominance
o Elevated CRP
o Note 10% of appendicitis has normal bloods

• Radiology
o Ultrasound
§ In young females an ultrasound of the RIF and pelvis can help rule out a gynaecological
cause of symptoms before proceeding to an appendicectomy, however the appendix cannot
always be visualised on such scans and therefore frequently cannot rule out appendicitis.
o CT Abdomen
§ CT scanning of the abdomen and pelvis is highly sensitive and specific and can reduce the
rates of negative appendicectomies.

Treatment
• Conservative
o Conservative management of acute appendicitis is treatment with antibiotics.
o There are three different scenarios in which conservative management may be undertaken:
§ Peri-appendiceal abscess or phlegmonous mass
• In the setting of an appendix mass, non-operative management with a view to
cooling down inflammation is the aim.
• Surgery in this setting carries an increased risk of adverse outcomes including post-
operative abscess formation, damage to surrounding structures and need for
extensive resection including ileo-caecal resection.
• The role of interval appendicectomy in this patient cohort is controversial and
practice varies between surgeons.
• There is a risk of occult neoplasm in the appendix which must be considered when
discussing the option of interval appendicectomy with patients.
§ Conservative management in the setting of acute uncomplicated appendicitis (when
confirmed on CT abdomen).
• This has been shown to be an acceptable alternative in randomised controlled trials.
However, there is a high recurrence rate.

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 • Approximately 30% of patients treated conservatively for acute uncomplicated
appendicitis will require an appendicectomy for recurrence within the first year.
§ In patients who are unfit for operative management, conservative management may be
considered.

• Surgical
o Laparoscopic appendicectomy is the preferred treatment for uncomplicated acute appendicitis.
o This normally involves a camera port near the umbilicus and one suprapubic port and one LIF port.
o The abdomen is insufflated with CO2.
o The appendix is mobilised, mesoappendix is clipped and divided and the appendix is usually tied
with a special suture which loops over it and is easy to secure.
o The appendix is usually removed in a bag to prevent contamination of the wound.
o Prior to laparoscopy, the treatment was an open appendicectomy. There are two main open
appendicectomy scars that you may see.
§ Gridiron incision
§ Lanz incision

83
Consent
• Ensure patient understands risks, benefits and alternatives
• In the case of acute appendicitis an alternative to surgery is conservative management, however the risks of
conservative management including risk of recurrence and failure of treatment need to be understood by
the patient. This risk is up to 30% interval appendicectomy within the year.
• Risks of surgery which the patient should be informed of include general risks of surgery and more specific
risks associated with appendicectomy.
• General risks: bleeding, surgical site infection, post-operative pain, venous thromboembolism, respiratory
infection, and anaesthetic risks.
• Specific risks of laparoscopic appendicectomy: conversion to an open procedure, pelvic/intraabdominal
abscess (up to 10%), damage to surrounding structures, leak from appendiceal stump, stump appendicitis,
the possibility of the need for more extensive resection and the possibility of a normal appendix on
histology.
• Clinical practice varies regarding removal of a macroscopically normal appendix with no competing
pathology and the consent should reflect the normal practice of the operating surgeon.

Post-operative Care
• Post-operative duration of antibiotics is controversial and varies depending on the degree of inflammation
intraoperatively.
• For simple appendicitis, a single dose at induction is sufficient.
• For perforated appendicitis, 5 days of antibiotics are required.

Follow up
• Follow up colonoscopy should be considered in patients over 40 with appendicitis.
• Histology should always be checked after appendicectomy.

84
Diverticular Disease

Diverticular disease is a common condition in which outpouchings arise in the colon where mucosa and submucosa
bulge through defects in the muscular wall. The insertion points of the vessels supplying the colon, the vasa recta,
are common sites for diverticula.

Definition
• Diverticula: Acquired sac-like protrusions through muscle wall.
o True diverticula involve all layers of the muscle wall e.g. Meckel’s Diverticulum.
o False diverticula do not involve all layers (submucosa and mucosa only) e.g. colonic diverticula.
• Diverticulosis: The presence of diverticula.
• Diverticulitis: Inflammation of diverticula
o Diverticulitis may be divided into uncomplicated or complicated based on clinical and radiological
(CT) features:
§ Uncomplicated: Simple inflammation of the diverticular segment.
§ Complicated: Associated abscess, perforation, peritonitis, stricturing, fistulae or
haemorrhage.

Pathophysiology
• The precise mechanism of development of colonic diverticular disease is unknown. The most common
theory is that a low fibre diet leads to increased pressure in the colon due to constipation, which then leads
to diverticula.
• Increased Pressure
o Diverticula most commonly occur in the sigmoid colon. The increased pressure theory is that
because of a low fibre diet there is increased intraluminal pressure over time and this leads to
building of mucosa and submucosa the site of weaknesses in the wall of the colon between the
taenia coli where the vasa recta penetrate.
• Diet and Obesity
o Diverticular disease is more common in Western countries, associated with low fibre diets and
obesity.
• Smoking
o More common in smokers. Complications of diverticular disease are more common in smokers also.
• Genetic Factors
o The majority of diverticulosis is left sided involving the sigmoid colon in the Western World, whereas
right sided diverticulosis is more common in Asian populations suggesting some genetic component.
• Other
o There are many other theories on the aetiology of diverticular disease including the role of the
microbiome and low grade inflammation.

Epidemiology
• As mentioned diverticulosis is more common in Western populations (studies of immigrant populations in
Western countries demonstrate this).
• Over 50% of people >80 will have colonic diverticula, but a much smaller proportion (2-25%)will develop
symptoms.
• Sigmoid/left sided diverticulosis is more common in Western populations, while right sided disease is more
common in African/Asian populations. Interestingly, as these countries become more westernised, the
location of the diverticula remains the same.
Genetics
• Difference in prevalence within ethnic groups within a region demonstrate a genetic component to
diverticular disease.

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History and Presentation
• The symptoms and signs vary depending on the underlying problem.

o Diverticulitis
§ History
• Left iliac fossa pain is the most common symptom of diverticulitis
• Other associated symptoms which may be present are diarrhoea and PR bleeding
§ Exam
• Pyrexia
• Tachycardia
• LIF tenderness

o Diverticular Abscess
§ History
• Left iliac fossa pain is the most common symptom, similar to diverticulitis
• Other associated symptoms – diarrhoea, PR bleeding, diaphoresis
§ Exam
• Pyrexia- may be a swinging pyrexia
• Tachycardia
• LIF tenderness

o Diverticular Stricture
§ History
• Left iliac fossa pain
• Constipation
• Obstipation if patient develops bowel obstruction
§ Exam
• LIF tenderness
• Abdominal distension if patient develops bowel obstruction

o Diverticular Bleed
§ History
• Sudden gush of painless bright red blood per rectum
§ Exam
• Bright red blood PR on digital rectal exam
• May have signs of haemodynamic instability e.g. tachycardia, hypotension

o Diverticular Fistula
§ Colovesical
• History
o Faeces in Urine
o Pneumaturia – patient may describe bubbles in the urine (“Champagne
urine”)
o Recurrent UTIs
§ Colovaginal
• History
o Faeces PV

86
Investigations
• FBC: High WCC, Hb (Hb may drop with diverticular bleed)
• U&E: Electrolyte disturbances secondary to diarrhoea.
• CRP High
• Blood Cultures: If pyrexial, to exclude sepsis
• Stool culture and sensitivity: Exclude infectious colitis.
• CT abdomen/pelvis with oral and IV contrast: Gold standard investigation for diagnosis and identifying
complications
• Colonoscopy: 4-6 weeks later as an outpatient. Main purpose is to exclude colon cancer. Also can help
confirm diagnosis of diverticular disease and out-rule other differential diagnoses e.g. colitis
• CT Colonography: If diverticular stricture causing luminal narrowing not passable with a colonoscope. Barium
enema an alternative investigation.

87
Colon Cancer

Risk Factors
• Age > 50
• Family history
• Genetic condition e.g. FAP, HNPCC
• Adenomatous polyps
• Inflammatory Bowel Disease
• Previous colorectal cancer
• Obesity
• Diet high in fat and red meat

Bowel Cancer Screening

• BowelScreen is offered to everyone in the age 60 to 69 age group in Ireland.
• They are sent a home test kit- FIT (Faecal Immunochemical Test)- in the post.
• 5% of people will have an abnormal FIT test and will be invited to a colonoscopy.
• Over time, the programme aims to expand to age 55 to 74.

Clinical Features
• Presentation
o Asymptomatic detection during screening
o Change in bowel habit- e.g. new onset constipation or diarrhoea
o Rectal Bleeding- bright red blood PR more common with rectal and left sided tumours, melaena with
right sided tumours
o Tenesmus – a feeling of incomplete evacuation- more common with a rectal tumour.
o Right sided tumours tend to present with darker blood mixed with the stool
o Bowel Obstruction
o Symptoms of anaemia- more common with right sided tumours. E.g. shortness of breath, fatigue
o Weight loss- concerning for metastases
• Examination
o Examination may be normal
o If there is a large tumour, there may be a palpable abdominal mass
o Mass on PR examination
o Cachexia
o Anaemia – pallor
o May present with a perforated tumour with peritonitis, or with an obstructed tumour with
abdominal distension

Investigations
• Bloods
o FBC & iron studies – Iron deficiency anaemia
o U&E
o LFTs ® PT/PTT
o CEA tumour marker – used after treatment of colorectal cancer as part of surveillance to assess for
recurrence. Not used as a screening or diagnostic test.
• Colonoscopy
o Colonoscopy is the most sensitive diagnostic test for colorectal cancer. It also allows for therapeutic
and diagnostic procedures, e.g. biopsy or polypectomy.
o It requires a patient to clear out the bowel with oral bowel preparation usually for 24 hours prior to
the test.
o Colonoscopy must reach the caecum which is identified by seeing the appendiceal orifice, the
triradiate fold and the ileocaecal valve.
o It carries a 1 in 500 risk of bowel perforation.

88
 • Alternatives to Colonoscopy
o CT colonography can be used as a safe alternative in patients for whom a colonoscopy is not
suitable. It requires full oral bowel preparation and oral contrast.
o Sigmoidoscopy is a limited colonoscopy that goes as far as the distal transverse colon usually. It is
used if there is a low index of suspicion for a right sided-tumour. It does not require full oral bowel
preparation, just an enema on the day of the procedure.

Staging
• Disease pattern to consider in staging
o Spread
§ Local spread by direct invasion
§ Lymphatic spread
§ Distant Metastases: haematogenous ( liver and lungs most commonly), transcoelomic
(peritoneal disease)
• Staging Investigations
o Standard staging for distant metastases in colon and rectal cancer is a CT Thorax/Abdomen and
Pelvis
o In rectal cancer, an MRI of the rectum is needed for local staging
o Other additional tests may be done to further evaluate abnormalities picked up on the CT, for
example an MRI of the liver or a PET scan to further evaluate for metastatic disease.
• Staging System
o The AJCC TNM system is used for colorectal cancer staging. It is broadly similar to the initial staging
system described by Cuthbert Dukes.
§ AJCC Stage I/Dukes A – Confined to bowel wall (T1/T2, N0, M0)
§ AJCC Stage II/Dukes B – Involves beyond the muscularis propria of the bowel wall (T3/T4,
N0/M0)
§ AJCC Stage III/Dukes C – Lymph node metastases (any T, N1/2, M0)
§ AJCC Stage IV/Dukes D – Distant metastases (any T, any N, M1)
o T, N, M
§ T1 submucosa
§ T2 muscularis propria
§ T3 subserosa
§ T4 adjacent structures

§ N1 1-3
§ N2 ³ 4

§ M1 distant metastases

o Other prognostic features include histological features

§ Tumour grade
§ Extramural invasion
§ Lymphovascular invasion
§ Tumour budding

89
 Blood Vessel
Spread to other
organs

Lymph Node

Stage 1
Stage 2

Stage 3

Stage 4

Management
• Surgery
o Surgical resection is the mainstay of management.
o A complete mesocolic excision is performed of the area, resecting the mesentery and the lymph
nodes associated with the area of the colon that is affected, e.g. with a caecal tumour, the ileocolic
artery territory.
o Surgical resection is based on the arterial supply.
§ Ileocolic
§ Right Colic
§ Middle Colic
§ Left Colic
§ Sigmoid
• Medical
o Adjuvant chemotherapy (chemotherapy after surgery) may be offered for Stage III and above
patients, or for high risk stage II patients.
o Radiotherapy is not used for colon cancer as the risk of small bowel radiation damage is too high.
• Rectal Cancer
o Rectal cancer management depends on how close the tumour is to the circumferential resection
margin(CRM).
o Rectal cancer surgery involves a total mesorectal excision, taking the entire envelope the rectum is
enclosed in, as this results in an oncological lymph node excision.

90
 o T3 tumours with a threatened CRM and T4 tumours are offered neoadjuvant (prior to surgery)
chemoradiotherapy.
§ The rectum below the peritoneal reflection should have a low risk of small bowel injury.
§ The standard used in Ireland is long course chemoradiotherapy with 12 weeks of
radiotherapy given with a small dose of chemotherapy agent 5-Fluorouracil (5-FU) as a
radiosensitiser. Another option is to use short course radiotherapy where the treatment is
given over 5 days.
§ The radiotherapy takes time to work and the effect of radiotherapy on the tumour is best
assessed at 8 to 12 weeks after the treatment finishes.
§ There are trials ongoing of giving up front full dose chemotherapy as well as radiotherapy
o A small proportion of patients who have neoadjuvant therapy have a complete pathological
response in which case a watch and wait approach is an option. More commonly patients go on to
have surgery
o Surgery for rectal cancer is an anterior resection or an abdominoperineal resection (APR).
o An APR involves removing the anal sphincters and is for tumours involving the sphincters. The
patients will have a perineal wound as well as abdominal wounds.

• Special Considerations
o Emergency Presentation
§ In the emergency setting with an obstructing tumour, options include forming a
defunctioning colostomy or stenting.

o Metastatic Disease
§ In the presence of liver metastases, neoadjuvant chemotherapy is often the first line
treatment, and consideration for surgical resection. Similarly for lung metastases.
§ For patients with intraperitoneal metastases, selected patients may be suitable for
cytoreductive surgery and hyperthermic intraperitoneal chemotherapy (HIPEC).

91
 Cancer Site Type of Surgical Anastomosis Risk of Leak
Resection
Caecum and Right Ileocolic < 5%
ascending colon Hemicolectomy
Transverse Colon Extended right Ileocolic < 5%
hemicolectomy
Splenic Flexure Extended right Ileocolic or < 5% and 2-5%
hemicolectomy or colo-colon respectively
left hemicolectomy
Descending Left hemicolectomy Colo-colon 2-5%
colon
Sigmoid Colon High anterior Colorectal 5%
resection
Upper rectum Anterior resection Colorectal 5 – 10%
with total
mesorectal excision
Lower rectum Low anterior Colorectal 15%
resection with total
mesorectal excision
and defunctioning
ileostomy

Anal verge Abdomino-peroneal Anal canal No leak

included excision of the excised and (but can get
rectum +/- colon sewn closed perineal wound
issues)

Follow up after colorectal cancer

• Follow up is with CT and colonoscopy, usually yearly, and with 6 monthly OPD and CEA.

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Familial Cancer Syndromes

Familial Adenomatous Polyposis (FAP)

• Characterised by the presence of multiple colorectal adenomatous polyps
o >100 polyps at colonoscopy
• Caused by mutation in APC gene
• In 90% of cases the APC gene on 5q21 is implicated
o APC is a protein encoded by the APC gene
o APC is a tumour suppressor protein
• Autosomal Dominant (AD) inheritance pattern, 1 in 4 cases have a de novo mutation
• 100% lifetime risk of colorectal cancer if APC gene positive
• 100% develop colorectal cancer by 40
• 100s of adenomas by age 16 ® mainly colon but also get duodenal polyps and need surveillance with a side
viewing endoscope, and extra gastrointestinal tumour sites, e.g. an association with desmoid tumours.
• Also associated with congenital hypertrophy of retinal pigment epithelium

• Variants
o Attenuated FAP ® less adenomas, CRC later
o Gardener Syndrome
§ Thyroid tumours
§ Osteomas of the skull
§ Dental abnormalities
§ Epidermal cysts
o Turcot’s Syndrome ® CNS tumours as well as polyposis and colonic tumours
• Management
o (Prophylactic) Panproctocolectomy. Ileal-pouch anal anastomosis is an option in these patients.
o At risk of gastric & duodenal Ca ® regular endoscopes

Hereditary Nonpolyposis Colorectal Cancer (HNPCC Lynch Syndrome)

• AD mutation causing Microsatellite instability/Mismatch repair protein deficiency.
• Lynch I ® R sided CRC
• Lynch II ® R sided CRC, gastric, endometrial, prostate, breast
• Amsterdam Criteria – Identify high-risk candidates for molecular genetic testing
o ³ 3 family members with HNPCC related cancers
o Over 2 generations
o At least 1 <50
o FAP has been excluded

• NICE guidelines recommend routine screening for microsatellite instability in colorectal cancer.
• MSI tumours tend to be right sided, poorly differentiated and rarely metastasise either to lymph nodes or
distant metastases.
• 10% of MSI tumours are associated with Lynch Syndrome and 10% of all colorectal tumours are MSI.
• Patients have a 50-60% risk of developing colorectal cancer in their lifetime
• Once diagnosed with Lynch syndrome colonoscopy screening is advised every 1-2 years from the age of 20-
25 and OGD 2 yearly from 30-35 years old

Peutz-Jeghers Syndrome
• AD STKII mutation
• Signs and Symptoms
o Mucocutaneous hyperpigmentation macules on palms, mouth
o Multiple GI hamartomatous polyps ® intussusception, haemorrhage
• Increased risk of cancer ® CRC, pancreas, breast, lung, ovaries, uterus

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Bowel Obstruction

Definitions
• Bowel Obstruction: Mechanical/functional obstruction of the GI tract inhibiting normal transit of enteric
contents. May be a partial or complete obstruction. Can be acute or subacute.
• Ileus: Disruption to normal gut motility due to a malfunction of peristalsis in the absence of a mechanical
obstruction. A common post-operative complication.
• Simple Obstruction: One obstruction point & no vascular compromise.
• Closed Loop: Bowel obstruction at two points, can result in ischaemia, necrosis or bowel perforation.
Surgical emergency requiring urgent diagnosis and surgical intervention.
• Strangulated: Bowel obstruction with compromised blood supply, Abdominal tenderness a common sign and
systemic features of toxicity such as pyrexia and blood indices including elevated inflammatory markers and
lactate.

Aetiology
• Small Bowel Obstruction: Majority are adhesional or secondary to a hernia. Other causes include bowel
strictures, Meckel’s diverticulum, bowel intussusception or malignancy.
• Large Bowel Obstruction: Colorectal neoplasia is most common. Other causes include diverticular stricture,
volvulus, hernias or strictures related to inflammatory bowel disease such as Crohn’s Disease
• Non-Mechanical Causes: Post-operative, peritonitis, drugs (opioids/antimuscarinics), Hypokalaemia,
Hyponatraemia, Hypomagnesaemia
• Mechanical Causes:
o Intraluminal: Impacted stool, foreign body, gallstones.
o Mural: Benign stricture, neoplasia, atresia, ileus, intussusception.
o Extramural: Hernia, adhesions, volvulus, extrinsic compression.

History
• Can be acute/subacute.
• Abdominal pain
o Constant localised pain may suggest perforation.
• Vomiting
o Early in high obstruction.
o Bilious contents if high obstruction
o Faeculent in distal obstructions

Symptoms
• Pain
• Absolute Constipation/Obstipation (faeces/flatus)
• Distension
• Vomiting

Signs
• Tachycardia, dehydration, hypovolaemia, fever
• Surgical scars, hernia, mass
• Bowel sounds
o Increased in mechanical obstruction
o Decreased in ileus
• PR: empty rectum, rectal mass, hard impacted stool

Investigations
• Bloods: High WCC, dehydration, electrolyte abnormalities, high amylase
• PFA: Dilated large bowel (haustrations) or small bowel loops (valvulae conniventes) Air/fluid levels
• Erect CXR: Presence of “free air” or pneumoperitoneum may indicate a perforation.

94
 • Gastrografin Studies: In a SBO scenario an oral bolus of gastrografin is administered and a PFA repeated 6-12
hours later, if contrast has reached colon, it is likely the SBO is resolving and the Gastrografin study may be
curative.

PFA Small Bowel Large Bowel

Obstruction (SBO) Obstruction (LBO)
Diameter >3cm >6cm
Location Central Peripheral
Markings Valvulae Conniventes Haustra
Large Bowel Gas Absent Present
Number of Loops Many Few
Fluid Levels Many, short Few, long

• 3, 6, 9 Rule
o >3cm SBO
o >6cm LBO
o >9cm Caecum obstruction
• Contrast CT
o Can identify cause.

Management
• Resuscitation
• “Drip & Suck”: Nasogastric tube (NGT) on free drainage
• IV fluids & catheterise (monitor UO).
o Important to monitor electrolytes.
• Analgesia
• Surgical Indications
o Closed loop obstruction
o Obstructing neoplasm
o Strangulation/sepsis/perforation
o Failure of conservative management
• Procedures
o Must consent for possible resection ± stoma
o SBO
§ Adhesiolysis
§ Bowel resection
§ Hernia repair.
o LBO
§ Resection of offending pathology which may require a Hartmann’s procedure
§ Segmental colectomy
§ Palliative bypass procedure

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Paralytic Ileus
• Adynamic bowel 2° to absence of normal peristalsis
• Decreased/absent bowel sounds
• Usually small bowel

• Causes
o Post-operative peritonitis
o Pancreatitis
o Drugs
o Pseudo-obstruction
o Metabolic dysfunction
o Mesenteric ischaemia

• Prevention
o Decreased bowel handling
o Laparoscopic approach
o Peritoneal lavage

• Management
o “Drip & Suck”
o Monitor electrolytes
o Treat underlying cause

Ogilvie’s Syndrome
• Pseudo-obstruction – acute dilatation of the colon
• Presents with signs and symptoms of mechanical obstruction, but no mechanical cause present
• Clinical features include abdominal distension, abdominal pain, nausea and vomiting.

• Cause
o Aetiology unknown
o Associated with elderly, cardiorespiratory disorders, pelvic surgery

• Investigations
o Contrast enhanced CT abdomen and pelvis to exclude mechanical obstruction

• Management
o Colonoscopic decompression
o Neostigmine ® Anti-cholinesterase

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Perianal Disorders

Haemorrhoids

Definition
• Dilatation of anal venous cushions
• Anal cushions positioned at 3, 7 & 11 o’clock (superior, middle and inferior rectal veins)

Aetiology
• Gravity & straining leads to engorgement & enlargement of cushions
• Hard stool disrupts connective tissue causing protrusion & bleeding
• Haemorrhoids above the dentate line are covered by mucosa and innervated by autonomic nerves and are
painless
• Haemorrhoids below the dentate line are covered by the anoderm, have somatic innervation and are very
sensitive
• Haemorrhoids may be gripped by the anal sphincter leading to thrombosis & strangulation, which may
ulcerate or infarct

Classification (Banov et al, 1985 and ASCRS 2018)

• Grade I: Never prolapse, only bleed.
• Grade II: Prolapse on defecation but spontaneously reduce
• Grade III: Prolapse on defecation but need digital reduction
• Grade IV: Remain permanently prolapsed and may have external components and may thrombose.

History
• Poor dietary habits, decreased fibre intake, decreased fluid intake.
• Constipation
• Straining when defecating.
• Important Caveats in History Taking in Haemorrhoids
o It is important to take a history of faecal incontinence and obstetric history as this may influence
your management options- haemorrhoidal tissue can contribute up to 30% of continence in women.
o It is also important to take a history that includes any red flags for colorectal cancer e.g. age over 50,
blood mixed with stool, tenesmus etc.
o Perianal tumours e.g. melanoma or SCC can masquerade as haemorrhoids.

Symptoms
• Fresh, painless/painful PR bleeding
• Painful = thrombosis
• Pruritis ani
• Prolapse

Signs
• DRE
o Can’t palpate haemorrhoids unless they are thrombosed - so a normal exam doesn’t preclude
haemorrhoids but it is important to outrule other differential diagnoses
• Purple/black lumps - external haemorrhoids
• Skin tags.

Causes
• 1°: Constipation w/ prolonged straining of hard stool
• 2°: Pregnancy and other causes of raised intraabdominal pressure

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Investigations
• DRE
• Sigmoidoscopy or Colonoscopy
• Proctoscopy

Management
• Conservative
o Increased fibre & fluid intake
o Minimise straining when defecating
o Sitz Baths for external haemorrhoids
• Medical
o Topical steroids e.g. Hydrocortisone
o Topical Analgesics e.g. Lidocaine
o Laxatives/stool softeners e.g. Lactulose
• Proctoscopy
o Sclerosant Injection
o Rubber band ligation
• Surgical
o Haemorrhoidectomy (Open/closed procedure)
§ Indicated for 3rd/4th degree haemorrhoids, or 2nd degree that has failed conservative/medical
management.
o Trans-anal dearterialization and hemorrhoidopexy is another option.

98
 Anal Fistula

Definitions
• Fistula: abnormal connection between two surfaces.
• Anal fistula: Abnormal connection between ano-rectal canal & skin.

Aetiology
• Chronic result of perianorectal disease.
• Associated with Crohn’s, Diverticular Disease, Rectal Cancer ± radiation proctitis, TB, HIV, LGV

History
• Anorectal disease

Symptoms
• Perianal pain
• Purulent discharge from perianal lesions
• Pruritus

Signs
• Inflamed perianal skin or induration around fistula
• External fistula opening may be visualised or palpated

Park’s Classification
• Superficial
• Type 1. Intersphincteric (65%)
• Type 2. Transphincteric (25%)
• Type 3. Suprasphincteric (5%)
• Type 4. Extrasphincteric

Levator Ani Muscle

Puborectalis Muscle

Internal Anal Sphincter

External Anal
Sphincter

Extrasphincteric Suprasphincteric
Transphincteric Intersphincteric Fistula
Fistula Superficial
Fistula Fistula (Parks Type 3)
(Parks Type 4) Fistula
(Parks Type 2) (Parks Type 1)

99
Goodsall’s Rule
• Anterior fistula tracks in a straight line
• Posterior fistulae have an internal opening at 6 o’clock and have a curved track

Investigations
• EUA anorectum
• MRI
•
• If concomitant abscess, bloods may be indicated

Management
• Surgical
o Fistulotomy with healing by secondary intention
o Fistulectomy excision
o Seton
§ This is a long-term stitch placed into the seton to stop abscesses forming – may be a vessel
loop or ethibond.
§ Two types
• Cutting - gradually cuts through the sphincter
• Draining - allows drainage

o Other options
§ Fibrin glue
§ Fistula plug
§ FILAC (laser)
§ LIFT procedure

100
 Pelvic Floor

Internal Anal Sphincter

External Anal Sphincter

Anal Canal

Seton
Peri-Anal Sepsis/Abscess
o Anal gland blockage ® infection ® abscess ® purulent discharge
o May develop from skin infection
o Associated with Crohn’s, DM, malignancy
o Presentation
§ Perianal mass
§ Cellulitic area
§ Fluctuant mass
§ Signs of sepsis
o Classification
§ Perianal
§ Ischiorectal
§ Intersphincteric
§ Supralevator
o Management
§ Antibiotics
§ EUA ® I&D
• May need interval repeat I&D if suspect fistula

101
Anal Fissure

Definition
• Tear of squamous epithelium in lower anal canal

Aetiology
• Trauma 2° to passage of hard stools
• Rare causes: associated with Crohn’s Disease, herpes simplex virus, anal cancer

History
• History of constipation/passing hard stools
• Diagnosis of Crohn’s Disease

Symptoms
• Excruciating pain (prevents patients from defecating)
• PR bleeding (bright red on paper)

Signs
• Posterior at 6 o’clock
• May be mucosal tag-sentinel pile present if chronic.
• Groin lymph node involvement suggestive of HIV infection.
• Often too painful to tolerate DRE

Management
• Conservative
o Increased fibre and fluid intake
• Medical
o Non-specific
§ Stool softeners e.g. lactulose, fybogel
§ Topical analgesia e.g. lignocaine
o Curative Aim
§ Topical GTN (relaxes sphincter)
§ Topical diltiazem 2% (calcium channel blocker)
• Interventional
o Botox injection (relaxes sphincter)
• Surgical
o Lateral internal sphincterotomy- rarely done

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Miscellaneous Anal Conditions

• Perianal Haematoma
o Thrombosed blood vessel of external venous plexus
o Tender blue lump at anal margin ® “external pile”
o Pain worsened by defecation/movement
o Management
§ Analgesia
§ Usually spontaneously resolves
§ Evacuation under anaesthetic- rare

• Proctalgia Fugax
o Young anxious men
o Crampy anorectal pain, worse at night
o Associated with CNV neuralgia
o Management
§ GTN cream

• Anal Warts
o Condylomata Accuminata
§ Caused by HPV
§ Managed by cryotherapy/surgery
o Condylomata Lata
§ Caused by Syphilis
§ Treated with Penicillin
§ Increased risk of anal cancer

• Hidradenitis Suppuritiva
o Form of acne involving apocrine glands
o Causes sepsis, sinuses, fistulae
o History of recurrent abscesses in groins and axillae
o Management
§ Setons and dermatology
§ Surgical excision rare
§ Recurrence usual

• Pruritis Ani
o 50% idiopathic
o Associated with poor hygiene, fungi, worms, haemorrhoids, anal fissure, fistulae, Crohn’s neoplasia
o Management: hygiene, antihistamines, cotton underwear, keeping area clean and dry, avoiding
creams

• Pilonidal Sinus
o Ingrown hair ® foreign body retention ® abscess formation
o Usually occurs in natal cleft
o Risk Factors
§ Male
§ Poor hygiene
§ Sitting
§ Overweight
o Presentation
§ Persistent discharge of purulent/clear fluid
§ Recurrent pain, abscesses
o Management
§ Hygiene

103
§ Shave
§ I&D if acute abscess
§ Elective excision of sinus

104
Anal Carcinoma

Risk Factors
• Female sex
• HPV Infection
• History of anorectal condyloma
• Cigarette smoking
• Receptive anal intercourse
• Ten or more lifetime sexual partners
• HIV Infection

Types of Anal Cancer

• Squamous Neoplasms
o Condylomata Acuminatum
o Anal intraepithelial neoplasia (AIN)
§ Precursor to invasive squamous anal carcinoma
o Bowen’s Disease
o SCC (80% of anal cancers)
• Adenocarcinoma
o Anorectal adenocarcinoma
o Paget’s disease
• Melanoma
• Neuroendocrine tumours
• Malignant Lymphoma
• Mesenchymal tumours

• Anal Margin Cancers – arise within the skin or distal to the squamomucocutaneous junction
o Well differentiated
o Keratinising lesions
o Commoner in Men
o Good Prognosis

• Anal Canal Cancers – arise in the mucosa

o Poorly differentiated
o Non-keratinising
o Commoner in Females
o Poor prognosis

Lymphatic Drainage
• Above dentate line ® Internal iliac lymph nodes
• Below dentate line ® Superficial inguinal lymph nodes

Presentation
• Pain
• Bleeding
• Pruritis Ani
• Faecal incontinence
• Rectovaginal fistula

Investigations
• US
• EUA + Biopsy
• CT/MRI

105
Management
• Chemoradiotherapy
• “Salvage” Abdominoperineal resection/Anterior resection and Total mesorectal excision if failure of
chemoradiotherapy

106
Stomas

Definition
• Stoma is derived from Ancient Greek for mouth. A stoma in abdominal surgery means an artificial opening of
a hollow organ to the surface, e.g. a colostomy or ileostomy.

Describing a Stoma - On inspection describe:

• Site: usually (but not always) an ileostomy is in the RIF and a colostomy in the LIF.
• Spout: an ileostomy is usually spouted, a colostomy usually is not
• Contents: it may be small bowel contents, faeces, urine (urostomy looks like an ileostomy but contains
urine) or if immediately post operatively serous fluid (the stoma can take time to start “working” post
operatively.
• Skin: is the surrounding skin healthy- in the exam setting you may need to comment that you would like to
take off the stoma bag to inspect the skin
• Lumens: is it a loop or an end stoma- in the exam setting, comment that you would like to digitally examine
the stoma with a gloved finger to see if there is one or two lumens as it may not be visible.
• Devices: Look at the stoma bag itself- is there a charcoal filter to reduce odour(usually used for a colostomy),
is it clear (usually is in the exam setting, but also early post operatively to be able to see the mucosa). Is
there a stoma rod? A stoma rod is a device that is sometimes used under a loop stoma
• Complications: comment if any evidence of complications e.g. mucosal necrosis, and prolapse
• Data: look at the fluid balance chart and see what the stoma output is. Over 1.5 litres per 24 hours is the
definition of a high output stoma. Look at the input of fluids and the overall fluid balance also.

Patients are seen by the stoma nurse preoperatively for elective surgery. They help determine a site that is easiest
for the patient to manage.

Ideal Site
• Healthy skin
• Away from umbilicus
• Avoid bony prominences, scars, skin creases
• Avoid belt line
• Reachable area to facilitate patient changing bag.
Rectus Muscle

Umbilicus

Stoma Sites

Stoma Sites

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 • When bringing a stoma out intraoperatively, the surgeon brings it out through the rectus muscle, avoiding
the inferior epigastric artery.

Common Types of Stoma in Colorectal Surgery

• Loop Ileostomy
o This is where a loop of ileum is brought to the surface with two lumens.
§ Site: RIF usually
§ Spout: Yes
§ Contents: Small bowel contents usually
§ Skin: look for excoriation from alkaline small bowel contents
§ Lumens: two- the proximal lumen is the active lumen that has small bowel contents coming
out of it
§ Devices: see if there is a stoma rod if early post operatively (usually removed at 72 hours
post op)
§ Data: look at the stoma output and see if this is a high output stoma- stoma output should
be less than one litre per day.

o Common indications for loop ileostomies, are in situations where a primary anastomosis is formed
that is deemed to be at risk of a leak, to reduce the risk of a clinically significant leak. For example, in
a low anterior resection, especially in patients who have received radiotherapy. The loop ileostomy
is brought out to protect the distal anastomosis. Three months post-operatively, the anastomosis is
tested by using a dye inserted rectally (a Gastrografin enema) to ensure there is no stricture or leak,
and the patient can be brought in for a reversal of ileostomy.
o Advantage of a defunctioning ileostomy is that it reduces the risk of a life-threatening leak.
o Disadvantages are that it involves the patient having to deal with having a stoma, the complications
of a stoma and also there is some evidence that defunctioning the bowel may affect long term bowel
function as an ileostomy is a risk factor for major low anterior resection syndrome (LARS).
o Reversal of a defunctioning loop ileostomy usually involves an incision locally around the stoma and
has a 3-5 day length of stay if no complications.
o Another stoma that can appear like a loop ileostomy is a loop jejunostomy. This may be fashioned
for example in the setting of severe ileocolic Crohn’s disease as a temporary measure to divert a
distal anastomosis. The more proximal the stoma, the higher the stoma output and the greater risk
of electrolyte abnormalities and dehydration.

Loop Ileostomy

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End Ileostomy
• Single lumen of ileum brought to the surface.
o Site: RIF usually
o Spout: Yes
o Contents: Small bowel contents usually
o Skin: look for excoriation from alkaline small bowel contents
o Lumens: One
o Devices: None
o Data: look at the stoma output and see if this is a high output stoma- stoma output should be less
than one litre per day.
• Common indications for an end ileostomy include a total colectomy, e.g. in Ulcerative Colitis or FAP.

End Ileostomy

• An end ileostomy would need a more major operation to “reverse” compared to a loop ileostomy. For
example, if it is an ulcerative colitis patient, an operation to form a J pouch would be needed.

• Stomas that may appear like an end ileostomy

o Urostomy
§ Don’t forget that a urostomy is fashioned with ileum and looks like an end ileostomy. It is
really important to check the contents of the stoma bag- a urostomy will be urine!
o End jejunostomy
§ This may be performed in the setting of having an extensive bowel resection e.g. after bowel
ischaemia.
§ These high stomas have a high stoma output and are associated with dehydration and
electrolyte disturbances.
§ In general, over 100cm of small bowel are required to be independent of total parenteral
nutrition.

Loop Colostomy
• This is when a loop of colon is brought to the surface.
o Site: it may be in the LIF (defunctioning loop sigmoid colostomy) or in the upper
abdomen(defunctioning loop transverse colostomy) on the right or left
o Spout: No
o Contents: Faeces
o Skin: usually don’t get excoriation as faeces rather than small bowel contents
o Lumens: two- the proximal lumen is the active lumen that has faeces coming out of it
o Devices: see if there is a stoma rod if early post operatively

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 Loop Transverse Colostomy

• Common indications would be in the presence of a distal obstructing colorectal tumour. May be a temporary
measure before other treatment and then definitive surgery. Another option in obstructing colon cancer
would be colonic stenting.
• Transverse colostomies have a higher rate of stoma prolapse than other stomas but are useful if the patient
has a closed loop obstruction with very distended bowel.
• Sigmoid colostomies may be fashioned laparoscopically if the patient isn’t very obstructed yet and have a
lower rate of prolapse.

End Colostomy
• Site: LIF usually
• Spout: No
• Contents: Faeces
• Skin: Usually don’t get excoriation as faeces rather than small bowel contents
• Lumens: One
• Devices: There will be no stoma rod as there is only one lumen.

Mucous Fistula
• A mucous fistula may be formed as well as an end colostomy - this is where the distal end of the bowel is
brought to the surface
• A mucous fistula allows release of colonic secretions e.g. mucous.
• These are usually brought to the surface in the context of severe colitis to prevent blow out of the rectal
stump after a total colectomy.

Other “stomas” you may encounter

• Feeding jejunostomy
o This is when a feeding tube is placed into the jejunum from the skin surface. This is commonly used
in oesophagogastric cancer.

110
 Feeding Jejunostomy

• Gastrostomy
o This may be for feeding, e.g. a Percutaneous Endoscopic Gastrostomy (PEG) or a RIG (Radiologically
inserted gastrostomy).
o It may also be used for Venting (i.e. allowing gastric decompression) usually in the palliative setting.
• Nephrostomy
o Diversion of urine from renal pelvis
• Cholecystostomy
o This is when a tube is inserted into the gallbladder to drain the gallbladder in the management of
cholecystitis when cholecystectomy is contraindicated.

Stoma Complications
• Early
o Dehydration/High Output, Ischaemia, Bowel Obstruction, Stenosis, Mucocutaneous separation
• Late
o Retraction, prolapse, herniation, peristomal skin ulceration/inflammation, bowel obstruction,
bleeding.
• Both
o Psychosexual issues
• High Output
o Output >1500mls /24 hours.
o Usually caused by decreased length of remaining bowel, enteric infection, residual disease in
remaining bowel, medications (e.g. laxatives, prokinetics) or radiation enteritis.
o Associated with dehydration, electrolyte depletion and malnutrition.
o Treatment involves careful attention to fluid balance, oral fluid restriction with IV fluid replacement,
electrolyte repletion, TPN and Loperamide/Codeine Phosphate.
• Ischaemia/Necrosis
o This is an early post-operative complication in the first week post-operatively.
o Associated with a foul smell, discolouration of mucosa and surrounding skin, and hard/dry mucosa.
o May also precede other stoma complications such as stenosis or prolapse.
o May be treated with debridement or surgical refashioning of the stoma.
o Stoma rod use is a risk factor for stoma necrosis.
• Mucocutaneous Separation
o If there is complete separation it will require surgical refashioning.
• Retraction
o Stoma recedes >0.5 cm below skin due to excessive tension or ischaemia.
o May be segmental or circumferential.
o Can be treated by local repair, or may require refashioning.

111
• Peristomal Skin Inflammation
o Can be caused by stoma complications (e.g. prolapse or herniation) or by improper stoma care.
o Usually can be treated with involvement of stoma nurse and careful attention to stoma care e.g.
barrier creams.
o Occasionally may need revision of stoma.
• Stoma Stenosis
o Usually caused by ischaemia or stoma prolapse/retraction.
o CD recurrence close to stoma can also contribute.
o Can be treated conservatively with increased fluid intake or laxatives.
o Dilatation is an option but usually excision of scar tissue or revision of stoma is the definitive surgical
treatment of choice.
• Prolapse
o Protrusion of bowel through stoma.
o Can be fixed or sliding.
o More commonly seen in end stomas than loop.
o Associated with parastomal herniation.
o May cause inadequate effluent outflow or bowel strangulation.
o In the emergency setting, reduce it with manual pressure. May use osmosis to assist e.g. using sugar
to reduce tissue oedema. Revision of the stoma surgically is the definitive treatment.
• Parastomal Hernia
o Common complication of stomas, can occur in up to 50%.
o More common in end stomas.
o More common in obese patients and those with COPD (increased intra-abdominal pressure and
repeated coughing).
o Indications for surgery are strangulation, obstruction and ischaemia.
o Local repair may be attempted but is associated with an increased risk of recurrence.

112
References
• Williams N, O'Connell P, McCaskie A. Bailey & Love's short practice of surgery. 27th ed. Boca Raton: CRC Press
- Taylor & Francis Group; 2018.
• Tavakkoli A, Szasz P. Acute appendicitis - Epidemiology | BMJ Best Practice US [Internet].
Bestpractice.bmj.com. 2020. Available from: https://bestpractice.bmj.com/topics/en-
us/290/epidemiology#referencePop7
• Kumar V, Abbas A, Aster J. Robbins basic pathology. 9th ed. Philadelphia, PA: Elsevier Saunders; 2012.
• Longmore M, Wilkinson I, Baldwin A, Wallin E. Oxford handbook of clinical medicine. 9th ed. Oxford: Oxford
University Press; 2014.
• Kumar P, Clark M. Kumar & Clark's Clinical medicine. 9th ed. London: Elsevier; 2017.
• Smink D, Soybel D. Management of acute appendicitis in adults [Internet]. Uptodate.com. 2020. Available
from: https://www.uptodate.com/contents/management-of-acute-appendicitis-in-adults
• Hayes D, Reiter S, Hagen E, et al. Is interval appendectomy really needed? A closer look at neoplasm rates in
adult patients undergoing interval appendectomy after complicated appendicitis [published online ahead of
print, 2020 Jul 16]. Surg Endosc. 2020
• Mohamed I, Chan S, Bhangu A, Karandikar S. Appendicitis as a manifestation of colon cancer: should we
image the colon after appendicectomy in patients over the age of 40 years? [published correction appears in
Int J Colorectal Dis. 2019 Feb 15;:]. Int J Colorectal Dis. 2019;34(3):527-531.
• Molecular Basis of Colorectal Cancer N Engl J Med 2009; 361:2449-2460
DOI: 10.1056/NEJMra0804588

113
5. Inflammatory Bowel Disease

• Mr Liam Devane

• Ulcerative Colitis
• Crohn’s Disease

114
Inflammatory bowel disease (IBD) is comprised of two major disorders: ulcerative colitis and Crohn’s disease.
Ulcerative colitis affects the colon and is characterised by inflammation of the mucosal layer whereas Crohn’s
disease can involve any component of the gastrointestinal tract from the mouth to the perianal area and is
characterised by transmural inflammation. These disorders have somewhat different pathologic and clinical
characteristics, but with substantial overlap. Their pathogenesis remains poorly understood with multiple genetic
and environmental factors implicated.

Patients are frequently young and those with indications for surgery are usually septic, and/or malnourished and/or
immunosuppressed. A specialised multidisciplinary team approach is optimal, including gastroenterologists,
colorectal surgeons, dieticians, IBD nurses & stoma nurses.

115
Ulcerative Colitis
• Ulcerative colitis is a chronic inflammatory condition characterized by relapsing and remitting episodes of
inflammation limited to the mucosal layer of the colon.
• It almost invariably involves the rectum, and the extent often involves more proximal segments of the colon
in a continuous fashion.
• Terms to describe extent of disease and sequentially inflamed segments are: proctitis, proctosigmoiditis, left
sided colitis, extensive colitis, pancolitis.

• Presentation
o Mild (70% at presentation)
§ Mucous & blood PR
§ £ 4 bowel movements per day
§ Faecal urgency, frequency & tenesmus
o Moderate (28%)
§ > 4 bloody stools/day
§ Abdominal pain
§ Low grade fever, minimal signs of toxicity
o Severe disease (<2%)
§ ≥6 bloody stools per day with severe cramps
§ Systemic toxicity – Fever, tachycardia, anaemia
§ Weight loss

• Extraintestinal Manifestations
o Musculoskeletal - arthritis/arthralgia, ankylosing spondylitis, osteoporosis
o Eye – uveitis, episcleritis, conjunctivitis
o Skin – erythema nodosum, pyoderma gangrenosum
o HPB – primary sclerosing cholangitis, autoimmune hepatitis

• Investigations
o Laboratory
§ FBC, U&E, CRP, LFTs, albumin, stool culture (out -ule infective colitis)
§ Faecal calprotectin
§ If considering biologic treatment – Mantoux, Quantiferon, Immunomodulatory viral screen
(HIV/HBV/HCV/VZV/EBV)
o Radiology
§ CT / PFA if systemically if systemically unwell to look for toxic megacolon
o Endoscopy
§ Colonoscopy (Sigmoidoscopy in acute setting)
§ Mayo grading 1 -3
§ Degree of erythema, bleeding, loss of vascular pattern, ulceration
o Biopsy
o Histology
§ Inflammation of mucosa & submucosa
§ Cryptitis & crypt abscesses
§ Ulceration

• Medical Treatment
o Goal is to induce remission (clinical & endoscopic) and maintain it.
o Mild – moderate disease
§ 5-aminosalicylic acid (5-ASA)
• Suppository or foam enema if proctitis/proctosigmoiditis
• Alternatively oral preparation
• Can be used in lower dose to maintain remission
§ Steroids
• Limited course if not responding to 5-ASA

116
 • Topical (suppository/enema) or oral
§ Biologics
• If fails to respond or steroid dependent
o Severe acute ulcerative colitis
§ Supportive care – usually requires hospitalisation
§ Correct electrolyte disturbance
§ Nutrition
§ +/- transfusion
§ LMWH – DVT prophylaxis
§ Steroids
• Oral or intravenous
§ Biologics – Anti-TNF
• To induce remission if no response to steroids
• To maintain remission if responds to steroids
§ Cyclosporine
• Alternative to biologic or if steroid contraindicated
• Large side effect profile

• Surgical Treatment
o Emergency Indications
§ Fulminant colitis not responding to medical treatment
§ Life threatening complications
• Toxic megacolon
o Non-obstructive dilation of colon (6cm in transverse) with associated
systemic toxicity (fever/tachycardia/leukocystosis)
• Perforation
• Severe haematochezia
o Elective Indications
§ Persistent symptoms despite best medical management
§ Increased risk of colorectal cancer
• Dysplastic polyps on surveillance colonoscopy
• Long standing disease (>10 years)

o Total Abdominal Colectomy with End Ileostomy

§ Emergency operation of choice – laparoscopic or open
• Entire colon removed and end ileostomy fashioned. The rectum is left in situ and
oversewn/stapled so the operation can be completed quicker in an unwell patient
• No restorative procedure is performed acutely as patients are unwell and frequently
immunosuppressed.
• Can later undergo a completion proctectomy [+/- ileal pouch anal anastomosis
(IPAA) with loop ileostomy and subsequent ileostomy closure (3-stage procedure)]
• In patients with persistent symptoms post op, the rectum can be treated with
topical steroids/5-ASA

117
 o Panproctocolectomy with ileal pouch anal anastomosis (IPAA)
§ Elective operation of
choice especially in
younger patients
§ Removal of rectum
and entire colon
§ Terminal ileum formed

20cm
into a ‘J pouch’ and
anastomosed to anus
§ Usually pouch is
defunctioned
with a temporary
loop ileostomy
(2-stage procedure)
§ IPAA complications include
pouchitis, faecal incontinence,
frequency and pouch failure Stapled “J” Reservoir

Pouch

Dentate
Line
Anus

o Panproctocolectomy with end ileostomy

§ For patients who don’t want reconstruction with IPAA
§ Older patients or patients with prior sphincter dysfunction that are not suitable for IPAA

o Total abdominal colectomy with ileorectal anastomosis

§ Not frequently performed for ulcerative colitis as rectum left in situ
§ Option for young females so pelvis is undisturbed to preserve fecundity
§ Also if there is a question of ‘indeterminate colitis’ or Crohn’s colitis, due to the high risk of
pouch failure with Crohn’s disease
§ Requires ongoing surveillance of rectum for cancer

118
Crohn’s Disease

• Crohn’s Disease is characterized by transmural inflammation and may involve any portion of luminal
gastrointestinal tract, from the oral cavity to the perianal area. There are many ways to classify Crohn’s
including age of disease onset, site of disease and behaviour of disease.

Montreal classification for Crohn’s Disease

Age at diagnosis
A1 below 16 years
A2 between 17 and 40 years
A3 above 40 years
Location
L1 ileal 80% (usually distal ileum)
L2 colonic 20% (unlike UC, 1/3 will have sparing of the rectum)
L3 ileocolonic 50%
L4 isolated upper disease* rare
Behaviour
B1 non-stricturing, non-penetrating
B2 stricturing Transmural inflammation often leads to fibrotic strictures
B3 penetrating Perforation, abscess, fistulae
p perianal disease modifier 33%

• Presentation
o Symptoms
§ Abdominal pain
• Common symptom regardless of disease distribution
• May be due to inflammatory disease
• May be due to strictures causing obstruction
§ Diarrhoea
• Common symptom, may fluctuate over long periods
• Various causes
o Impaired fluid absorption by inflamed bowel
o Bile salt malabsorption by diseased terminal ileum
o Entero-enteric fistulas bypassing absorptive surface area
o May have gross blood in stool or microscopic blood
§ Systemic symptoms
• Fatigue very common
• Weight loss – due to malabsorption or decreased intake
• Fever uncommon, may indicate abscess/perforation
§ Other GI symptoms
• Oral aphthous ulcers
• Oesophageal disease – dysphagia, odynophagia
• Gastroduodenal disease (15%) - similar symptoms to peptic ulcer disease
§ Extraintestinal manifestations
• Joints - Arthritis/arthropathy 20%
• Eye - uveitis/iritis/episcleritis 5%
• Skin – erythema nodosum/pyoderma gangrenosum 10%
• Primary sclerosing cholangitis 5%
• Renal stones – calcium oxalate / uric acid stones
• Bone loss

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• Features of transmural inflammation
o Strictures
§ Recurrent inflammation can result in fibrotic strictures causing obstruction
o Fistulas
§ Transmural inflammation may cause a sinus tract and penetrate serosa giving rise to fistula
(abnormal tract between two epithelial-lined organs)
§ Indolent process, usually doesn’t present with acute pain
§ Fistula to bladder (enterovesical), skin (enterocutaneous), bowel (enteroenteric) or vagina
(enterovaginal)
o Abscess / Phlegmon
§ Sinus tract may cause abscess formation with acute symptoms – pain/fever
§ May present with a phlegmon (a walled-off inflammatory mass)
o Perianal disease
§ Affects 30-40% of patients
§ Perianal abscess – requires emergency drainage
§ Perianal fistula may require seton drainage
§ Severe perianal disease may impair sphincter function and continence or cause anal stenosis

• Investigations
o Laboratory
§ FBC, U&E, CRP, LFTs, B12, Vitamin D, albumin, stool culture (if diarrhoea)
§ Faecal calprotectin
§ If considering biologic treatment – Mantoux, Quantiferon, Immunomodulatory viral screen
(HIV/HBV/HCV/VZV/EBV)
o Radiology
§ MR Enterogram to evaluate extent of bowel disease
§ CT Abdomen/Pelvis if abscess or perforate suspected
§ MRI pelvis to evaluate perianal disease
o Endoscopy
§ Colonoscopy with intubation of terminal ileum
§ OGD
§ Capsule endoscopy may be considered but not if suspicious of stricture
§ Mayo grading 1 – 3
• Degree of erythema, loss of vascular pattern, ulceration
§ Biopsy
o Histology
§ Transmural inflammation
§ Non-caseating granulomas in 50% of cases
§ Ulceration

• Medical Treatment
o Goal is to induce remission (clinical & endoscopic) and maintain it. Any focus of sepsis should be
controlled prior to medical treatment – i.e. drainage of perianal or abdominal abscess.
o Low risk with mild disease
§ Mild symptoms, lack of systemic signs of inflammation
§ Superficial ulcers, limited anatomic involvement, age >30 years
§ No perianal disease, no prior intestinal resection, no penetrating/structuring disease
§ Observation – if incidental finding and patient asymptomatic, repeat scope in 6mnth
§ Oral 5-aminosalicylic acid (5-ASA)
• If responds, can be used in lower dose for maintenance of remission
§ Oral steroids
• Should be tapered when remission is achieved
• If unable to stop then biologic/immunomodulator should be started
§ Biologics / Immunomodulator
• Usually not used in low-risk disease unless steroid dependent

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 § Dietician input
o High risk with moderate/severe disease
§ Moderate/severe symptoms, systemic signs of inflammation
§ Deep ulcers, long segment/diffuse bowel involvement, age <30 years
§ Perianal disease, prior intestinal resection, penetrating/structuring disease
§ Steroids
• Limited course if rapid symptom relief required
• Bridge to long term maintenance treatment
§ Biologics
• Anti TNF (e.g. infliximab, adalimumab)
• Anti Il 12/23 (ustekinumab)
§ Immunomodulator
• Azathioprine, 6-mercaptopurine, methotrexate
• May be given in combination with biologic
§ Supportive care
• Antibiotics if complicated by infection
• Fluid / electrolyte replacement
• Dietician input

• Surgical Treatment
o Crohn’s Disease is a chronic, incurable inflammatory disorder that is mainly managed medically.
However, 50% of patients with Crohn’s will have at least one surgical procedure. Because Crohn’s
disease often recurs, bowel resection should be performed with the goal of preserving as much
bowel as possible.
o Emergency indications
§ Bowel perforation
• Localised perforations are contained and may be initially treated with antibiotics +/-
radiologic drainage
• Free perforations require emergency resection +/- anastomosis and/or stoma
• Patients that are malnourished, on steroids, unstable or have a lot of contamination
should have a stoma rather than anastomosis
§ Abscess refractory to non-operative management
• More complicated abscess involving rectus sheath or retroperitoneum are less likely
to resolve with non-operative management
• Perianal abscesses require emergency drainage
§ GI bleed refractory to non-operative management
• More likely in Crohn’s colitis – may be difficult to localise source of bleeding
§ Fibrotic stricture causing bowel obstruction
• An alternative to surgery in subacute obstruction is endoscopic dilation if the
stricture is <5cm
• Surgical management of short strictures can be a stricturoplasty, longer strictures
require surgical resection.
• Occasionally, acute obstruction can be due to a combination of inflammation and
fibrosis – steroids occasionally used to reduce inflammation and relieve acute
symptoms to plan an elective operation

o Elective indications
§ Enteric fistula refractory to medical therapy
• Small bowel resection of affected segment
• May require repair of bladder/vagina
§ Small bowel or colorectal cancer/dysplasia
• Colorectal cancer much more common than small bowel
• Regular endoscopic surveillance is required
§ Persistent symptoms refractory to medical therapy
• Choice of surgery is dependent on the location and extent of disease
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o Small bowel surgery
§ Stricturoplasty
• Short strictures – bowel opened longitudinally and closed transversely to widen
lumen and preserve bowel
§ Small bowel resection
• Longer strictures / diseased segments of bowel
• Preserve as much healthy bowel as possible
• Anastomosis unless contraindicated
§ Ileocolic resection
• Terminal/distal ileal disease close to ileocaecal valve requires resection of valve with
caecum/ascending colon to perform ileocolic anastomosis

o Colorectal surgery
§ Segmental colectomy
• Suitable for very select patients with either isolated colonic stricture or solitary
segment of colonic disease
§ Total colectomy with ileorectal anastomosis
• For 2 or more involved segments of colon
• If rectum is spared, ileorectal anastomosis can be performed
• Ileorectal anastomosis can be delayed if resection is performed emergently
§ Total proctocolectomy with end ileostomy
• For patients with disease of colon and rectum
• Or patients with longstanding Crohn’s with a premalignant/malignant lesion
§ Proctectomy
• For isolated rectal disease
• Closure of perineum and end colostomy

o Post-operative management
§ Most patients eventually relapse with either clinical or endoscopic findings. 5-year rate of
recurrence is 25%. 10-year rate of recurrence is 35%
§ If low risk - Ileocolonoscopy at 6-12 months and recommence medical therapy if recurrence
§ If high risk – immunosuppressive therapy post op with Ileocolonoscopy at 6-12 months to
tailor treatment
§ Many will require subsequent surgery
§ Multiple resections risk short gut syndrome – intestinal failure, <200cm small bowel.

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6. Hernias

• Mr Ian S. Reynolds

• Inguinal Hernia
• Femoral Hernia
• Epigastric Hernia
• Umbilical Hernia
• Paraumbilical Hernia
• Incisional Hernia
• Spigelian Hernia
• Obturator Hernia
• Consent for Hernia Surgery

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Definition
• A hernia is a protrusion of a viscus or part of a viscus through an abnormal opening in the walls of its
containing cavity where it normally resides.
• Internal hernias occur when a segment of intestine herniates through a defect in the mesentery and cause
symptoms resulting in a hernia entirely within the peritoneal cavity.

Epidemiology
• Estimated incidence is 3-4% of the male population
• Lifetime risk of developing an inguinal hernia estimated to be 27% in men and 3% in women
• More than 1 million hernia operations take place in the United States, of which 80% will be for inguinal
hernias

Pathophysiology and Risk Factors

• Arise due to conditions that increase intra-abdominal pressure - most arise slowly over time, but some can
be precipitated by a single forceful event.
• Increased risk:
o People whose occupation requires frequent heavy lifting
o Recurring cough resulting in constant increases in intra-abdominal pressure
o Persistent straining at the time of micturition or defaecation
o Smoking
§ May result from reduced synthesis of type I and type III collagen associated with smoking
o Obesity
o Inguinal hernias
§ A patent processus vaginalis can predispose to the development of a hernia.
o Incisional hernias
§ Previous operation/wound complications/conditions associated with impaired wound
healing e.g. diabetes/steroid use
• The hernia consists of the hernial orifice and three other components – the sac, the coverings of the sac and
the components of the sac.
o The hernial orifice is the defect in the innermost aponeurotic layer of the abdomen.
o The sac is made of an outpouching of parietal peritoneum and consists of a mouth, neck, body and
fundus. The wider the diameter of the neck the less likely a hernia is to strangulate.
o The coverings of the sac will be derived from the layers of the abdominal wall through which the
hernia passes.
o The most common contents encountered in a hernial sac are the greater omentum, small intestine
and large intestine.
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Potential Complications of Hernias
• The majority of hernias are reducible meaning that the hernia will return to its normal containing cavity
when the patient lies down or it can be reduced by the patient or the surgeon.
• Occasionally a hernia will be irreducible meaning that the contents of the sac cannot be returned to their
normal containing cavity, however there are no other complications. Hernias are usually irreducible due to
adhesions between the sac and its contents or overcrowding within the sac.
• An obstructed hernia is an irreducible hernia containing intestine that is obstructed from without or within,
there is however no interference to the blood supply of the bowel. These patients have colicky abdominal
pain, vomiting, obstipation and abdominal distension and they also tend to have pain over the hernia site. If
left untreated for long enough, an obstructed hernia has the potential to become strangulated.
• A strangulated hernia is one in which the blood supply of its contents is impaired, the result is that the
contents at first become ischaemic and then progress on to develop gangrene.

History and Presentation

• Incidental finding when attending for another reason.
• Many patients will present with gradual enlargement of a lump in the groin or on the abdominal wall.
• Hernias are associated with a range of symptoms such as discomfort and pain related to the contents of the
sac and the pressure on surrounding tissues.
o Traditionally hernia pain has been described as being worse at the end of the day and relieved at
night time when the patient is in the supine position in bed.
• The majority of patients will initially present to their general practitioner and be referred onto a general
surgeon for management of their hernia.
• In some cases hernias will present to the hospital as an acute emergency.
o Typically these patients present with pain from strangulation of the hernia or with symptoms and
signs of intestinal obstruction (vomiting, abdominal distension, obstipation).
o As well as pain and symptoms of obstruction they will usually have a palpable lump at the site of the
hernia.
o Patients who present to the hospital emergently should be seen and dealt with quickly due to the
risk of intestinal ischaemia, gangrene, sepsis and death if the problem is not corrected in a timely
fashion.

Clinical Features and Clinical Examination

• The majority of ventral abdominal wall hernias (epigastric, umbilical, paraumbilical, incisional and port-site)
will have similar clinical features and should be easy to examine and diagnose.
• The patient will usually present with a lump over the area of concern.
• For the most part the lump will usually be more obvious in the standing position and it may fully or partially
reduce with the patient supine.
• When a hand is placed over the lump and the patient is asked to cough a palpable cough impulse will be felt
over the lump if it is a hernia.
• When examining patients with a hernia of the ventral abdominal wall you should describe the site and size of
the hernia. The size of the maximum dimensions of the external component can be estimated or measured
using a ruler on the skin.
• Deeper palpation may allow you to feel the hernial orifice from which the neck of the hernial sac is
protruding.
• Differential Diagnoses
o Divarication of the rectus abdominus muscle
o Rectus sheath haematomas and
o Benign and malignant neoplasms e.g. lipomas, desmoid tumours and rarely fibrosarcomas of the
abdominal wall.
• Examination of groin hernias (inguinal and femoral) should determine:-
o Whether or not a hernia is present
o Whether the hernia is inguinal or femoral
o If it is an inguinal hernia whether it is direct or indirect

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Investigations
• Investigations often are not necessary for the diagnosis and management of hernias in the elective setting.
• The majority of hernias can be diagnosed based on the history and clinical examination alone.
• In the elective setting where there is some uncertainty about the presence of a hernia imaging can be
obtained e.g. US or CT. The goal of imaging in these cases is to determine whether or not there is a hernia
and if so what are the contents of the hernia.
• Preoperative assessment prior to elective hernia surgery
o FBC, U&E and coagulation screen
o A type and screen (group and hold) may be required for some larger hernias or hernias being
repaired via a laparoscopic approach
o ECG, echocardiogram, chest X-ray and pulmonary function tests.

• The diagnosis and management of hernias in the emergency setting differs in several ways when compared
to the elective setting. As always all patients should have a clinical history taken and a thorough physical
examination should be performed
• In the emergency setting a full abdominal examination should be undertaken to look for signs of obstruction
proximal to the hernia. In patients who present late with gangrene or perforation there may be signs of
peritonism if any of the extruded bowel content has been able to track back into the peritoneal cavity.
o Blood tests that should be performed include a full blood count, urea & electrolytes, C-reactive
protein, coagulation screen and a group and crossmatch for 2 units if a laparotomy is anticipated.
o A lactate can be taken from venous or arterial blood and if raised it might be an indicator of bowel
ischaemia.
o A plain film of the abdomen (PFA) will show dilated loops of bowel proximal to the herniated
segment if obstruction is present.
o An erect chest X-ray is standard imaging that is performed in most emergency abdominal
presentations. In the case of a perforation air may or may not be visible under the diaphragm on an
erect chest X-ray.
o A CT scan can be obtained if any uncertainty exists about the diagnosis or if further imaging is
required
o The patient should have adequate fluid resuscitation, an NG tube should be placed if there are signs
of obstruction and a urinary catheter should be placed.

Management
• In the elective setting hernias can be managed conservatively or surgically.
• Patients should be counselled about the risks and benefits of each option and where feasible they should be
offered an operation to fix their hernia in the near future.
• There are some patients who have substantial medical comorbidities that preclude them from undergoing
operative repair of their hernias under general anaesthetic. It is reasonable in this cohort of patients to
recommend a conservative approach although some consideration should be given to an operative approach
using local anaesthetic or spinal anaesthesia where the risk of strangulation is considered to be high (e.g.
femoral hernias).
• Patients with reducible inguinal hernias can be informed that the risk of strangulation is less than 1% per
year.
• Conservative Management
o Ask the patient to present to the emergency department if they develop symptoms or signs of
obstruction or strangulation.
o Analgesia can be provided to those patients who get occasional discomfort or pain from their
hernias.
o Hernia truss or a hernia belt that helps to keep the hernia reduced during the daytime while they are
up.
• Surgical Management
o Surgical repair of hernias can be performed using sutures only or with a mesh.
o The basic principles of all hernia operations is that the repair should be tension free and where
possible the surgeon should avoid suturing together tissues that are not normally in apposition.

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o Most sutured repairs are carried out using non-resorbable monofilament sutures (e.g. polypropylene
sutures).
o There are a wide range of options available for mesh repairs and the choice of mesh is often based
somewhat on evidence and somewhat on surgeon preference and experience. The majority of
meshes are synthetic and they should only be used during clean operations. If the patient is found to
have contamination from a perforation at the time of their surgery the surgeon should consider
postponing definitive repair of the hernial defect until a later date.

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Inguinal Hernias
• Inguinal hernias can be direct or indirect.
• An indirect hernia travels through the deep ring (lateral to the inferior epigastric vessels) into the inguinal
canal alongside the spermatic cord and in some cases can exit through the superficial ring into the scrotum.
• A direct hernia comes directly through the posterior wall of inguinal canal (medial to the inferior epigastric
vessels). Direct hernias come through Hesselbach’s Triangle.
o Boundaries of Hesselbach’s Triangle
§ Lateral border = inferior epigastric artery
§ Medial border = rectus abdominis muscle
§ Inferior border = inguinal ligament
• Rarely patients can have a pantaloon type hernia which consists of direct and indirect components.

• Males are 20 times more commonly affected with inguinal hernias when compared to females.
• In adult males 65% of inguinal hernias are indirect and 55% are right sided.
• In 12% of cases the hernia is bilateral.
• Direct hernias become more common as patients get older. The risk factors are the same as for all hernias
described above.
• In the elective setting patients typically present with a lump in the groin, pain or discomfort in the groin, a
dragging sensation or pain in the testicle.
• Most inguinal hernias can be diagnosed clinically as described above and ultrasound, CT or MRI are rarely
required to confirm the diagnosis.

• Boundaries of the Inguinal Canal

o Anterior Wall
§ Aponeurosis of the external oblique, reinforced laterally by the medial fibres of the internal
oblique muscle.
o Posterior Wall
§ Transversalis fascia, reinforced along its medial one-third by the conjoint tendon
o Roof
§ The arching fibres of the transversus abdominis and internal oblique muscles.
o Floor
§ The medial one-half of the inguinal ligament, reinforced medially by the lacunar ligament.
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 o In adults the canal is about 3.75cm long and directed downwards and medially from the deep
inguinal ring (a U-shaped condensation of transversalis fascia) to the superficial inguinal ring (a
triangular aperture in the aponeurosis of the external oblique muscle).

• Contents of the Inguinal Canal

o In women the contents consist of the round ligament of the uterus, the genital branch of the
genitofemoral nerve derived from L1 and L2 and the ilio-inguinal nerve derived from L1.
o In men the contents of the inguinal canal consist of the spermatic cord and the ilio-inguinal nerve
derived from L1
§ The spermatic cord contains the following structures:
• Vas Deferens
• Artery to Vas Deferens
• Testicular artery
• Pampiniform plexus of veins
• Cremasteric artery
• Cremasteric vein
• Genital branch of the genitofemoral nerve
• Sympathetic and visceral afferent nerve fibres,
• Lymphatics
• Remnants of the processus vaginalis.

• Other Definitions
o Midpoint of the Inguinal Ligament: Point halfway along the inguinal ligament which is the midpoint
between the pubic tubercle and ASIS. 1cm above this point corresponds to the deep inguinal ring.
o Mid-Inguinal Point: Point halfway along a line joining the ASIS and the midline (i.e. pubic symphysis).
This point corresponds to the location of the femoral artery.

• Patients should be offered operative repair for their inguinal hernia as long as they are medically fit for an
operation.
o Open Approach
§ The Lichtenstein procedure - a tension free hernioplasty.
§ In this operation indirect hernial sacs will be separated from the cord, the sac contents will
be reduced into the peritoneal cavity and the sac will be transfixed with a suture and
excised.
§ In the case of direct hernias, the sacs will be reduced and in some cases the posterior wall
will be sutured to keep the sac in place while the mesh is placed.
§ In both direct and indirect hernias a mesh should be placed without tension to reinforce the
posterior wall of the inguinal canal.
o Laparoscopic Approach
§ Transabdominal Pre-Peritoneal (TAPP) Approach
• Involves reducing the hernia and placing a mesh over the defect laparoscopically
from within the peritoneal cavity. The
§ Totally Extraperitoneal (TEP) Approach
• Involves creating a space in front of the peritoneum and behind the other layers of
the abdominal wall and reducing the hernia and placing a mesh over the defect from
within this space.
o The choice of operation will be dependent on surgeon preference and the techniques that he/she
were exposed to during their training.
o The recurrence rate for the Lichtenstein and laparoscopic approaches should be less than 2%. Only
50% of recurrences will happen within 2 years

• Inguinal hernias can present in the emergency setting with obstruction, strangulation and in some cases
gangrene and bowel perforation. The diagnosis will usually be made clinically, however, CT can be used if
there is any uncertainty.

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 • The patient should be consented for the repair of the hernia and the consent should also include the
potential need to perform a bowel resection and anastomosis, to convert to a lower midline laparotomy and
in extremely rare circumstances where the patient is extremely unwell from a perforation to fashion a stoma
instead of performing a bowel anastomosis.
• Most emergency presentations of inguinal hernias will be dealt with through a standard groin incision. It may
be advisable not to use prosthetic mesh if there is any contamination from bowel content, in a case like this
a definitive repair of the hernia with placement of mesh can be performed weeks or months later when the
patient is well and there are no signs of ongoing infection.
• In the setting of patients presenting with an irreducible inguinal hernia some surgeons will advocate trying to
reduce the hernia. In the rare circumstances where the hernia can be reduced the patient should be
observed for 6-12 hours to ensure that a gangrenous or perforated segment of bowel has not been reduced
into the peritoneal cavity.

Femoral Hernias
• Femoral hernias pass through the femoral ring and into the femoral canal.
• The femoral ring is the entrance to the femoral canal and is extremely narrow with three of its four
boundaries formed by rigid ligaments explaining why femoral hernias are extremely susceptible to
strangulation (40% of femoral hernias present for the first time with strangulation).

• Boundaries of Femoral Ring

o Anterior: Inguinal ligament
o Posterior: Pectineal ligament
o Medial: Lacunar ligament
o Lateral: Femoral vein

• The femoral canal is the most medial compartment of the femoral sheath
o Approximately 1.25cm long
o Usually contains lymphatics, the lymph node of Cloquet, loose connective tissue and fat.
• Weight loss can result in a reduction of fat in the femoral canal and predispose to the development of a
hernia.
• Femoral hernias account for 20% of hernias in women and 5% of hernias in men.
• Female patients with femoral hernias are usually elderly and have had children.
• Male patients with femoral hernias tend to present between the ages of 30 and 45.
• The right side is affected twice as often as the left.
• While femoral hernias are more common in women than men the most common groin hernia in women is
still an inguinal hernia.
• Patients presenting electively usually present with a small palpable lump, they occasionally present with pain
or a dragging sensation.
• In the emergency setting femoral hernias present with signs and symptoms of strangulation and gangrene
can rapidly develop. Obstruction is not always present and a Richter’s type hernia (only one intestinal wall
protrudes through the defect resulting in partial obstruction) can occur frequently.
• There are a number of approaches to repairing a femoral hernia.
o Elective
§ A low approach (Lockwood operation) can be taken.
• This approach involves a groin incision below the inguinal ligament directly over the
hernia.
• The contents of the sac can be reduced and the defect can be repaired by suturing
the inguinal ligament to the pectineal ligament using non-absorbable sutures or a
piece of polypropylene mesh can be rolled and placed into the femoral canal and
sutured in place.
§ A high approach (McEvedy operation) can also be taken
• A vertical incision is made over the femoral canal and continuing upwards above the
inguinal ligament.

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 •
The hernia is dealt with in the preperitoneal space and the defect is again closed by
suturing the conjoined tendon to the iliopectineal ligament using a non-absorbable
suture or by covering the defect with a mesh.
• The benefit of this operation is that a bowel resection can be performed using this
incision as the peritoneal cavity can easily be opened.
§ Laparoscopic TEP approach
o Emergency
§ Lower midline laparotomy
• Reduce the hernia under direct vision and try and close the hernial defect from
inside the abdomen.
• This approach could also facilitate a bowel resection if it was required.

Epigastric Hernias
• Epigastric hernias occur through the linea alba at any point between the xiphoid process and the umbilicus.
• They usually commence as a protrusion of extraperitoneal fat and one theory suggests that this tends to
occur at sites where blood vessels pierce the linea alba creating a point of potential weakness.
• The cause of these hernias is more likely due to weaknesses of the linea alba secondary to abnormal
decussation of fibres of the aponeurosis.
• Sometimes multiple hernial orifices can be present.
• These hernias usually just contain extraperitoneal fat and sometimes omentum, although possible they
rarely contain intestine.
• They occur most frequently in manual workers between the ages of 30 and 45.
• They are often symptomless and occasionally present with pain due to strangulation of the fatty contents.
• The operation for these hernias can be undertaken through a vertical or transverse incision.
• The defect in the sheath is defined using diathermy.
• The sac and its contents can either be reduced or divided and removed using diathermy and suture ligation
as needed.
• Small defects (<4cm) can be repaired using non-absorbable sutures. Larger defects (>4cm) can be reinforced
with a mesh.

Umbilical Hernias
• These hernias tend to occur in infants and children partly from failure of the round ligament (obliterated
umbilical vein) to cross the umbilical ring and partly from absence of the umbilical fascia.
• Umbilical hernias occur equally in both sexes, however, they are seen eight times more frequently in African
infants when compared to Caucasian infants.
• These hernias become more prominent when the child cries.
• Obstruction and strangulation is extremely rare below the age of three.
• Conservative management should be advised for umbilical hernias in children under the age of two and
parents should be reassured that 95% of these hernias will resolve spontaneously.
• In children older than two the hernia is unlikely to resolve and an open approach should be used to either
reduce or ligate and transfix the sac and close the hernial defect with interrupted absorbable sutures.

Paraumbilical Hernias
• These hernias occur in adults and unlike in a true umbilical hernia the sac does not come through the
umbilical scar, instead it is a protrusion through the linea alba just above or below the umbilicus.
• As these hernias enlarge they become round or oval in shape and tend to sag downwards, they can become
quite big.
• The neck of the sac is usually much narrower than the body and stomach and the sac often contains greater
omentum but can also contain small intestine or transverse colon.
• These hernias are five times more common in women than in men and they tend to occur between age 35
and 50.
• Obesity and multiple pregnancies are the most important risk factors for these hernias.
• The omentum will often form adhesions within the sac and make these hernias irreducible.
• Patients will usually present with a painful swelling around the umbilicus.

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 • Large hernias may cause a dragging pain and traction on the stomach or transverse colon and may cause
gastrointestinal symptoms such as colic due to transient obstruction.
• The diagnosis of paraumbilical hernias is often made clinically and usually does not require any imaging.
• Due to the risk of strangulation the surgeon should recommend repairing these hernias to almost all
patients, the exception being those with major medical co-morbidities where the potential risks of an
elective repair outweigh the benefits.
• If the defect is small a sutured repair can be performed
• A ventral patch type mesh can be used to repair larger (>4cm) or recurrent defects.
• Some surgeons use a laparoscopic approach to repair these hernias in the elective setting, however, an open
operation using a small curved incision below the umbilicus is the most straightforward approach.
• A similar incision can be used to deal with strangulated paraumbilical hernias which are frequently
encountered. The incision and hernial orifice can be widened if a bowel resection and anastomosis is
required.

Incisional Hernias
• Incisional hernias are a diverse group of hernias and they can occur at any site where an incision has been
made or even in sites where a transabdominal drain has been placed.
• Risk factors
o Obesity
o Postoperative cough
o Postoperative vomiting
o Postoperative abdominal distension (e.g. in the setting of an ileus),
o Postoperative wound infection
o Diabetes
o Use of steroids or other medications that impair wound healing (e.g. chemotherapy).
o Patients that are malnourished, have a malignancy, jaundice, anaemia or hypoproteinaemia are all
at increased risk of developing incisional hernias.
o Vertical incisions are more likely to result in incisional hernias when compared to transverse
incisions.
o Emergency operations, particularly those for obstruction, peritonitis or in the rare instances when
operations for severe necrotising pancreatitis are performed are more likely to result in incisional
hernias when compared to elective operations.
• Incisional hernias often begin as a symptomless partial disruption of the deeper layers of a laparotomy
wound during the early postoperative course.
• The hernia may occur through only part of the incision or through its entire length (often the lower end).
• Incisional hernias tend to increase steadily in size over time.
• Most have a wide neck and do not necessarily require treatment.
• Intestinal obstruction can occur and strangulation is possible if loops of bowel protrude through a defect
with a narrow neck.
• For patients without symptoms who don’t mind the cosmetic appearance a conservative approach can be
taken, a truss can be tried but is often not needed.
• Operations on incisional hernias can be difficult as there is often a lot of adhesions and multiple
enterotomies can easily be made in the bowel during the dissection.
• The operation will involve freeing the obstructed segment from the incisional hernia. In the setting of
strangulation a bowel resection and anastomosis may be required.
• The fascial layers can be closed using non-absorbable sutures or a mesh can be used for larger defects.
• A laparoscopic approach can also be used in the elective setting using composite mesh to occlude the defect
after the hernial contents have been reduced.

Spigelian Hernias
• Spigelian hernias are a rare type of ventral hernia and account for 0.1-2% of all ventral hernias.
• They occur equally in men and women and tend to present in the 5th and 6th decade of life.
• These hernias occur due to a defect in the Spigelian aponeurosis which is composed of the transversus
abdominus and internal oblique aponeuroses.

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 • The borders of the Spigelian aponeurosis are the rectus abdominus muscle medially and the linea
semilunaris laterally.
• Spigelian hernias can occur anywhere along the length of the Spigelian aponeurosis, however they tend to
occur below the level of the umbilicus and above the level of the superior iliac spines (the area between
these two landmarks is known as the Spigelian hernia belt).
• These hernias may be asymptomatic and identified as an incidental finding when imaging is obtained for
another reason.

Obturator Hernias
• Obturator hernias are another rare type of hernia representing <1% of all abdominal wall hernias.
• They occur six times more frequently in women than in men and tend to occur between the ages of 70 and
90.
• Right sided obturator hernias are more common than left sided hernias and this is believed to be because
the left obturator foramen is covered by the sigmoid colon.
• These hernias occur when the abdominal contents herniate through the obturator foramen into the
obturator canal.
• Clinical diagnosis is difficult and patients with this type of hernia will usually require a CT scan to make or
confirm the diagnosis.

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Consent for Hernia Surgery
• When asked about consent for any procedure always break up the potential risks and complications into
those that are common to all procedures (general risks) and those that are specific for the procedure being
undertaken (specific risks).

• General Risks
o Reaction to anaesthetic or any medication used before, during or after the procedure
o Damage to teeth or airway during intubation
o Vocal cord damage from the endotracheal tube
o Pain (acute and chronic)
o Bruising, bleeding, the need for a blood transfusion, the need for return to theatre to deal with
bleeding
o Infection (superficial wound infection or deep infection)
o Wound dehiscence
o Nerve injury (associated with incorrect positioning on the operating table or insufficient padding of
at risk areas)
o Deep vein thrombosis
o Pulmonary embolus
o Myocardial infarction
o Stroke
o Death (although rare, even elective procedures are associated with a risk of mortality)

• Specific Risks
o Damage to bowel, bladder or major blood vessel (these three complications may require a bigger
procedure such as a laparotomy to be carried out to repair the damage)
o Recurrence of the hernia (either acutely or in the long-term)
o Ischaemic orchitis (due to damage to the testicular artery of pampiniform plexus of veins)
o Urinary retention
o Mesh infection (this is serious and will often require removal of the mesh),
o Extrusion of mesh through the skin
o Adherence of bowel to the mesh which can result in an obstruction or even development of a fistula
o Development of a seroma or haematoma (seromas and haematomas can be managed conservatively
or can be drained).

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References

• Gray’s Anatomy for Students 4th Edition. Richard L. Drake, A. Wayne Vogl, Adam W.M. Mitchell.

• Last’s Anatomy: Regional and Applied 12th Edition. Chummy S. Sinnatamby.

• Bailey & Love’s Short Practice of Surgery 27th Edition. Norman S. Williams, P. Ronan O’Connell, Andrew
McCaskie. [Excellent reference text that can be used to gain more details on most surgical topics. It’s a
worthwhile purchase for anyone interested in reading more about surgery and definitely for those
planning on pursuing a career in surgery].

• Schwartz’s Principles of Surgery 11th Edition. F. Charles Brunicardi. [Excellent reference text that can be used
to gain more details on most surgical topics. This book contains even more details than Bailey & Love’s
and provides nice overviews of relevant surgical anatomy and physiology at the start of most chapters.
This is the textbook recommended by a lot of American Medical Schools and would be considered
essential reading for a lot of surgical residency programmes in the USA. It’s a great book for those
interested in surgery but contains much more than you need for your finals in surgery].

• Clinical Cases and OSCEs in Surgery 3rd Edition. Manoj Ramachandran, Marc A. Gladman. [A must have for all
students in my opinion. Contains a lot of detail for such a small book and provides simple instructions on
how to carry out most of the clinical exams that you will encounter in both short and long cases. It even
deals with most of the questions you will face in your clinical exams. It can be purchased for a reasonable
price and will still be useful when you undertake your membership exams in medicine, surgery or general
practice].

• Amid PK, Shulman AG, Lichtenstein IL. The Lichtenstein open "tension-free" mesh repair of inguinal hernias.
Surg Today 1995;25(7):619-25. doi:10.1007/BF00311436.
o [The original Lichtenstein paper, not mandatory reading but those interested in surgery may enjoy
it].

• There are several other surgical textbooks such as Clinical Surgery 3rd Edition by Michael M. Henry &
Jeremy N. Thompson and Principles and Practice of Surgery 7th Edition by O. James Garden & Rowan W.
Parks. These books provide less detail than Bailey & Love’s or Schwartz’s but they would be adequate for
your surgical finals. You may find that this surgical handbook provided to you by UCD provides just as much
information as these two texts but in a more focused way.

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7. Vascular Surgery

• Ms Aoife Kiernan, Mr Thomas Aherne, Mr Nawar Masarani, Mr Ahmed Hassanin

• Abdominal Aortic Aneurysm (AAA)

• Carotid Artery Disease (Extracranial Cerebrovascular Disease)
• Acute Lower Limb Ischaemia (ALI)
• Peripheral Arterial Disease (PAD)
• Vascular History and Examination
• Incisions
• Ulcers
• The Diabetic Foot
• Charcot Foot
• Varicose Veins
• Lower Limb Deep Venous Thrombosis (DVT)

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Abdominal Aortic Aneurysm (AAA)

Definition
• Abnormal dilatation of the abdominal aorta, exceeding the normal diameter by >50% (diameter >3cm is
considered aneurysmal as the maximal normal abdominal aortic diameter is 2 cm).

Epidemiology
• The prevalence of abdominal aortic aneurysm (AAA) in men over 65 years is around 7–8%.
• The condition is thought to be six times greater in men than in women.

Pathophysiology
• 90% are thought to represent a degenerative or non-specific process.
• Abdominal aortic aneurysms exhibit familial clustering. This raises the possibility of both genetic and
environmental aetiological factors.
• Aneurysms are more prevalent amongst smokers.
• Abdominal aortic aneurysms are characterised histologically by destruction of elastin and collagen in the
tunica media and tunica adventitia.
• Four pathological mechanisms are thought to play central roles in AAA development: proteolysis of
connective tissue, inflammation, biomechanical stress and genetic influences.

History and Clinical Presentation

• About 75% of aortic aneurysms are asymptomatic and are discovered incidentally either as a pulsatile
abdominal mass on physical examination or on abdominal imaging done for another reason.
• A small proportion will present with symptoms related to pressure on adjacent structures (Back/flank pain,
ureteric compression, caval compression).
• Most of the clinical symptoms due to aortic aneurysm are related to aneurysm rupture or embolism of
mural thrombus.

Risk Factors
• Advanced age
• Male sex
• Positive family history of AAA
• Smoking (ten-fold increased risk)
• Uncontrolled hypertension
• Hyperlipidaemia

Complications
• Aneurysm rupture is associated with an estimated overall mortality of 90% and a significant proportion of
patients (over 50%) will not reach hospital.
• Embolism: patients with embolisation of thrombus from an aortic aneurysm may also present with acute
ischaemia of the lower limb.

Investigations
• Abdominal ultrasound (U/S): An initial imaging modality to detect the AAA, non-invasive, available, no
radiation or contrast exposure. However, cannot show the morphology or the extension of the AAA so it is
not adequate to plan surgical/endovascular repair.
• CT Angiogram of the Aorta (CTA): high accuracy in sizing the aneurysm diameter, extension, morphology,
aneurysm relation with the renal arteries (neck), detect any leak or rupture, and used to plan the repair
(suitability for endovascular aortic repair (EVAR)).

Screening
• Men above 65 years with risk factors should be screened for AAA (NICE guideline, UK).
• The rate of aneurysm growth and rupture is directly related to its size. The risk of rupture jumps significantly
when the size of the AAA exceeds 5.5cm (repair is indicated).

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Surveillance of Asymptomatic AAA

Current surveillance guidelines

3cm – 4.4cm Annual surveillance with U/S
4.5cm – 5.4cm 3 monthly U/S surveillance
5.5cm or greater Repair (OSR / EVAR)

Aneurysm Repair
• The repair can be an elective procedure (open surgical repair (OSR) or EVAR) when the aneurysm size is
exceeding the 5.5 cm threshold or when the rate of growth is >1cm per year, or an emergency repair (OSR or
EVAR) in the case of rupture or symptomatic aneurysm.

Open Surgical Repair (OSR)

• Done through midline incision (laparotomy) with mortality around 5%.
• The aneurysm is replaced with synthetic graft either tube, or bifurcated (Aorto-bi-Iliac, Aorto-bi-Femoral)

OSR Complications
• Early
o Bleeding
o MI (Myocardial Ischemia)
o Respiratory complications
o Renal failure
o Colonic ischemia
o Lower limbs ischemia
o DVT (Deep Venous thrombosis)/PE (Pulmonary Embolism)
o Abdominal compartment syndrome (in ruptured AAA)
o Impotence in men
• Late
o Anastomotic breakdown
o Graft infection
o Abdominal wall incisional hernia
o Small bowel obstruction (adhesions)
o Aorto-enteric fistula (upper GI bleeding)

Endovascular Aneurysm Repair (EVAR):

• The stent graft is delivered through groin incisions to exclude the aneurysm.
• Must be done using radiation and nephrotoxic contrast is used.
• No Aortic clamping is needed, less early postoperative mortality than OSR, but higher re-intervention rate
due to endoleak which requires lifelong surveillance with US or CTA.

EVAR Complications
• Early
o Endoleaks (persistent flow between the graft and the aneurysm sac, the aneurysm is not fully
excluded)
o There are five types of endoleak:

Type I Leak at attachment sites of graft proximal or distal

Type II Filling of aneurysmal sac by collateral vessels (IMA, Lumbar)
Type III Leak through defect in graft
Type IV Leak through fabric of graft due to porosity
Type V Expansion of aneurysm sac without evidence of leak on imaging

o Atheroembolization during graft insertion (organ infarction, limb ischemia)

o Vessels injury with guidewires and catheters

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 • Late
o Graft migration/dislocation
o Graft kinking/occlusion
o Pseudoaneurysms
o Graft infection

Ruptured Abdominal Aortic Aneurysm:

• Vascular emergency with extremely high mortality.
• The rupture can be free into the abdominal cavity (immediate death), or can be contained retroperitoneally
(gives time to transfer patient to hospital for management, OSR or EVAR).

Clinical Presentation
• The classical patient is a male above 65 years old.
• Sudden onset of abdominal, back, or flank pain.
• Collapse, hypotension.
• A known history of AAA under surveillance can be present, or the rupture might be the first presentation of
unknown AAA.
• Aggressive resuscitation should be avoided as it may convert a contained rupture to a free rupture.
• The principle of Permissive Hypotension is applied where the systolic BP is kept between 70-80 mmHg to
maintain vital organs perfusion.
• Urgent repair must be done to save life either with OSR or EVAR.

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Carotid Artery Disease (Extracranial Cerebrovascular Disease)

• Atherosclerotic disease of the carotid arteries can cause stroke or transient ischemic attacks (TIAs).
• Stroke is the third commonest cause of death and a major cause of neurological disability.

Definitions
• Stroke It is defined as acute loss of focal cerebral function with symptoms exceeding 24 hours (or leading to
death), with no apparent cause other than of vascular origin.
• A transient ischaemic attack (TIA) has the same definition, but lasts < 24 hours.

Epidemiology
• In the UK, the annual incidence of stroke is 2:1000 and 150 000 patients will suffer their first stroke each
year.

Aetiology
• About 80% of strokes are ischaemic and 20% haemorrhagic (intracerebral/subarachnoid).
• Approximately 80% of ischaemic strokes affect the carotid territory.
• The main cause of ischaemic, carotid territory stroke is thromboembolism of the internal carotid artery (ICA).

Risk Factors
• Advanced age
• Smoking
• Hypertension
• Ischemic heart disease
• Cardioembolic source
• History of TIA
• Diabetes
• Peripheral vascular disease
• Hypercholesterolemia

Clinical Presentation
• Asymptomatic Carotid Disease: carotid stenosis without stroke or TIA, carotid bruit can be detected.
o The presence/absence/quality of a bruit does not correlate with degree of stenosis.
• Symptomatic Carotid Disease: The carotid plaque can rupture and cause stroke / TIA, or death.
• Carotid territory classical symptoms:
o Hemimotor/hemisensory signs
o Monocular visual loss (amaurosis fugax)
o Higher cortical dysfunction (dysphasia, visuospatial neglect etc.)
• FAST is an acronym used as a mnemonic to help detect and enhance responsiveness to the needs of a
person having a stroke. The acronym stands for:
o Facial drooping
o Arm weakness
o Speech difficulties
o Time to call emergency services.

Investigations
• Duplex ultrasound (DUS)
• Contrast enhanced MRA (CEMRA)
• CT Angiogram (CTA)
• Digital subtraction Angiography (DSA)
• Echocardiogram (detect cardiac embolic source)
• ECG/ Telemetry (Arrhythmias)

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Treatment/Management: Best Medical Therapy (BMT) vs Surgery

• Asymptomatic Disease
o BMT including Aspirin, Clopidogrel, Statins, smoking cessation, control of blood pressure and
diabetes.

• Symptomatic Disease
o In patients with limited neurology post stroke and who are acceptable risk for intervention
o Surgery - Carotid Artery Endarterectomy (CEA)
§ Removing the atherosclerotic plaque from the ICA +/- patch repair, +/- use of shunt during
surgery to maintain cerebral perfusion.
• Can be done under GA or local.
• Incision along anterior border of sternocleidomastoid muscle.
§ Complications
• Cranial nerve injury (Vagus, Glossopharyngeal, Hypoglossal)
• Wound complications (hematoma that can compromise airway, or infection)
• Perioperative stroke
• Restenosis of the carotid artery
• Patch infection
o Endovascular Treatment (Carotid Artery Stent, CAS)
§ Performed under local, through common femoral artery (CFA)
• Puncture at the groin
• Higher periprocedural stroke rate.
• Protection devices or filters may be used.
§ Complications
• Cerebral hyper-perfusion syndrome (headache, cerebral bleed, death)
• Intra-cranial hemorrhage
• Atherosclerotic embolization
• Stent thrombosis
• Carotid dissection
o Contraindications to CEA/CAS
§ Total carotid artery occlusion
§ Severe neurological deficit after stroke (poor recovery)
§ Severe comorbidities (unfit patient)

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Acute Lower Limb Ischaemia (ALI)

Definition
• Sudden decrease in limb perfusion that threatens limb viability. (TASC 2008)*
(*TASC 2008 Trans-Atlantic intersociety Consensus meeting 2008)

• Acute lower limb ischaemia is associated with high risk of limb loss, up to 30-50% at 30 days.

Causes
• Thrombosis
o Atherosclerosis (Acute-on-chronic Ischaemia) most common cause of ALI. Often patient has a history
of intermittent claudication.
o Popliteal aneurysm
o Bypass graft occlusion
o Endovascular stent occlusion
• Embolism
o Atrial fibrillation
o Mural thrombosis
o Vegetations
o Proximal aneurysm
o Atherosclerotic plaque
• Rare Causes
o Dissection
o Trauma
o Intra-arterial drug injection
o Iatrogenic.
_______________

Clinical Features (6 P’S)

• Pain, pallor, pulselessness, perishing cold, paraesthesia, paralysis

Rutherford’s Classification
Category Description Capillary Muscle Sensory Loss Doppler Signals
Refill Paralysis Arterial Venous
I Not Intact None None Audible Audible
Viable immediately
threatened
IIa Salvageable if Intact/ None Partial Inaudible Audible
Threatened promptly slow
treated
IIb Salvageable if Slow/ Partial Partial/ Inaudible Audible
Threatened immediately absent complete
treated

III Needs primary Absent/ Complete Complete Inaudible Inaudible

Irreversible amputation mottling tense
compartment

Initial Management
• If clear evidence of acute ischaemia on history and exam, do not delay definitive treatment and give IV
heparin 5000 units bolus

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 • Patients usually have other significant comorbidities: IHD, renal disease.
• Give O2
• IV access and fluids if dehydrated.
• Bloods – FBC, U&E, coagulation profile, troponin, glucose, group & save.

Management Options
• Category III Irreversible Leg Ischemia
o Resuscitate and stabilize before considering amputation.
• Category IIb Immediately Threatened
o Start with Initial management with urgent CTA followed by urgent revascularization with surgery
(thromboembolectomy +/- bypass surgery)
• Category IIa (threatened) and Category I (viable) limb
o Revascularization options include endovascular catheter directed thrombolysis in addition to open
surgical thromboembolectomy and bypass.

Complications of Reperfusion
• Mostly occur after delayed revascularization, >6hrs from the onset of ALI, particularly in category IIb/III
disease.
• Post revascularization swelling.
• Rhabdomyolysis
o Elevated K+, elevated CPK, renal impairment, myoglobinuria.
o Treat with aggressive IV fluids, diuresis with Mannitol, alkalinisation of urine.
• Compartment syndrome – prevent and treat with 4-compartment fasciotomy.

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Peripheral Arterial Disease (PAD)

Definition
• Chronic decrease of the arterial blood supply of the limbs (most commonly the legs) due to atherosclerotic
stenosis or occlusion of the vessels
• Primary pathological cause is atherosclerosis
• Less common causes include
o Popliteal artery entrapment
o Fibromuscular dysplasia
o Vasculitides (Buerger’s disease, Takayasu arteritis)

Symptoms
• Intermittent Claudication: Muscular pain (most commonly in calves and/or buttocks) brought on by exercise
and relieved by rest
o Caused by demand for oxygen by muscles during exertion in the context of reduced blood supply
• Critical Limb ischaemia
o Rest pain > 2 weeks
§ Pain in the forefoot when lying flat at night, classically relieved by hanging leg over side of
bed
o Tissue loss (ulcers, gangrene, necrosis)
• Pallor of the lower limb
• Reduced temperature of the lower limb
• Burning sensation, paraesthesia
• Leriche Syndrome: Aortoiliac occlusion causing classical triad
o Buttock/thigh claudication
o Absent/reduced femoral pulses
o Erectile dysfunction

Risk Factors
• Non modifiable factors (male, age>55, family history of vascular disease)
• Smoking (most important risk factor)
• Hypertension
• High Cholesterol
• Diabetes
• Previous Stroke / Myocardial infarct / Angina
• Hyperhomocysteinemia

Classification

Fontaine Classification
I Asymptomatic
II Intermittent Claudication: Can be further classified into IIA
(claudication distance>200m) and IIB (claudication
distance<200m)
III Rest Pain
IV Tissue Loss (ulcers, gangrene, necrosis)

Differential Diagnoses to consider apart from Intermittent Claudication:

• Spinal stenosis
• Osteoarthritis
• Symptomatic Baker’s Cyst
• Nerve root entrapment (e.g. Sciatica)

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Diagnosis

• History Taking
o Full cardiovascular history and risk factors (smoking, hypertension, diabetes, dyslipidaemia)
o Pain character, site, claudication distance and rest time
• Examination
o Inspection: trophic changes and scars of previous surgery
o Palpation: of all pulses and capillary refill time
o Buerger’s test and sign

Investigations
• Ankle-Brachial Pressure Index (ABPI): Ratio of peak systolic doppler ankle pressure to arm pressure

ABPI interpretation
1.2-0.9 Normal
0.9-0.5 Intermittent claudication
<0.5 Rest pain
<0.3 Tissue loss
>1.3 Calcified arteries (typically seen in diabetics) - False
elevation, incompressible vessels
• Duplex Ultrasound
• CT Angiogram/MR Angiogram
• Digital Subtraction Angiography DSA

Management
• Best Medical Therapy (BMT)
o Successful in 75% of Fontaine Stage I and II intermittent claudicants
o Consists of three parts
§ Risk Factor Modification
• Smoking cessation (CRUCIAL)
• Physical exercise
• Dietary modification
§ Medical Treatment
• Antiplatelet therapy (Aspirin, Clopidogrel)
• Statin: lowers cholesterol, improves walking distance, reduces rate of major vascular
events
• Control BP
• Tight glycaemic control
§ Exercise
• Regular supervised exercise program

• Endovascular and Surgical Interventions in Stage III and IV Fontaine’s classification or if failed BMT
o Endovascular
§ Angioplasty +/- stenting.
§ In many cases, procedures can be performed as day case procedures.
§ Procedures can also be performed under local anaesthesia

o Surgical
§ Endarterectomy
§ Bypass procedures used for disease not best managed by endovascular techniques
• Can use synthetic graft (e.g. PFTE/Dacron) or vein graft (the best option e.g. GSV).
• Examples of bypass procedures
o Anatomical: Fem-pop bypass, fem-distal bypass, aorto-bifem bypass
o Extra-anatomical: axillo-bifem bypass, fem-fem crossover
• Amputation if non-viable limb
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Vascular History and Examination
• Atherosclerosis is a systemic disease.
• A patient is likely to have associated coronary artery disease.
• The risk factors are the same regardless of the vascular territory, although diabetes and smoking in particular
increase the risk in the lower limbs.
o For an outline of a vascular history, please see Figure 11.1 in Vascular and Endovascular surgery at a
Glance, first edition by Morgan McMonagle & Matthew Stephenson.

Examination
• Follow the format of inspection, palpation, (percussion), auscultation
• There are three relevant vascular exams to study
o Peripheral vascular exam of the lower limb
o Varicose veins
o Ulcers
• When examining pulses, generally start at the feet and move up to finish with the abdominal aorta.
o Know the landmarks for each pulse (Dorsalis pedis, posterior tibial, popliteal artery, femoral artery,
aorta)
• Special tests
o Buerger’s angle and test.
§ Ask the patient to raise their leg off the bed, inspect for ulceration.
§ Keep raising slowly.
§ If leg blanches: note the angle – this is Buerger’s angle; if it is less than 30° this indicates
severe ischaemia.
§ Ask the patient to swing the leg out of bed to see if it becomes hyperaemic (pink/purple) if
so – Buerger’s positive
• In an exam scenario, state that you would also
o Examine the rest of the cardiovascular system
o Examine the venous system in the legs
o Check the sensation
o Check the ABPI (ankle brachial pressure index, see PAD section)

146
Incisions used for access in vascular surgical procedures

147
Ulcers

Definition
• An ulcer is a breach of the continuity of the skin, epithelium or mucous membrane caused by sloughing of
necrotic inflammatory tissue and which fails to heal.

Causes
• Venous
• Arterial
• Mixed arterial & venous disease
• Neuropathic
• Diabetes
• Vasculitis - Buerger's disease, Takayasu's arteritis
• Malignancy- (‘Marjolin ulcer- SCC’) consider if ulcer does not heal with adequate medical management
• Lymphoedema

It is important to ask about both arterial, neuropathic and venous risk factors for ulceration

Clinical Features of Arterial, Neuropathic & Venous Ulcers

Examination Arterial Ulcer Neuropathic Ulcer Venous Ulcer
Pulses Absent Present Present
Skin Perfusion Cool, prolonged Normal and warm Normal and warm
capillary refill
ABPI Reduced (<0.5) Normal Normal
Ulcer Location Pressure and friction Pressure areas Medial (or lateral)
areas (heel & toes) malleolus (gaiter area)
Ulcer Margin ‘Punched out’ well ‘Punched out’ well Large and irregular
defined defined ‘sloped’
Depth Deep Deep Superficial
Size Small Small Large
Base Black necrotic tissue Clean granulating (pink) Yellow wet appearance
(dry or wet) wound ‘sloughy’
Exudate Minimal Minimal Moderate to large
Skin Pale, thin, hairless, Healthy Signs of venous
friable hypertension (Varicose
veins, haemosiderin
deposition,
lipodermatosclerosis)
Oedema Minimal Minimal Moderate to severe
Pain Ischaemic rest pain Insensate Painful

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 Arterial Ulcer Neuropathic Ulcer Venous Ulcer
Pathophysiology Poor arterial supply Limb prone to injury Chronic venous
resulting in tissue without detection given hypertension leads to
hypoxia. Decreased reduced sensation. tissue oedema with
perfusion also leaves There may be venous congestion. The
these prone to infection associated chronic joint skin is vulnerable to
with poor healing destruction and minor trauma or
ability. malformation spontaneous
(Charcot’s joint’) breakdown with poor
healing ability.
Cause PVD Diabetes Venous hypertension
Diabetes Ischaemic neuropathy VV
mellitus(macro-and (post ALI) DVT
microvascular Alcoholic neuropathy Congenital absence of
occlusion) Vit B12 deficiency deep veins (Klippel-
Arterial trauma Medications Trenaunay syndrome)
Arterial embolism
Vasculitis
Investigations Wound swab Wound swab Wound swab
ABPI +/-Nerve conduction Venous duplex
Arterial Duplex studies for initial +/-ABPI
+/- CT/MR angiogram diagnosis
+/-ABPI if pulses not
palpable
Management Correction of poor Relieve pressure areas Compression bandage
tissue perfusion As per Treat infection Leg elevation
chronic PVD in patients Generally irreversible Class II stocking when
with critical limb Good diabetic control healed
ischaemia +/-Skin graft
Treat infection Consider
VV surgery if possible
once ulcer healed to
reduce recurrence rate

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The Diabetic Foot

• The diabetic foot is a challenging condition requiring a multidisciplinary team approach, often including
vascular surgery, endocrinology, diabetic nurse specialist, nephrology, podiatry, tissue viability, and
orthotics.

Aetiology of Diabetic Foot

• Neuropathy (sensory and autonomic neuropathy)
• Vasculopathy (macro-and micro-vascular disease)
• Infection

Pathophysiology
• Neuropathy
o Loss of posterior spinal columns – decreased joint position and vibration
o Eventually loss of lateral spinal tracts – decreased sensation of pain and temperature
o Autonomic neuropathy – shunting of blood from skin contributes to vulnerability, leading to ulceration
and poor healing

• Vasculopathy
o Macrovascular refers to PAD – atherosclerosis is often diffuse and multilevel throughout lower limb,
vessels are often smaller and heavily calcified (especially tibial vessels)
o Microvascular – non-atherosclerotic disease affecting other vessels (skin, retina, kidney).
Hyperglycaemia-related thickening of the basement membrane in arterioles causing impaired oxygen
diffusion

Risk Factors for Diabetic Foot

• Previous ulcers/amputations
• Diabetic neuropathy - stocking distribution, Charcot’s joint
• Poor glycaemic control
• Associated peripheral arterial disease
• Smoking
• Evidence of other diabetic complications e.g. Renal/visual impairment.

Clinical Features
• Ischaemic ulcers commonly on pressure points (toes, heels).
• Evidence of sensory loss -chronic friction can lead to callus formation which predisposes to ulcers
• If arterial disease is present, foot may be cool with reduced/absent pulses.
• Infection is more common in diabetics, it can progress quickly and travels proximally through foot along
tendons to involve joint. Sepsis control often includes incision and drainage, broad-spectrum antibiotics, +/-
amputation
• ABI may be falsely elevated (due to calcified vessels). Toe pressures are a useful adjunct in determining
perfusion in this population

Investigations
• ABIs / Toe Pressures/ TcPO2(transcutaneous pO2)
• Duplex US
• CT Angio / MR Angio if co-existing arterial disease suspected
• Check blood glucose level and HBA1c, renal function, BP

Management
• Best done at a specialist multidisciplinary clinic
• Regularly inspect feet
• Appropriately fitted footwear & avoid walking barefoot
• Podiatry/Chiropodist for debriding calluses and for nail care

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 • If infected ulcer
○ Broad spectrum antibiotics
○ +/- Debridement of dead tissue
○ +/- Amputation of non-viable digits if adequate arterial supply for healing of amputation
○ X-ray/MRI to rule out underlying osteomyelitis
• Consider revascularization if significant arterial disease
• Consider amputation if no response to medical or other surgical treatments

Neuropathic Ulcers
• Caused by trauma to insensate foot
• Punched out appearance
• Located over pressure points or calluses
• Surrounded by inflammatory tissue
• Frequently painless due to neuropathy

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Charcot Foot
• Chronic, progressive, degenerative arthropathy as a result of a loss of sensory innervation of the affected
joint and its ligaments.

Pathophysiology
• Neuropathic arthropathy – loss of protective joint and sensory reflexes allows minor trauma and chronic
pressure maldistribution to go undetected.
• Joints (ankle and foot- metatarsal-phalangeal) become painlessly destroyed resulting in deformity,
osteoarthropathy and new bone formation.
• Motor neuropathy – muscle wasting and loss of arch architecture, in-drawing of toes (‘hammer’ or ‘claw’
toes)
• Autonomic neuropathy – shunting of blood away from skin. Feet are dry and prone to callus formation over
pressure areas.

Clinical Features
• Sensory neuropathy – pin-prick & light touch, loss of temperature sensation, loss of proprioception and
vibration sense
• Grossly deformed, swollen ankle joint
• Fallen arches ‘flat foot’
• +/- ulceration
• Acute - warm, red, swollen, painful (can be confused with cellulitis)

Management
• Usually multidisciplinary approach – vascular, endocrine, podiatry, orthotics, TVN
• Non-Surgical
o Immobilization - cast, removeable boot, brace, non-weight bearing
o Orthotics – custom-made shoes after the bones have healed to reduce recurrence and risk of
ulceration
• Surgical (uncommon)
o Realignment or bony fusion

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Varicose Veins

Definitions
• Varicose veins: subcutaneous superficial veins that are tortuous and dilated measuring >3mm when
examined in the standing position. They are the result of underlying venous incompetence.
• Venous incompetence: dysfunctional venous emptying, leading to venous hypertension, most commonly
associated with underlying valvular failure

Epidemiology
• Very common presentation
• Predominantly affects the legs (trunk, pelvis and upper limbs may also be affected)
• 20-40% of the general population report varicose veins (some epidemiological studies report rates up to 80%
among the general population)
• 5-10% report skin changes associated with chronic venous disease
• 1% present with venous ulceration
• Female preponderance

Risk Factors
• Increasing age
• Pregnancy
• Prolonged standing
• Obesity
• Family history
• Previous deep venous thrombosis

Aetiology and Anatomy

• Functioning deep and superficial veins permit outflow of blood from the lower limb. In normal anatomy this
anti-gravitational effect occurs using a system of one-way valves, which prevent reflux of blood and the
muscle pump (muscular contraction which propagates venous blood towards the heart). Chronic failure of
these systems results in an increased peripheral vessel hydrostatic pressure. This increases the permeability
of peripheral venules via wall shear stress leading to extravasation and chronic interstitial inflammation. This
inflammatory cascade causes peripheral oedema, skin damage and subsequently ulceration.
• The deep veins traverse the leg closely aligned to the course of the lower limb arteries and connect with the
Great Saphenous Vein (GSV) at the groin (saphenofemoral junction) and the Small Saphenous Vein (SSV) in
the popliteal fossa (saphenopopliteal fossa) both of which are located superficially.
• The GSV runs along the medial aspect of the leg from groin to the medial malleolus while the SSV runs
downs the centre of the calf from the popliteal fossa to the lateral malleolus. Incompetence of these veins
typically leads to varicose veins and as such they are the focus of surgical treatment.
• Valve failure can be primary (most common) related to valvular degeneration over time, or secondary
related to obstruction (DVT, obesity, pregnancy), or congenital (Klippel-Trenaunay)

Symptoms Signs
• Heaviness • Telangiectasia
• Aches and cramps • Varicose veins
• Restlessness • Swelling
• Itchiness • Haemosiderin deposition
• Pressure feeling • Eczema
• Lipodermatosclerosis
• Ulceration

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Complications of Venous Incompetence
• Impaired quality of life due to symptoms
• Bleeding
• Superficial thrombophlebitis
• Skin changes leading to ulceration
• Deep venous thrombosis

Investigation
• Trendelenburg’s and Perthe’s tests are largely obsolete, with ultrasound routinely used to assess venous
disease
• Venous Colour Duplex
o Used to identify location of venous reflux (GSV/SSV)
o Used to assess the deep veins for incompetence or obstruction

Classification of Disease
• Clinical Etiological Anatomical Pathological (CEAP) classification: (only the clinical component is routinely
used in practice as below)
o C0: no visible or palpable signs of venous disease
o C1: Telangiectasia or reticular veins
o C2: Varicose veins; distinguished from reticular veins by a diameter of 3mm or more
o C3: Oedema
o C4: Changes in skin and subcutaneous tissue secondary to CVD
§ C4a: Pigmentation or eczema
§ C4b: Lipodermatosclerosis or atrophie blanche
o C5: Healed venous ulcer
o C6: Active venous ulcer

Treatment
• Conservative
o Aims to reduce the effects of chronic venous hypertension. This can be achieved using
o Leg elevation to augment venous return
o External compression using graduated compression stockings (Class 2*). This compress to a greater
extent at the ankle with reducing pressure proximally
or
o Multilayer compression bandaging* which is largely reserved for refractory swelling or venous
ulceration
§ These can only be applied provided the limbs arterial circulation is normal i.e. palpable pedal
pulses.
• Surgical
o This may be performed as an open surgical or endovenous procedure.
o These interventions focus on removing the incompetent superficial venous system (either GSV or
SSV) from the limbs venous return with a view to redirecting flow through a functioning deep
system.
o Open surgery
§ Involves high ligation of either the SFJ or SPJ and stripping of the GSV.
§ Stripping of the SSV is rarely performed due to the risk of sural nerve injury.
§ Open surgery typically requires a general anaesthetic.
§ This approach carries a higher risk of wound infection, bruising, peri-operative pain and
requires a longer period of recovery.
§ Importantly, it carries a similar rate of recurrence to endovenous intervention.

• Endovenous Intervention
o Now widely recommended as the first line intervention for superficial venous disease with a range of
minimally invasive “keyhole” approaches carrying similar procedural efficacies.

154
 o All these interventions can be performed under local anaesthesia and involve cannulation of the
target vessel using ultrasound.
o Once a cannula is in situ a probe can be inserted into the GSV or SSV to a point 3cm distal to the
junction with the deep vein.

• Thermal Ablation (Radiofrequency Ablation or Laser Ablation)

o Involves the passage of a heater probe into the GSV or SSV
o The probe tip is then heated to a temperature of at least 120 degrees Celsius
o This induces venous endothelial injury, inflammation and subsequent vessel thrombosis
o Tumescent anaesthesia is placed circumferentially around the treated vessel to protect surrounding
structures from heat-induced injury
o Alternatively mechanochemical ablation induced endothelial injury using a combination of trauma
and chemical irritation to the vein wall while cyanoacrylate based closure glues the vessel closed

• Ultrasound-Guided Foam Sclerotherapy

o This technique involves the injection of sclerosant into the vein to induce chemical phlebitis and
vessel occlusion
o It is a second line agent as its efficacy is lower than other endovenous interventions

• Stab Avulsions
o Used to remove residual superficial tributaries following GSV or SSV ablation or stripping

Complications of Venous Interventions

• Deep venous thrombosis
• Pulmonary embolus
• Phlebitis
• Bruising
• Paraesthesia
• Stroke (rare)
• Headache (foam)
• Recurrent disease
• Skin staining
• Skin burns (thermal ablation)

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Lower Limb Deep Venous Thrombosis (DVT)

Definition
• The presence of thrombus within a deep vein

• Common in surgical patients, with up to 50% of patients affected after some surgical procedures
• Trauma, orthopaedic and pelvic interventions are at higher risk. Prophylaxis using low molecular weight
heparin (LMWH) should always be considered unless contraindicated
• Commonly affected sites
o Below knee tibial veins (many asymptomatic)
o Infra-inguinal veins (popliteal, superficial or profunda femoris)
o Pelvic (left iliac veins at greater risk than right due to external compression from the right common
iliac artery - May Thurner Syndrome)
o Mesenteric veins
o IVC (may be congenital related to atresia)
o Hepatic veins (Budd-Chiari syndrome)
o Central veins (related to central line insertions or external compression of the subclavian, internal
jugular and SVC)

Risk Factors
• Surgery
• Immobility
• Pregnancy
• Cancer
• Covid-19
• OCP
• Elevated BMI
• Previous DVT
• Underlying thrombophilia
• External venous compression
• Superficial thrombophlebitis

Presentation Differential diagnosis of the acutely swollen leg

• Swelling of the affected limb • Cellulitis
• Pain and tenderness • Bakers Cyst rupture
• Heaviness • Deep venous thrombosis
• Congested appearance • Musculoskeletal injury
• Dilated subcutaneous veins

Investigations
• D-Dimer
o High sensitivity, low specificity. Should only be used in patients with a low clinical suspicion of DVT
o If negative d-dimer and low clinical suspicion the negative predictive value of d-dimer is 99%
o If positive d-dimer and low clinical suspicion therapeutic low molecular weight heparin should be
administered if ultrasound cannot be performed immediately or perform immediate diagnostic
ultrasound
o All patients with medium to high clinical suspicion should undergo ultrasound which if negative
should be repeated in 1 week

• Duplex Ultrasound
o Characterized by an absence of flow and non-compressible vein

• Consider other contributing pathology if no obvious cause, such as CT-TAP to outrule malignancy,
thrombophilia screening or imaging to identify external vessel compression

4
 • Wells Score
o Used to assess clinical risk of DVT
§ 3 or more = high risk
§ 1-2 = intermediate risk
§ 0 = low risk
Cancer 1 point
Immobilisation 1 point
Major surgery or bedbound 1 point
Tenderness in deep vein distribution 1 point
Calf swelling >3cm between legs 1 point
Pitting oedema 1 point
Distended subcutaneous veins 1 point
Alternative diagnosis more likely - 2 points

Treatment
• Anticoagulation: initially with LMWH, then warfarin or alternative novel oral anticoagulant
o 3 months duration if transient reversible risk factor
o 6-12 months if unknown cause
o Indefinite if recurrent DVT

• Catheter directed thrombolysis using tissue plasminogen activator

o Reserved for those with severe, symptomatic disease and underlying large truncal vein (iliac,
subclavian) occlusion secondary to DVT.
o Must be performed within 14-days as chronic thrombus unlikely to clear beyond this

Prophylaxis in Hospital
• Early mobilization post operatively
• Hydration
• Low molecular weight heparin (prophylactic dose)
• Thrombo-embolic deterrent (TED) stockings
• Sequential compression devices

Complications of DVT
• Post-thrombotic syndrome
• Pulmonary embolus
• Stroke (via patent foramen ovale)
• Mesenteric ischaemic
• Liver failure (Budd-Chiari)
• Phlegmasia cerulea dolens
• Phlegmasia alba dolens

157
8. Breast Disorders

• Mr. Andrew McGuire

• Breast Cancer
• Benign Breast Disease

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Breast Cancer

Overview
• Breast cancer is the second most common cancer diagnosed worldwide, affecting approximately 1 in 10
women in Ireland
• Majority of cases are diagnosed between the ages of 50 to 70
• Incidence increases with age
• 1% are male
• Up to 5% of patients will have distant metastases at time of presentation, most common first site is bone,
followed by liver, lung and brain.

Aetiology
• Genetics
o Majority of cases are sporadic
o 5-10% are hereditary (BRCA1 and BRCA2 genes)
o BRCA1 gene confers a 60-90% life time risk
o BRCA2 gene confers a 45-85% life time risk
o 10% are familial, likely due to combination of inherited genes
• Risk Factors
o Early menarche
o Late menopause
o Nulliparity
o Obesity
o Hormone replacement therapy (HRT)
• Precursors
o Ductal carcinoma in situ (DCIS) and lobular carcinoma in situ (LCIS) are both associated with
increased risk of developing invasive breast cancer.
o Atypical ductal hyperplasia (ADH) and atypical lobular hyperplasia (ALH) are also associated with an
increased risk of developing invasive cancer
• High Risk Family History
o Two first/second degree (one must be first degree) under the age of 50
o Three first/second degree (one must be first degree) under the age of 60
o Four first/second degree (one must be first degree) at any age
o Male breast cancer with one female with one first/second degree relative with breast cancer at age
50 or under

Pathology
• Nearly all breast cancers are adenocarcinoma
• Graded 1-3 based on level of differentiation (i.e. well differentiated, moderately differentiated, poorly
differentiated)
• Invasive ductal carcinoma is the most common (75%)
• Invasive lobular carcinoma is the next most common (15%). Invasive lobular carcinoma tends to be
multicentric, can be bilateral, and size can be underestimated on mammogram and ultrasound
• Rarer types of breast cancer include Medullary, Tubular, Mucinous, Inflammatory
• Ductal cancer in-situ is a pre-malignant condition, that can become invasive if left untreated. Ductal
carcinoma in situ is treated as an invasive cancer and requires excision with clear margins.
• Rarer cancers of the breast include forms of sarcoma (angiosarcoma or phylloides tumours)

Receptor Markers
• The estrogen receptor (ER) and progesterone receptor (PR) are hormone receptors that are expressed in 60-
65% of all breast cancers
• The HER2 receptor is one of a family of four epidermal growth factors, over-expressed in about 30% of
breast cancers

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Breast Cancer Subtypes
• Using hormone receptor and HER2 receptor status, breast cancer can be divided into four subtypes (see
table)

Molecular Subtypes
Breast Cancer Subtype
ER/PR HER2 % of breast cancers

Luminal A + - 50-60%

Luminal B HER2 + + 10-20%

HER2+ (non-luminal) - + 15-20%

Triple negative - - 10-20%

Screening/Detection
• Symptomatic patients are referred by their GPs, and the referrals are categorised as urgent (seen within 2
weeks), semi-urgent (seen within 6 weeks), or routine (seen within 12 weeks).
• Symptomatic patients undergo triple assessment:
o Clinical Exam
§ S score [1 (benign) to 5 (definite malignancy)].
§ All symptomatic patients over 35 years old all have a mammogram performed.
§ Patients with an S score >3 will also undergo a focused ultrasound
o Imaging
§ R score [1 (normal) to 5 (definite malignancy)].
§ Patients with an R score > 3 will have a core biopsy performed
o Core Biopsy
§ C score [1 (normal tissue) to 5 (definite malignancy)]
• All patients who have had biopsies are discussed at a breast multi-disciplinary team meeting
• Breastcheck is the national breast cancer screening program.
• Breast screening is offered to all women in Ireland from ages 50-65 years. These women are invited to have
a mammogram every two years.

Imaging
• Mammography
o Two view (CC and MLO) digital mammography is the gold standard, with an overall sensitivity of 85%
and specificity 89%
o Performed in all patients over 35 years old. Sensitivity is reduced in younger women and women
with dense breast tissue
• Ultrasound
o All patients with palpable lumps will also undergo a focused ultrasound
o Also used to assess for axillary lymph node involvement
• MRI
o Used in patients with lobular breast cancer and for high-risk screening
o Higher sensitivity than mammography but higher false positive rates.
• CT
o Used to stage Breast cancer, to assess for distant metastasis.
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Diagnosis
• Core Biopsy
o Usually ultrasound guided under local anaesthetic
o Can distinguish cell type, grade and receptor status
o Can be used for Oncotype assessment (21 gene panel scoring system used in early luminal A breast
cancers with <2 nodes positive, to assess if chemotherapy would be beneficial to increase survival)
o Not able to distinguish fibroadenoma from a phylloides tumour
• Stereotactic Biopsy
o X-ray guided core biopsy used for ultrasound occult lesions or calcifications
• Excisional Biopsy
o Performed under general anaesthetic
o Wire-guided procedure for non-palpable lesions

Staging
• TNM classification, based on tumour size, number of nodes involved and evidence of distant metastases.
• T Staging
o T1 <2cm
o T2 2-5cm
o T3 >5cm
o T4 extends to skin/chest wall
• N Staging
o N0 No nodes
o N1 Mobile ipsilateral node
o N2 Fixed ipsilateral nodes
o N3 Infra/supra clavicular or internal mammary node(s)
• M staging
o M0 No distant disease
o M1 Distant disease

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Treatment

Surgery
• Wide local excision (breast conserving surgery)
o Typically done for smaller tumours
• Mastectomy
o Complete excision of all breast tissue
o Can be simple, skin-sparing or nipple-sparing, depending on need for reconstruction
o Used for larger tumours or multifocal tumours
• Sentinel Lymph Node Biopsy (SLNB)
o Used for patients with node-negative disease on imaging
o About 20% will be positive
o Consists of injection of either a blue dye, a radioisotope (technetium 99) or combination of both into
the breast tissue followed by excision of the first one or two axillary nodes draining the breast tissue.
• Axillary Node Clearance
o The removal of all axillary lymph nodes draining the breast
o Three levels of nodes, categorised by their location to pectoralis minor - inferolateral (level I),
posterior (level II) and superomedial (level III)
o Performed for patients who are node-positive on SLNB or on imaging
o Lymphoedema occurs in 20-40% of patients postoperatively
o Risk of injury to long thoracic nerve, which can lead to a winged scapula
• Distant Metastasis
o Generally treated with systemic therapy, but some liver and lung metastasis maybe suitable for
wedge excision

Reconstruction
• Can be implant-based, autologous tissue-based, or a combination of both
• Autologous tissue can include pedicled flap (Latissimus Dorsi) or free flap (DIEP)

Chemotherapy
• Given in the adjuvant setting to reduce the risk of distant spread, usually as a combination of drugs
• The most common drugs used are anthracyclines (doxorubicin & epirubicin), taxanes (paclitaxel &
docetaxel), fluorouracil (5-FU) and cyclophosphamide.
• Adjuvant chemotherapy can be given to patients with large tumour, node positive disease, distant disease,
young age or to patients with high Oncotype Dx scores.
• Increasingly given prior to surgery (neoadjuvant chemotherapy) for large tumours to reduce tumour size and
make tumour more amenable to breast conserving surgery.
• Large variation in response rates based on tumour subtype, with highest pathological complete response
(pCR) rates seen in HER2 over-expressing tumours (50%).
• Targeted anti-HER2 therapy (Trastuzuamab) is used for HER2 receptor positive tumours
• Oncotype DX
o Used in patients with early Luminal breast cancer to determine if chemotherapy will give added
survival benefit.
o It is a 21 gene panel that gives a score between 0-100. Patients with score >26 are deemed high-risk
and should receive adjuvant chemotherapy

Hormone Therapy
• Given to patients who have ER and/or PR positive breast cancers to reduce the risk of local and distant
recurrence.
• Given for 5 years usually.
• CTS5 calculator (based on tumour size, grade, number of lymph nodes involved and patient age) is used to
assess patients who should have extended hormone therapy (>5 years)
• Tamoxifen prevents estrogen binding to receptors, resulting in its inhibition.
o Used in pre-menopausal women
o Increased risk of endometrial cancers, hot flushes and thromboembolic events
162
 • Aromatase inhibitors inhibit the synthesis of oestrogen from androgens
o Used in post-menopausal women as shown to have increased disease free survival rates compared
to tamoxifen

Radiotherapy
• Primarily used to reduce local recurrence of breast cancer.
• Radiotherapy can be given locally to the chest wall post-surgery or regionally in the axilla
• Patients who have breast conservative surgery (BCS / WLE) will have whole breast radiotherapy (WBRT) in
the adjuvant setting.
• ACOSOG ZOO11 trial showed that in patients with two or less positive lymph nodes undergoing BCS with
WBRT, survival was equivalent to patients who had axillary lymph node dissection.

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Benign Breast Disease

Lumps
• Fibroadenoma
o Benign growth with epithelial and fibrous component
o Most common in women <30 years old, but can occur at any age
o Usually presents as a painless, mobile, discrete lump in the breast
o Diagnosis: clinical exam, ultrasound +/- core biopsy (i.e. triple assessment)
o Most treated non-operatively but surgical excision recommended if over 3cm, increasing in size,
symptomatic or for cosmesis.

• Breast Cysts
o Benign fluid filled sacs
o Usually present as discrete lumps that can be painful, and may be tender.
o Investigation is with ultrasound and can be aspirated.

• Fat Necrosis
o Necrosis of the fatty breast tissue usually due to trauma
o Can present with pain and a discrete tender lump
o Diagnosed with mammogram and ultrasound

Nipple Discharge
• Mostly physiological
• Can be secondary to duct ectasia (benign widening of milk ducts)
• Persistent spontaneous discharge or blood-stained discharge needs investigation with mammogram and
ultrasound to assess for a papilloma
• Patients with normal imaging but continued discharge should have subareolar exploration to evaluate for
DCIS.

Gynaecomastia
• Benign growth of breast tissue in males
• It is most commonly caused by male oestrogen levels that are too high or are out of balance with
testosterone levels
• Mostly due to natural hormone changes, such as around puberty or at 50-70 years old
• Can be triggered by certain drugs such as marijuana, spironolactone, steroids or anti-androgens used to treat
BPH or prostate cancer
• Can also be brought on by liver disease, hyperthyroidism or certain tumours
• Investigations
o Bloods
§ LFTS,TFTs, LDH, prolactin, beta HCG and alpha-feta protein
o Imaging
§ Ultrasound if under 35 years old or mammogram if older to out-rule male breast cancer
• Management
o Treat underlying cause if possible
o Usually patient can be re-assured and managed non-operatively
o Subcutaneous mastectomy can be done for cosmetic reasons

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9. Endocrine Disorders

• Ms. Carolyn Cullinane

• Differential Diagnosis of Neck Swelling

• Thyroid Gland Anatomy
• Goitre
• Grave’s Disease
• Thyroid Cancer
• Parathyroid Disease
• Adrenal Gland
• Cushing’s Syndrome
• Pheochromocytoma

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Differential Diagnosis of Neck Swelling

Anterior Triangle of the Neck (Sternocleidomastoid muscle, mandible, midline)

• Lymphadenopathy
• Goitre
o Moves on swallowing
• Thyroid Nodule
• Branchial Cyst
o At anterior border of SCM
o Presents in those under twenty years old
o Contains cholesterol
• Dermoid Cyst
o In the midline
§ Presents in those under twenty years old
• Carotid Body Tumours
o Strong pulsation
o ‘Goblet’ sign on angiography
• Thyroglossal Cyst
o Embryological remnant
o Always midline
o Moves with protrusion of the tongue

Posterior Triangle of Neck (Sternocleidomastoid muscle, Trapezius, Mid one-third of clavicle)

• Lymphadenopathy
• Cervical Rib
o Subclavian steal syndrome
• Pharyngeal Pouch
o Dysphagia and bad breath.
o N.B Beware of these at endoscopy
• Cystic Hygroma
o Benign proliferation of lymph vessels.
o Presents in infancy.
o Transilluminates brightly.

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Thyroid Gland Anatomy

• The thyroid gland is composed of a central isthmus, which overlies the second and third tracheal rings and two
lateral lobes, which extend from the side of the thyroid cartilage to the sixth tracheal ring.
• The thyroid gland spans from C5 and T1.
• The gland is enclosed in the pretrachael fascia (along with oesophagus and pharynx), which is attached to the
larynx. The thyroid moves up on swallowing. It is covered by the strap muscles and overlapped by the
sternocleidomastoids.
• Two nerves lie in close proximity to the gland, in the groove between the trachea and oesophagus lies the
recurrent laryngeal nerve which supplies the intrinsic muscles of larynx and vocal cords
• Deep to the upper pole lies the external branch of the superior laryngeal nerve which supplies the cricothyroid
muscle, a tensor of the vocal cords
• Three arteries supply the gland: the superior thyroid artery, from the external carotid (first branch), the inferior
thyroid artery, from subclavian artery and an anatomical variant thyroidea ima artery exists in 10% of the
population
• Three veins drain the gland, the superior, middle and inferior thyroid veins. The superior and middle thyroid
veins drain into the internal jugular veins. The inferior thyroid vein drains into the brachiocephalic vein.
• The lymphatic drainage of the thyroid is multidirectional and extensive. It drains into peri-thyroid nodes and
from there into prelaryngeal, pretracheal, and paratracheal nodes. Laterally, the gland drains unto the superior
and inferior deep cervical nodes.
• There are four parathyroid glands, two superior and two inferior, which are situated on the lateral surface of the
thyroid lobes
• The thyroid gland originates from the foramen caecum at the base of the tongue and descends into the neck.
The track left behind usually closes, although a portion of the epithelial may persist and form a cyst (thyroglossal
cyst) usually in the late adolescent. The connection to the tongue means that the cyst will move on protrusion of
the tongue.

167
168
Goitre
• Thyroid goitres can be either toxic (associated with hyperthyroidism) or non-toxic (euthyroid/hypothyroid).
• They are also described as either diffuse and smooth or multinodular.
o Grave’s Disease
§ Toxic, diffuse and smooth
o Hashimoto’s thyroiditis
§ Non-toxic, diffuse and smooth
o Plummer’s Disease
§ Toxic and multinodular (rare)
• Non-toxic and multinodular goitres are most common and particularly seen in elderly.
o Patient will complain of hoarseness, cosmetic appearance, stridor from tracheal compression or
from recurrent laryngeal nerve compression.

Investigations
• Thyroid Function Tests – TSH, T3 and T4
o Hyperthyroid = decreased TSH, increased T3 and T4
o Hypothyroid = increased TSH, decreased T3 and T4
• Autoantibodies
o Grave’s Disease = TSH receptor/thyrotropin receptor stimulating Ab
o Hashimoto’s = anti-TPO and anti-thyroglobulin Ab

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Grave’s Disease
• Grave’s disease is caused by autoantibodies that bind to the thyrotropin receptor (TSHR-Ab), stimulating
growth of the thyroid and overproduction of thyroid hormone. This can lead to thyrotoxicosis.

• Symptoms and Signs

o Cardiovascular: High output heart failure, mitral valve prolapse, arrythmias
o GI: Weight loss, diarrhoea, malabsorption
o Eyes: proptosis/exophthalmos, lid lag, stare
o Nervous system: Hyperreflexia, proximal muscle weakness, developmental delay
o Bone: osteoporosis
o Skin: pretibial myxoedema

• Investigations
o First line
§ TFT’s, TSH receptor/thyrotropin receptor stimulating Ab
o Second line
§ Antithyroid peroxidase (anti-TPO) and antithyroglobulin (anti-Tg) antibodies
o Other investigations
§ Radioactive iodine scans
• Management
o Medical
§ Thionamides
• The goal of thionamide therapy in Graves' hyperthyroidism is to attain a euthyroid
state within three to eight weeks.
• This can be followed by ablative therapy with radioiodine or surgery, by
continuation of the drug for one to two years with the hope of attaining a remission,
or for long-term therapy.
• Choice of thionamide = methimazole (can cause agranulocytosis, monitor FBC), PTU
can be used in pregnancy
§ Radioiodine
• Radioiodine is less expensive than surgery and may be preferred as definitive
therapy of hyperthyroidism in non-pregnant patients except in patients with
moderate or severe orbitopathy.
• Radioiodine can be administered as a capsule
o Surgery
§ Primarily indicated in patients who have an obstructive goitre or a very large goitre.
§ In patients with moderate to severe, active orbitopathy who desire definitive therapy for
their hyperthyroidism
§ Total thyroidectomy
• Collar incision
• Complications: bleeding, nerve damage, hypothyroidism, thyroid storm
§ Pre-operative Lugol’s iodine solution can be administered 1 week pre-op to reduce thyroid
levels.

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Thyroid Cancer
• Follicular Epithelial-Derived Cancers
o Papillary (differentiated) Cancer – 85%
§ Lymphatic spread
o Follicular (differentiated) Cancer – 12 %
§ Haematogenous spread
o Anaplastic (undifferentiated) Cancer - <3%
§ Very poor prognosis
• Non-Follicular Epithelial-Derived Cancers
o Medullary thyroid cancer originates in the calcitonin producing parafollicular C-cells that
predominate in the upper thyroid poles. Associated with MEN 1 syndrome.
o Lymphoma

• Papillary and follicular cancers are considered differentiated cancers, and patients with these tumours are
often treated similarly, despite numerous biologic differences.

Differentiated Thyroid Cancers

• Initial Evaluation
o Radiation exposure
o Family history
o Personal history
o Thyroid symptoms: heat intolerance/ cold intolerance, weight loss/weight gain, lethargy/irritability,
palpitations, GI upset
• Imaging
o The initial and most valuable thyroid imaging study is cervical ultrasound (US) which is widely
utilized to characterize thyroid nodules and guide practitioners in recommending fine-needle
aspiration biopsy (FNAB).
o US is useful in localizing concurrent parathyroid disease (which is diagnosed biochemically) and is
critical in the preoperative evaluation of cervical lymph node (LN) disease and surgical planning.
o CT or MRI with intravenous contrast should be used preoperatively as an adjunct to US in selected
patients with clinical suspicion for advanced locoregional thyroid cancer.
• Fine Needle Aspiration Biopsy
o This is usually performed under ultrasound guidance.
o This is a cytological diagnostic test.
o Thyroid FNAB results are classified into 1 of the 6 conventional Bethesda System categories, and the
associated risk of malignancy or premalignancy (e.g., non-invasive follicular thyroid neoplasm with
papillary-like features, NIFTP) is used to guide clinical management.
o FNAB results are discussed at multi-disciplinary meeting and pre-operative management plans are
decided.

Bethesda Cytopathologic Approximate Malignancy Suggested treatment (Prior

Category Category expected Rate to availability of molecular
frequency testing)
I Non-diagnostic/ 5-11% 1-4% Repeat FNA
Inadequate/ Benign
II Benign 55-74% 0-3% US Follow-Up
III Atypia/ Follicular lesion 5-15% 5-15% Repeat FNA or US follow-up
of undetermined or lobectomy
significance
IV Follicular neoplasm/ 2-25% 15-30% Lobectomy
suspicious for follicular
neoplasm
V Suspicious for 1-6% 60-75% Lobectomy or Thyroidectomy
malignancy
VI Malignant 2-5% 97-99% Near-total Thyroidectomy

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Indications for Thyroid Surgery
• Risk of malignancy
• Hyperthyroidism - despite medical optimization
• Goitre/Nodule compression symptoms: hoarseness, dysphagia, SOB
• Cosmesis

Pre-Operative Management
• Rendering the patient euthyroid
o Most cases of thyrotoxicosis are initially managed with anti-thyroid drugs, which block the
synthesis of thyroid hormone.
o Carbimazole restores serum hormone levels to normal within 4 – 8 weeks in the majority of cases.
o A lower maintenance dose may then be prescribed for a year, following which more than 50% of
patients will be rendered euthyroid, which will require no further therapy.
o Importantly, carbimazole may cause a reversible neutropenia. The white blood count should
therefore be monitored once every three months for the duration of treatment.
o Beta – adrenergic blocking drugs, such as propranolol, rapidly control the symptoms of
thyrotoxicosis.
o In patients who are undergoing a thyroidectomy for hyperthyroidism, potassium iodine (Lugol’s
iodine) is given for ten days pre-operative to reduce the vascularity of the gland.
• Where compressive symptoms or the possibility of malignancy are the indication for surgery the vocal cords
should be checked pre-operatively via indirect laryngoscopy. This is to document any abnormalities before
the surgery that may otherwise be deemed a complication of the surgery if not noticed pre-op.

Surgery
• Low transverse collar incision along a skin crease (for cosmetic reasons to hide scar) approximately 2cm
above the sternal notch.

• Tumour <1 cm without extrathyroidal extension and no lymph nodes

o When surgery is planned for unilateral intrathyroidal differentiated thyroid cancer <1 cm, a thyroid
lobectomy is preferred unless there are clear indications to remove the contralateral lobe
§ e.g., clinically evident thyroid cancer in the contralateral lobe, previous history of head and
neck radiation, strong family history of thyroid cancer, or imaging abnormalities that will
make follow-up difficult.
• Tumour 1 to 4 cm without extrathyroidal extension and no lymph nodes
o For intrathyroidal tumours between 1 and 4 cm, the initial surgical procedure can either be a total
thyroidectomy or thyroid lobectomy.
o Total thyroidectomy would be chosen either based on patient preference, the presence of
ultrasonographic abnormalities in the contralateral lobe (nodules, thyroiditis in the contralateral
lobe, or nonspecific lymphadenopathy that will make follow-up difficult), or on a decision by the
treatment team that radioiodine therapy may be beneficial either as adjuvant therapy or to facilitate
follow-up.
• Tumour ≥4 cm, extrathyroidal extension, or metastases
o Total thyroidectomy is recommended if the primary tumour is 4 cm in diameter or greater, there is
extrathyroidal extension of tumour, or there are metastases to lymph nodes or distant sites.
• Any tumour size and history of childhood head and neck radiation
o Total thyroidectomy should also be performed in all patients with thyroid cancer who have a history
of exposure to ionizing radiation of the head and neck, given the high rate of tumour recurrence
with lesser operations in these patients.

Complications
• Bleeding
• Scarring
• Recurrent nerve palsy
• Hypothyroidism- patients with total thyroidectomy need thyroxine replacement post op
• Hypocalcaemia (due to removal of parathyroid gland)
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Adjuvant therapy
• External beam radiation or radioactive iodine for high risk tumours.

Monitoring post op
• Year one post op
o Serum Thyroglobulin (Tg)
o Anti-thyroglobulin Antibody
o TSH (should be kept suppressed so it doesn’t stimulate growth of thyroid gland).

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Parathyroid Disease

Parathyroid Glands
• Four in total, two superior and two inferior.
• In most patients, the inferior and superior parathyroid glands will both be supplied by branches of the
inferior thyroid artery.
• The parathyroid glands are usually in close approximation with, but function independently of, the thyroid
gland.
• The parathyroid glands produce parathyroid hormone (PTH), which is one of the two major hormones
modulating calcium and phosphate homeostasis; the other hormone is calcitriol (1,25-dihydroxyvitamin D).
• PTH also stimulates the conversion of calcidiol (25-hydroxyvitamin D) to calcitriol in renal tubular cells,
thereby stimulating intestinal calcium absorption.

Hyperparathyroidism
• Primary
o Adenoma 85%
o Hyperplasia 15%
• Secondary
o Low serum calcium e.g. Renal failure
• Tertiary
o Occurs when there is long-standing secondary ↑PTH and the gland becomes autonomous leading
to unregulated secretion of PTH

Symptoms of Hypercalcaemia
• “painful bones, renal stones, abdominal groans, and psychic moans”
o Bones: fractures
o Stones: renal stones
o Moans: GI upset
o Psychiatric overtones: depression

Investigations
• Bloods: High serum calcium, High/normal PTH, High ALP, Low PO4
• ECG: Prolonged QT
• X-Rays: Osteitis Fibrosa Cystica
• DEXA: Osteoporosis (T Score <.2)

Indications for surgery for primary hyperparathyroidism

• Symptomatic
• Serum Ca >3mmol/l, hypercalciuria (>400mg/day)
• ↓creatinine clearance by 30%
• Renal stones
• ↓bone density
• Young patient <50yo
• Pre-op imaging to localize “hot” parathyroid gland; modalities should be concordant.
o USS neck
o Sestamibi scan
o CT Neck

Surgery
• Minimally invasive parathyroidectomy for single hot gland, USS neck is performed morning of surgery to
mark localization on neck
• Four gland exploration is performed when the gland cannot be localized pre-op.

Complications
• Similar to thyroid surgery

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Post-Op
• Calcium and PTH bloods in recovery
• Monitor for signs of hypocalcaemia
o Chvostek’s sign
§ Twitching of facial muscles in response to tapping over the area of the facial nerve.
o Trousseau’s sign
§ Carpopedal spasm caused by inflating a blood pressure cuff to a level above systolic for
three minutes

Medical Management of Hyperparathyroidism

• Cinacalcet is a calcimimetic agent which directly lowers PTH levels by increasing the sensitivity of the calcium
sensing receptor to extracellular calcium.

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Adrenal Gland

Anatomy

• Retroperitoneal Endocrine Glands closely adherent to the medial aspect of the superior pole of the kidney
• Adrenal Cortex: Coelomic epithelium
• Adrenal Medulla: Ectodermal / Neural Crest
• Migration during fetal development can lead to the presence of accessory or ectopic tissue
• Right Adrenal
o Lower than the left due to the liver
o Pyramidal shape
o Single vein draining directly into the IVC
• Left Adrenal
o Higher and larger than right
o Lunate in shape
o Drains via the left adrenal vein to the left renal vein
• Arterial Supply - similar bilaterally
o Superior: Branch off the inferior phrenic artery
o Middle: Branch off the Aorta
o Inferior: Branch off the renal artery
o Form a plexus of vessels in capsule of the cortex which descend into the medulla forming extensive
dilated capillary network
o Allows rapid response to hormonal secretion

Physiology
• Cortex (85% of the gland)
o Zona Glomerulosa: Aldosterone
o Zona Fasciculata: Cortisol / DHEA
o Zona Reticularis: Cortisol / DHEA
§ All derived from cholesterol
• Negative feedback loop provides control
• Medulla (15% of the gland)
o Functions as a post-ganglionic sympathetic neurone
o Secretes Adrenaline / Noradrenaline
o ‘Fight or flight’ response

Hormones
• Aldosterone
o Mineralocorticoid
o Contributes to blood pressure homeostasis
o Secreted in response to
§ Decrease in blood volume (Majority)
• Direct response of BARO receptors in sympathetic nerves attached to adrenal
• Decrease in renal artery perfusion increases RENIN production
• Renin converts angiotensinogen to angiotensin I which is converted in the lung by
ACE to angiotensin II
• Direct effect on the secretion of ALDOSTERONE
§ Increase in Serum potassium

• Cortisol
o Cortisol secretion is predominantly under the control of ACTH (Anterior pituitary)
o ACTH is secreted in response to cortisol-releasing factor produced in the hypothalamus
o Cortisol has a circadian rhythm/variation
o Secreted to order but only 5% is unbound and active
o Half-life: 80 – 120 mins

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 o Forms part of the stress response, mobilising substrates from stores/reducing inflammation and
reducing blood pressure

• Catecholamines
o Direct control from the sympathetic nervous system
o Mediates the stress response
o Derived from tyrosine in the adrenal medulla with a noradrenaline (20%) / adrenaline (80%) split,
the conversion of which is under control of cortisol
o Broken down by monoamine oxidase and secreted in the urine
o Effects are mediated through α and ß receptors and include increasing HR, BP and PVR and induce
the breakdown of fat, glycogen and protein

Assessment of Disease
• Clinical history and examination
• Screening biochemical investigations
• Confirmatory biochemical investigations
• Radiological Localisation

Primary Hyperaldosteronism/ “Conn’s Syndrome”

• Discovered in 1955 by Jerome Conn
• Epidemiology
o 0.05 – 13%
o Commonest cause of secondary hypertension
o Women > Men
o 30 – 50 years of age

Clinical Presentation
• Refractory hypertension
o Headache
• Hypokalaemia
o Malaise, muscle weakness, paraesthesia, cramps, polyuria, polydypsia
• Cardiac Abnormalities
o Left ventricular hypertrophy
o Increased risk of MI / Stroke
• Metabolic abnormalities
o Insulin resistance leading to glucose intolerance
o Increased BMI

Aetiology
• Primary Hyperaldosteronism
o Aldosterone-producing adrenal adenoma (50-66%)
o Idiopathic bilateral adrenal hyperplasia (30-50%)
o Others
§ Adrenocortical carcinoma producing aldosterone (<1%)
§ Unilateral adrenal hyperplasia (5%)
§ Familial hyperaldosteronism (Type I and II) (1%)
• Secondary Hyperaldosteronism
o Renal artery stenosis
o Congestive heart failure
o Cirrhosis
o Pregnancy

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Indicators to Perform Testing
• Drug resistant hypertension/ grade 2 or 3 hypertension
• Hypertension with adrenal incidentaloma
• Hypertension with hypokalaemia
• Family hx of hyperaldosteronism or <20 year or <40 years with cardiovascular accident

Screening Investigations
• Hypokalaemia (although NOT mandatory)
• Elevated aldosterone levels (> 15 – 20ng / dL)
• Suppressed renin levels
• Elevated plasma aldosterone concentration: Plasma renin activity ratio (>20 – 30)

Localisation to determine Unilateral / Bilateral Disease

• CT Abdomen
o Thin cut adrenal protocol
o Hypodense lesions
o Sensitivity: 90%
• MRI Scan
o Not widely used: contra-indications to CT
• Adrenal Venous Sampling
o Most accurate method of determining laterality of disease BUT invasive with complications

Medical Management
• Potassium replacement
• Anti - Hypertensives
• Spironolactone

Surgery
• Open/laparoscopic adrenalectomy
• If less than <5cm in size suitable for laparoscopic retroperitoneal approach
• If larger than 5cm transabdominal laparoscopic approach

Surgery Outcomes
• Hypertension
o 75% improvement in hypertension control
o 33% no anti-hypertensive medication
o 66% reduction in the number of anti-hypertensive medication
o Dependent upon:
§ Early age at diagnosis
§ Short duration of hypertension requiring less than two anti-hypertensives
§ No family history of hypertension
• Potassium Levels
o 95% of patients have normalisation of potassium levels

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Cushing’s Syndrome

The hypercortisolaemia in Cushing's syndrome is usually due to a corticotropin (ACTH)-producing pituitary tumour
(Cushing's disease), ectopic ACTH secretion by a nonpituitary tumour, or cortisol secretion by an adrenal adenoma or
carcinoma.

Classification of Endogenous Cushing’s Syndrome in Adults

Micronodular adrenal
Macronodular adrenal hyperplasia
hyperplasia 1% Adrenocortical
1% carcinoma
7%
ACTH-INDEPENDENT 20%
Adrenal Adenoma
9%

Ectopic ACTH
9%

Pituitary Cushings
Syndrome
73%

ACTH-DEPENDENT 80%

Adrenal Adenomas
• Some functional adenomas hypersecrete cortisol and cause Cushing's syndrome.
• Approximately 10 percent of cases of overt Cushing's syndrome are due to adrenal adenomas.
•
Clinical Features
• Catabolic Effects
o Proximal myopathy
o Striae
o Bruising
o Osteoporosis
• Glucocorticoid Effects
o Diabetes Mellitus
o Obesity
o Mineralocorticoid effects
o Hypertension
o Hypokalaemia

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 • Appearance
o Moon face
o Acne and hirsutism
o Interscapular and supraclavicular fat pads
o Centripetal obesity
o Striae
o Thin limbs
o Bruising
o Thin skin

Investigations
• First Line: 24-hour urinary free cortisol
• Late night serum or salivary cortisol
o Highest in the AM, lowest at midnight
• Dexamethasone suppression tests
• ACTH (but ACTH degrades very quickly following venepuncture)
• Localisation
o CT, MRI
• DEXA scan

Treatment
• Cushing’s Disease
o Trans-sphenoidal excision of ACTH-producing pituitary tumour
• Adrenal Adenoma/Cancer
o Adrenalectomy
§ Virtually all patients with adrenocortical adenomas are cured by surgery.
§ Postoperative glucocorticoid therapy is needed because excess cortisol secretion has
suppressed corticotropin-releasing hormone (CRH) and corticotropin (ACTH).
• Ectopic ACTH
o Tumour excision,
o Metyrapone (inhibits cortisol synthesis)

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Pheochromocytoma
• Catecholamine-secreting tumours that arise from chromaffin cells of the adrenal medulla and the
sympathetic ganglia are referred to as "pheochromocytomas" and "catecholamine-secreting
paragangliomas" ("extra-adrenal pheochromocytomas"), respectively.

• Epidemiology
o 0.2% of people with hypertension

• 40% are familial, these cases are more likely to be paragangliomas or bilateral pheochromocytoma
o There are several familial disorders associated with adrenal pheochromocytoma, all of which have
autosomal dominant inheritance
§ Von Hippel-Lindau (VHL) syndrome,
§ Multiple endocrine neoplasia type 2 (MEN2)
§ Neurofibromatosis type 1 (NF1)

Rule of 10’s
• 10% Familial (although it is more like 20-40%)
• 10% Bilateral
• 10% Malignant
• 10% Extra-adrenal

Clinical Presentation
• Typical triad
o Headache, sweating, tachycardia
• Palpitations
• Tremor
• Dyspnoea
• Weakness
• Blurred vision
• Asymptomatic

Investigations
• Twenty four hour urinary metanephrines and catecholamines
• Plasma fractionated metanephrines
• CT/MRI will detect almost all pheochromocytomas over 3cm in size
o Increased vascularity
o Hounsfield unit (usually >20)
o Delayed contrast wash out
o High signal intensity on T2 weighted images
• Metaiodobenzylguanidine [MIBG]) scintigraphy
o Compound resembling adrenaline is taken up by adrenergic tissue
• FDG-PET scan- good to detect metastatic disease

Medical Treatment
• Alpha Blockade
o Phenoxybenzamine
§ Irreversible, non-selective, long acting alpha blocker.
§ Side effect: blocked nose
o Doxazosin
§ Selective alpha-1 blocker
§ Less side effects
o Aim for postural BP drop. Perform lying/standing BP pre-op to check
• Beta Blockade
o Once alpha blockade achieved can start beta blocker pre-op e.g. propranolol
• Also initiate volume repletion with IV fluids

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Surgery
• Laparoscopic/Open adrenalectomy
• Careful intra-operative BP monitoring to prevent hypertensive crisis once manipulating pheochromocytoma
• Patients can be hypotensive once disconnected from pheochromocytoma (i.e. adrenal vein clipped)

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References
• https://www.uptodate.com/contents/treatment-of-pheochromocytoma-in-adults
• https://www.uptodate.com/contents/overview-of-the-treatment-of-cushings-syndrome
• https://www.uptodate.com/contents/diagnosis-of-primary-aldosteronism
• https://www.uptodate.com/contents/search?search=thyroid%20cancer
• Patel K N et al. Executive Summary of the American Association of Endocrine Surgeons Guidelines for the
Definitive Surgical Management of Thyroid Disease in Adults. Ann Surg 2020;271:399 – 410
• Zollinger’s Atlas of Surgical Operations 10th ed.

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10. Urology

• Ms Sorcha O’ Meara

• Urinary Tract Stones

• Acute Urinary Retention
• Benign Prostatic Hyperplasia (BPH)
• Prostate Cancer
• Renal Neoplasms
• Transitional Cell Carcinoma/Urothelial cell Carcinoma
• Testicular Tumours
• Acute Testicular Pain

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Urinary Tract Stones

Epidemiology
• Lifetime prevalence 12% men, 7% in women.
• Rates are increasing in Western Societies.
• See intrinsic risk factors for more details.

Pathophysiology
• Supersaturation of urine - too much solute and not enough solvent. In the majority of cases this is
idiopathic/due to extrinsic risk factors, but some patients have underlying metabolic abnormalities such as
hypercalcaemia, renal tubular acidosis, or cystinuria.

Classification
• Classified by predominant composition
Composition % of all Renal Calculi
Calcium oxalate 80-85%
Uric acid 5-10%
Calcium phosphate + oxalate 10%
Struvite (associated with infection) 2%
Cystine 1%

History and Presentation

• Incidental diagnosis during investigation for other issue.
• Renal colic (occurs when a stone has passed into the ureter) – acute onset severe 10/10 flank pain that
radiates to the groin. Waxes and wanes. Patients will struggle to sit comfortably and will pace/walk around.
Can be associated with vomiting, nausea or haematuria.
• Haematuria – non-visible (on urinalysis or dipstick) or visible.
• Infectious complications
o Recurrent UTIs if there is a large/staghorn stone in the kidney.
o Urosepsis secondary to an obstructing stone that has dropped into the ureter - Urological
emergency!
• In your history remember to ask about risk factors as below.

Risk Factors
Intrinsic
Age – peak incidence 20-50 years old
Sex – Male:Female 1.3:1
Previous stone formation – 10% annual recurrence rate
Genetic – 25% of stone formers report a family history.
More common in Caucasian and Asian populations.
Inherited conditions – cystinuria and familial renal tubular
acidosis.
Extrinsic/Environmental
Low fluid intake (<1200mls/day)
Hot climates/hot working environment
Diet – High animal protein, high salt intake. NB not
associated with high calcium diet!
Summer Season
Occupation – Sedentary occupations

Complications
• Recurrent UTIs
• Pain secondary to obstructing stones
• Urosepsis
• Renal failure
• Complications of procedures

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Investigations
• Imaging
o CT KUB (non-contrast CT of kidneys, ureters and bladder) – very accurate method of diagnosing
renal and ureteric stones. Allows determination of size and location of stone.
o Plain film X-RAY KUB – Very small stones, struvite or cystine stones may not be visible.
o Renal Ultrasound – variable sensitivity for diagnosing stones, however may show hydronephrosis if
there is an obstructing ureteric stone.
• Laboratory
o FBC, renal profile, CRP, Coagulation studies – initial work up to assess for infection, evidence of renal
impairment form obstruction, and coagulation anomalies if considering intervention.
o Bone profile, urate/uric acid, Parathyroid hormone – basic metabolic work up in all stone
presentations to evaluate for possible underlying metabolic abnormalities.
o Urine for culture and sensitivity.
o Recurrent stone formers should have a 24 hour urine collection, and be referred to nephrology for a
full work-up.

Treatment
• Depends on the stone location, size and presence of sepsis.
• Obstructing ureteric stone + Sepsis – urological emergency!
o Treat with sepsis 6
o Urgent decompression – percutaneous nephrostomy in interventional radiology or stent insertion by
urology in theatre.
§ The rationale is to relieve the obstruction by providing a way for the kidney to drain.
o Definitive treatment of stone at a later date after sepsis has settled.
• Obstructing ureteric stone (no sepsis)
o Analgesia – NSAIDs are best.
o Small stone, normal bloods, and pain manageable with analgesia à discharge with analgesia and
outpatient follow up.
§ 68% of stones <5mm will pass spontaneously.
§ Medical expulsive therapy with tamsulosin (alpha blocker) can increase stone passage rate.
o Large stone (>5mm), abnormal bloods, unmanageable pain à treatment.
§ Ureteroscopy + laser fragmentation of stone under general anaesthetic.
§ ESWL (extracorpeal shockwave lithotripsy) can be used for proximal stones, however it is not
always readily available.
• Non-obstructing stone (usually in the kidney)
o Watchful waiting – if small stone with no symptoms.
o ESWL - externally generated shock waves are focused at the stone under x-ray guidance. No
sedation or anaesthesia needed. Best for stones <1cm
o FURS – Flexible ureterorenoscopy. Small camera passed via urethra to kidney with stone then
lasered/basketed. Under general anaesthesia. Can require multiple procedures if very hard or large
stone.
o PCNL – Percutaneous nephrolithotomy. Large stones, failed FURS or ESWL, Staghorn stones. Under
general anaesthesia a tract is developed between the skin and the kidney collecting system. A
camera can then be used to visualise the stone and lasers, ultrasound and other instruments can be
used to break up the stone.
o Open surgery – usually only if other treatments have failed, patient has complex stone burden, or
body habitus that precludes endoscopic surgery.
E.g. Pyelolithotomy, nephrolithotomy, nephrectomy.

Don’t forget the basic metabolic profile in all patients as discussed in investigations. All patients should also be given
stone prevention advice – e.g. fluid intake of 3 litres per day, low salt diet

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Acute Urinary Retention

Definition
• Painful inability to void with relief of pain following drainage of bladder by catheterization.

Pathophysiology
• Normal micturition requires: Bladder à
1. Afferent input to brainstem and cerebral cortex External
2. Co-ordinated relaxation of external sphincter Sphincter à
3. Sustained detrusor contraction
4. A clear outlet from the bladder along the urethra. Urethra à
• Interruption of any these processes can cause urinary retention

Differential Diagnosis
Male * Female* Both Sexes
Benign Prostatic Enlargement (BPH) Pelvic prolapse Bladder outlet obstruction –
haematuria, pelvic fracture causing
disruption of urethra.
Malignant enlargement of prostate (prostate Pelvic mass CNS causes – MS, transverse myelitis,
cancer) sacral cord/nerve injury.
Urethral stricture Fowler’s syndrome Diabetic neuropathy
*These relate to interruption of part 4 in the micturition cycle! Drugs (anti-cholinergics), pain, post-
operative retention.

History and Presentation

• Unable to void, with urgency (need to go) and suprapubic discomfort.
• May have had history of preceding obstructive LUTS (Lower urinary tract symptoms); urgency, frequency,
poor flow, post terminal dribble, nocturia, sensation of incomplete emptying.
• May have had history of preceding UTI symptoms: frequency, urgency, dysuria, small volume voids,
temperature/general malaise.
o The presence of a UTI can exacerbate underlying risk factors and cause an acute presentation of
retention.
• Remember to ask about baseline LUTS, neurological symptoms, co-morbidities and medication history to
help in your differential diagnosis.

Risk Factors
• The potential causes are all risk factors as above.
• In men advancing age is a risk factor, as is the presence of baseline bothersome LUTS, and previous
retention.
• The presence of a UTI or constipation can exacerbate underlying causes.

Clinical Features
• Vital signs usually are normal.
• On exam, patient may be distressed, with palpable bladder above pubic bone.
• DRE and external genitalia should be inspected. DRE may show enlarged prostate.

Complications
• Pain
• Urinary tract infection and urosepsis
• Obstructive kidney injury as the kidneys cannot drain,
• Post obstructive diuresis
• Electrolyte abnormalities.

187
Investigations
• Lab investigations: FBC and CRP for signs of infection and to check haemoglobin if patient had haematuria,
renal profile to check for electrolyte abnormalities or deranged renal function.
o PSA should NOT be checked in acute setting as can be falsely elevated secondary to instrumentation
etc. Ensure is checked at 6 weeks post event.
• Ultrasound kidneys to assess for hydronephrosis.
• Depending on differential diagnosis MRI spine and full urodynamic studies may be required.

Treatment
• Initial treatment is urethral catheterisation. Then investigate potential causes and treat as appropriate.
• Trial of void (TOV) without catheter when investigations complete and exacerbating factors managed.
• Some conditions (e.g. MS, spinal cord injury) may require long term catheterisation with catheter changes
every three months.

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Benign Prostatic Hyperplasia (BPH)

Definition
• Benign enlargement of the prostate.

Epidemiology and Risk Factors

• Affects men, risk increases with age and with family history.
• 88% of 80 year olds have BPH on autopsy.

Pathophysiology
• BPH is characterized by an increase in epithelial and stromal cell numbers in the peri-urethral/ central zone
of the prostate. This causes lower urinary tract symptoms by compressing the bladder outlet/urethra.
• Hyperplasia is dependent on the action of testosterone which either acts directly on the androgen receptor
on the prostate, or is converted to its more potent form dihydrotestosterone by 5-alpha-reductase.

History and Presentation

• History should focus on duration of preceding lower urinary tract symptoms, which are usually obstructive in
nature.
• May present as a GP referral to outpatients with Obstructive/Voiding LUTS Irritative/Storage LUTS
LUTS or an elevated PSA, or with an episode of Poor flow Frequency
acute retention, or with UTIs secondary to Nocturia Urgency
incomplete bladder emptying. Post terminal dribble Urge incontinence
• Ensure to ask about family history as well as co- Incomplete emptying Small volume voids
morbidities and medications. Hesitancy
• IPSS score (International Prostate Straining
Symptom Score) useful to determine severity of Intermittent flow
symptoms.

Clinical Features
• Symptoms as above.
• Exam is usually unremarkable except may show an enlarged prostate with a smooth gland.
o Check for a palpable bladder – may have chronic retention.

Complications
• Acute urinary retention
• Chronic retention
• UTIs
• Haematuria
• Obstructive kidney injury
• Complications of catheterisation/treatment

Investigations
• History and physical exam including DRE
• Labs: PSA, renal profile, urine culture and sensitivity
• Flow rate and post void residual bladder scan
o Done in urology outpatients
o Gives objective flow rate and shows if patient is adequately emptying their bladder

Treatment: Conservative/Surgical
• Treatment depends on patient symptoms and co-morbidities.
• Watchful waiting – suitable in patients who are managing their symptoms, with normal bloods and normal
post void residual.
o Ensure take appropriate fluid history and advise reducing alcohol, caffeinated drinks.

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• Medical treatment – patients with bothersome LUTS
o Alpha blockers (tamsulosin, silodosin) – relax smooth muscle in prostatic urethra and at bladder
neck to relieve bladder outlet obstruction.
§ Side effects: postural hypotension, retrograde ejaculation, dizziness, constipation
o 5-alpha-reductase inhibitors (finasteride) – block the conversion of testosterone to DHT and thus
slowly reduce the size of the prostate (can take months)
§ Side effects: Loss of libido, impotence.
§ Artificially reduce PSA – important in prostate cancer or screening. Should have baseline PSA
taken before starting.
o Combined treatment with both. Usually we start with an alpha blocker, assess response and then
add in finasteride if no improvement.

• Surgical treatment – patients with failed medical management or who have obstructive kidney injury
secondary to bladder outlet obstruction (hydronephrosis on ultrasound or elevated creatinine).
o Transurethral Resection of Prostate (TURP)
§ Endoscopic (via urethra) resection of prostate to relieve obstruction.
§ Complications: bleeding, TUR syndrome, incontinence, failure to relieve symptoms,
recurrence of symptoms at future date, damage to urethra/bladder, infection, GA/Spinal
anaesthesia risk.
o Open prostatectomy (Millin/Freyer prostatectomy)
§ Open resection of prostate
§ Used for very large gland (>100cc).
o New treatments
§ Urolift, STEAM, Rezum – ongoing research into same.

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Prostate Cancer

Definition
• Malignancy of the Prostate

Epidemiology
• Second most commonly diagnosed male cancer. Rates are increasing, likely secondary to an increase in PSA
testing.
• More common in Western nations and in North America.
• More common in black men, rare in Asian men.
• In Ireland 5-year survival is 92%.

Pathophysiology
• As with BPH, growth of prostate cancer is largely due to the influence of testosterone and DHT.
• The majority are adenocarcinoma of the prostate (95%).
• Usually affects the periphery of the gland, which is why lesions may be palpable on DRE and it is less likely to
cause LUTS compared to BPH.
• Can spread locally through the prostate capsule (locally advanced).
• Most commonly metastases to bone – sclerotic lesions affecting axial skeleton most commonly.

History and Presentation

• May present in multiple ways.
o Most commonly is through referral to the rapid access prostate service from the GP due to an
elevated PSA or abnormal DRE.
o May be completely asymptomatic.
o Locally advanced disease can present with urinary retention or haematuria.
o Metastatic disease can present with pathologic fractures, weight loss, pain or signs and symptoms of
nerve compression.
• History should focus on baseline LUTS and erectile function with measurement of IPSS and IIEF (International
Index of Erectile Function) scores to give objective baseline.
o As mentioned previously many men will be asymptomatic.
o Always ensure to take full history including medical and surgical history, medications, family history
and social history as may impact treatment decisions.
• Clinical exam may be unremarkable
o Ensure to note any systemic signs
such as cachexia or joint pain.
o Ensure DRE is performed in
presence of chaperone.
o Gland may have palpable nodules
or be “craggy,” but can also feel
benign.

Risk Factors
• Western countries
• Black populations
• Increasing age – prevalence is 29% in fifth decade and 67% in ninth decade.
• Family History

Complications
• Usually related to locally advanced or metastatic disease as mentioned previously.
• Complications related to treatment.

Investigations and Staging

• Full history and physical exam
• Labs: PSA blood test
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• Imaging:
o Multiparametric MRI of prostate: Most useful method to image prostate. Given PIRADS score, rated
from 1-5 with 1 being low risk for malignancy with 5 a very high risk of malignancy.
o Bone scan to evaluate for metastatic disease.
o CT TAP to evaluate for metastatic disease.
• Biopsy of prostate – usually transrectal ultrasound (TRUS) guided biopsy, however increasing use of
transperineal biopsies.
o Greatest risk is of TRUS sepsis, which is minimal in transperineal biopsy.
o Other side effects include pain, bleeding, haematospermia, further investigations required.
o Gleason score used for histological diagnosis and grading of prostate cancer, with the two most
common tissue patterns present used to give an overall grade.
§ E.g. 3+4=7
§ However not the same as 4+3=7, which is considered more severe as 4 is the predominant
tissue pattern type.

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Gleason’s Pattern Scale

• Staging using TNM criteria

Treatment
• Many factors influence the treatment of prostate cancer including the Gleason grade, the stage, patient age
and co-morbidities.
• Conservative approaches
o Watchful waiting – usually in older men, regular PSA checks every 6/12. No active treatment unless
develops symptoms or PSA dramatically increases.
o Active Surveillance – Usually in young men with localised disease that is low risk.
§ Repeat biopsy at one year, 6 monthly PSA checks and DRE.
• Surgical Treatment
o Localised disease, no metastases.
o Robot assisted laparoscopic prostatectomy or open radical prostatectomy.
o Complications
§ Bleeding, infection, scarring, hernia, pain, GA risks.
§ Incontinence, impotence, recurrence of disease, bladder neck contracture.
§ Require 6 monthly PSA surveillance life-long.
§ PSA should be undetectable post operatively.
• Radiotherapy
o Localised disease with no metastases à same oncological outcomes as with surgery, however
requires multiple hospital visits.
o Side effects
§ Impotence, incontinence, radiation cystitis, radiation enteritis/colitis, pain, disease
recurrence.
o Require regular PSA surveillance life-long.
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 o External beam or brachytherapy.
o Palliative radiotherapy can also be given in locally advanced disease or to bony metastases.
• Medical treatment
o Usually reserved for metastatic disease, or older patients, or those with significant co-morbidities
unsuitable for major surgery.
o Androgen deprivation therapy is first line
§ LHRH agonists, LHRH antagonists and antiandrogens.
• The aim being to reduce testosterone production and induce prostate cancer cell
apoptosis.
• Usually a depot injection
§ Side effects: reduced libido, erectile dysfunction, hot flushes, wight gain,
fatigue, gynaecomastia, anaemia.

Rapid Access Prostate Clinics

• For men aged between 50-70 with…
• Elevated PSA or abnormal DRE
o Usually two PSA checks six weeks apart required.
o Lower limits for black men
• 8 units around the country
• Seen by consultant urologist within six weeks of referral

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Renal Neoplasms

Epidemiology and Risk Factors

• 2-3% of all cancers
• Highest incidence in Western countries.
• Risk factors: smoking, obesity, haemodialysis, family history.
• 5-10% are hereditary: Birt-Hogg Dube syndrome, Von-Hippel Lindau syndrome, hereditary papillary renal
carcinoma.

Pathophysiology
• Most common are renal cell carcinomas
o Subtypes include clear cell, papillary and chromophobe.
• Wilms’s tumour (nephroblastoma) usually presents in children.
• Rarely can be metastases from other site, lymphoma or sarcoma.
• Differential diagnosis: renal cyst, TB, oncocytoma.

History and Presentation

• Majority are an incidental diagnosis (50%).
• “Classic” triad of flank pain, haematuria and palpable abdominal mass presents in 6-10%.
• Paraneoplastic syndromes – anaemia, polycythaemia (ectopic EPO secretion), hypertension (renin),
Cushing’s syndrome (ACTH), hypoglycaemia (insulin), hypercalcaemia (PTH-like substance)
• Metastatic disease – cachexia, weight loss, abdominal pain, bone pain or cough.

Clinical Features
• Full medical history, as above may be asymptomatic.
o Check for systemic symptoms, haematuria, flank pain and symptoms of paraneoplastic syndrome.
• On Exam
o May be normal
o Ensure to ballot kidneys and palpate for abdominal masses.
o Check for palpable lymph nodes and bilateral lower limb oedema.
o External genitalia in presence of chaperone – left sided varicocele

Complications
• Metastases – lung metastases, bone metastases, venous involvement can cause lower limb oedema.
• Paraneoplastic syndromes as above.

Investigations
• Labs: FBC, LFTs, bone profile, and renal profile
o Looking for paraneoplastic syndromes and need to assess baseline renal function.
• Imaging: Triple phase renal CT and CT thorax to allow for initial staging.
o DMSA scan to assess split function if there are bilateral tumours, or a reduced eGFR.
• Biopsy: do not routinely biopsy unless there is a question regarding diagnosis.
• Staged using TNM criteria.

Treatment
• Immunotherapy
o Metastatic disease has poor prognosis, but survival can be improved with immunotherapy
(interferon alpha)
• Surgery
o Localised disease are offered a partial nephrectomy or radical nephrectomy depending on the size
and location of the tumour.
§ Open, laparoscopic or robot-assisted, depending on centre.
§ Complications
• Bleeding, infection, failure, scarring, hernia, pain, GA risks.

4
 • Long term renal failure, disease recurrence, incomplete resection, damage to
surrounding structures, urinary leak.
o Require minimum of 5 year follow up with CT/ultrasound and renal profile check depending on final
histology.
• Conservative
o Active surveillance can be considered in patients with a tumour <3cm, especially if they have co-
morbidities or are elderly.
o Radiofrequency ablation is also an option in this cohort.

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Transitional Cell Carcinoma/Urothelial cell Carcinoma

Definition
• Malignancy affecting the urothelium – lines the urinary tract from the renal pelvis to the urethra.

Epidemiology and risk factors

• More common in western nations, Caucasian populations and men more than women.
• Risk factors include smoking, exposure to ionising radiation or arsenic, and occupational exposure to amines
or hydrocarbons (textile industry).
• Other risk factors include lower socioeconomic status.

Pathophysiology
• Majority of bladder cancer is transitional cell/urothelial cell carcinoma (95%)
• Squamous cell carcinoma accounts for 4% and is associated with schistosomiasis infection or chronic
irritation of bladder.
• Other rare types: Metastases to bladder, adenocarcinoma.
o Can get local invasion from cervical, uterine, prostate and rectal cancer.

History and Presentation

• Painless visible/frank haematuria is the most common presentation (85%).
• Asymptomatic non-visible/microscopic haematuria diagnosed on routine urine dipstick in 4-16%.
• Irritative LUTS
• Recurrent UTIS
• Locally advanced or metastatic disease: lower limb swelling, weight loss, bone pain, retention secondary to
obstruction.

Clinical Features
• General exam may show pallor or cachexia, look for signs of tobacco use.
• Abdominal exam may show palpable bladder.
• DRE – may reveal a pelvic mass involving the prostate.

Complications
• As above, usually related to locally advanced or metastatic disease.

Investigations
• Full history and physical exam.
• Labs
o Urine culture and sensitivity, urine cytology.
o FBC, renal profile, coagulation studies – evaluate for complications and plan for treatment.
• Imaging:
o US kidneys or CT urogram to allow evaluation of renal pelvis and ureters and ensure no involvement.
o CT thorax to evaluate for metastatic disease.

• Cystoscopy:
o All patients with haematuria should undergo work up as
above as well as flexible cystoscopy under local
anaesthesia.
o If abnormality present a biopsy can be taken, however
most will proceed to a transurethral resection of bladder
tumour (TURBT) under general anaesthesia.
§ Tumour is staged using TNM classification.
§ Broadly speaking can be broken down into
metastatic, muscle-invasive or non-muscle
invasive.

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Treatment
• Conservative
o Only discussed in patients who are very frail or with extensive co-morbidities.
• Surgical treatment
o TURBT – endoscopic (via urethra) resection of visible bladder tumour under GA.
§ Needed in all cases initially for histological
diagnosis and grading.
§ Patients with non-muscle invasive disease
need surveillance flexible cystoscopies at
regular intervals to ensure no recurrence.
§ Complications
• Bleeding, infection, GA risks, pain.
• Damage to bladder or urethra,
recurrence of disease, repeat
procedures required.
o Radical cystectomy and ileal conduit formation
§ Used for muscle invasive disease
§ Usually open procedure under GA
§ Complications
• Bleeding, infection, scarring, hernia, GA risks, pain
• Damage to surrounding structures, damage to vasculature, stoma complications
(skin damage, hernia, prolapse, retraction, stenosis), disease recurrence.
• Radiotherapy
o Offered in palliative setting or In patients with muscle invasive disease not suitable for major
surgery.

• Chemotherapy
o Systemic chemotherapy offered in neo-adjuvant setting for muscle invasive disease, can also be
offered In metastatic setting.
o Intravesical (into the bladder) chemotherapy in the form of BCG or mitomycin can be given for Cis,
or high grade disease.

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Testicular Tumours

Epidemiology
• Most common solid cancer in men aged 20-45.
• Considered the most curable cancer
• Caucasian most common

Pathophysiology
• Classified by the WHO as follows:
o Germ cell tumours 90%
§ Most common
§ Seminoma 48%
§ Non-seminomatous germ cell tumours (NSGCTs) 42%
• Teratoma, yolk sac, choriocarcinoma.
§ Mixed germ cell tumours 10%
• Leydig cell, Sertoli cell, sex cord stromal tumours.
o Non germ cell tumours (10%)
§ Epidermoid, adenomatoid, carcinoid, lymphoma, metastatic.
• Staged using TNM criteria.

History and Presentation

• On history be sure to elucidate: length of symptoms, change in size of mass, pain/painless, associated LUTS,
sexual history, recent trauma, previous medical and surgical history.
• May present as GP referral or ED referral due to painless mass or swelling in scrotum, may complain of a
dragging sensation.
o 10% present with symptoms of metastatic disease à weight loss, neck lump, SOB, haemoptysis,
bone pain.
o Recent trauma may be a red herring à led to self-exam at which stage lump was noted.

Risk Factors
• History of cryptorchidism – 1.3 times increased risk of testicular cancer, which persists even if has been
corrected, and in opposite side.
• Family history
• Most common in Caucasians
• Contralateral testicular cancer
• Maternal oestrogen exposure
• HIV
• History of subfertility

Clinical Features
• General exam – supraclavicular nodes, chest and abdominal exam. Ensure there are no inguinal scars
suggesting correction of cryptorchidism .
• Exam of external genitalia – always offer chaperone.
o Exam contralateral testes first
o Assess size, mass, painful or painless.
§ Hard mass arising from testicle is suggestive of malignancy

Complications
• If not identified in timely manner can result in metastatic disease which affects treatment and prognosis.

Investigations
• History and physical exam.
• Labs
o Tumour markers – alpha fetoprotein, b-HCG, LDH.
§ 51% have raised tumour markers on presentation
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 • Used for diagnosis and prognosis
§ Seminomas – 10% have elevated bHCG, seminomas do not secrete AFP.
10-20% have elevated LDH.
§ NSGCTS – AFP in 50-70%, b-HCG in 40%
§ Choriocarcinoma – b-HCG 100% cases
§ Embryonal carcinoma 40-60% elevated b-HCG.
• Imaging
o Urgent ultrasound testes – approximately 100% sensitivity for detection of testicular tumours.
o Staging CT TAP

Treatment
• Surgical – radical inguinal orchidectomy +/- insertion of testicular prosthesis.
o Offer sperm banking prior to same.
§ Retroperitoneal lymph node dissection - specialist centres
• If nodes present on follow-up imaging.
• Adjuvant Chemotherapy if there are nodes, metastases or high risk features on histology (gemcitabine,
cisplatin)
• All patients need surveillance post-op with tumour markers at one week, and at least annual imaging.

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Acute Testicular Pain

Acute onset testicular pain in a young man should be considered an emergency!

Differential Diagnosis and Clinical Features

• Testicular torsion – time sensitive, can lead to ischaemia of testes if not resolved.
o Describe acute onset of unilateral testicular pain, severe.
o May be associated with vomiting.
o May have had preceding episodes.
o Usually young men (<30)
o On exam is usually distressed with tender testes. May be high rising, have a thickened cord and
absent cremasteric reflex.
• Testicular tumour
o Heavy or dragging sensation of testes, may have palpable mass or have noticed increased size of
testes.
• Epididymitis/orchitis
o Related to UTI or STI.
o Acute onset of testicular pain, usually a persistent pain worse with movement and relieved with
elevation. May have overlying scrotal erythema and may be hot to touch. Tender and swollen on
examination.
§ Important to ask about risk factors such as unprotected intercourse and UTI symptoms.
• Hydrocele
o Patent processus vaginalis or trauma causes collection of fluid around the testes.
o Usually chronic issue with dull intermittent pain, can cause discomfort if very large.
o Unable to palpate testes separately from hydrocele, trans-illuminates on exam.

• Varicocele
o Dilated venous plexus, usually idiopathic but can be associated with renal tumours or other tumours
obstructing drainage of testicular vein.
o May cause intermittent or dull pain.
o Palpable as “bag of worms” sperate to the testes.
• Trauma – Can cause haematoma and sometimes even rupture of testicle.
• Other causes: may be referred pain from appendicitis, hernia, or other intra-abdominal cause.

Investigations
• US testes is best step to investigate pain or swelling of scrotum
o However, if suspicion of testicular torsion remember this is a clinical diagnosis – straight to surgical
exploration!!

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 • Other investigations; urine culture and STI screen if considering epididymo-orchitis.

Treatment:
• Depends on the cause.
• Torsion – emergent scrotal exploration + orchidopexy (fixation of testicle).
• Epididymitis/orchitis – treat with antibiotics depending on local protocols and cause (UTI vs STI).
• Hydrocele – can be managed conservatively or be offered surgical repair with Jaboulay or Lords procedure if
bothersome.
• Varicocele – managed conservatively or offered testicular vein embolization or ligation if bothersome.
• Trauma – exploration if concerned about testicular rupture, otherwise conservatively managed with rest,
elevation and analgesia.

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References
• https://sketchymedicine.com/2012/02/tnm-staging-for-prostate-cancer/
• https://www.cancerresearchuk.org/about-cancer/prostate-cancer/stages/tnm-staging

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11. Cardiothoracic Surgery

• Mr Adam Daly, Mr Joseph McLoughlin, Professor David G Healy

• Cardiac Surgery
o Referral pathway to Cardiac Surgery Services
o Cardiopulmonary Bypass (CPB)
o Workup for Cardiac Surgery
o Coronary Artery Bypass Grafting (CABG)
o Acute Aortic Dissection
• Thoracic Surgery
o Pneumothorax
o Chest Drain Insertion
o Surgery for Lung Cancer

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Cardiac Surgery

Cardiac surgery and cardiology are complementary specialist services that treat patients with heart disease. There is
significant overlap between topics in cardiac surgery and elsewhere in the in the curriculum (e.g. acute coronary
syndromes covered in the medical/cardiology curriculum) - these will not be discussed in detail.

A baseline knowledge of cardiology is a prerequisite to a student’s rotation in cardiac surgery (i.e. students should
have a reasonable understanding of common cardiology conditions, history/examination findings and
investigations).

Instead, this chapter in cardiac surgery serves to provide students with details specific to cardiac surgery, not
covered elsewhere in the curriculum. This chapter aims to develop students’ understanding of the process by which
patients come to receive Cardiac Surgery services. This aims to benefit you in practical life as a doctor, rather than
provide a rote learning source without deeper understanding. Students should revise cardiac surgery while revising
cardiology and vice versa. Tips for examination are in italics.

This chapter highlights

• The pathway to Cardiac Surgery
• The typical workup patients undergo prior to cardiac surgery
• Critical elements of cardiac surgery
• The most common operations performed
• Key topics expected of medical students (e.g. valve choice)

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Referral pathway to Cardiac Surgery Services
• Patients undergoing cardiac surgery often present with cardiorespiratory symptoms and signs as described
in Tally & O’Connor. Students must familiarise themselves with this.
• Students should be familiar with New York Heart Association and Canadian Cardiovascular Score
classification systems.
• In history taking, students should specifically ask for cardiac risk factors (hypertension, hypercholesterolemia,
diabetes, smoking history, family history, rheumatic fever, peripheral vascular disease, transient ischaemic
attacks/stroke).
• History, examination, investigations (blood investigations, CXR, ECG) will determine whether the patient
presentation is cardiac in nature or not.
• Patients are then referred to Cardiologists who determine if further, more specialised investigations are
required.
• Patients with significant cardiac conditions potentially amenable to surgery are then discussed by the
Cardiology team at the combined CardioThoracic-Cardiology Conference (CTC) where the patients’
treatment options are discussed.
• If surgery is deemed to be potentially beneficial, the patient will meet with a surgeon who will revisit the
history, examination, investigations, discuss the diagnosis, management options (conservative, cath lab
approach, surgery), pros and cons of options and discuss the risk of surgical intervention.
• Occasionally, patients present requiring emergent cardiac surgery. Ad hoc discussion between referring
cardiology team or emergency department team and on call cardiac surgery services occurs, bypassing the
CTC.

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Critical elements of Cardiac Surgery

Cardiopulmonary Bypass (CPB)

• This is used in the majority of cardiac surgery cases. While on CPB, venous blood drains into the
cardiopulmonary bypass machine (rather than into the heart and lungs) and is pumped back to the patient’s
aorta via a large venous cannula (e) and large arterial cannula.
• The CPB machine can oxygenate blood, warm & cool blood as required and pumps blood through systemic
circulation, effectively acting as the patient’s heart and lungs during surgery.
• CPB permits a bloodless operating field, permits manipulation of the heart, reduces myocardial oxygen
demand and provides control of systemic blood pressure.
• CPB is managed by specialist staff known as perfusionists.
• Steps for placing a patient on CPB include
1. Heparinising the patient (using large dose unfractionated heparin to prevent clot formation with
blood/CPB tubing interface)
2. Placing an arterial cannula. This is usually in the ascending aorta. This is then connected to the
arterial return line from the CPB machine
3. Placing a venous cannula. This is usually placed in the right atrium or superior vena cava and inferior
vena cave. This is then connected to the venous line to the CPB machine.
4. Antegrade +/- retrograde cardioplegia cannulae are then sited (see below)
5. CPB is then commenced by draining the patients venous blood into the CPB machine via venous
cannula and then returning it to the patient via the arterial line
6. Once stable on CPB, the patient’s lungs can be deflated.
7. A cross clamp can be applied to the aorta proximal to the aortic cannula to isolate the heart from
blood
8. Cardioplegia can then be delivered to arrest the heart.

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Students should be able to draw a schematic of the CPB circuit.

Myocardial Protection
• Protecting the heart against ischaemia is crucial to surviving heart surgery. If there is a significant mismatch
between myocardial oxygen demand and myocardial oxygen supply, the myocardium will infarct.
• Myocardial protection is achieved by reducing the oxygen demands of the heart by:
1. Reducing the workload of the heart by off-loading the heart while on CPB (i.e. CPB is doing the work
for the heart)
2. Reducing the temperature of the heart by topical cooling
3. Arresting the heart (asystole) by using a high potassium solution called cardioplegia. This can be
delivered antegrade (i.e. via a cannula in the aortic root which delivers cardioplegia into the
coronary arteries) or retrograde (i.e. via a cannula in the coronary sinus which delivers cardioplegia
into the cardiac veins)

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Workup for Cardiac Surgery

• The workup required to proceed with cardiac surgery is dependent on the specific procedure being
undertaken but there are several important investigations required for almost all cardiac operations. These
are in addition to “routine bloods, chest x-ray, ECG” etc.

“Routine workup”
• Coronary angiogram – This is used to assess for the presence and/or extent of coronary artery disease. It is
used for pre-operative planning in coronary artery bypass operations. In select circumstances CT coronary
angiogram is an acceptable alternative.

• Echocardiogram – This establishes the pre-operative function of the heart, assess for the presence / severity
of valvular heart disease and assess for any other cardiac abnormalities (i.e. ASD, VSD).
o A trans-thoracic echocardiogram is first line and required for all cardiac interventions.
o A trans-oesophageal echo gives more detailed information which can be important in operative
planning. This is most common in cases of suspected infective endocarditis and in complex valvular
disease.

• Carotid Doppler Ultrasound – If certain risk factors present, such as the presence of symptomatic carotid
disease, carotid bruit, smoking history or age >70yo. This assesses for carotid artery stenosis. Significant
carotid disease increases peri-operative stroke risk. Patients with significant carotid disease (see vascular
chapter) need to be reviewed by a vascular surgeon pre-operatively. In rare instances a carotid
endarterectomy is performed at the same time as the cardiac surgery.

• Pulmonary Function Tests – If significant smoking history or shortness of breath. This helps establish a
baseline of the patients lung function and helps differentiate between cardiac and respiratory shortness of
breath. This is particularly important in patients with significant lung disease.

• Dental Review – This is only required for valvular cardiac surgery. A dentist assessment for evidence of
dental disease which would increase the risk of the patient developing infective endocarditis. Some patients
require dental extraction in advance of their operation.

“Specific situational pre-op investigations”

• CT Aorta – This provides important dimensions of the patients ascending aorta. This guides the decision of
whether to replace the ascending aorta. Used in cases of aortic surgery or redo cardiac surgery.

• Cardiac MRI - Multiple uses but often used to assess myocardial viability (i.e. is the myocardium likely to
recover after revascularisation.

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Common Cardiac Surgeries
• The most common cardiac surgeries performed are Coronary Artery Bypass Grafting and Valvular Heart
surgery.
• Less commonly, but critically, surgery for acute type A dissection is an emergent life-saving procedure.

Coronary Artery Bypass Grafting (CABG)

• Coronary artery bypass grafting is the surgical option for coronary artery revascularisation in patients with
coronary artery disease.
• Patients with coronary artery disease can present acutely with Acute Coronary Syndromes (STEMI, NSTEMI,
Unstable Angina) or with chronic symptoms, termed) Chronic Stable Ischaemic Heart Disease (progressive
angina/dyspnoea on exertion).
• Diagnosis is confirmed with coronary angiography or CT coronary angiography.
• There are multiple indications for CABG surgery, the details of which are found in either the American or
European cardiology guidelines. The details between choosing best medical therapy, percutaneous
intervention and surgery are complex and beyond the scope of undergraduate medicine. Broadly speaking,
patients with complex multivessel coronary artery disease, diabetes, reduced left ventricular function should
be considered for surgical revascularisation.
• The major steps of the procedure include:
o Harvest of conduit – arterial or venous conduit. Left internal mammary artery (almost always used),
long saphenous vein (examine for varicose veins), radial artery (perform Allen’s test).
o Heparinisation – The patient is given a large dose of unfractionated heparin for anticoagulation. This
facilitates safe use of cardiopulmonary bypass and reduces the risk of clot formation in the system.
o Cannulation – The heart and great vessels are cannulated to connect the patient to the
cardiopulmonary bypass circuit. Typically this is a cannula in the ascending aorta delivering blood to
the body and one in the right atrium which diverts blood from the body back to the heart lung
machine.
o Cardiopulmonary Bypass (CPB) – the cardiopulmonary bypass machine is started and takes over the
work of the heart and the lungs. It circulates blood around the body, provides gas exchange and
controls the patient’s core temperature through cooling and warming of blood.
o Aortic Cross Clamping – A clamp is placed across the ascending aorta. This prevents blood from
entering back into the heart from the cannula in the aorta.
o Cardioprotection - The heart is now ischaemic and a cardioplegia solution is administered to the
heart. This is a high potassium cold solution that causes the heart to arrest. The patient’s core body
temperature is also lowered. Both of these actions reduce the metabolic rate of the heart, reducing
its oxygen demand and thus providing protection from ischaemia. Additionally, reducing the
workload of the heart by placing the patient on CPB also reduces the myocardial oxygen demand
(when the heart is not arrested obviously)
o Grafting – The conduit is then used to create each bypass graft. A small opening is made distal to the
blockage on the coronary artery, one end of the conduit is stitched to cover this opening. The
opposite end is stitched to an opening made on the ascending aorta.
o Once all the required grafts have been finished the cross- clamp is removed from the ascending
aorta. Blood the re-enters the heart, this washes the cardioplegia solution out. Following this, the
heart will spontaneously begin to beat again. Once the function of the heart has returned the
patients is weaned off the cardiopulmonary bypass machine, the cannulae are removed and the
chest is closed.

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Valvular Heart Disease
• Surgical intervention can be required for any of the four heart valves. This may be due to stenosis,
regurgitation or a combination of both.
• Valves can become infected and develop infective endocarditis with large valvular vegetations.
o Students should be familiar with infective endocarditis, presenting symptoms, signs and diagnostic
criteria (Duke’s criteria) although this is a more common subject in medical examinations (unless
your examiner is a cardiac surgeon!).
• The most common valvular heart surgery performed includes aortic valve replacement (most commonly for
aortic stenosis) and mitral valve repair/replacement (most commonly for mitral regurgitation).
• Patients present with symptoms of progressive dyspnoea on exertion, angina, syncope, or symptoms of left
or right heart failure.
• Diagnosis is confirmed with echocardiography.
• Detailed discussion of indications for surgery can be found in ESC guidelines but again are beyond the scope
of undergraduate medicine.
• In general, patients with severe symptomatic valvular heart disease meet criteria for intervention.
• Students should know the definition of
o Severe aortic stenosis (defined by ECHO)
§ Mean gradient >40mmHg
§ Aortic valve area <1cm2
§ Aortic jet velocity >4m/s

Valve Replacement Options

• Biological
o Made from bovine / porcine pericardium.
o Do not require lifetime anticoagulation.
o Valves last between 12 – 15 years before valve failure requiring intervention. This is age and activity
dependant i.e. younger active patients are more likely to encounter structural valvular degeneration
earlier than older inactive patients.
• Mechanical
o Made from titanium and carbon. Designed to last for the duration of the patient’s life without valve
failure. Require lifelong anticoagulation with warfarin (NOACs are currently contraindicated) to
prevent valve thrombosis and stroke.
o Warfarinisation itself provides a 1-2% risk per patient year of a major bleeding of thrombotic event.
The target INR is determined by the Cardiac Surgeon and target INRs vary depending on multiple
factors. Confirm with Cardiac Surgeons if undocumented and if uncertain. Generally, INR target 2.5
for mechanical aortic valve, INR target 3 for mechanical tissue valve.
• TAVI – Transcatheter Aortic Valve Insertion
o This is a minimally invasive method of performing a valve replacement of a biological valve. It is
currently primarily used in older patients who are considered medium-high risk for surgical aortic
valve replacement. It is also considered in elderly patients.
o It is expected that this technique will be used for less high risk patients in the future. It can also be
used to replace bioprosthetic valves that have been surgically inserted – this can prevent the patient
undergoing a redo cardiac operation.

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Acute Aortic Dissection
• This is a group of life threatening conditions. It involves a tear in the inner layer of the wall of the aorta
(intima) and blood travelling between the intima and media, through a “false lumen”.
• The most common classification system is the Stanford Classification
o Type A dissection: involves the aorta proximal to the left subclavian artery
o Type B dissection: involves the aorta distal to the left subclavian artery
• De Bakey classification is less commonly used.

• Type A dissections represent a Cardiothoracic Surgery emergency. Mortality rate approximates 1% per
hour with nearly half of patients dead within 48hours.

• Patients commonly present with severe, tearing chest/back/interscapular pain.

• They may present with collapse or in shock.
• Patients may present with evidence of end organ malperfusion due to abnormal blood flow through the false
& true lumen. Therefore, patients may present with stroke, ischaemic limbs or ischaemic bowel.

• A low index of suspicion is required.

• Diagnosis is made by CT aorta with contrast.

• Surgery aims to reduce the fatal complications of

o Aortic rupture
o Cardiac tamponade
o Myocardial infarction
o Acute severe aortic incompetence

• During surgery, the patient is placed on CPB. The segment of aorta with the intimal tear is resected and
replaced with an interposition graft and blood flow is restored to the true lumen.

Practical tips in managing acute Type A dissection

• Low index of suspicion & early diagnosis with CT aorta
• Type A dissectionà contact Cardiothoracic surgery emergently
• Involve anaesthesia/ICUà will need invasive monitoring i.e. arterial line for continuous blood pressure
monitoring and central venous cannula
• Aim heart rate & blood pressure control to prevent propagation of dissection
o Aim heart rate <80
o SBP 100-120
§ Achieve this using firstly IV beta-blocker infusion (e.g. labetalol/esmolol) and secondly
arteriodilator (e.g. nipride).
§ If not beta blocked first, will have reactive tachycardia and propagate dissection
• If hypotensive, treat with fluids/blood/vasopressors as appropriate. This will be by a senior doctor.
• Once accepted by Cardiothoracic Surgery centre, do NOT delay transfer and transfer emergently. Should be
transferred with
o Arterial line
o Central line
o Urinary catheter
o Senior doctor
Complications
• General
o Bleeding/transfusion (approx. 30%),
o Pain
o Scar
o Infection
o GA
o DVT/PE

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• Specific
o Arrhythmia
o MI
o Permanent pacemaker
o AKI (dialysis)
o CVA
o Death

• EUROScore II is a risk prediction model used to calculate the operative mortality of a procedure for an
individual patient.

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Thoracic Surgery

Pneumothorax
• A pneumothorax is a collection of air within the pleural cavity. This air compresses the lung affecting its
function.
• Types
o Spontaneous
§ A pneumothorax that occurs in the absence of any external event. They can be either:
• Primary spontaneous – in the absence of known lung disease
o Typically: tall, thin males between years 10 – 30.
o Smoking and cannabis smoking increases risk.
• Secondary spontaneous – in the setting of known lung disease
o COPD, bullous disease, lung malignancy

o Traumatic
§ This is from air entering the pleural space following chest trauma causing disruption to the
lung or airways. This can be seen following blunt or penetrating trauma. It is frequently
associated with rib fractures, a haemothorax may also be present.
§ Iatrogenic pneumothorax is a special case of traumatic pneumothorax, it can occur from
procedures such as; lung biopsy, central line insertion, pacemaker insertion or mechanical
ventilation.

• Management of pneumothorax is often with the insertion of a pleural chest drain to remove the air from the
pleural space. The British Thoracic Society (BTS) guidelines outline the algorithm for this.

• Tension Pneumothorax
o This is a subset of any of the above types of pneumothorax.
o The pressure of the air in the pleural cavity increases and begins to compress the mediastinum.
o As the intrathoracic pressure increases the mediastinum is forced to the contralateral side.
o This can cause kinking of the SVC and IVC resulting in dramatically reduced venous return and
cardiac arrest.
o It is a medical emergency that must be identified and managed immediately.
o Signs & Symptoms
§ Dyspnoea, chest pain, agitation, tachycardia, hypotension, reduced Sp02, tracheal deviation
(away from pneumothorax), reduced ipsilateral air entry, hyper-resonant percussion and
engorged neck veins.
o Tension pneumothorax should be diagnosed on clinical examination.
o Management
§ Urgent needle decompression in the second intercostal space, mid clavicular line.
§ This buys time for definitive chest drain placement.
§ A chest drain should be placed to further decompress the pleural cavity and to manage any
ongoing air leak from the lung/ airway.
§ A surgical pleurodesis procedure should be considered on the index admission to prevent
recurrence.

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Chest Drain Insertion
• Chest drains are inserted for evacuation of:
o Air (pneumothorax)
o Fluid (blood, pleural effusion, chyle) from the pleural cavity.
• There are varying types of chest drains available and varying methods of insertion.
• The type of fluid of being drained dictates the calibre of the drain required.
o Simple pleural effusions can be managed with a smaller calibre drain, whereas as haemothorax / pus
may require a wider drain as the fluid is more viscus and can cause smaller drains to block.

• Seldinger Technique
o This technique refers to the insertion of a drain / cannulae into a space over a guidewire. Drains can
be inserted using this technique with the help of image guidance (US/ CT) or by using surface
anatomical landmarks.

• Triangle of Safety
o This outlines an area of the chest wall where chest drains can be most safely inserted. The landmarks
are:
§ Anterior border of the latissimus dorsi
§ Lateral border of the pectoralis major muscle
§ Line superior to the horizontal level of the nipple
§ Apex below the axilla

• Chest Drain Removal

o The decision to remove a chest drain is a clinical decision based on
§ Absence of air leak
§ Satisfactory volume of chest drain output (dependent on clinical scenario)
§ Satisfactory radiological findings

• Terminology
o Oscillation “swing” – this refers to the rise and fall of the water in the water seal chamber or fluid in
the drainage tubing. It is caused by the changing intra-pleural pressures with respiration. Lack of
oscillation can indicate blockage/ kinking of the drain system.
o Bubbling – This is the existence of bubbles in the under-water seal chamber. Presence of bubbles
indicates air leaking from the lung. They can occur with breathing alone or only seen on coughing.
The severity of the bubbling is associated with the degree of air leak at that moment.

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Surgery for Lung Cancer

• Lung cancer is responsible for more deaths than any other cancer.
• Patients with lung cancer often present with advanced, incurable disease. Students should have knowledge
of how lung cancer presents form their respiratory module.

• Surgery in lung cancer can be for

o Diagnosis (e.g. open biopsy)
o Cure (e.g. lung resection in “early” stage lung cancer)
o Palliation (e.g. pleural drainage and pleurodesis for malignant pleural effusion)

• Patients with suspected lung cancer are referred initially to the Rapid Access Lung clinic.
• Depending on patient clinical history, findings and risk profile, patients undergo investigations to assess for
lung cancer (i.e. confirm/exclude diagnosis and to stage the cancer)
o Imaging: CXR, CT thorax, PET-CT (to assess nodal/distant metastasis)
o Bronchoscopy: endobronchial tumour
§ Can be performed with ultrasound-Endobronchial ultrasound - to assess enlarged lymph
nodes.
§ Can also be used to perform bronchoscopic biopsy of suspicious lymph nodes or central lung
masses i.e. masses near the airways)
o Tissue Diagnosis
§ CT guided biopsy
§ Bronchoscopic biopsy
§ Open surgical biopsy
• Patients are discussed at a Lung Cancer MDT with CardioThoracic Surgeons, Respiratory physicians,
Oncologists, Radiation Oncologists, Radiologists and Pathologists present.
• Diagnosis and potential treatment options are discussed.
• If surgery is considered, the patient meets with a surgeon who revisits their diagnosis, treatments options,
risks benefits and alternatives.
• The surgeon’s priority on clinic visit is to determine:
o 1. Is the cancer resectable and
o 2. Is the patient operable

• Resectability
o A patient is deemed to have “resectable disease” if
§ The lung cancer is potentially curable by surgical resection
§ The tumour can be removed completely with clear margins (i.e. no macro- or micro-scopic
evidence of residual disease)

• Surgery offers the best chance of cure in patients with “curative disease”.
o Stage I / II non – small cell lung cancer, and in limited cases of stage III disease, is considered
potentially curative with surgical resection. Essentially, this refers to patients with lung cancer that
has limited nodal spread and no distant metastasis. The earlier the stage, the better the survival.
• Students should have a basic understanding of TNM staging (See IASLC Lung cancer staging for details)
• Alternatives to surgery include Stereotactic Radiation (SABR), chemo therapy, radiation or a combination.
o This offers a lower chance of cure in patients with “resectable” disease but may be considered an
alternative in patients who are deemed high risk or who decline surgery.
• Operability
o Operability essentially refers to “fitness for surgery”. If a patient is deemed “operable” they are
deemed to have a reasonable chance of survival with a reasonable quality of life. Operability is
determined by assessing:
a. Lung function
b. Comorbidities
c. Functional status

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• Lung function is assessed subjectively by patient history and objectively by the 6 minute walk test (6MWT)
and pulmonary function tests (PFTs)
• Predicted postoperative lung function based on the patient’s preoperative PFTs (FEV1, DLCO) and on the
estimated amount of lung to be resected (e.g. if a patient is to undergo pneumonectomy, they will lose
approximately half their lung function and therefore their predicted postoperative lung function will be
approximately half their preop lung function).
o Predicted FEV1 or DLCO <40% is deemed high risk and <30% is generally considered prohibitive.

• Surgical Technique
o Surgical approaches include minimally invasive surgery (robotic or VATS) or open techniques using a
thoracotomy incision.
o The extent of the lung resection required depends both on the characteristics of the primary
malignancy and the patients pre – operative lung function.
o Options include:
§ Wedge resection – lesion is excised with small around of surrounding normal lung. This can
be performed if the diagnosis is uncertain.
§ Segmentectomy – anatomical pulmonary segment is excised including vessels and bronchus.
Lung sparing procedure in patients with poor pulmonary function.
§ Lobectomy – lobe is excised in full. This is the considered the gold standard oncological
resection.
§ Pneumonectomy – entire lung is excised. Only performed when lesser resections are
insufficient.
o Mediastinal lymph node dissection is also performed to establish the patient’s pathological nodal
staging and guide the need for adjuvant therapies.

• Complications
o Pain including chronic pain
o Mortality (~ 2-3%, 6-7% if pneumonectomy)
o Bleeding
o Pneumonia
o Prolonged air leak (> 5 days) from chest drains
o Damage to structures (oesophagus, recurrent laryngeal nerves, Vagus nerves, thoracic duct, heart,
diaphragm)

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References
• Mater Misericordiae University Hospital Department of Cardiothoracic Surgery
o https://www.mater.ie/services/cardiothoracic-surgery/
• European Guidelines (useful for cardiac surgery guidelines)
o www.eacts.org/resources/clinical-guidelines/
• British Thoracic Society (useful for thoracic surgery guidelines)
o https://www.brit-thoracic.org.uk/quality-improvement/guidelines/
• CTSNet (Useful for videos/explanations)
o https://www.ctsnet.org/
• American Association for Thoracic Surgery
o https://www.aats.org/aatsimis/AATSWeb
• Society for Thoracic Surgeons
o https://www.sts.org/

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12. Trauma

• Dr Micheal Sheehan, Dr Izabella Kinga Orban, Dr Enda Hession, Dr Jeffrey Mulcaire, Dr Jessica Lynch

• ATLS
• Head Trauma
• Thoracic Trauma
• Abdominal Trauma

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ATLS

1. Overview
2. Primary Survey
3. Secondary Survey
4. Shock
5. Definitive Care

Overview
• ATLS is for urgently and systematically evaluating the trauma patient. It is designed to help clinicians focus on
life-threatening conditions and minimize the risk of missed injuries.
• Trauma is a leading cause of death in developed countries. It is also a major killer of the elderly - “silver trauma”
describes their higher rates of mortality and morbidity.
• The ABCDE mnemonic defines the specific order of evaluations and interventions that should be followed in
all injured patients and age groups.

o Airway with cervical spine protection

o Breathing
o Circulation with haemorrhage control
o Disability or neurologic status
o Exposure (undress) and Environment (temperature control)

• The management of a trauma patient requires a team and a team leader.

• The patient’s care begins before the arrival of the patient by the pre-hospital emergency medical team. They
usually pre-alert the incoming trauma to the receiving hospital, allowing time for the Emergency Department
staff and trauma team to get ready for the casualties.
• The trauma team usually comprises of airway doctor and airway nurse, primary survey doctor, circulation
nurse, monitoring nurse, doctor for procedures, a scribe.
• A trauma team, including general surgery, orthopaedic surgery etc. should present by the arrival of a major
trauma patient.
• The blood bank and radiology department should be informed early to facilitate the patient’s care.
• The team leader is not involved in hands-on management of the patient – he or she usually stands at the end
of the bed and directs and supervises the patient’s care. Most of the time in a major trauma scenario a lot of
problems are addressed simultaneously by different team members.
• The team members must give feedback after each task performed to the team leader, ensuring closed-loop
communication.
• Before the arrival of the paramedics, the team leader should allocate team members for each role. The
transfusion laboratory should be informed as blood products may be needed urgently and the major
haemorrhage protocol depending on each situation might need to be activated.

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• On the arrival of the patient, the team leader takes the handover which includes details of:
o Mechanism and time of injury
o Injuries found and suspected
o Symptoms and signs
o Treatment initiated

• The management of every trauma patient comprises:

o Primary survey
o Resuscitation
o Secondary survey
o Initiation of definitive care

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Primary Survey

1. Airway Maintenance with Cervical Spine Protection

• The assessment of the airway should begin by introducing oneself to the patient and asking the patient’s
name and what happened to them.
• An appropriate response gives you information about their airway -able to speak clearly, their breathing -
not severely compromised; and their GCS - no major decrease in the conscious level. If there is an
inappropriate answer:
o Check the patency of the airway – the airway may be obstructed by the tongue, a foreign body,
aspirated material, tissue oedema, or expanding hematoma inspect the airway for foreign bodies
(dentures, loose tooth) provide suctioning if needed.
o Look for possible facial/mandibular/tracheal or laryngeal fractures that can obstruct the airway.
o Chin-lift, jaw-thrust to optimize airway: by grasping the angles of the lower jaw one hand on each
side and displace the mandible forward. Restrict spinal motion.
o Use airway adjunct: OPA if there is no gag reflex.
• Supplemental oxygen must be administered to all trauma patients.
• Maintaining oxygenation and preventing hypercarbia are critical in managing trauma patients, especially
those who have sustained head injuries.
• Patients can vomit at any time – be prepared to roll the patient on spinal precautions to the lateral position
and provide suctioning.
• A definitive airway should be established if there is any doubt about the patient’s ability to maintain airway
integrity. Patients with severe head injuries and a GCS < 8 require definitive airway (a cuffed tube below
the vocal cords.)
• Assume a cervical spine injury in patients with blunt multisystem trauma, especially those with altered
level of consciousness or blunt injury above the clavicle. Every effort must be made to keep the cervical
spine inline. The patient’s head and neck should not be moved.
• The 10th edition of ATLS recommends drug-assisted intubation instead of rapid sequence intubation (RSI)
and the use of video laryngoscopy.

2. Breathing and Ventilation

• Assess the adequacy of oxygenation and ventilation. Respiratory rate, breathing effort, oxygen saturation.
• Agitation suggests hypoxia, hypercarbia causes obtundation. Cyanosis is a late sign.
• Inspect the chest for signs of injury, including asymmetric or paradoxical movement (e.g., flail chest),
auscultate breath sounds at the apices and axillae, and palpate for crepitus and deformity.
• Look at the trachea, JVP.
• Life-threatening conditions: tension pneumothorax (compromises ventilation and circulation), cardiac
tamponade, massive haemothorax should be addressed once recognised during the primary survey.
• FAST scan (Focused Assessment Sonography in Trauma) could be used to facilitate diagnosing the above
conditions without delay.
• NB! Distended neck veins, muffled heart signs and hypovolaemia – Beck’s triad = cardiac tamponade.
Point of care ultrasound may be diagnostic.
• Decreased breath sounds, hyper resonance on percussion and shock = tension pneumothorax.
• Treat tension pneumothorax with needle decompression with a large-bore (14 gauge or larger) needle, in
the 5th ICS MAL for adults, 2nd ICS for a child, followed by tube thoracostomy (size 28 – 32 Fr chest drain
for haemothorax).

3. Circulation with Haemorrhage Control

• Check the patient’s skin colour, temperature, capillary refill time, HR, BP and apply cardiac monitors.
• Significant haemorrhage occurs in any of five sites: external, intrathoracic, intraperitoneal, retroperitoneal,
and pelvic or long bone fractures.
• The management of these may include decompression, pelvic binders, splint application and surgical
intervention.
• Insert two large-calibre cannula – black, 16 Fr where possible. If difficulty getting IV access, consider a
central line.

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 • Bloods should be drawn for group and crossmatch and baseline haematologic studies, coagulation profile
and pregnancy test for all females of childbearing age.
• VBG to assess lactate for presence and degree of shock.
• IV fluid therapy with crystalloids – initially 20 ml/kg bolus isotonic fluids up to 1L max. If class III or IV
haemorrhage – blood products.
• Patients with obvious severe or ongoing blood loss should be transfused immediately with O negative
blood.
• TXA / tranexamic acid – 1 g over 10 mins followed by TXA infusion 1 g over 8 hours if trauma < 3 hours and
no other contraindications.
• Consider the reversal of anticoagulant agents once more information is available and consult
haematology.
• Consider transfusing platelets even with normal platelet count. Where available, monitor
thromboelastography and thromboelastometry.
• NB! Elderly patients who take anticoagulants are at higher risk of bleeding.

4. Disability
• A quick assessment of the patient’s GCS, size of the pupils, reaction to light, lateralizing signs, and spinal
cord injury level.
• Maintain spinal immobilization for all patients with the potential for spinal cord injury. The presence of a
motor deficit or a spinal cord sensory level indicates the need for imaging of the brain, spinal cord, and
their vascular supply.

Glasgow Coma Scale

Eye Opening 4 - Spontaneously
3 - To speech
2 - To pain
1 - No response
Verbal 5 - Oriented to time, person and place
Response 4 - Confused
3 - Inappropriate words
2 - Incomprehensible sounds
1 - No response
Motor Function 6 - Obeys commands
5 - Moves to localised pain
4. Flex to withdraw from pain
3 - Abnormal flexion
2 - Abnormal extension
1 - No response

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 5. Exposure and Environment
• Undress the patient for assessment but cover with warm blankets afterwards or consider external
warming to prevent hypothermia.
• Intravenous warmed fluids with the fluid infuser and Bair Hugger.

Adjuncts used during the Primary Survey

• ECG
o Dysrhythmias, atrial fibrillation, ST-segment changes – can indicate a blunt cardiac injury.
o PEA can indicate tamponade, tension pneumothorax or profound hypovolaemia.
o Bradycardia, aberrant conduction – hypoxia and hypo-perfusion should be suspected immediately.
o Extreme hypothermia also produces dysrhythmia.
• Urinary Catheter
o If blood at the urethral meatus, perineal ecchymosis or high riding/non-palpable prostate: do not
catheterise the patient.
o Urethral integrity should be confirmed by retrograde urethrogram before catheter insertion.
• Gastric Catheter/NG tube
o To reduce distension of the stomach and prevent further vomiting.
• Bloods pressure, pulse oximetry, blood gas
• X-Ray
o AP chest radiograph.
• FAST Scan
o To detect free fluid – blood in the abdomen. *See Abdominal Trauma section for further reading.*
o NB! A negative FAST scan does not rule out intraperitoneal bleeding.
o The eFAST (extended FAST scan) is now standard care for evaluation of pneumothorax. Sensitivity of
the eFAST for pneumothorax: 86 – 98%, specificity 97 – 100%.

Secondary Survey
• Full head-to-toe examination with a reassessment of all the vital signs.
• Inspect, palpate, percuss, auscultate and consider additional imaging.
• History
o Allergies
o Medications
o Past illnesses/pregnancy
o Last meal
o Event/Environment related to the injury

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 • Injury types can help predict possible injuries

Mechanisms of Injury and Suspected Injury Pattern

Mechanism of Injury
Frontal impact automobile
collision
• Bent steering wheel
• Knee imprint, dashboard
• Bull’s-eye fracture,
windscreen
Suspected Injury Pattern
• Cervical spine fracture
• Anterior flail chest
• Myocardial contusion
• Pneumothorax
• Traumatic aortic disruption
• Fractured spleen or liver
• Posterior fracture/dislocation
of hip and/or knee

Side impact automobile collision • Contralateral neck sprain

• Cervical spine fracture
• Lateral flail chest
• Pneumothorax
• Traumatic aortic disruption
• Diaphragmatic rupture
• Fractured spleen/liver/kidney,
depending on side of the
impact
• Fractured pelvis or acetabulum

Rear impact automobile collision • Cervical spine injury

• Soft tissue injury to neck

Ejection from vehicle • Ejection precludes meaningful

prediction of injury patterns
but places patient at greater
risk from virtually all injury
mechanisms

Motor vehicle impact with a • Head injury

pedestrian • Traumatic aortic disruption
• Abdominal visceral injuries
• Fractured lower
extremities/pelvis

Shock
• First step: recognize the presence of shock = Inadequate tissue perfusion and oxygenation
• Identify the probable cause of the shock state
• Stop the bleeding and replace the volume loss
• Haemorrhage is the most common cause of shock in the injured patient.
• NB! If patient is cold and tachycardic, they are shocked.
• Two major types of shock
o Haemorrhagic: is defined as an acute loss of circulating blood volume. In an average adult, this
represents approx. 7% of body weight. The blood volume of a child is 8% to 9 % of body weight.
o Non-Haemorrhagic
§ Cardiogenic: myocardial dysfunction caused by blunt cardiac trauma or tamponade
§ Neurogenic: isolated intracranial injuries do not cause shock. Classic picture: hypotension
without tachycardia or cutaneous vasoconstriction. The failure of fluid resuscitation to
restore organ perfusion suggests either continuing haemorrhage or neurogenic shock.
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 § Septic shock due to infection – if the patient’s arrival to the emergency department was
delayed for several hours.

CONDITION ASSESSMENT MANAGEMENT

Tension • Tracheal deviation Needle decompression
Pneumothorax • Distended neck veins Tube thoracostomy
• Tympany
• Absent breath sounds
Massive • Tracheal deviation Venous access
Haemothorax • Flat neck veins Volume replacement
• Percussion dullness Surgical
• Absent breath sounds consultation/thoracotomy
Tube thoracostomy
Cardiac • Distended neck veins Venous access
Tamponade • Muffled heart sounds Volume replacement
• Ultrasound Thoracotomy
Pericardiocentesis
Intraabdominal • Distended abdomen Venous access
Haemorrhage • Uterine lift, if pregnant Volume replacement
• Ultrasound Surgical consultation
Displace uterus from vena
cava
Obvious • Identify the source of Direct pressure
External external bleeding Splints
Bleeding Closure of actively bleeding
scalp wounds

Haemorrhage Control
• Warmed isotonic electrolyte solutions – normal saline or Hartmann’s can be used. This provides transient
intravascular expansion and further stabilizes the vascular volume by replacing the fluid loss.
o The latest guidelines recommend judicious use of IV fluids - 1 L.
o The patient’s response is observed during this initial fluid administration and further therapeutic and
diagnostic decisions are based on this response.
• Persistent infusion of large volumes of fluid and blood to achieve normal blood pressures is not a substitute
for definitive control of bleeding.
o NB! Excessive fluid administration can exacerbate the lethal triad of coagulopathy, acidosis and
hypothermia.
• In penetrating trauma, delaying aggressive fluid resuscitation until definitive control may prevent additional
bleeding.
• Balancing the goal of organ perfusion with the risks of rebleeding by accepting lower than normal blood
pressure has been termed permissive hypotension. The goal is balance, not the hypotension.
• The latest guidelines recommend early resuscitation with blood products.

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 Estimated Blood Loss Based on the Patient’s Initial Presentation
CLASS I CLASS II CLASS III CLASS IV
Bloods Loss Up to 750 750 – 1500 1500 – 2000 > 2000
(mL)
Blood Loss Up to 15% 15% - 30 % 30% - 40% > 40%
(%)
Pulse Rate < 100 100 – 120 120 – 140 > 140
Systolic BP Normal Normal Decreased Decreased
Respiratory 14 – 20 20 – 30 > 35 > 35
Rate
Urinary > 30 20 – 30 5 – 15 Negligible
Output
(mL/hr)
CNS/Mental Slightly Mildly anxious Anxious, Confused,
Status anxious confused lethargic
Initial Fluid Crystalloid Crystalloid Crystalloid and Crystalloid and
Replacement blood blood
Base Deficit 0 to -2 mEq/L -2 to – 6 mEq/L -6 to – 10 - 10 mEq/L or
mEq/L less
o Massive Transfusion
§ Defined as > 10 units of pRBCs within the first 24 hours of admission.
o Coagulopathy
§ Severe injury and haemorrhage results in the consumption of coagulation factors and early
coagulopathy.
o NB! Massive fluid resuscitation results in dilution of platelets and clotting factors along with the
adverse effect of hypothermia on platelet aggregation and the clotting cascade, contributes to
coagulopathy.

Special Considerations
• Children, elderly and pregnant woman have different pathophysiology. Resuscitation of this subgroup of
patients warrants special care.
• Athletes may manifest signs of shock late.

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 • Pregnancy
o Sudden decrease in the maternal intravascular volume can cause reduced foetal oxygenation against
normal maternal vital signs.
o Displace the uterus to the left side, relieving the pressure on the inferior vena cava.
o All pregnant Rh-negative trauma patient should receive Rh immunoglobulin therapy unless the injury
is remote from the uterus (within 72 hours).
o NB! Intimate partner violence in pregnancy.

• Geriatric patients have a limited physiologic reserve and may have difficulty generating an adequate response
to injury.
o Normal blood pressure and heart rate can represent relative hypotension in the elderly patient.
o The high mortality rate reflects the decreased physical reserves of the elderly due to changes of
ageing, comorbidities.
o The use of anticoagulation and beta-blockers can blunt cardiovascular response to hypovolaemia.
o Features that affect the management of the airway in the elderly include dentition, nasopharyngeal
fragility, macroglossia and cervical arthritis.

• Paediatric trauma: smaller body mass, head disproportionately larger.

o Skeleton is more pliable, check babies’ fontanelles.
o Thermal energy loss is a significant stress for the infants.
o Large occiput, large tongue, and short neck.

Definitive Care
• Transfer should be considered whenever the patient’s treatment needs exceed the capability of the receiving
institution.
• Appropriate personnel should transfer the patient to the receiving hospital with close monitoring throughout
transfer.
• Optimal preparation for transfer includes direct communication between the receiving and referring doctor –
using the ISBAR template, documentation of every intervention and safe transfer by escorting by adequate
medical personnel.

I Identification
S Situation
B Background
A Assessment
R Recommendation

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Intracranial Injuries

1. Introduction
2. Anatomy
3. Physiology
4. Classification of Head Injuries
5. Assessment
6. Management

Introduction
• One of the most common trauma presentations to ED
• 90% of prehospital trauma-related deaths involve head injury
• Those who receive medical treatment:
o 75% mild injuries
o 15% moderate injuries
o 10% of severe injuries

Anatomy
• Cranial Anatomy
o Scalp - highly vascular, can result in major blood loss
o Skull - anterior fossa contains frontal lobes, middle fossa contains temporal lobes, posterior fossa
contains lower brainstem and cerebellum
o Meninges- cover brain and consist of three layers
§ Dura - tough fibrous membrane, adheres internal surface of the skull, meningeal arteries lie
between the dura and internal surface of the skull (extradural space). An overlying skull
fracture can lacerate these arteries causing an extradural haematoma. The middle
meningeal artery is the most commonly injured, located over temporal fossa
§ Arachnoid mater - thin and transparent, subdural space between dura and arachnoid,
bridging veins travel from brain surface to venous sinuses (major venous drainage of brain)
within dura, subdural haematoma may develop if they tear
§ Pia mater - firm attachment to the brain surface, CSF fills space between arachnoid and pia
(subarachnoid space), this cushions brain and spinal cord, location of subarachnoid
haemorrhage
o Brain
§ Cerebrum - right and left hemispheres separated by falx cerebri (a fold of meningeal layer of
dura mater descending vertically into longitudinal fissure), left hemisphere contains
language centre in virtually all right-handed and >85% left-handed people. The frontal lobe
controls emotions, executive function, motor function and speech expression on the
dominant side. Parietal lobe controls sensory function and spatial orientation. The temporal
lobe controls certain memory functions. The occipital lobe controls vision.
§ Brainstem - contains midbrain, pons and medulla. Midbrain and upper pons contain reticular
activating system responsible for the state of alertness. The medulla connects with the
spinal cord and contains vital cardiorespiratory centres.
§ The cerebellum - balance and coordination, connects to the spinal cord, brainstem and
cerebral hemispheres
§ Ventricular system - CSF filled spaces and aqueducts within the brain. Consists of four
ventricles- two lateral ventricles, third ventricle and fourth ventricle. CSF continuously
produced within ventricles and absorbed over brain surface. Presence of blood within CSF
can impair its reabsorption and increase ICP. Ventricles usually symmetrical and can be
shifted by brain oedema and mass lesions readily identified on CT.
o Intracranial Compartments
§ Tough meningeal partitions separate brain into regions. The tentorium cerebelli divide the
intracranial cavity into supratentorial and infratentorial compartments. The midbrain passes
through an opening called tentorium hiatus. Oculomotor nerve containing parasympathetic
fibres that constrict pupil run along the edge of tentorium and can be compressed with
temporal lobe herniation causing pupillary dilatation or “blown pupil”.
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Physiology
• Intracranial pressure - a major determinant of cerebral perfusion pressure (CPP)
o CPP = MAP – ICP (MAP= mean arterial pressure, ICP= intracranial pressure)
o Increased ICP will reduce CPP and can cause or exacerbate ischaemia
o Normal ICP is approximately 10mmHg
o Pressure greater than 22mmHg if sustained or refractory to treatment is associated with poor
outcome

• Monro-Kellie Doctrine
o The cranium is a rigid box that cannot expand, therefore the total volume of intracranial contents
must remain constant for ICP to remain normal
o ICP rises when normal intracranial volume increases
o There is a degree of pressure buffering initially as CSF and venous blood is compressed out of the
‘container’
o Once the limit of CSF and venous blood displacement reached- ICP rapidly increases

• Cerebral Blood Flow (CBF)

o Cerebral oxygen delivery dependent on CPP and arterial oxygen content
o Cerebral autoregulation usually impaired early stages after cerebral injury
o CPP = MAP - ICP
o MAP of 50 - 150mmHg is autoregulated to maintain constant CBF
o Severe traumatic brain injury can impair this so that brain cannot adequately compensate for
changes in CPP
o If MAP too low - ischaemia and infarction
o If MAP too high - brain swelling with increased ICP
o Cerebral blood vessels can dilate or constrict responding to changes in partial pressures of oxygen
(PaO2) and partial pressures of carbon dioxide (PaCO2) in the blood
o Enhance CPP and CBF by reducing increased ICP, maintaining normal MAP and intravascular volume
and ensuring adequate oxygenation and ventilation
o Lesions increasing intracranial volume need to be evacuated early

Head Injury Classification

• Various classifications e.g. severity of injury or morphology
o Severity of injury
§ Glasgow coma scale (GCS)
Glasgow Coma Scale
Eye Opening 4 - Spontaneously
3 - To speech Memory Aid
2 - To pain
• 6 - Cylinder Motor
1 - No response
Verbal 5 - Oriented to time, person and place • Jackson 5
Response 4 - Confused • 4 Eyes
3 - Inappropriate words
2 - Incomprehensible sounds
1 - No response
Motor Function 6 - Obeys commands
5 - Moves to localised pain
4. Flex to withdraw from pain
3 - Abnormal flexion
2 - Abnormal extension
1 - No response

§ GCS <8 - generally accepted as the definition of coma or severe brain injury
§ GCS 9-12 - moderate brain injury
§ GCS 13-15 - mild brain injury

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 § When calculating GCS if right/left or upper/lower motor asymmetry, use the best motor
response to calculate the score

• Morphology
o Skull Fractures - can occur at cranial fault or skull base
§ Signs of basilar skull fractures - periorbital ecchymosis (racoon eyes), CSF from the nose
(rhinorrhoea) or ear (otorrhea), retro auricular ecchymosis (Battle’s sign)

o Intracranial Lesions - diffuse or focal, commonly coexist

§ Diffuse injuries - mild concussion to severe hypoxic and ischaemic insults
§ Concussion - transient non-focal neurological injury commonly with LOC
§ Severe diffuse injury typically results from prolonged shock or apnoea, or the result of high-
velocity impact or deceleration injuries which may produce multiple punctate haemorrhages
throughout the cerebral hemispheres, these are "shearing injures" referred to as diffuse
axonal injuries and typically occur between the border of the grey and white matter
§ Focal injuries include epidural hematomas, subdural haematomas, contusions, and
intracerebral haematomas

§ Extradural (AKA epidural) Haematoma

§ Relatively uncommon, approx. 0.5% of patients with brain injuries
§ Biconvex or lenticular in shape- push adherent dura away from the inner aspect of the
skull
§ Often at the temporal or temporoparietal region from a tear to the middle meningeal
artery from fracture
§ Classically a lucid interval may occur, from the time of injury to neurological
deterioration
§ Treatment: Surgical evacuation

§ Subdural Haematoma
§ More common than extradural
§ Often appear to conform to contours of the brain, crescent-shaped or curved, (think
sUbdural = cUrved)
§ Often result from the shearing of bridging blood vessels of the cerebral cortex
§ May be:
• Acute - symptoms within 48 hours
• Subacute - symptoms within 3-14days
• Chronic - symptoms after 2 weeks or longer
§ Treatment: Craniotomy and clot evacuation to reduce the mass effect

§ Contusions and Intracerebral Haematomas

§ Cerebral contusions quite common, 20-30% of severe brain injuries
§ Contusions can evolve to form intracerebral haematomas over hours to days requiring
immediate surgical evacuation
§ Patients with contusions typically undergo repeat imaging to evaluate for changes

Assessment of Patients
• Detailed history including
o Mechanism
o Time of injury
o Loss of consciousness
o Nausea and vomiting
o Amnesia - retrograde, antegrade
o Headache
o Seizures
o Witnesses
o Focal neurology
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 o Past Medical History
o Drugs - anticoagulants and antiplatelets
• Examination
o GCS
o Primary and secondary survey
o Pupils equal and reactive
• Imaging
o Nice Head CT guidelines
§ https://www.nice.org.uk/guidance/cg176/resources/imaging-algorithm-pdf-498950893

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Management of Intracranial Injuries
• Three priorities
o Resuscitation, rapid diagnosis of brain lesion resulting from a head injury, prevention of secondary
brain insults
• Imperative to achieve rapid cardiopulmonary stabilisation
• A systematic approach (ABCDE) *See ATLS section*
• Secondary survey - head to toe assessment and treat as appropriate
• Medical Therapies - the primary aim is to prevent secondary brain injury
o IV fluids, blood, and blood products as appropriate to maintain normovolaemia
o Hyperventilation - normocarbia normally preferred, hyperventilation will reduce PaCO2 causing
cerebral vasoconstriction, use only in moderation and for as limited a period as possible. It may be
necessary to hyperventilate the patient to manage acute neurological deterioration while other
treatments are initiated e.g. hyperventilation will lower ICP with expanding intracranial haematoma
before emergent craniotomy.
o Anticoagulation Reversal - coagulation studies
§ Antiplatelet agents – give platelets
§ Warfarin - FFP, vitamin K, prothrombin complex concentrate
§ Heparin - protamine sulphate
§ Direct thrombin inhibitors e.g. dabigatran- idarucizumab
§ Other NOACs - PCC
o Mannitol - used to reduce elevated ICP
§ Do not give if hypotensive, acts as an osmotic diuretic, need to correct hypovolemia first
o Hypertonic saline - used to reduce elevated ICP
o Anticonvulsants - posttraumatic epilepsy occurs in approximately 5% of admitted patients with
closed head injuries and up to 15% with severe head injuries. They can inhibit brain recovery so
should only be used if necessary
o Sedation and analgesia reduce cerebral oxygen demand and prevent coughing and straining which
can increase ICP
o Nurse patient at 30 degrees and position head and neck in a neutral position to optimise venous
drainage of the brain
o Maintain normothermia
o Prevent hyperglycaemia
o Tranexamic acid (See CRASH 3 trial)

• Surgical Management
o Scalp lacerations - clean and inspect thoroughly before stapling or suturing
o Depressed skull fractures - often require surgical intervention
o Intracranial mass lesion - neurosurgical input, craniotomy required
o Penetrating brain injury - prophylactic broad-spectrum antibiotics, neurosurgical input

• Brain Death - no possibility of recovery

o GCS = 3
o Non - reactive pupils
o Absent brainstem reflexes e.g. oculocephalic, gag reflex, corneal reflex
o No ventilatory effort
o Absence of confounding factors e.g. hypothermia, drug or alcohol intoxication
o Consider organ donation with family

Discharge Advice for Patients with a Head Injury

• Stay with someone for 48 hours
• Give the patient an advice card and tell to return if:
o Confusion
o Drowsiness
o Seizures
o LOC

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o Visual disturbance
o Headaches
o Vomiting

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Thoracic Trauma

1. Background
2. Primary Survey
3. Secondary Survey

Background
• Thoracic trauma is a significant cause of mortality
• Less than 10% of blunt chest injuries and only 15% to 30% of penetrating chest injuries require operative
intervention, but emergency management (ATLS) saves lives
• Thoracic trauma causes
o Lung contusions
o Haematomas
o Alveolar collapse
o Changes in intrathoracic pressure relationship
§ Tension pneumothorax
§ Open pneumothorax
• Physiological consequences of thoracic trauma
o Hypoxia
o Hypercarbia
o Respiratory acidosis (caused by hypercarbia)

Primary Survey: Immediately Life-Threatening Thoracic Injuries

• A: Airway Problems
o Airway Obstruction
§ Potential types of injury
• Laryngeal injury
• Posterior dislocation of the clavicular head
• Penetrating trauma from knives or bullets
§ Causes
• Swelling
• Bleeding
• Vomitus

o Assessing for obstruction

§ Inspect
• Inspect the oropharynx for foreign body
• Respiratory distress
• Stridor or hoarseness
§ Palpate
• Feel for crepitus over the anterior neck and chest wall (feels like crunching Rice
Krispies)
• Palpate for defect over sternoclavicular joint
§ Auscultate
• Listen to all lung fields to assess air movement

o Management
§ Suction blood and vomitus from airway
§ Often a temporary fix pre definitive airway placement (early intubation with endotracheal
tube)
§ Reduce a posterior dislocation or fracture of the clavicle if this is the cause of obstruction

• Tracheobronchial Tree Injury

o Injury to the trachea or the major bronchus is unusual but potentially fatal
§ Tension pneumothorax
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 § Tension pneumopericardium
o Presentation
§ Haemoptysis
§ Cervical subcutaneous emphysema
§ Tension pneumothorax
§ Cyanosis
o Management
§ Intubation
§ Chest drain insertion
o If a tracheobronchial injury is suspected, obtain immediate cardiothoracic consultation
§ Diagnosis confirmed with bronchoscopy
§ Operative intervention may be immediate or delayed, depending on the stability of the
patient.

• B: Breathing Problems
Action Findings
Inspect Expose Patient Chest and Neck
Neck veins
• Distended
• Flat
• Normal
Chest Wall Expansion
• Equal or not
• Adequate or hypoventilation
• Obvious deformity or injury
Palpate Tenderness
• Rib fracture
Crepitus/subcutaneous emphysema
Defect of the chest wall
Auscultate Breath sounds equal bilaterally or not
Added sounds
• Effusion
• Contusion

Tension Pneumothorax
• “One-way valve” leak occurs from the lung or through the chest wall
• Air is forced into the pleural space with no escape, collapsing the affected lung
• If the mediastinum is displaced to the opposite side
o Decreased venous return
o Compression of the opposite lung
o Obstructive shock may result
o Decreased venous return à Reduced cardiac output

• Causes
o The most common cause is mechanical ventilation in patients with lung injury
o As a result of simple pneumothorax following penetrating or blunt trauma

• On Examination
o Vitals
§ Tachypnoea
§ Tachycardia
§ Hypotension
o Chest pain
o Tracheal deviation AWAY from the side of the injury
o Unilateral absence of breath sounds
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 o Elevated hemithorax without respiratory movement
o Hyperresonant to percussion
o Neck vein distension
o Cyanosis (late manifestation)
o Extended focused assessment with sonography in trauma (eFAST)
§ Absence of lung sliding
§ See https://www.youtube.com/watch?v=rnLwPhidvZA for example

• Management
o CLINICAL DIAGNOSISà DO NOT WAIT FOR RADIOLOGICAL CONFIRMATION
o Immediate decompression
§ Needle decompression
• Large bore cannula
• 5th intercostal space, slightly anterior to the mid-axillary line
• Beware cannula may kink, or chest wall may be too thick to effectively reach the
pleural space
• Continuously reassess
o Finger thoracostomy may be performed if needle decompression is unsuccessful
o Chest drain insertion is mandatory after needle or finger decompression

Open Pneumothorax
• Large chest wall injuries that remain open can result in an open pneumothorax
• Equilibration between intrathoracic pressure and atmospheric pressure is immediate
• Air follows the path of least resistance
• When there is an opening in the chest wall that is ≥2/3 the diameter of the trachea, air passes preferentially
through the chest wall defect with each inspiration
• Effective ventilation is thereby impaired à Hypoxia and hypercarbia

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• On Examination
o Chest wall wound with noisy air movement

• Management
o Close defect with sterile dressing large enough to overlap the edges of the wound
o Tape dressing ONLY on 3 sides to provide a flutter valve effect
o As the patient breaths, the dressing occludes air entry
o As the patient exhales, the open end allows air to escape from the pleural space
o Insertion of a chest drain remote from the wound site
o Surgical closure of skin wound

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 • C: Circulation Problems
Action Findings
Inspect Expose Patient Chest and Neck
Neck Veins
• Distended
• Flat
• Normal
Chest Wall Expansion
• Equal or not
• Adequate or hypoventilation
• Obvious deformity or injury
Skin
• Mottled
• Cyanosis
• Pallor (? Bleeding)
• Cold or warm
• Central cap refill time (2 sec normal)
Palpate Central and Peripheral Pulses
• Quality
• Rate
• Regularity
• Peripheral may be absent in
hypovolemia
Auscultate Breath Sounds Equal Bilaterally or Not
Added Sounds
• Effusion
• Contusion
Heat Sounds
• Muffled or normal
• Regular or irregular

• Major thoracic injuries that affect circulation and should be recognized and addressed during the primary
survey are
o Massive haemothorax
o Cardiac tamponade

Massive Haemothorax
• Accumulation of >1500ml blood in one side of the chest (or more than 1/3 of the patients’ blood volume)
• Cause
o Penetrating or blunt trauma that disrupts the systemic or hilar vessels
o Can compromise respiratory efforts by compressing the lung and preventing adequate oxygenation
and ventilation
• On Examination
o Chest wall dull to percussion
o Decreased chest wall expansion on the affected side
o Absent or decreased air entry
o Vital Signs
§ Tachypnoea
§ Tachycardia
§ Hypoxia
§ Hypotension
§ Signs of shock

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 o Neck Veins
§ Flat due to hypovolemia
§ Maybe distended if there is associated tension pneumothorax. Neck veins will not be
distended in haemothorax alone.

• Management
o Establish large calibre intravenous lines
o Infuse crystalloid, give blood as soon as possible
o Chest drain insertion (28-32 French) and drainage of haemothorax
§ 5th intercostal space
§ Anterior to the mid-axillary line

o Where possible, blood from the chest tube can be collected in a device suitable for autotransfusion
o Emergency surgery consultation advised

Indications for Urgent Thoracotomy

The immediate return of 1500 mL or more of blood
Initial output <1500ml, but continued loss of >200ml/hr for 2-4 hrs
Incomplete evacuation of blood from the chest
Persistent need for blood transfusion
Penetrating anterior chest wounds medial to the nipple line and posterior wounds medial to the
scapula (the mediastinal “box”)
• The possible need for thoracotomy because of potential damage to the great vessels, hilar
structures, and the heart, with the associated potential for cardiac tamponade
NB: Colour of the blood is a poor indicator of the necessity for thoracotomy

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 Differentiating Tension Pneumothorax and Massive Haemothorax
Condition Physical Signs
Breath Percussion Tracheal Neck Veins Chest
Sounds Position Movement
Tension Decreased or Hyperresonant Deviated Distended Expanded
Pneumothorax Absent away immobile
Massive Decreased Dull Midline Collapsed Mobile
Haemothorax

Cardiac Tamponade
• Compression of the heart by an accumulation of fluid in the pericardial sac
• Pericardial sac
o Fibrous structure
o A small amount of fluid or blood can restrict cardiac activity and interfere with cardiac filling
• Causes
o Penetrating (most common) or blunt chest wall injuries
§ Pericardium to fill with blood from the heart, great vessels, or epicardial vessels
• Signs
o Classical Triad
§ Muffled heart sounds
§ Hypotension
§ Distended neck veins
• May be absent due to hypovolemia
o Kussmaul’s Sign
§ A rise in venous pressure with inspiration when breathing spontaneously
§ A true paradoxical venous pressure abnormality that is associated with tamponade
o Pulseless electrical activity (PEA) on ECG in a trauma patient in cardiac arrest may indicate cardiac
tamponade
• eFAST can effectively identify cardiac tamponade or pericardial effusion
o 90-95% accurate
o Beware à concomitant haemothorax may result in both false positive and false negative exams
• Management
o IV fluid will improve cardiac output transiently while preparations are made for surgery
o If surgical intervention is not possible, pericardiocentesis can be therapeutic, but it does not
constitute definitive treatment for cardiac tamponade.
§ Subxiphoid pericardiocentesis with aspiration
§ Because complications are common with blind insertion techniques, pericardiocentesis
should represent a lifesaving measure of last resort in a setting where no qualified surgeon is
available to perform a thoracotomy or sternotomy

Traumatic Cardiac Arrest

• Trauma patients who are unconscious and have no pulse are considered to be in circulatory arrest
o Hypovolemia
§ PEA seen on ECG
o “True” cardiac arrest
§ Ventricular fibrillation
§ Asystole
• Causes of traumatic circulatory arrest
o Severe hypoxia
o Tension pneumothorax
o Profound hypovolemia
o Cardiac tamponade
o Cardiac herniation
o Severe myocardial contusion
• Remember, a cardiac event may have preceded the traumatic event

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 • Signs
o Known blunt or penetrating trauma
o Unconscious
o No pulse
• 1.9% will survive if closed CPR is performed
• 10% survival and higher have been reported with circulatory arrest following penetrating and blunt trauma
• Management
o Start CPR
o ABC management
o 2 X Large-bore IV cannulas (Intraosseous if unable to get IV)
o Secure airway with an endotracheal tube (if expertise available)
o Administer mechanical ventilation with 100% oxygen
o To alleviate potential tension pneumothorax
§ Perform bilateral finger or tube thoracostomies
o Monitor ECG and oxygen saturation
o Rapid fluid (ideally blood) resuscitation
o Administer epinephrine (1 mg) if ventricular fibrillation is present
o A resuscitative thoracotomy may be required if there is no return of spontaneous circulation (ROSC)
§ Only if the loss of output is witnessed and <10min have passed

Secondary Survey
• The secondary survey of patients with thoracic trauma involves
o In-depth physical examination
o Ongoing ECG
o Pulse oximetry
o Arterial blood gas (ABG) measurements
o Chest computed tomography (CT) scan in selected patients with suspected aortic or spinal injury
• Chest X-Ray
o Lung expansion
o Absence of lung markings
o Presence of fluid
o Mediastinal widening
o A shift in the midline
o Loss of anatomical detail
o Rib fractures
§ Fractures of 1st or 2nd rib suggest significant force delivered to the chest
o Extended FAST (eFAST) has been used to detect both pneumothoraces and haemothoraces

Potentially Life-Threatening Injuries

Simple pneumothorax
• Pneumothorax results from air entering the potential space between the visceral and parietal pleura
• A ventilation-perfusion defect occurs because the blood that perfuses the nonventilated area is not
oxygenated
• Causes
o Blunt trauma (most common)
o Penetrating trauma
• Signs
o Decreased air entry to the affected side
o Hyperresonance
o Tachypnoea
o No tracheal deviation (no tension)
o Dyspnoea
• Investigations
o Upright expiratory chest x-ray (if no concerns re thoracic spine)
o CT Thorax if appropriate

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 • Management
o Observation and aspiration of a small, asymptomatic pneumothorax may be appropriate
§ <3cm
o Chest drain insertion
§ Fifth intercostal space, just anterior to the midaxillary line
§ After inserting a chest tube and connecting it to an underwater seal apparatus with or
without suction
§ Chest x-ray examination is done to confirm appropriate placement and re-expansion of the
lung
o Avoid positive pressure ventilation unless the chest drain is inserted

Haemothorax
• <1500ml blood
• Signs
o Decreased chest wall movement
o Penetrating injuries evident
o Decrease air entry to the affected side
o Dullness to percussion on the affected side
o Typically no signs of shock as not massive
• Causes
o Laceration of the lung, great vessels, an intercostal vessel, or an internal mammary artery from
penetrating or blunt trauma
o Thoracic spine #
• Management
o Supine chest x-ray (If possible)
§ A small amount of blood will be identified as a homogeneous opacity on the affected side
o CT Thorax (if appropriate or if haemothorax suspected on plain film)
o If <1500ml, bleeding is often self-limiting and does not require operative management
o An acute haemothorax that is large enough to appear on a chest x-ray may be treated with a 28-32
French chest tube
o The chest tube evacuates blood, reduces the risk of a clotted haemothorax, and allows for
continuous monitoring of blood loss

Rib Fractures, Flail Chest and Pulmonary Contusion

• Injuries to the ribs are often significant
o Pain breathing typically results in shallow breathing
o Reduced ventilation and oxygenation, and ineffective coughing
o Atelectasis and pneumonia is much more likely with pre-existing lung conditions
• A flail chest occurs when a segment of the chest wall does not have bony continuity with the rest of the
thoracic cage
o Two or more adjacent ribs fractured in two or more places
o It can also occur when there is a costochondral separation of a single rib from the thorax
• A pulmonary contusion is a bruise of the lung, caused by thoracic trauma
• A pulmonary contusion can occur without rib fractures or flail chest, particularly in young patients without
completely ossified ribs
• Children have far more compliant chest walls than adults and may suffer contusions and other internal chest
injuries without overlying rib fractures
• Pulmonary contusion is most often encountered with concomitant rib fractures, and it is the most common
potentially lethal chest injury
• Rib fractures and contusions can cause respiratory failure over time.
• Observation of abnormal respiratory motion and palpation of crepitus from rib or cartilage fractures can aid
the diagnosis
• Management
o Chest X-ray may suggest multiple rib fracture
o If flail chest is suspected, CT Thorax is indicated

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 o Analgesia
§ IV or PO Opioids
§ Local anaesthetic administration (Paravertebral or serratus anterior nerve blocks)
• Avoids the potential respiratory depression common with opioids
o Humidified oxygen
o Adequate ventilation
o Cautious fluid resuscitation
o Patients with significant hypoxia (i.e., PaO2 < 60 mm Hg [8.6 kPa] or SaO2 < 90%) on room air may
require intubation and ventilation within the first hour after injury
§ COPD and CKD increase the likelihood of requiring early intubation and mechanical
ventilation

Blunt Cardiac Injury

• Can result in myocardial muscle contusion, cardiac chamber rupture, coronary artery dissection and/or
thrombosis, and valvular disruption.
• Causes
o Road traffic collision (50%)
o Pedestrian vs vehicle
o Motorcycle accidents
o Fall from height >6 metres
• Clinically Significant Sequelae
o Hypotension
o Dysrhythmia
o Wall-motion abnormality on echo
• ECG Changes are Variable
o ST changes
o Premature ventricular contractions
o Unexplained sinus tachycardia
o New atrial fibrillation
o Bundle branch block
• The use of troponin in diagnosing blunt cardiac injury is inconclusive
• Patients with a blunt injury to the heart diagnosed by conduction abnormalities (an abnormal ECG) are at
risk for sudden dysrhythmias
o Monitor for the first 24 hours
o After this interval, the risk of a dysrhythmia appears to decrease substantially
• Patients without ECG abnormalities do not require further monitoring

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Traumatic Aortic Disruption
• Seen most commonly after falling from height >6 metres or road traffic collision (deceleration injury)
• Frequently fatal
• If identified promptly and treated expeditiously survivors can recover

• Signs of traumatic aortic disruption on x-ray

o Widened mediastinum
o Obliteration of the aortic knob
o Deviation of the trachea to the right
o Depression of the left mainstem bronchus
o Elevation of the right mainstem bronchus
o Obliteration of the space between the pulmonary artery and the aorta (obscuration of the
aortopulmonary window)
o Deviation of the oesophagus (nasogastric tube) to the right
o Widened paratracheal stripe
o Left haemothorax
o Fractures of the first or second rib or scapula
• If an aortic injury is suspected à CT aortogram
• Management
o Open repair involves resection and repair of the torn segment or, infrequently, primary repair
o Endovascular repair is the most common option for managing aortic injury and has excellent short-
term outcomes

Traumatic Diaphragmatic Injury

• More common on the left side because of the liver protecting the diaphragm on the right
• Chest x-ray findings
o Elevated right hemidiaphragm
o Diaphragmatic injuries are frequently missed initially
§ Misinterpreted as showing an elevated diaphragm, acute gastric dilation, loculated
hemopneumothorax, or subpulmonic hematoma
• CT can occasionally miss injury
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 • Diagnostic laparotomy can help evaluate in an indeterminate case
• Treatment is by direct repair
• Care must be taken when placing a chest tube in patients with suspected diaphragm injury, as tubes can
inadvertently injure the abdominal contents that have become displaced into the chest cavity

BluntOesophageal Rupture
• Most commonly results from penetrating injury
• Linear tear in the lower oesophagus, allowing leakage into the mediastinum
• The resulting mediastinitis and immediate or delayed rupture into the pleural space causes empyema
• Signs
o Particulate matter may drain from the chest tube after the blood begins to clear
o Mediastinal air also suggests the diagnosis, which often can be confirmed by contrast studies or OGD
(oesphagogastroduodenoscopy)
• Treatment
o Wide drainage of the pleural space and mediastinum
o Direct repair of the injury
o Repairs performed within a few hours of injury improve the patient’s prognosis

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Abdominal Trauma

1. Anatomy
2. Epidemiology
3. Mechanism of injury
4. Assessment of Blunt Abdominal Trauma
5. Assessment of Penetrating Abdominal Trauma
6. CT
7. FAST
8. Indications for Emergency Laparotomy
9. Specific Injuries
10. Pelvic Trauma

Anatomy
• There are four regions of the abdomen to consider in penetrating abdominal injuries:

i. Thoracoabdominal area
ii. Anterior abdomen
iii. Flanks
iv. Back

• The pelvic cavity contains the lower part of the intraperitoneal and retroperitoneal spaces, enclosed by the
pelvic ring. It contains the rectum, bladder, iliac vessels, and female internal reproductive organs.

Epidemiology
• Blunt abdominal trauma accounts for 80% of abdominal injuries seen in the Emergency Department. Most
blunt abdominal trauma cases (75%) are related to motor vehicle collisions.
• The prevalence of intra-abdominal injury in patients presenting to ED with blunt abdominal trauma is
approx. 13%.
• Blunt abdominal trauma has a mortality rate of approximately 8.5%.
• Almost 2/3 of blunt abdominal injuries occur in males, with a peak incidence in patients aged 14 – 30 years.
• As many as 30% of penetrating chest injuries traverse the diaphragm, potentially injuring abdominal
structures.

Mechanisms of Injury
• Blunt abdominal injury may occur because of:
o Rapid severe increase in intra-abdominal pressure
o Direct blow
o Restraint (e.g. lap belt)
o Ejection from a vehicle
o Crush injuries
o Shearing injuries
o Deceleration injuries
• Penetrating abdominal injury may occur because of:
o Stabbing
o Gunshot wounds
o Explosions/blast injuries – from high-velocity fragments
o Impalement

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Assessment of Blunt Abdominal Trauma

Primary Survey
• Abdominal and pelvic injuries may cause life-threatening haemorrhage.
• Initial examination of the abdomen is best performed in the circulation phase of the primary survey.
• Manage as per ATLS

Secondary Survey

Inspection
• Abrasions
• Bruising
• Seat belt marks
• Lap belt sign (= 30% chance of mesenteric or intestinal injury)
• Retroperitoneal haemorrhage (Cullen’s sign = ecchymosis of the peri-umbilical area; Grey-Turner’s sign =
ecchymosis of the flank)
• Blood at urethral meatus/perineal bruising

Palpation
• Fullness indicates haemorrhage
• Crepitation of the lower ribcage indicates potential hepatic or splenic injury
• Peritonism indicates rupture of a hollow viscus with leakage of contents into the peritoneal cavity
• DRE: High riding or non-palpable prostate in men indicates urethral injury

Assessment of Penetrating Abdominal Trauma

• Any patient with penetrating abdominal trauma should be fully undressed and examined carefully as
wounds may be obscured by body habitus, clothing or bleeding or be concealed in the axilla, scalp, perineum
or groin.
• All patients with penetrating abdominal trauma must be log rolled to evaluate for wounds to the
back/flanks.

Assessment for Peritoneal Penetration

• Evaluation of penetrating abdominal trauma in patients without indications for immediate laparotomy may
include:
o Local wound exploration
o Plain radiograph
o Computed tomography
o Serial physical examination
o Ultrasonography
o Laparoscopy
• Serial physical examination is 94% sensitive for detecting the presence of intraabdominal injury in patients
with penetrating trauma.
• All patients with a wound that penetrates the anterior rectus fascia must be observed for a minimum of 12
hours.
• Any patient >65 years of age, on anticoagulation, with significant medical comorbidities, or with other
significant injuries, should be observed for a minimum of 24 hours.
• Intoxicated patients should be observed until after the effects of the intoxicating substance have resolved.
• Prior to discharge, several criteria must be met:
o Mentally capable of making informed medical decisions
o Unremarkable physical exam (reasonably isolated discomfort at the wound site is allowed)
o Vital signs normal and no concerning trends
o Passing urine
o Tolerating PO fluids
o Mobilising normally
o Safe discharge environment
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 • Local wound exploration: Involvement of the abdominal fascia is considered a positive result.
• Erect CXR: Subdiaphragmatic free air is indicative of peritoneal perforation; however, a normal examination
does not rule it out.
• FAST (Focused Assessment with Sonography for Trauma): The presence of free fluid in the abdomen is
indicative of peritoneal perforation/intraperitoneal organ injury, however, a normal examination does not
rule it out.
o Focused Assessment with Sonography for Trauma (FAST)
§ The FAST scan is a point-of-care ultrasound examination performed at the time of
presentation of a trauma patient.
§ The main aim of a FAST scan is to identify intra-abdominal free fluid (assumed to be
haemoperitoneum in the context of trauma). This helps to make decisions about further
management.
§ The sensitivity of FAST scanning is ~90% & specificity is ~95% for detecting intraperitoneal
free fluid. The sensitivity for detecting solid organ injury is much lower. It has now largely
replaced diagnostic peritoneal lavage as the preferred initial assessment for assessment of
haemoperitoneum.
§ Four regions are assessed during a standard FAST scan:
• 1. Subxiphoid transverse view: to assess for pericardial effusion and left lobe of liver
injuries
• 2. Longitudinal view of the right upper quadrant: to assess for right lobe of liver
injuries, right kidney injury and fluid in the hepatorenal recess (Morrison's pouch).
The hepatorenal recess is the deepest part of the peritoneal cavity when lying
supine and is, therefore, the most likely place for fluid to accumulate in a patient
lying flat.
• 3. Longitudinal view of the left upper quadrant: to assess for splenic injury and left
kidney injury
• 4. Transverse and longitudinal view of the suprapubic region: to assess the bladder
and fluid in the pouch of Douglas
§ It may take up to 500mls of free fluid for the FAST to be positive – if initially negative but
high suspicion for intraabdominal injury/haemorrhage consider repeat examination after a
period of time.
§ An 'extended FAST' or 'eFAST' may also be performed looking at the left and right thorax and
helps to assess for the presence of pneumothorax and haemothorax.
• CT abdomen is highly sensitive (97%) for peritoneal violation. The major advantage of CT is the ability to
diagnose the injured organ(s) and to quantify the severity of injuries.
o Computed Tomography (CT)
§ CT Advantages
• Defines the severity of organ injury and potential for nonoperative management
• Detects severity and source of haemoperitoneum rather than just presence/absence
• Often able to detect active bleeding
• Ability to assess retroperitoneum and vertebral column
• Ability to concurrently scan other areas (e.g. brain, thorax)
• Negative imaging generally good indicator of the absence of clinically significant
injury
§ CT Disadvantages
• Insensitive for mesenteric, bowel, and pancreatic duct injuries
• IV contrast required – potential for allergic reactions
• High cost
• Difficult to obtain/potentially unobtainable in haemodynamically unstable patients
• Radiation exposure

Indications for Emergency Laparotomy

• Blunt abdominal trauma with haemodynamic instability with a positive FAST scan or clinical evidence of
intraperitoneal bleeding
• Blunt or penetrating abdominal trauma with a positive DPL
249
 • Penetrating abdominal wound with haemodynamic instability
• Gunshot wounds traversing the peritoneal cavity or visceral/vascular retroperitoneum
• Evisceration
• Bleeding from the stomach, rectum or genitourinary tract following penetrating trauma
• Peritonitis
• Free air or rupture of hemidiaphragm on CXR
• Contrast-enhanced CT demonstrating ruptured gastrointestinal tract, intraperitoneal bladder injury, renal
pedicle injury, or a severe visceral parenchymal injury after blunt or penetrating trauma

Specific Injuries

Grading of Liver Injury

Grade Description of Injury
I Small (<10% involvement, <1cm)
II Moderate (10-50%, <10cm)
III Large (>50%, >10cm or expanding)
IV Large with parenchymal disruption (>25% of a hepatic lobe)
V Large with parenchymal disruption (>75% of a hepatic lobe) or Juxtahepatic
venous injury
VI Hepatic avulsion

Grading of Splenic Injury

Grade Description of Injury
I Small (<10%, <1cm)
II Moderate (10-50%, <5cm)
III Large (>50%, >5cm or expanding)
IV Large with partial devascularisation (>25%)
V Complete devascularisation of spleen
Both splenic and liver injuries can be managed conservatively in the absence of haemodynamic instability.

Renal Injury
• Most genitourinary injuries are not immediately life-threatening
• Renal pedicle injury can lead to life-threatening haemorrhage and renal ischaemia
• Assessment
o Clinically significant injuries will have ≥1 of the following:
§ Microscopic haematuria (-> 20% of renovascular injuries and ~5% of renal injuries do not
have microscopic haematuria)
§ Flank tenderness and/or swelling
§ Haemodynamic instability
§ Fracture of lower posterior ribs, lower thoracic or lumbar vertebrae
• Imaging
o Gold standard = CT abdomen with IV contrast
o Renal angiography rarely necessary

Grading of Renal Injuries

Grade Description of Injury
I Haematuria, no parenchymal involvement, subcapsular
II Non-expanding, confined to retroperitoneum, <1cm, no urinary extravasation
III >1cm, involving renal cortex, no urinary extravasation or collecting system involvement
IV Cortex, medullary and collecting system or vascular involvement
V Shattered or avulsed kidney

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 • Management
o Most (95%) renal injuries (grades I-III + most grade IV) can be managed conservatively
o Surgical management required for ongoing active haemorrhage, haemodynamic instability or urinary
extravasation
o Grade V injuries often require nephrectomy
o Interventional radiology to stent dissected arteries or embolise bleeding vessels is an alternative to
surgical management

Duodenal Injuries
• Direct blow to abdomen (**bicycle handlebars**)
• Bloody gastric aspirate
• Subdiaphragmatic free air on erect CXR

Pancreatic Injuries
• Direct blow to epigastrium with compression of pancreas against vertebrae
• Amylase
o Early normal amylase does not exclude injury
o Elevated amylase may be from non-pancreatic sources
• CT
o IV and oral contrast
o False negatives up to 8hrs post-injury

Hollow Viscus Injuries

• Injured intestinal structures frequently missed as may produce only minimal haemorrhage
• High index of suspicion in:
o Chance fractures (50% are associated with intra-abdominal injury)
o Seat belt sign (30% chance of mesenteric or intestinal injury)

Pelvic Trauma

Aetiology
• Pelvic fractures mostly result from high-energy mechanisms
o Road traffic collision (~50%)
o Pedestrian vs motor vehicle (~30%)
o Fall from height (~10%)
o Motorbike collision (~4%)
o Other e.g. sports injury, low energy fall (~6%)

• Associated major injuries are common

o Intra-abdominal organs (28%), including aortic injury
o Bladder & urethral injury (5-20%)
o Hollow viscus injury (13%)
o Rectal injury (up to 5%)
o Vaginal tears (<5%)

• Morbidity and mortality from pelvic fractures is high, with an overall mortality of 10-30%, which rises to 50%
in patients with pelvic fractures and haemodynamic instability.

• There are 4 potential sources of haemorrhage from pelvic fractures

o Surfaces of fractured bones
o Pelvic venous plexus
o Pelvic arterial injury
o Extra-pelvic sources

• Venous haemorrhage is said to account for 90% of bleeding from pelvic fractures.

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 • Pelvic volume is approximately 1.5L.
• Disruption of the pelvic ring in severe fractures creates a loss of tamponade effect.

Assessment
• If a pelvic binder has been applied in the prehospital setting for suspicion of serious pelvic injury, do not
remove, stabilise the patient and proceed with imaging
• Inspect for ecchymosis, asymmetry, wounds
• Palpate the pubic symphysis, iliac crests, posterior sacroiliac joints, sacrum and ischial tuberosities
• Gently compress the iliac crests to feel for instability – this should be done cautiously to avoid worsening
haemorrhage/dislodging clot, ideally by the most senior doctor present
• Digital rectal examination – assessing for rectal injury (e.g. frank blood, palpable wounds/tears), bony
fragments/palpable fractures, anal sphincter function, boggy/high riding prostate in males (indicative of
urethral injury)
• Examine perineum for perineal/scrotal haematoma or blood at urethral meatus (indicative of urethral injury)
• Examine lower limbs for length discrepancy, rotation, and abnormal neurology
• Examine the abdomen for signs of associated intra/retroperitoneal injury

Management
Haemodynamically Stable Patient
• Perform CT abdomen/pelvis with IV contrast
• A pelvic 'blush' indicates active arterial haemorrhage
• Treatment of choice is angiography with selective embolisation of actively bleeding artery
• Surgical fixation as required under orthopaedic team

Haemodynamically Unstable Patient

• Resuscitation with blood products (activation of massive transfusion protocol may be required)
• Involve general surgery, orthopaedic and intensive care teams
• AP pelvis XR (if normal, rules out significant pelvic fracture as the cause of haemodynamic instability)
• eFAST: If positive – emergency laparotomy with pelvic stabilisation and/or pre-peritoneal packing

252
References
• https://www.litfl.com/trauma-mortality-and-the-golden-hour/
• https://www.uptodate.com/contents/initial-management-of-trauma-in-adults
• ATLS Student Course Manual, 9th Edition. 2012
• ATLS Student Course Manual, 10th Edition. 2018 https://viaaerearcp.files.wordpress.com/2018/02/atls-
2018.pdf
• Henry S. ATLS 10th edition offers new insights into managing trauma patients. Bulletin of the American
College of Surgeons [Internet][published 01 Jun. 2018.
• Gomersall C, Joynt G., Cheng C, Yap F, Lam P, Torrance J et al. Basic Assessment and Support in Intensive
Care. United Kingdom: BASIC; 2019.
• National Institute for Health and Care Excellence, Head Injury, Nice Clinical Guideline, London. 2014
• Ekeh AP, Peterson W, Woods RJ, et al. Is chest x-ray an adequate screening tool for the diagnosis of blunt
thoracic aortic injury? J Trauma 2008;65:1088–1092.
• Rhee PM, Acosta J, Bridgeman A, et al. Survival after emergency department thoracotomy: review of
published data from the past 25 years. J Am Coll Surg 2000;190(3):288–298
• Davies G, Lockey D. Thirteen survivors of prehospital thoracotomy for penetrating trauma: a prehospital
physician-performed resuscitation procedure that can yield good results, trauma. Injury Infection and Critical
Care 2011;70:75–8
• European Resuscitation Council Guidelines for resuscitation 2015 section 4. Cardiac arrest in special
circumstances. Resuscitation. 2015;95:148-73
• Royal College of Surgeons of Edinburgh, Consensus Statement 2018: Management of Traumatic Cardiac
Arrest

253
13. Plastic Surgery

• Ms Laoise Coady, Ms Stephanie Bollard, Ms Christine Quinlan

• Wound Management and Principles of Reconstruction

• Skin Lesions
• Burns
• Upper Limb
• Reconstruction
o Breast
o Head and Neck
o Lower Limb
o Perineal
o Chest Wall

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Wound Management & Principles of Reconstruction

Wound Healing

Wound – disruption of normal anatomical relationship of tissues as a result of injury

Definitions
• Laceration – cut or tear
• Contusion – skin in-tact but injured “bruised”
• Abrasion – superficial skin removed “grazed”
• Crush – compression (Can result in contusions & lacerations)
• Puncture – laceration where depth is expected to be greater than width/opening (dog bites/stab wounds)
• Avulsion – tissue forcefully separated from surrounds

Wound Healing – The process by which normal anatomy is restored

All of these processes overlap, though different aspects more dominant at different times

1. Haemostasis
Immediately within minutes, coagulation
o Vasoconstriction
o Platelet aggregation – release vasoactive amines & growth factors e.g. serotonin, PDGF, EGF, platelet
factor IV
o Activation of clotting cascade
o Deposition of fibrin – scaffold for other cells to enter wound
o Granulation tissue formation
• Proliferation of new vessels looping in and out of wound
• Stimulated by growth factors released in clot
2. Inflammation/Lag Phase
Days 1 – 4, cellular recruitment & increased vascular permeability, damage limiting
o Complement activation
o Polymorphonuclear cells infiltrate due to chemotaxis
• e.g. Neutrophils
• Phagocytosis of debris/bacteria
o Mononuclear cells
• e.g. macrophages/monocytes
• growth factors for collagen production stimulating fibroblasts
o Stimulation of epithelialization
• Migration of epithelial cells from edge of wound or remaining dermal appendages begins
within hours (1mm/day)
• Primary closure in surgery – complete in 48 hours
3. Proliferative Phase
Days 4 – Week 3, reparative phase – granulation tissue & collagen
o Fibroblast proliferation
• Synthesis of collagen, increasing tensile strength
o Ongoing re-epithelialisation
o Ongoing angiogenesis
4. Remodelling Phase
Week 3 onward, maturation & strengthening
o Steady state of collagen synthesis & breakdown (MMPs) resulting in better organisation and
stronger cross links
o Scar contracts and flattens
o Peak strength at 60 days – 80% pre-injury

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Wound Closure Types
1. Primary Intention
• Wound closure by direct approximation of wound edges
2. Secondary Intention
• Wound left open to heal spontaneously (i.e. remains in inflammation stage until closed)
• Depends on contraction and epithelialisation

Factors Affecting Wound Healing

1. Local Factors (Often modifiable)
• Infection
• Ischaemia/poor blood supply
• Foreign body
• Haematoma/Seroma
• Mechanical (tension/shearing forces)
• Previous irradiation
2. General (Often non-modifiable)
• Smoking
• Chronic disease
• Steroid use
• Nutritional deficiencies
• Age

II) Abnormal Scarring

• Hypertrophic Scarring - Red, raised enlarged scar remaining within the boundaries of original injury
• Sites – areas of tension: back, shoulder, sternum
• Treatment
o Pressure garments
o Silicone sheeting
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 o Steroid injections
o Re-excision (may reoccur)
• Keloid Scarring – Red raised often pruritic scar extending beyond boundaries of original injury
• Sternum, deltoid, earlobes, more common in darker skin groups
• Treatment
o Pressure garments
o Silicone
o Steroid injections
o Surgical excision – very likely to reoccur
o Radiation therapy

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Principles of Wound Management

General Principles

Goal – obtain a closed wound as quickly as possible to prevent infection and secondary deformity
• Clean surrounding skin
• Debridement of clot, debris, necrotic tissue
Convert chronic contaminated wounds into acute clean freshly debrided wound
• Assess wound
o Is there tissue loss?
Which tissues require reconstruction – i.e. what is your defect?
o Is there damage to underlying structures? (nerve/tendon/bone)
• Antibiotics – follow local guidelines
• Immunisation – Consider need for tetanus
• Closure & Dressing - when clean & appropriate

Dressings
The Ideal Dressing should
• Maintain a moist environment at wound interface
• Remove exudate
• Act as a barrier to micro-organisms
• Leave no foreign particles in wound
• Provide mechanical protection
• Be easy to remove without trauma to wound
There is no single dressing ideal for all wounds – there are multiple different types

Negative Pressure Wound Therapy, i.e. Vacuum-Assisted Closure Device

• Consists of open-pore foam sponge, semi-occlusive cover, fluid collection system & suction pump
• Changed typically every 24-36 hours
• Mechanism of Action
o Direct Effects
• Maintains moist and warm environment
• Closed system generates pressure gradient, promoting fluid transport and decreasing
oedema
• Draws the edges of the wound together/apposes skin grafts
• Removes exudates and infectious materials
o Indirect Effects
• Increased blood flow
• Diminished inflammatory response (decreased MMP documented)
• Promotes granulation tissue formation by facilitating cell migration and proliferation
• Advantages
o Can anticipate and manage pain at change of dressings pre-emptively (only every 2-3 days vs. saline
dressing)
o Easy to tailor and maintain in position
o Accelerated wound healing
• Disadvantages
o Portable pump – must carry
o Expensive – but quicker wound closure leads to decreased dressing changes
• Contraindications
o Exposed vital structures – organs/vessels or vascular grafts
Increases risk of tissue erosion, causing enteric fistula/haemorrhage
Generally reserved until granulation tissue layer/flap/graft covers
o Ongoing infection
o Devitalized/malignant tissue
o Adhesive allergy
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Reconstructive Ladder

Definitions
• Graft – A segment of tissue detached from its blood supply at the donor site, transferred to another site,
and dependent upon revascularisation from the recipient site.

• Flap – A segment of tissue transferred from one site to another with its vascular supply (a pedicle) intact.

The important distinction between a flap and a graft is blood supply.

E.g. a free flap is completely detached from its blood supply, but as it is transferred with a pedicle that is
anastomosed elsewhere, it is not dependent upon revascularisation.

The principle of the reconstructive ladder is to outline a hierarchy of different reconstructive techniques of
increasing complexity.

Secondary Intention
Primary Closure
Delayed Primary Closure
Skin Grafts
Local Flap
Regional Flap
Free Flap

The benefit of this outline is allowing the surgeon to select the most simple option (or combination of options)
suitable for reconstruction of a given defect.
In practice, certain ‘rungs’ on the ladder are often skipped for aesthetic or functional purposes.

259
Skin Grafts
• A segment of tissue detached from its blood supply at the donor site, transferred to another site, and
dependent upon revascularisation from the recipient site.

• Classified as split-thickness or full-thickness depending on amount of dermis included

Split Thickness Skin Graft (SSG) Full Thickness Skin Graft (FTSG)
Includes Epidermis & part of dermis Epidermis & all of dermis
Donor Most often thigh Neck, supraclavicular area, pre-
Can be buttock/scalp/back auricular

Donor Healing Re-epithelisation from dermal Must be primarily closed.

appendages No dermal appendages left.
Graft Take Easier take, shorter distance for Slower vascularisation
i.e. how well it heals imbibition of nutrients
Contraction More secondary contracture More primary contracture
i.e. reduction in size contracts once placed on wound immediately contracts upon harvesting
of graft bed/over time during (elastin in dermis intact)
remodelling
Cosmesis Poor Better cosmesis
Recipient areas Large areas e.g. burns Hands, face, fingers – better cosmesis
and less contracture
Other Can mesh to cover larger areas
(Also prevents accumulation of
fluid beneath)

Skin Graft Healing or “Take”

• 4 Stages of Graft Take
o Adherence
• Sticks to wound bed by fibrin
o Imbibition (0-48 hours)
• Passive absorption of nutrients from wound bed below by diffusion
o Revascularisation
• Inosculation (48-72 hrs) – vessels in graft connect with vessels in wound bed (ends line up
& join)
• Neovascular Ingrowth (Day 3-5) – new vessels, revascularisation of graft
o Remodelling

• Requirements for Survival

A skin graft will fail or “not take” due to anything that disrupts one of these 4 stages and needs to be placed
on a clean & well-vascularised wound bed
o Well-vascularised wound bed
• Required for imbibition.
• Bone/cartilage unsuitable, though can survive on well vascularised
periosteum/perichondrium
o Contact between graft & bed
• Required for imbibition & inosculation
• Haematoma/collection obstruct these processes (meshing can help)
• Shearing i.e. sliding of graft, will disrupt inosculation – must be well secured

o Clean bed
• Low bacterial count required
• Graft Review
o Check Graft approx. D5 post op to assess “take”
o Donor site for Split graft left for 2 weeks
260
Flaps
• A segment of tissue transferred from one site to another with its vascular supply (a pedicle) intact.
• Can classify in many ways
o Blood Supply
• Random Blood Supply – supply by dermal/subdermal plexus
Kept within certain length:width to ensure blood supply (2:1)
e.g. Most local flaps on face rotation/transposition or advancement flaps
• Axial Blood Supply – well defined artery and vein supplying flap
e.g. gracillis flap, Transverse Rectus Abdominal Myocutaneous (TRAM) Flap
o Anatomic Location
• Local – raised from tissue adjacent to the defect, sharing an edge
Described then based upon type of movement used to place into defect
e.g. Most local flaps on face
• Regional – tissue in vicinity but not adjacent to defect
Interpolated into defect crossing over or under normal tissue
e.g. Latissimus dorsi or TRAM in breast reconstruction
• Distant – donor site is far from defect
Most commonly used now is Free Flap where the named vessels are detached from donor
and re-anastomosed to a recipient vein and artery at the recipient site
e.g. Deep Inferior Epigastric Perforator flap in breast reconstruction
o Composition
• Single component – muscle/skin/bone
• Multiple components
e.g. fasciocutaneous – radial forearm flap
myocutaneous – TRAM flap
• Remember where the flap is taken from also leaves a donor site defect that must be closed.
This can also be closed using any step on the reconstructive ladder.

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Skin Lesions

Benign

Skin lesions can arise from any of the constituents of the skin.
• Dermis
• Epidermis
• Cysts
• Vascular Tumours
• Subcutaneous Fat
• Melanocytic Proliferations

Dermal Tumours
• Skin Tag (Acrochordon)
o Outgrowth of normal skin.
Pedunculated lesions
common at sites of friction

• Dermatofibroma
o Most common cutaneous soft
tissue lesion
o Present as solitary, firm
nodules approximately 0.3-
1cm in diameter
o Often hyperpigmented
o Most commonly located on
lower extremities
o Characteristic dimple when
pinched
o Treatment only if
symptomatic, diagnosis in
doubt or for cosmetic reasons

Epidermal Tumours
• Seborrheic Keratosis
o Benign proliferation of
immature keratinocytes
o Develop after age of 50
usually
o Present as round/oval lesions
with a verrucous surface and
stuck-on appearance
o Treatment only if
symptomatic, diagnosis in
doubt or for cosmetic reasons

262
Cysts
• Epidermal Cysts
o Most common cutaneous
cysts
o Present a skin coloured
nodules with a visible central
punctum
o Occur anywhere on the body
o May remain stable or
progressively enlarge
o Treatment
§ May resolve
spontaneously, but
tend to recur
§ Incision and drainage
when lesion is
inflamed
§ Oral antibiotic
therapy may be
required if significant
surrounding cellulitis
§ Excision when not
inflamed

• Pilar Cysts
o Slow growing, firm
subcutaneous nodules
o Derived from the root sheath
of the hair follicle
o Most commonly found on the
scalp
o Can be sporadic or hereditary
with autosomal dominant
transmission

Vascular Tumours
• Pyogenic Granuloma
o Benign vascular tumour of the
skin or mucous membranes
o Characterised by rapid growth
o Friable – bleeds after minor
trauma
o Cause unknown – trauma and
medication reported as
triggers
o Spontaneous regression may
occur, however treatment
(surgical excision) is usually
required due to bleeding and
ulceration

263
Tumours of Subcutaneous Fat
• Lipoma
o Most common benign soft-
tissue neoplasms
o Mature fat cells enclosed in a
fibrous capsule
o Present as painless, soft
subcutaneous nodules
o Clinical diagnosis – ultrasound
can confirm
o Malignant transformation to
liposarcoma is rare
o Treatment only if symptomatic,
diagnosis in doubt or for
cosmetic reasons

Melanocytic Proliferations
• Melanocytic Naevi
o Proliferation of cutaneous
melanocytes
o Present as pigmented macules,
papules or plaques
o May be flesh-coloured or pink

• Solar Lentigo
o Proliferation of melanocytes
secondary to solar damage
o Uniform hyperpigmentation in
areas of chronic sun exposure
§ Face, Shoulders, Backs,
Hands
o Flat, oval evenly pigmented
macules
o Treatment only if symptomatic,
diagnosis in doubt or for
cosmetic reasons

264
Malignant
Basal Cell Carcinoma
• Arises from basal layer of epidermis
• Most common non-melanoma skin
cancer (NMSC)
• Slow growing, metastases rare, locally
invasive
• Incidence increases with age
• Risk Factors
o UV Radiation from
sunlight/tanning beds/PUVA
o Fair skin/red hair/blue eyes
(Fitzpatrick Skin Type I/II)
o Immunosuppression
o Family history
o Previous BCC
o Gorlin Syndrome
• Presentation
o Nodular
§ 80% of cases
§ Pearly/pink/flesh
coloured papule
§ Telangiectasia within
papule Nodular BCC
§ Rolled edges with
central ulceration
o Superficial
§ 15% of cases
§ M>F
§ Scaly pink/red
macules/patches
§ Can be pigmented
o Morpheaform
§ 5-10%
§ Smooth flesh
coloured
Superficial BCC
papules/plaques
§ Can present as
indented scar-like
lesions
• Treatment
o Surgical excision
o Moh’s micrographic surgery
o Radiotherapy
o Topical Creams – 5-
Fluorouracil/Imiquimod

• Prognosis
o Risk of developing subsequent Morpheaform BCC
BCCs
§ 15% will develop
another primary BCC
within one year
§ 35% within five years

265
Actinic Keratosis
• Proliferation of atypical epidermal
keratinocytes
• Occasionally progress to SCC (60% of
SCCs arise from Actinic Keratoses)
• Present as rough, erythematous, scaly
macules and patches
• Risk factors: chronic sun exposure, fair
skin (Fitzpatrick Skin Type I/II), male
sex, immunosuppression
• Treatment
o Cryotherapy
o Topical: 5-Fluorouracil,
Imiquimod
o Surgical excision

266
Squamous Cell Carcinoma
• Arises from epidermal keratinocytes
• Second most common NMSC
• Metastases can occur – spread via
lymphatics
o Lesions on lips and ears
metastasize early and are
associated with poor prognosis
• Risk Factors
o UV Radiation from
sunlight/tanning beds/PUVA
o Fair skin/red hair/blue eyes
(Fitzpatrick Skin Type I/II)
o Immunosuppression
o Family history
o Smoking
o Chronic inflammation
• Presentation
o SCC in Situ (Bowen’s Disease)
§ Presents as erythematous
scaly patch/plaque
o Invasive SCC
§ Clinical appearance
correlates to the level of
tumour differentiation
§ Well differentiated
lesions: hyperkeratotic
papules/plaques/nodules
§ Poorly differentiated
lesions: show areas of
necrosis, haemorrhage,
ulceration
§ Neurological symptoms
e.g. paraesthesia,
numbness, stinging may
be present in those with
histological perineural
invasion
• Treatment
o Surgical excision
o Moh’s micrographic surgery
o Radiotherapy
o Cryotherapy
o Topical Creams – 5-
Fluorouracil/Imiquimod (SCC in
Situ)
• Prognosis
o Five year cure rate >90%
o Survival rate markedly reduced for
those with regional and distant
metastases
§ Lymph node metastases:
25-35% survival at 5 years
§ Distant Metastases: <10%
survival at 5 years
o Risk of subsequent skin cancer –
SCC/BCC/Melanoma

267
Melanoma

• Malignant neoplasm of melanocytes

• Most serious form of skin cancer
• 80% of all skin cancer deaths
• Incidence increases with age
• Majority of melanomas arise de novo

• Risk Factors
• UV Radiation from sunlight/tanning beds/PUVA
• History of childhood sunburn
• Fair skin/red hair/blue eyes (Fitzpatrick Skin Type I/II)
• Immunosuppression
• Family history
• >50 melanocytic naevi
• Atypical naevi
• Previous skin cancer

• Presentation
• ABCDE
o Asymmetry
o Border irregularities
o Colour variegation (red/blue/black/grey/white)
o Diameter ≥6 mm
o Evolution – Change in colour, size, shape of pre-existing lesion
• Ugly Duckling Sign – presence of a lesion which does not match the patient’s naevus phenotype
• Glasgow Seven Point Checklist (Any major feature or ≥3 minor features is an indication for referral)
o Major
• Change in size/new lesion
• Change in shape
• Change in colour
o Minor
• Diameter ≥7mm
• Inflammation
• Crusting or bleeding
• Sensory change
• Metastatic melanoma may present with palpable lymph nodes

268
Pathological Subtypes
• Superficial Spreading Melanoma
• Most common (~70%)
• Most common on back in men
and lower extremities in women
• Present as variably pigmented
macule with and irregular border

• Nodular Melanoma
o 15-30% of all melanomas
o Present as darkly pigmented
polypoid or pedunculated
papules or nodules
o Most are thicker than 2mm at
the time of diagnosis

• Lentigo Maligna Melanoma

o 10-15% of all melanomas
o Arises in areas of chronic sun-
damage – common in elderly on
face
o Begins as a tan/brown macule,
enlarges over years and may
develop darker asymmetric
areas

269
• Acral Lentiginous Melanoma
o <5% of melanomas
o Most common among dark
skinned individuals
o Arise on palmar, plantar and
subungual surfaces

Acral Lentiginous Melanoma

Subungual Melanoma

• Others

Amelanotic melanoma Uveal melanoma

Spitzoid melanoma Desmoplastic melanoma

270
• Staging
• Breslow Thickness
o Depth of tumour measured from the epidermis to the thickest part of the lesion
o Most important prognostic factor
o Five Year Survival
Depth 5 Year Survival
(%)
In Situ 95-100
<1 mm 95-100
1 – 2 mm 80-95
2 – 4 mm 60-75
> 4mm 50

• American Joint Committee on Cancer (AJCC) Tumour, Node, Metastasis (TMN) Staging System Eight
Edition
o T0: Unknown/Completely regressed primary tumour
o Tis: Melanoma in situ
o TX: Tumour thickness cannot be assessed e.g. biopsy by shave excision
o T1: ≤1mm
• T1a: <0.8mm without ulceration
• T1b: <0.8mm with ulceration or 0.8-1.0mm with or without ulceration
o T2: >1.0-2.0mm
• T2a: without ulceration
• T2b: with ulceration
o T3: >2.0-4.0mm
• T3a: without ulceration
• T3b: with ulceration
o T4: >4mm
• T4a: without ulceration
• T4b: with ulceration

• Management
• Diagnosis
o Excisional biopsy with 2mm margins of normal skin and subcutaneous fat
o Lesion is staged based on biopsy result and lymph node involvement
o All patients with a diagnosis of primary invasive cutaneous malignant melanoma should be
discussed at a multidisciplinary team meeting
• Surgery
o Wide local excision down to muscle fascia
o Margin based on Breslow Thickness of Tumour
Breslow Excision
Thickness Margins
In Situ 5mm
<1mm 1cm
1.01-2mm 1-2cm
2.1-4mm 2-3cm
>4mm 3cm
o Sentinel lymph node biopsy for melanomas stage T1b and greater
o Sentinel lymph node biopsy for melanomas >4mm for purposes of staging/adjuvant therapy
if recommended at MDM

• MSLT-1, MSLT2, DeCOG Trials

o Historically elective lymph node dissection was suggested as optimal management based on
the fact that melanoma metastasized initially to regional lymph nodes.
271
 o Elective lymph node dissection is associated with significant morbidity, therefore sentinel
lymph node biopsy was introduced to assess what patients had nodal disease and would
therefore benefit from lymph node dissection.

• Multicentre Selective Lymphadenectomy Trial I (MSLT-I)

o Patients randomised to wide excision alone or wide excision with sentinel
node biopsy
o Those who had wide excision alone underwent completion lymph node
dissection upon discovery of nodal recurrence while those who had a
positive sentinel node biopsy underwent completion dissection.
o Results: No statistically significant melanoma-specific disease free survival
difference between the two arms; Improved survival in those with early
lymph node dissection for lymph node metastases in intermediate thickness
melanomas

• German Dermatologic Cooperative Oncology Group-Selective Lymphadenectomy

Trial (DeCOG-SLT)
o Compared the survival of sentinel node positive patients with melanoma
with and without completion lymph node dissection
o Results: No difference in survival outcomes between patients treated with
completion lymph node dissection or nodal observation following positive
sentinel lymph node biopsy
o Trial was underpowered but concluded that completion lymph node
dissection should not be performed in those with sentinel lymph node
metastases £ 1mm

• Multicentre Selective Lymphadenectomy Trial II (MSLT-II)

o Aimed to determine whether completion lymph node dissection improved
melanoma specific disease free survival in patients with sentinel lymph node
metastases vs observation of the nodal basin with ultrasound follow up
o Those with a positive sentinel node biopsy were randomised into two
groups
§ Completion lymph node dissection
§ Observation with nodal ultrasound – lymph node dissection
performed if nodal recurrence
o Results: small but significant difference in disease free survival in those who
underwent lymph node dissection. No difference in distant metastasis-free
survival
o Concluded that careful US surveillance is safe for patients with melanoma
sentinel lymph node metastases. Dissection improves regional nodal control,
provides staging information and decreases recurrence slightly, however,
there is additional morbidity for the patient

o Positive sentinel lymph node biopsy

• Clinical observation with Ultrasound Surveillance – immediate completion lymph
node dissection provides no survival benefit
• Completion lymphadenectomy if subsequent evidence of regional lymph node
recurrence (in absence of distant metastases)

• Adjuvant Therapy
o Immunotherapy
• Anti-programmed cell death 1 [PD-1] Antibodies e.g. pembrolizumab, nivolumab
• Anti-cytotoxic T-lymphocyte-associated protein 4 [CTLA-4] antibody - ipilimumab
o Targeted therapy
• BRAF V600 mutation - dabrafenib plus trametinib

272
 • KIT mutation – imatinib
o Radiation therapy
• Palliative role
• Areas of symptomatic local disease e.g. brain metastases
o Chemotherapy in patients whose disease has progressed after optimal treatment with other
systemic therapies

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Burns

Aetiology
• Thermal burns are caused by boiling water, flames or contact with hot objects.
• Chemical burns occur after contact with household/industrial chemicals.
• Electrical injuries (low voltage, high voltage and lightning strike) result in thermal burns secondary to heat
generation.
• Frostbite results in cold thermal injury
• Flame burns are the most common cause of burns in adults.
• Scalds are the most common cause of burns in children.

Assessment of Depth of Burns

Severity of the burn will depend on it depth, size, location and patient comorbidities.

Depth Colour Blisters Capillary Sensation Healing

Refill
Epidermal Red No Present Present Yes
Superficial Pale Pink Yes - small Present Painful Yes
Dermal
Mid-Dermal Dark Pink Yes - large Sluggish Painful; Usual
Sensation to
light touch
may be lost
Deep Dermal Blotchy Red – Sometimes Absent Absent No
fixed staining
Full Thickness White No Absent Absent No
(leathery
appearance)

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Estimation of Total Body Surface Area of Burn

• Rule of Nines
o Divides the body surface into areas of nine percent or multiples of nine percent
o Exception – perineum » 1%
o Paediatric Rule of Nines for children
• Palmar Surface
o Use for small burns
o Palmar surface (fingers and palms) of patient’s hand » 1% TBSA
• Lund and Browder Chart
o Most accurate method
o Takes into consideration the age of the patient

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276
Principles of Burn Management

1. First Aid
2. Primary Survey
3. Secondary Survey
4. Further Management

1. First Aid
• Stop the burning process
• Cool the burn wound
• First aid is effective only within the first three hours from the time of the burn

Thermal Burns
• Stop the burning process
o Remove the person from the source of the burn
o “Stop, Drop and Roll” method for flame burns
• Remove clothing and jewellery
• Cool the burn
o Cool running water for 20 minutes
o DO NOT USE ice or iced water
o Limited water: cool compress or cover burn with cling film and cool asap within 3 hours of injury
• Warm the patient
o Need to keep the patient warm to prevent hypothermia
• Cover the burn
o The cooled burn should be covered with loose strips of cling film or any clean lint free cloth or non-
adherent dressing

Chemical Burns
• Remove chemical agent
• Irrigate
• Treat
o TOXBASE for agent-specific decontamination and treatment information

Electrical Burns
• Manage life threatening conditions as per ATLS protocol
• Cool injury site after electrical source has been controlled
• Prolonged monitoring is not required if there is no history of cardiac arrest, abnormal rate/rhythm,
unconsciousness

Cold Burns (Frostbite)

• Manage life threatening conditions as per ATLS protocol e.g. hypothermia, severe trauma
• Rewarm in circulating water at 37°C to 39°C with a mild antibacterial agent e.g. chlorhexidine for at least 30
minutes within 12 hours of injury
• Once all injured tissues have regained sensation and are soft and pliable to touch and are red-purple in
appearance rewarming is complete
• Elevate injured area to reduce swelling

2. Primary Survey
• A Airway Maintenance and C-Spine Control
• B Breathing and Ventilation
• C Circulation with Haemorrhage Control
• D Disability – neurological status
• E Exposure and environmental control
• F Fluid Resuscitation

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3. Secondary Survey
• Head to toe examination
• History

o A - Allergies
o M - Medications
o P – Past Illnesses
o L – Last Meal
o E – Events/Environment related to Injury

• Mechanism of Injury

4. Further Management
• Analgesia
• Tetanus immunisation
• Enteral feeding if indicated
• Proton pump inhibitors – reduce incidence of stress ulceration
• DVT prophylaxis
• Conservative Treatment
o Simple dressings for small superficial/mixed thickness burns
• Surgery
o For full thickness burns
o Excision down to viable tissue
o Skin grafting

Fluid Resuscitation

• Fluid resuscitation is indicated in adults with >15% TBSA burns and children with >10% TBSA burns
• Burn injury results in fluid sequestration into the area of injury.
• This process becomes generalised when the size of the burn exceeds 20-30% TBSA.
• Oedema combined with continuing evaporative loss from the moist burn surface results in decreased plasma
volume, which in turn leads to intravascular hypovolaemia.
• Hartmann’s Solution is the internationally accepted choice for initiation of resuscitation.

Parkland Formula

3-4ml Hartmann’s Solution x Bodyweight (kg) x % TBSA

• Calculated volume is given over the first 24 hours from the burn
o Half is given in the first 8 hours and the other half is given over the next 16 hours
o Calculation of fluid requirements commences at the time of the burn and not at the time of
presentation.

• Children are given maintenance fluids 5% Glucose in 0.45% NaCl in addition to resuscitation fluids.
o 100ml/kg up to 10kg plus
o 50ml/kg from 10-20kg plus
o 20ml/kg for each kg over 20kg
• Adequacy of fluid resuscitation should be monitored by urine output (Insert a urinary catheter) and altered if
necessary.

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Complications

• Circumferential Burns/Full thickness Burns

o In full thickness and deep dermal burns the skin is unable to expand due to progressive oedema
o Circumferential full-thickness burns can lead to distal ischaemia
o The burn wound (eschar) needs to be released surgically by incising burnt skin down to the
subcutaneous fat
§ Escharotomy
• To allow adequate ventilation
• To prevent ischaemia

• Inhalational Injuries
o Fire in an enclosed space
o Upper airway burns
o Ensure patent airway
o High flow oxygen
o Monitor frequently for respiratory deterioration

• Renal Compromise
o Acute tubular necrosis and acute kidney injury secondary to hypovolaemia and increased secretion
of stress mediators e.g. aldosterone, vasopressin angiotensin
o Can progress to renal failure with metabolic acidosis and myoglobinuria.

• Infection
o Common cause of morbidity and mortality in burn patients.
o Burn wound is susceptible to colonisation by endogenous and exogenous organisms
o Eschar provides a favourable environment for microbial colonisation and proliferation
o Treatment should include burn wound care (dressings), antimicrobial therapy (topical +/- systemic)
and burn wound excision/debridement

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Basic Upper Limb Anatomy Notes

• In order to examine the hand, a basic knowledge of the anatomy of the hand is essential. Much of this can
be gleaned from your core anatomy texts, but a quick revision of the basic tenets of hand anatomy will add
to your learning during your plastics rotation. It is also important for the plastic surgery portion of your
exams!

Skin
• On the hand, the skin of the palm differs from dorsal skin
• The palmar skin is thick, glabrous and non-pliable. It contains a high number of sensory nerve fibres and
sweat glands. It is also closely adherent to the underlying fascia
• The dorsal skin is looser, thinner and attached to underlying fascia by loose areolar tissue

Fascia
• The palmar fascia has a complex arrangement in the hand and digits, the greater details of which are beyond
the scope of the undergraduate syllabus. However a basic knowledge will help your understanding of
common conditions such as Dupuytren's.
• The palmar fascia originates from the palmaris longus in the proximal palm
• It fans out from here and fibres run in multiple directions - longitudinal, vertical, oblique and transverse -
depending on the location
• Fibrosis of the palmar fascia is what gives rise to the clinical presentation of Dupuytren's Disease

Tendons
• Movement at the wrist is controlled by flexors, running along the volar surface of the forearm, and extensors
which run dorsally
• The wrist flexors are flexor carpi radialis and flexor carpi ulnaris
• The wrist extensors are extensor carpi radialis brevis, extensor radialis longus and extensor carpi ulnaris
• In the hand, movements of the digits are controlled by both intrinsic and extrinsic muscles
o Flexion of the digits is controlled by the extrinsic flexor digitorum profundus tendons (one to each of
the 4 digits from index to little) which flex the distal interphalangeal joints (DIPJ), and the flexor
digitorum superficialis tendons (one to each of the 4 digits from index to little although it can be
absent in approximately 20% of little fingers) which flex the proximal interphalangeal joints (PIPJ)
o Flexion of the IPJ of the thumb is controlled by the flexor pollicis longus
o Extension of the thumb IPJ is controlled by extensor pollicis longus
o Extensor pollicis brevis and abductor pollicis longus are responsible for thumb metacarpophalangeal
joint (MCPJ) extension and radial deviation of the hand at the wrist
o Extension of the DIPJ and PIPJ of the index to little fingers is controlled by the extensor digitorum
communis (EDC) tendons
o The index (extensor indicis proprius) and little (extensor digiti minimi) fingers also have an additional
extensor tendon, both of which lie ulnar to the EDC. These tendons can perform independent
extension of these digits, in the absence of EDC (e.g. EDC laceration)
o The intrinsic muscles of the hand (4 dorsal interossei, 3 palmar interossei, 4 lumbricals and thenar
and hypothenar muscles) work together to perform more fine movements of the hand
o Specifically, the complex arrangement of the lumbricals and interossei, together with the extensor
tendons of the digit, are responsible for MCPJ flexion together with PIPJ extension of the index to
little fingers
o The adductor pollicis muscle, together with extensor pollicis longus, perform a similar function in the
thumb

Nerves
• All interosseous muscles of the hand are supplied by the deep branch of the ulnar nerve, except for the LOAF
muscles (lateral 2 lumbricals, opponens pollicis, abductor pollicis brevis and the superficial head of flexor
pollicis brevis) which are supplied by the median nerve
• More proximally the ulnar nerve also supplies the flexor carpi ulnaris and the flexor digitorum profundus
muscles to the little and ring fingers

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 • The median nerve supplies all other wrist and digital flexors, including flexor pollicis longus which is
innervated by the anterior interosseus branch of the median nerve
• All extensors of the wrist and digits are supplied by the radial nerve
• Each digit is supplied by a radial and ulnar neurovascular bundle, on the volar surface, containing a digital
artery and digital nerve (sensory) - these lie superficial, radial and ulnar, respectively, to the flexor sheath
and gross integrity is examined by testing sensation on either side of the digit

Vessels
• The two main arteries supplying the hand are the radial artery and the ulnar artery, both of which branch
from the brachial artery in the proximal forearm
• The radial artery is the dominant blood supply to the thumb and radial index finger and to the deep palmar
arch
• The ulnar artery is the dominant vessel supplying the superficial palmar arch which supplies the middle, ring
and little fingers via common digital arteries (the ulnar digital artery to the little finger usually arises
separately directly from the arch) which then branch into ulnar and radial digital arteries to each digit

Bones
• 8 carpal bones make up the carpus, the proximal row of which articulates with the distal forearm to form the
wrist joint
• From the carpus, 5 metacarpal bones form the proximal bone structure of the hand
• In the thumb, 2 phalanges articulate at the IPJ, while all other digits have 3 phalanges (proximal, middle and
distal)
• 2 sesamoid bones are found at the volar surface of the thumb MCPJ

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Hand Examination
• The key to an efficient hand exam is a good history as it will often elicit key findings to help make an accurate
diagnosis and direct you towards the parts of the hand exam that are relevant

• Important points in any hand history include

o Age
o Handedness
o Occupation
o History of presenting complaint

• In trauma scenarios important to know

o Mechanism of Injury
o Lacerations: what caused the wound, was it sharp/serrated/crush or burst type injury
o Time of injury
o Functional deficit e.g. can they bend/extend the affected digit
o Sensory loss
o Treatment to date

• In less acute scenarios e.g. Dupuytren's, carpal tunnel it is important to clarify the degree of functional
deficit
o Work
o ADLs
o Use of walking aids
o Hobbies
o Medications - especially anti-coagulants and arthritis medications (which may indicate degree to
which chronic conditions like RA have already been treated and therefore may now merit surgical
intervention)
o Smoking history

Examination
• Broadly speaking the hand examination can follow the sequence of "Look, Feel, Move, Measure and Special
Tests"

• Look
o Without touching the patient ask them to hold both hands out and inspect before asking them to
turn the hands over to view the other sides
o Observe
§ Scars
§ Swelling
§ Deformity
§ Contractures
§ Vascular status of the hand/digits affected

• Feel
o Always ask the patient, before you touch them, whether they have pain anywhere
o Clean your own hands with alcohol gel
o Feel any swellings or abnormalities to characterise (size, shape, consistency, mobility, pulsatility,
fluctuance, surrounding skin)
o Check sensation in the distribution
§ Median nerve
§ Ulnar nerve
§ Radial nerve
§ For a hand injury check the sensation of the digital nerves (radial and ulnar in each digit) to
each digit distal to the wound

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• Move
o Always active before passive to avoid inadvertently hurting the patient - allowing them to show you
their active movements first gives a good indication of how far you can passively move them without
difficulty
o Test range of motion at each joint
o Flexion
§ For digits test FDP and FDS separately
§ Isolate each FDP by holding the PIPJ in full extension and blocking its movement.
§ Ask the patient to flex to DIPJ to check FDP function.
§ If movement present but painful, it may indicate a partial tendon laceration in the case of an
open injury (NB FDS can be congenitally absent in the little finger in up to 10-20% of
patients, and may be unilateral or bilateral)
§ To test FDS check PIPJ flexion
§ For the thumb isolate FPL by blocking MCPJ movement
o Extension
§ Digits
• Begin by assessing any extensor lag at the DIPJ, PIPJ or MCPJ
• Gross examination of extension of the digits can be tested by asking the patient to
straighten each digit individually however the DIPJ (mallet injury) can be tested by
isolating the joint and the PIPJ (central slip injuries) can be assessed using a special
test called Elson's test
• Independent extension of the index (EIP) and little (EDM) can be tested by asking
the patient to make a fist then straightening these two digits while the other digits
remain in a fist
§ Thumb
• In the thumb, continuity of the EPL tendon is confirmed by asking the patient to lift
the thumb from a resting flat position on a table, directly upwards.
• To test interosseous muscle function ask the patient to abduct and adduct the digits
- this can then be repeated against resistance to abduction, with the examiner
placing resistance to the ulnar surface of the little finger and the radial surface of the
index
• In the case of the thumb: check abduction (away from palm) and adduction (towards
palm)
o Where a joint injury is suspected, check for joint stability by gently moving in volar/dorsal and
radial/ulnar planes
o With passive motion check can deformities be corrected. In the case of a flexion deformity if it
cannot be corrected then this is known as a contracture

• Your examination to this point will have secondarily confirmed the motor function of the median (FPL via
anterior interosseus nerve) and thumb abduction (recurrent branch to APL), ulnar (flexion in ulnar 2 digits
and adduction of thumb) and radial nerve (extensors) however further special tests noted below can give
further detail on nerve injuries.

• Measure
o This will be dictated by your history and your exam to date
§ Flexion contractures can be measured in degrees with the use of a goniometer
§ Flexion: Express this as degrees of movement from neutral
§ Extension: Express this as degree to which full extension cannot be achieved (e.g. -10
degrees)

• Special tests
o Nerves
§ Ulnar nerve
• Froment's test will confirm the presence or absence of motor function of the deep
branch of the ulnar nerve which supplies the adductor of the thumb

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 • Wartenberg's sign: Inability to adduct the little finger (due to unopposed action of
EDM on little finger)
§ Tendons
• Central slip injuries: Elson's test

• To complete the hand examination, summarise your findings and note any special investigations you might
like to request such as imaging or nerve conduction studies.

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Hand Trauma

Tendon Injuries
• While the commonest individual components of upper limb injuries are described below, in reality upper
limb trauma often comprises a combination of several of these elements and therefore treatment will be
tailored to the specific patient and injury pattern

• Flexors
o Injured in volar lacerations of the hand, wrist and distal forearm
o Generally treated by primary repair unless very delayed presentation in which case secondary
procedures (2-stage reconstruction/arthrodesis) may be considered
o Post-operative hand therapy (splinting and physio) central to rehabilitation following repair to
facilitate the delicate balance between tendon adhesion formation (which results from excessive
immobilisation) and rupture (may results from too much mobilisation)
o Flexor injury can result in prolonged (2-3 months) period off sporting/driving/occupational activities

• Extensors
o Injured in dorsal lacerations
o Again, primary repair favoured and the method of repair will differ according the level at which the
tendon is cut as along their course they vary from flat to cylindrical in shape
o NB Injuries proximal to the level of the juncturae tendinum may not result in an apparent clinical
deficit
o Rehabilitation less complex but hand therapy central to successful recovery
o Usually necessitates less time off activities following injury than flexor tendons

• Nerve Injuries
o Commonly seen in volar injuries
o Repair of the mixed major nerves (ulnar, median and radial) requires careful approximation of the
epineurium under microscope magnification
o Evidence now suggests that these nerves have a reproducible topographical pattern of motor and
sensory fibres so the aim of careful alignment is to optimise recovery
o Repair of major nerve branches or digital nerves (sensory) can be performed under loupe of
microscopic (surgeon preference) magnification. Again end to end epineural repair is the preferred
method to reduce the risk of painful neuroma formation and optimise the chances of recovery

• Fractures
o Specific fracture patterns are beyond the scope of the undergraduate syllabus however basic
principles of fracture management apply to hand fractures
o In contrast to other areas of the body, hand fractures are often open and frequently associated with
tendon, nerve or vascular injury
o Associated injuries need to be taken into account when considering the optimal choice of fixation to
balance the need for early mobilisation of tendons and protection of nerve and vascular repairs
o Rigid fixation is achieved with plates or screws and this will permit early movement of digits but not
all fractures are amenable
o Kirschner wires (k-wires) are also commonly used to fix fractures but require a longer period of
immobilisation
o All of these are placed under x-ray guidance.

• Vascular Injuries
o Any vascular injury to the upper limb resulting in distal ischaemia is a surgical emergency
o Digits tolerate ischaemia for longer periods than the hand and forearm, due to the absence of
muscle within the finger, but surgical revascularisation should be performed urgently where possible
o Type of injury will determine likelihood of successful end to end vessel repair (rotating
blades/mechanical saws may result in substantial intimal injury and tissue loss which may make a
tension-free repair difficult, compared to clean-cut/guillotine type injuries)

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• Amputations
o Upper limb amputations that may be considered for replantation include digits, partial or whole
hand amputations and forearm amputations
o Ring avulsion/degloving injuries are less likely to be successfully replanted owing to stretch and
consequent intimal damage of the vessels
o In injuries proximal to the digits (hand/forearm), prolonged ischaemia time may result in muscle
necrosis and make limb salvage unlikely - in this case, elective amputation/terminalisation may be
preferable. Such a decision will always be undertaken by a multi-disciplinary trauma team
o Replantation of digits may be undertaken following amputation if conditions are favourable
o Sharp, clean cut injuries at a level distal to FDS insertion
o Appropriately transported digit (wrapped in damp gauze/towel which is placed in a plastic
bag/container which is placed on ice - NB placing the digit directly in ice can cause irreversible
vascular injury which may preclude successful replantation)
o Compliant patient with good understanding of the necessary post-operative monitoring and
rehabilitation
o Relative indications for digital replantation
§ Thumb amputation (due to its importance in grip and overall hand function)
§ Multiple digit amputation
§ Any digit in children
o Post-operative monitoring of a replanted digit will include regular clinical evaluation for signs of
arterial or venous compromise and any changes should prompt urgent review by the surgical team

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Dupuytren’s Disease

What is Dupuytren's Disease?

• Dupuytren's disease is an abnormal progressive thickening of the palmar and digital fascia
• It is not an abnormality of the tendons but the fascial layer lying superficial to these

What causes it?

• There are no known causes other than genetics and race
• Very often hereditary
• The myofibroblast is the causative cell - infiltrates the fascia and causes it to become contractile resulting in
cords and palmar pits
• However some "associations" described which are, at best, tenuous e.g. anti-epileptic drugs, liver disease,
pneumatic machinery use

Who gets it?

• Men > Women
• Usually older age
• Commonest in races of Celtic and Nordic descent - "Viking disease"
• Commoner in diabetics

How is it diagnosed?
• Clinical diagnosis - no investigations usually required
• Important points in history
o Age
o Handedness
o Occupation
o Family history
o Smoking (thought to be commoner in smokers due to association with ischaemia/effect on
microvasculature)

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 • Important points to note on examination
o For diagnosis
§ Visible and palpable cords, nodules, palmar pits and joint contractures - PIPJ/MCPJ
§ Overlying skin can also be involved
§ Ectopic disease in the form of "Garrod's pads" on the dorsal PIPJ can also be present
§ Most commonly ring finger but can affect any digit
§ "Hueston's Table-top" test to demonstrate contractures
§ Goniometer can be helpful to calculate degree of joint contracture present to calculate
urgency of treatment and to measure progression
o For bonus points, also inspect for
§ Scars, skin grafts - evidence of previous surgery which may complicate future treatment and
indicate severity of the disease if it has recurred
§ Evidence of associated pathologies (e.g. diabetics can also more commonly get carpal
tunnel syndrome and trigger finger as well as Dupuytren's)
§ Shoulder mobility - this may affect surgical plan/patient positioning if surgery is required
• The intricate anatomy of the palmar and digital fascia (the details of which are beyond the scope of this
undergraduate syllabus) and what elements are involved in the disease process will determine the clinical
presentation e.g. normal longitudinal fascial bands, when diseased, become contracted thickened cords
resulting in MCPJ and PIPJ contracture

Dupuytren's Diathesis
• Dupuytren's disease associated with Peyronie's disease (penile fascia) and Ledderhose disease (plantar
fascia), family history and Northern European ethnicity
• In those with the diathesis, Dupuytren's tends to occur earlier in life and more severely, can often be
bilateral and tends to recur more commonly

How is it treated?
• Treatment of Dupuytren's will be determined by the severity of the disease
• Disease is broadly classified as mild, moderate or severe (British Society for Surgery of the Hand)
• Broadly speaking MCPJ contracture of 30 degrees or more merits intervention, and any degree of PIPJ
contracture (the PIPJ capsule and volar plate tend to shorten in flexion meaning that if left flexed for a
prolonged period, the likelihood of achieving an extended joint is diminished, so best to intervene as soon as
possible when this sign is present. In contrast, the MCPJ collaterals stretch in flexion so can tolerate
contracture over longer period and still remain amenable to surgical correction)

• Mild (no contracture or MCPJ contracture but less than 30 degrees)

o If no functional sequelae of mild disease, observe patient clinically and no intervention required
unless deterioration

• Moderate (MCPJ contracture > 30 degrees and/or PIPJ contracture and/or contracture of 1st webspace
which limits webspan)
o Non-surgical
§ Historically, Collagenase (Clostridium Histolyticum) injections e.g. Xiapex, were offered as an
alternative to surgery for this group however this is no longer licensed for use outside of
USA for Dupuytren's
o Surgical
§ Limited/segmental fasciectomy - i.e. excision of defined portion of diseased fascia within the
palm
§ Regional fasciectomy - i.e. excision of all accessible disease fascia within palm and into digits
§ Needle fasciotomy: Percutaneous, repeated penetration of the disease fascia using a needle
which weakens the cord and allows for rupture by passive extension. This risks damage to
the neurovascular bundles as it is performed blindly and recurrence rates are higher than in
open surgery. However it may be an option in surgically unfit patients

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 • Severe (MCPJ contracture > 60 degrees and/or PIPJ contracture)
o Surgical
§ Regional fasciectomy
§ Dermofasciectomy - i.e. regional fasciectomy with excision of overlying skin - usually
resurfaced with full thickness skin graft from adjacent site within operative field (e.g. medial
arm) but healing by secondary intention also described (McCash Technique - not commonly
used due to concerns re secondary scar contracture/deformity - less predictable than FTSG)

• Splinting, steroid injection also described but there is little evidence to support their use in the management
of Dupuytren's
• There is some emerging evidence that anti-TNF alpha drugs may play a role in disease management in the
future

Complications of Surgical Treatment

• Wound healing - if skin is involved, skin flaps raised to perform fasciectomy can be thin and occasionally
necrose - usually managed expectantly and allowed to heal by secondary intention if this occurs
• Neurovascular injury - if "spiral cords" develop, can be intimately associated with ulnar and radial
neurovascular bundles so patients must be warned of risk of injury to sensory nerves and vasculature,
including risk of sensory loss and devascularisation of digit - especially if revision surgery
• Period of time off work to permit recovery
• Night splint (for up to 6 months post-operatively depending on hand therapy protocols in place in each unit)
• Disease recurrence

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Nerve Compression Syndromes

Median Nerve

Carpal Tunnel Syndrome

• Aetiology
o Carpal tunnel syndrome is the compression of the median nerve within the carpal tunnel
o The carpal tunnel is formed by: the carpal bones forming the deep surface, the transverse carpal
ligament (TCL) forming the roof, the pisiform and hamate forming the ulnar border and the scaphoid
and lunate forming the radial border
o It contains the 4 FDS tendons, the median nerve, the 4 FDP tendons and the FPL tendon
o Although causes are often cited in textbooks, it is rare that a direct cause is found for compression of
the median nerve within the carpal tunnel and it can be attributed to postural issues such as
repeated flexion of the wrist due to occupational or recreational activities
o Pregnancy, diabetes, inflammatory conditions and thyroid disease can also predispose
o Less common causes include space occupying lesions within the carpal tunnel and trauma (e.g.
fractures and perilunate dislocation)

• Epidemiology
o Carpal tunnel syndrome is the commonest nerve entrapment syndrome
o Commoner in females 3:1

• Diagnosis
o History
§ Symptoms
• Sensory
o Paraesthesia in the distribution of the median nerve distal to the carpal
tunnel (but can radiate proximally)
o Pain
o Nocturnal symptoms are common - patients describe waking with symptoms
and the need to "shake out" the hands to obtain relief
• Motor
o Reduced grip strength

o Examination
§ Look
• Thenar eminence wasting can be seen in more advanced cases
• Swellings or bruising around the carpal tunnel may indicate tumour, trauma or
haematoma
• Scars may indicate previous surgery to the area
§ Feel
• Check sensation in the distribution of the median nerve (take-off of palmar
cutaneous branch usually proximal to carpal tunnel so palmar sensation may be
preserved)
§ Move
• As well as a general hand exam, specifically examine function of the ABP muscle by
asking the patient to abduct the thumb while feeling the muscle mass with your
other hand to confirm contraction
§ Measure
• No specific measurements are required in the diagnosis of carpal tunnel
§ Special Tests
• Tinel's: Tapping with a finger over the carpal tunnel elicits altered sensation or
paraesthesia

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 • Phalen's: With elbows bent the dorsum of both hands are pressed together to
narrow the space within the carpal tunnel - any altered sensation within a
continuous of minute of wrist flexion is positive
• Reverse Phalen's: Can also alter the space within the carpal tunnel using this test;
the reverse of Phalen's: elbows bent and wrists flexed
• Durkan's Compression: Continuous compression over the carpal tunnel induces
altered sensation or paraesthesia

• Investigations
o Nerve conduction studies
o A negative test does not outrule compression, but positive findings will confirm a diagnosis
o Prolonged distal motor latency
o Slowed sensory conduction velocity
o Reduced amplitude of compound action potentials
o Occasionally, retrograde degeneration i.e. nerve is affected proximal to the compression

• Treatment
o Treatment is broadly subdivided into non-operative and operative methods
o Non-Operative
§ Splinting (e.g. Futura splint with wrist in slight dorsiflexion) to widen the diameter of the
carpal tunnel positionally and steroid injection
§ Suitable for those who do not wish to have surgery or who are unfit, or for likely temporary
compressions e.g. pregnancy
§ Long term benefits are not sustained
o Operative
§ Open Carpal Tunnel Release
• The gold standard for the management of carpal tunnel syndrome
• Can be performed under local anaesthetic
• Short procedure, well tolerated
• Vertical skin incision and transverse carpal ligament is released under direct vision
§ Complications include
• Wound issues
• Scar sensitivity
• Pillar pain (pain attributed to adjustment of carpal arch following release of TCL - will
usually settle spontaneously but may take several months)
• Nerve injury - especially in the setting of aberrant recurrent branch or palmar
cutaneous branch anatomy
• CRPS

Pronator Syndrome

o Rare
o Intermittent compression of the nerve more proximally
o Nerve conduction studies may be normal as the compression is intermittent
o Treatment: trial of splint; open release if non-operative management unsuccessful

Anterior Interosseus Syndrome

• Rare.
• Can also arise as a result of inflammation, in the absence of physical nerve compression
• Motor deficit only: FPL, radial 2 FDPs and PQ all paralysed
• Often idiopathic
• Key examination finding: cannot make an "O" sign with the index and thumb on the affected side (FPL/FDS
not functioning)
• Usually settles with non-operative management

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Ulnar Nerve

Cubital Tunnel Syndrome

• Aetiology
o Cubital tunnel syndrome is the compression of the ulnar nerve at the elbow at any of a number of
sites along the cubital tunnel
o The cubital tunnel is formed by the medial epicondyle of the humerus and the olecranon, the elbow
joint and the deep fascia of the FCU (Ligament of Osborne extends up from this deep fascia)
o Again, a specific cause for this may not be found but space occupying lesions, trauma and
subluxation of the nerve from the cubital tunnel can predispose
o Elbow flexion stretches the ulnar nerve and causes the cubital tunnel to narrow

• Epidemiology
o 2nd commonest nerve entrapment syndrome

• Diagnosis
o History
§ Pain
§ Paraesthesia/sensory deficit in distribution of ulnar nerve

o Examination
§ Look
• Intrinsic muscle wasting is a late sign
§ Feel
• Can occasionally feel subluxation of the ulnar nerve out of the cubital tunnel with
elbow flexion
§ Move
• Intrinsic and thumb adductor weakness
§ Measure
• N/A
§ Special Tests
• Tinel's over cubital tunnel
• Froment's
• Wartenberg's

• Investigations
o Nerve conduction studies

• Treatment
o Operative
§ Open cubital tunnel decompression - there is some debate around whether the nerve itself,
during decompression should be left in situ or transposed anteriorly to avoid tension during
elbow flexion - while there is no strong evidence to support anterior transposition over in-
situ decompression, it is often advisable to perform this in severe cases so to ensure that if
there is no resolution, all surgical options have been exhausted
§ Like in carpal tunnel syndrome, although decompression may not alleviate all symptoms, it
should prevent the condition from worsening

Ulnar Tunnel Syndrome

• Compression of the ulnar nerve at the level of Guyon's canal at the wrist
• Rare
• Can affect either the deep motor branch or sensory branch or both depending on the level of compression -
the zone of compression will dictate symptoms and signs

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• Can be due to repetitive trauma/stretch (e.g. motorbike users/cyclists/hook of hamate fractures) and space
occupying lesions (e.g. ganglia)
• Ulnar Paradox
o This describes the "paradox" whereby a more distal ulnar injury or compression results in a more
marked clinical presentation
o A distal injury, distal to where the nerve supplies FDP will result in paralysis of the intrinsic muscles
resulting in unopposed FDP action leading to a "claw" of the ulnar 2 digits - if the nerve was affected
more proximally then the FDP would not flex and therefore there would not be clawing

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Radial Nerve

Wartenberg's Syndrome

• Rare
• Sensory only: compression of superficial sensory branch of radial nerve at distal forearm

Posterior Interosseus Syndrome

• Rare
• Results in loss of digital and thumb extension
• Wrist extension is preserved as the branch to ECRL is usually proximal to the level of compression

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Infectious Flexor Tenosynovitis

• Infectious flexor tenosynovitis is an infection of the synovial flexor sheath

• It is usually a surgical emergency (in selected very early cases the condition may occasionally be treated with
a trial of conservative management with high elevation and IV antibiotics but this is not common) as the
condition can progress quickly and lead to irreversible necrosis of the contents of the flexor sheath and the
surrounding structures
• Often the source of the infection will either be unknown or trivial (a small scratch or often a seemingly
innocuous penetration of the skin with sharp items such as thorns, glass or blades) but once established a
flexor sheath infection has the potential to spread proximally into the palm and secondarily to other digits
• The treatment is washout (and, in very advanced cases, surgical debridement) of the sheath, IV antibiotics
(tailored to microbiology specimens obtained intra-operatively) and high elevation
• In some cases, particularly where a streptococcus species is the causative bacteria, repeated washouts may
be required before resolution
• Often the residual digit may be swollen and stiff and intensive hand therapy, following the acute phase of
the infection, is essential to achieve the best functional outcomes

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Breast Reconstruction

• Breast reconstruction post mastectomy provides social, emotional, psychological and functional
improvement such as improved self-esteem, body image and quality of life to patients who undergo them.

• Breast reconstruction post mastectomy can be immediate or delayed.

o Immediate can be considered in most patients undergoing mastectomy
o Contraindications to immediate reconstruction include multiple poorly controlled comorbidities and
inflammatory breast cancer
o Advantages of Immediate Reconstruction
§ Streamlined surgical process
§ Psychological benefit
o Disadvantages of Immediate Reconstruction
§ Prolonged operating time
§ Necrosis of mastectomy skin flaps can affect the aesthetic result
§ Pre/Post-operative radiotherapy can adversely affect the reconstruction
o Advantages of Delayed Reconstruction
§ Assured clear oncological margins prior to reconstruction
§ Allows completion of adjuvant treatment
o Disadvantages of Delayed Reconstruction
§ Additional surgery
§ Limited options post radiotherapy

Options for Breast Reconstruction

• Implant
o Can be performed in one or two stages
§ One Stage Reconstruction: A permanent implant – saline or silicone is inserted
§ Two Stage Reconstruction: A tissue expander is placed first and filled to the desired volume
gradually. The tissue expander will be changed for a permanent implant at a later date.
o Implants can be placed either subpectorally, prepectorally, or subglandularly.
o Acellular dermal matrix (ADM) e.g. Strattice can be used to reinforce the lower pole of the breast
during implant reconstruction

• Autologous
o Flap based reconstruction can be either with free flaps or pedicled flaps.
o Free flaps are moved to the breast area as a free tissue transfer and the artery and venous supply of
the flap are attached to an artery and vein at the mastectomy site by microsurgery.
o Pedicled flaps remain attached to their native blood supply and are rotated into the breast area.

o Free Flaps
§ Deep Inferior Epigastric Artery Perforator (DIEAP) Flap
• Includes skin and fat
§ Transverse Rectus Abdominus Musculocutaneous (TRAM) Flap
• Includes skin, fat and muscle
§ Gluteal Musculocutaneous and Perforator (SGAP & IGAP) Flap
• Includes skin and fat
§ Transverse Upper Gracillis (TUG) Flap
• Includes skin, fat and muscle

o Pedicled Flap
§ Latissimus Dorsi (LD) Flap
• Includes skin, fat and muscle
• Smaller volume flap, therefore is combined with an implant for optimal volume
§ Transverse Rectus Abdominus Musculocutaneous (TRAM) Flap
• Includes skin, fat and muscle

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 • Choice of Reconstruction
o Patient Choice
o Clinical Factors
§ Patient must have ample tissue at the donor site e.g. abdomen, thigh, gluteal region,
posterior thorax
§ History of radiation to breast – autologous reconstruction is preferred if the patient has a
history of radiation to the breast because of local tissue effects from radiation therapy
§ Multiple scars on the breast from biopsy scars can compromise implant reconstruction due
to risk of skin necrosis
§ Adequate vasculature e.g. in DIEP Flaps – CT Angiogram performed first!

Obtaining Symmetry
• Mastopexy, breast reduction or breast augmentation can be done to achieve symmetry with the
reconstructed breast.
• Contour defects can be improved with lipofilling/fat grafting
o Process of relocating autologous fat to change the volume and profile of tissues
o Liposuction from abdomen, thighs, flanks is performed
o Fat is processed (by sieve or using Revolve System)
o Processed fat is injected into area of concern to improve contour
o Approximately 50% of transferred fat survives
o Patient should be advised that several procedures may be required for the desired effect.

Nipple Reconstruction
• This is performed once patient is happy with both breasts and reconstructive process is complete.
• The nipple is reconstructed under local anaesthetic with a local flap e.g. C to V flap
• The patient then undergoes tattooing to recreate the areola
• 3D tattooing of the nipple and areola is another option

C to V Flap

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Head and Neck Reconstruction
• The majority of head and neck cancers are squamous cell carcinomas found in the mucosal surfaces of the
upper aerodigestive tract.
• Head and neck cancers arise from five basic areas in the head and neck region – oral cavity, pharynx
(nasopharynx, oropharynx, hypopharynx), larynx, nasal cavity and paranasal sinuses and salivary glands.
• A multidisciplinary team including surgeons, radiation oncologists, medical oncologists, dentists, speech
therapists, is involved in treatment planning.
• Following discussion at MDT, patients are treated with either definitive radiation therapy or primary surgery
dependent on anatomical area of cancer and impact of surgery on speech and swallow.
• Current standard of care is primary reconstruction of maxillary, tongue, mandibular and palatal defects
following ablative surgery.
• Approach to reconstruction will depend on defect to be reconstructed

• Common Flaps and Reconstructive Applications

Flap Reconstructive Application
Anterolateral Thigh Floor of mouth, Tongue ,
Face
Radial Forearm Floor of mouth, Tongue, Face
Fibula Mandible, Maxilla

• Anterolateral Thigh Flap

o Used in floor of mouth, tongue and face reconstruction
o Harvested as a subcutaneous, fasciocutaneous, myocutaneous or adipofascial flap based on
perforators from the descending branch of the lateral circumflex femoral vessels
o The ALT is considered a chimeric flap – consists of multiple independent flaps with independent
vascular supply; these pedicles are all linked to one common source vessel.
• Radial Forearm Flap
o Used in floor of mouth, tongue and face reconstruction
o Useful for thin soft tissue replacement or mucosal loss
o Can be harvested as a fasciocutaneous, septocutaneous, adipofascial or osteocutaneous flap,
dependent on reconstruction needs
o Radial artery provides blood supply via perforators that pierce the antebrachial fascia to supply
subcutaneous fat and skin
o Donor site closed with split thickness skin graft
• Fibular Osteocutaneous Flap
o Used in mandibular and maxillary reconstruction
o Can be harvested with a skin paddle for intraoral or skin defects
o Blood supply is from the peroneal artery and its perforators

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Lower Limb Reconstruction
• Complex open lower limb fractures should be managed by a multidisciplinary team including orthopaedic
and plastic surgeons at specialist centres where possible.
• Initial treatment for open lower limb fractures is as per the BAPRAS guidelines
o ABCDE
o Haemorrhage control via direct pressure
o Wounds handled only to remove gross contaminants, photograph and seal from the environment
o Limb is splinted
o Antibiotics and tetanus
o X-Rays
• Early debridement of all devascularised tissue is the most important surgical procedure when managing
open lower limb fractures
• Internal fixation is safe in minimally contaminated open fractures
• External fixation is used in cases of significant contamination, bone loss and comminution

Gustilo Classification
Gustilo Description Treatment
Grade
I Open fracture with clean wound Irrigation, debridement, ORIF/EF, Primary
<1cm Closure
II Open fracture with wound >1cm Irrigation, debridement, ORIF/EF, Primary
but <10cm without extensive soft- Closure
tissue damage
III Open fracture with extensive soft
damage
III A Adequate soft tissue coverage of Irrigation, debridement, ORIF/EF, Primary
fractured bone, despite extensive Closure or STSG/Local Flap
soft tissue laceration/flaps, or high
energy trauma, irrespective of
wound size;
Contaminated – farm injuries are
automatically at least Gustilo IIIA
III B Extensive soft tissue injury with Irrigation, debridement, ORIF/EF
periosteal stripping and bone Often requires free tissue transfer/local
exposure. muscle flaps or perforator based flaps
III C Open fracture associated with Irrigation, debridement, ORIF/EF, vascular
arterial injury requiring repair, repair
irrespective of degree of soft tissue Often requires free tissue transfer/local
injury muscle flaps or perforator based flaps

• Timing of Soft Tissue Reconstruction

o Local flaps can be safely performed at the same time as skeletal fixation.
o Internal fixation should only be undertaken if soft tissue coverage can be performed also
o Free flap reconstruction should be performed on scheduled trauma lists at specialist centres.
o Definitive soft tissue reconstruction should be undertaken within the first seven days after injury

• Choice of Soft Tissue Reconstruction

o Depends on the extent and location of the injury
§ Split-Thickness Skin Grafts
• Can be used to cover exposed muscle or soft tissue and occasionally bone with
healthy periosteum or tendon with healthy paratenon
§ Local Flaps
• Fasciocutaneous or muscle flaps for small to moderate defects

299
 • Local flaps are available in the proximal or middle third of the leg; defects of distal
third of leg generally always require free tissue transfer
• Fasciocutaneous flaps are used to cover small defects of bone, exposed vessels or
tendons
• Local muscle flaps are used to cover defects with exposed bone, artery, nerve or
tendon e.g. lateral or medical gastrocnemius flap, soleus flap
§ Free Flaps
• Can be used once debridement of all the devitalised tissue is completed if there is an
appropriate recipient artery e.g. rectus abdominis flap, latissimus dorsi flap

300
Perineal Reconstruction
• Perineal reconstruction is indicated for acquired defects e.g. post-surgical excision of gynaecological,
colorectal or urological malignancies, trauma and infectious processes e.g. Fournier’s Gangrene and
congenital defects e.g. Müllerian or Wolffian Aplasia
• Aim is to achieve a healed wound in a one stage reconstruction
• Usually performed with local or regional flaps from the abdomen or legs. Choice of flap is based on defect
o Vertical Rectus Abdominis Myocutaneous Flap (VRAM)
o Inferior Gluteal Artery Perforator Flap (IGAM)
o Gracilis Flap
o Posterior Thigh Flap
o Pedicled anterolateral thigh flap

301
Chest Wall Reconstruction
• Causes of chest wall defects include sternal dehiscence post sternotomy, trauma, infection, tumour excision,
iatrogenic injuries such as radiotherapy and congenital deformities
• Aims of chest wall reconstruction are to restore chest wall rigidity, obliterate dead space, protect
intrathoracic organs, maintain physiological pulmonary function, provide soft tissue coverage, minimise
deformity and permit adjuvant radiotherapy if indicated.
• Reconstruction involves replacing what has been removed during resection
o Bone/Cartilage
§ “Bone Replacement”
• Necessary if greater than 4 ribs have been excised or the defect is >5cm
• Mesh
o Synthetic mesh: e.g. polypropylene knitted mesh, Gore Tex, Vicryl, Marlex
o Methyl methacrylate “sandwich” between two mesh sheets
• Bioprosthetic materials
o Xenograft e.g. Veritas bovine pericardium, Strattice porcine dermis
o Allograft e.g. Alloderm -acellular human tissue matrix derived from
cadaveric tissue
• Titanium
o Soft Tissue
§ Local
• Pectoralis Major Flap
§ Regional
• Latissimus Dorsi Flap
• Rectus Abdominis Flap
• Omentum – used particularly where dead space obliteration is required
§ Free Flap
• Anterolateral Thigh

302
References

• UpToDate – Overview of benign lesions of the skin

• UpToDate – Epidemiology, pathogenesis, and clinical features of basal cell carcinoma
• UpToDate – Treatment and prognosis of basal cell carcinoma at low risk of recurrence
• UpToDate – Epidemiology, natural history and diagnosis of actinic keratosis
• UpToDate – Treatment of actinic keratosis
• UpToDate – Cutaneous squamous cell carcinoma (cSCC): Clinical features and diagnosis
• UpToDate – Treatment and prognosis of low-risk cutaneous squamous cell carcinoma
• UpToDate – Melanoma: Clinical features and diagnosis
• UpToDate – Surgical management of primary cutaneous melanoma or melanoma at other unusual sites
• UpToDate – Overview of the management of advanced cutaneous melanoma
• UpToDate – Evaluation and treatment of regional lymph nodes in melanoma
• DermNet NZ - https://dermnetnz.org
• British Burn Association – Emergency Management of Severe Burns
• UpToDate – Emergency care of moderate and severe thermal burns in adults
• UpToDate – Overview of surgical procedures used in the management of burn injuries
• UpToDate – Burn wound infection and sepsis
• UpToDate – Overview of complications of severe burn injury
• British Society for Surgery of the Hand (BSSH). BSSH Evidence for Surgical Treatment 1
• Dupuytren’s Disease. London: BSSH; 2010.
• Grabb and Smith’s Plastic Surgery 7th Edition
• BAPRAS and British Orthopaedic Association (BOA) Standards for the management of Open Fractures of the
Lower Limb

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14. Orthopaedic Surgery

• Ms Laoise Coady

• Principles of Orthopaedic Surgery

• Upper Limb Injuries
• Lower Limb Injuries
• Compartment Syndrome
• Pelvic Fractures
• Back Pain
• Cauda Equina Syndrome
• Osteoarthritis
• Septic Arthritis

304
Principles of Orthopaedic Surgery

Definitions
• Fracture
o A break in the continuity of the bone cortex
o Usually occur in the setting of trauma as a result of mechanical forces which exceed the bone’s
ability to withstand them.
o Insufficiency fractures can occur due to metabolic (e.g. osteoporosis) or genetic (e.g. osteogenesis
imperfecta) abnormalities which make the bones more prone to fractures from forces that would
not be sufficient to cause fractures in normal bones
o Stress fractures can occur in the setting of chronic abnormal stresses (e.g. running) which results in
an accumulation of microfractures
o Pathological fractures occur in bones which have lesions e.g. metastasis or bone cyst which focally
weakens the bone
• Open Fracture
o A fracture exposed to the external environment
• Closed Fracture
o No communication with the external environment
• Reduction
o Manipulation of a fracture in order to restore normal alignment at the fracture site
• Fracture Dislocation
o Fracture associated with joint dislocation

Types of Fracture
• Greenstick
o Seen in young children <10 years – soft bone bends and breaks; usually mid diaphysis
• Comminuted
o Fracture in more than two parts
• Avulsion
o Fragment of bone tears away from main mass of bone e.g. trauma to ligament/tendon
• Transverse
o Fracture orientated perpendicular to the axis of the bone
• Wedge/Compression
o Hyperflexion injury to vertebral body as a result of axial loading
• Oblique
o Oblique orientation across the bone
• Spiral
o Spiral fracture path; usually in diaphysis of long bones

Bony Injury Description

• Name of bone injured
• Region of bone injured – epiphysis/physis/metaphysis/diaphysis/tubercle/epicondyle
• Pattern of fracture – transverse/oblique/spiral/segmental/comminuted
• Presence of compression
• Presence of displacement
o Type and degree: angulation/translation/rotation/shortening
• Presence of any pre-existing pathology
• Associated joint pathology
o Dislocation
o Subluxation
• Condition of overlying tissues – open or closed fracture

305
Principles of Fracture Management
• Clinical Assessment
o Life or Limb Threatening Injury/Major Trauma – ATLS Protocol
o Focused History
§ A: Allergies
§ M: Medications
§ P: Past medical/surgical history
§ L: Last meal
§ E: Events that lead to injury - mechanism of injury
o The mechanism of injury is important as injury patterns can be associated
with particular mechanisms e.g. fall on outstretched hand (FOOSH) is
associated with a distal radius fracture or a scaphoid fracture.

o Examination
§ Look, Feel, Move, Special Tests
§ Neurovascular examination
• Distal pulses
• Capillary refill
• Motor function
• Sensation

• Radiographic Assessment
o Two Views – anterior-posterior (AP) and lateral
o Two Joints – above and below fracture

• Immobilisation
o Reduce fracture
§ Stabilises the fracture, thus reducing pain, restoring normal anatomical relationships and
preserving blood supply
§ Aids in bone healing and remodelling and helps to avoid malunion
§ Reduces chance of non-union of bones
§ Reduces risk of osteoarthritis
o Immobilise with cast/splint/internal fixation/external fixation
§ Unstable fractures or poorly reduced fractures will require operative intervention
§ Open Reduction Internal Fixation (ORIF)
• Fracture site is exposed and immobilised internally using plates and screws or other
fixation devices
§ Closed Reduction
• Fracture site is manipulated and reduced without exposing the fracture site
• Immobilisation is achieved with cast/brace/surgical device
o Kirschner Wires – K-wires can be placed percutaneously to immobilise the
fracture (they are removed at a later date)
o Intramedullary nails can be inserted via incisions remote to the fracture site

• Pain Management
o Immobilisation, ice, elevation, analgesia

• Wound Care
o Open fractures will require antibiotics and tetanus cover

• Patient Education

• Follow-up care
o Rehabilitation – mobilisation/physiotherapy

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Stages of Fracture Healing
• Three stages
o Inflammatory
§ Haematoma formation – provides building blocks for healing
§ Resorption of bone which has lost blood supply at fracture edges
§ Osteoprogenitor cells form new bone
o Reparative
§ New blood vessels form to supply cartilage which forms across fracture site
§ Complete immobilisation is preferred in the inflammatory and early reparative stages to
allow neovascularisation
§ Once neovascularisation is complete progressive loading and stress across the fracture site
will augment callus formation
§ Callus forms as endochondral bone around the fracture
§ Clinical union occur late in reparative phase
o Remodelling
§ Endochondral callus becomes ossified
§ Bone undergoes structural remodelling

• Factors affecting rate of fracture healing

o Age
o Poor nutrition
o Diabetes Mellitus
o Hypothyroidism
o Arteriovascular disease
o Smoking
o Medications: NSAIDs, Glucocorticoids, Ciprofloxacin
o Degree of local trauma
o Inadequate reduction and immobilisation
o Infection

307
Open Fractures
• Open fractures are fractures exposed to the external environment as a result of trauma to the overlying soft
tissue and skin.
• Most commonly as a result of high velocity trauma

• Management
o ATLS Protocol
o Assess neurovascular status
o Reduce fracture and repeat neurovascular assessment
o Remove gross contamination
o Photograph wound
o Dress wound
o Backslab to immobilise fracture
o IV Antibiotics as per local hospital guidelines
o Tetanus
o Early surgical management
§ Debridement
• Immediate in grossly contaminated wounds or associated vascular compromise
• Within 12 hours of injury for solitary high energy open fractures
• Within 24 hours of injury for all other low energy open fractures
§ Definitive Internal Fixation
• Only when can be immediately followed by definitive soft tissue coverage
§ Definitive soft tissue coverage/closure
• Within 72 hours of injury if not performed at the same time as debridement
o Monitor tibial fractures for signs of compartment syndrome

Gustilo Classification
Gustilo Description
Grade
I Open fracture with clean wound <1cm
II Open fracture with wound >1cm but
<10cm without extensive soft-tissue
damage
III Open fracture with extensive soft
damage
III A Adequate soft tissue coverage of
fractured bone, despite extensive soft
tissue laceration/flaps, or high energy
trauma, irrespective of wound size;
Contaminated – farm injuries are
automatically at least Gustilo IIIA
III B Extensive soft tissue injury with
periosteal stripping and bone exposure.
III C Open fracture associated with arterial
injury requiring repair, irrespective of
degree of soft tissue injury
Treatment
Irrigation, debridement, ORIF/EF, Primary
Closure
Irrigation, debridement, ORIF/EF, Primary
Closure
Irrigation, debridement, ORIF/EF, Primary
Closure or STSG/Local Flap
Irrigation, debridement, ORIF/EF
Often requires free tissue transfer/local
muscle flaps or perforator based flaps
Irrigation, debridement, ORIF/EF, vascular
repair
Often requires free tissue transfer/local
muscle flaps or perforator based flaps

308
Upper Limb Injuries

Scaphoid Fracture
• Most commonly fractured carpal bone
• Usually occurs after fall on outstretched hand (FOOSH)

• Presentation
o History: FOOSH
o Symptoms: Wrist pain
o Examination
§ Wrist swelling
§ Pain worse on movement
§ Anatomical snuff box tenderness dorsally
§ Scaphoid tubercle tenderness volarly

• Imaging
o X-Rays: AP, Lateral, Scaphoid View (30 degrees wrist extension, 20 degrees ulnar deviation)
o If x-rays are clear repeat in 14-21 days if high clinical suspicion of scaphoid fracture
o CT for further evaluation of fracture –location/displacement/ angulation/fragment size/ evaluation
of union or non-union
o MRI for occult fractures

• Treatment
o Non-Operative
§ Cast immobilisation
• Stable non-displaced fractures
• Normal X-Ray but high level of suspicion
o Operative
§ Percutaneous screw fixation
§ Open reduction internal fixation (ORIF)

• Complications
o Non-union
o Malunion
o Avascular necrosis

Distal Radius Fracture

• Most common orthopaedic injury
• Bimodal Distribution
o Young Patients: High energy injury
o Older Patients: Low energy injury e.g. FOOSH
• Intraarticular in 50%
• Colles’ Fracture: Dorsally displaced extra-articular distal radius fracture – “dinner fork deformity”
• Smith’s Fracture: Volarly displaced extra-articular distal radius fracture

• Risk Factors
o Previous distal radius fracture
o Osteoporosis

• Presentation
o History: FOOSH
o Symptoms: wrist pain, swelling and deformity
o Examination
§ Swelling
§ Ecchymosis

309
 § Tenderness
§ Deformity (if displaced)
§ Range of motion limited by pain
§ Important to do neurovascular assessment to assess integrity of the median nerve (? carpal
tunnel compression)

• Imaging
o X-Rays: AP, Lateral, Oblique
o CT: evaluate intra-articular involvement; surgical planning
o MRI if concern for soft tissue injuries

• Treatment
o Non-Operative
§ Closed reduction and splint/cast immobilisation
o Operative
§ Closed reduction and percutaneous pinning (CRPP) with K-Wires
§ Open reduction internal fixation (ORIF) e.g. volar or dorsal plating
§ External fixation – indicated in open or highly comminuted fractures

• Complications
o Median nerve injury
o Ulnar nerve injury
o Tendon rupture e.g. Extensor pollicis longus, Flexor pollicis longus
o Non-union
o Malunion
o Osteoarthritis

Proximal Humerus Fracture

• Common in elderly with osteoporosis following a fall on an outstretched arm
• Seen in younger patients, often in association with neurovascular and soft tissue injuries following high
energy trauma

• Risk Factors
o Osteoporosis
o Female Sex (2:1 F:M)
o Epilepsy
o Diabetes

• Presentation
o History: FOOSH, High energy trauma e.g. RTA, electrical shock, seizure
o Symptoms: Pain, swelling, decreased range of motion
o Examination
§ Ecchymosis
§ Swelling
§ Tenderness
§ Neurovascular assessment - > Axillary nerve injury – paraesthesia over deltoid (regimental
patch)

• Imaging
o X-Rays: AP, Scapular Y, Axillary
o CT: further evaluation; surgical planning
o MRI: can identify associated rotator cuff injury

310
 • Classification
o Neer Classification
§ Divides the proximal humerus into four parts and classifies the fracture based on the
displacement
§ Four Parts: Humeral Head, Greater Tuberosity, Lesser Tuberosity, Humeral Shaft
§ Displacement is on a per part basis
§ One-part Fracture
• Fracture lines involve 1 – 4 parts
• None displaced
§ Two-part Fracture
• Fracture lines involve 2 – 4 parts
• One displaced
§ Three-part Fracture
• Fracture lines involve 3 – 4 parts
• Two displaced
§ Four-part Fracture
• Fracture lines involve more than 4 parts
• Three displaced

• Treatment
o Non-Operative
§ Sling immobilisation
o Operative
§ Closed reduction and percutaneous pinning (CRPP) with K-Wires
§ Open reduction internal fixation (ORIF)
§ Intramedullary nail
§ Arthroplasty – hemiarthroplasty/reverse total shoulder

• Complications
o Avascular necrosis
o Nerve injury – axillary nerve, suprascapular nerve, musculocutaneous nerve
o Non-union
o Malunion
o Long head of biceps tendon injuries
o Rotator cuff injuries
o Osteoarthritis
o Infection
o Adhesive capsulitis

Clavicular Fracture
• 75% midshaft
• 25% distal

• Presentation
o History: fall or direct blow to the lateral shoulder
o Symptoms: anterior shoulder pain
o Examination
§ Tenderness
§ May have skin tenting (impending open fracture)
§ May have deformity
§ Neurovascular exam

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 • Imaging
o X-Rays: Upright AP of Bilateral Shoulders, 15° cephalic tilt (Zanca view - determines inferior/superior
displacement)
o CT: evaluates fracture further, identifies vascular injury

• Treatment (non-displaced fractures)

o Non-Operative (90%)
§ Sling immobilisation
§ Gentle ROM exercises at 2-4/52
§ Strengthening at 6-10/52
o Operative (for open fractures, displaced fractures, vascular injury)
§ Closed reduction and intramedullary fixation
§ Open reduction internal fixation

• Complications
o Pneumothorax
o Neurovascular injury – brachial plexus, subclavian artery/vein
o Non-union

Shoulder Dislocation
• Shoulder dislocations account for ~50% of all major joint dislocations
o Anterior dislocation 95-97%
o Posterior dislocation 2-4%
o Inferior dislocation 0.5%

• Presentation
o History
§ Anterior dislocation: blow to abducted, extended and externally rotated arm
§ Posterior dislocation: blow to anterior portion of the shoulder, axial loading of adducted,
internally rotated arm, muscle contractions post electrocution or seizure
o Symptoms: pain, reduced range of motion, bruising, distorted shoulder contour
o Examination
§ Anterior dislocation
• Arm abducted and externally rotated, prominent acromion, loss of usual rounded
appearance
• Neurovascular exam (? axillary nerve injury)
§ Posterior dislocation
• Posterior shoulder prominence, anterior flattening, prominent coracoid process.
• Arm held in internal rotation; cannot externally rotate
• Humeral head palpable posteriorly

• Imaging
o X-Rays: AP, Scapular Y View, Axillary View
§ Lightbulb sign: posterior dislocation – humeral head is internally rotated, hence tuberosities
do not project laterally resulting in circular appearance of the humeral head
o CT: to evaluate chronic dislocation
o MRI: assess for associated rotator cuff tears, detachment of anteroinferior larum (Bankart’s Lesion)
damage to humeral head (Hill-Sachs lesion)

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• Treatment
o Non-Operative
§ Anterior Dislocation
• Prone Technique
• External Rotation Technique
• Scapular Manipulation
• Upright Technique
• Stimson Technique
§ Posterior Dislocation
o Operative
§ Indicated if repeated dislocations or persisting symptoms of instability
§ Anterior Dislocation
• Arthroscopic or open
o Repair of Bankart defect with tightening of capsule
o Grafting may be necessary for large Hill-Sachs lesions or bony defects of the
glenoid)
§ Posterior Dislocation
• Repair of damaged labrum and tightening of the posterior capsule
• Open reduction if <25% defect of articular surface of humeral head
• Dislocation older than 3/52

• Complications
o Stiffness
o Recurrence
o Nerve injury – axillary or suprascapular
o Adhesive capsulitis

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 Lower Limb Injuries

Hip Fractures
• Commonest fracture in the elderly
• 80% in women
• Bimodal distribution –
o High energy trauma/RTA in young patients
o Low energy fall in elderly
• 20-30% mortality risk in the first year post fracture
o Early surgery within 48 hours will decrease mortality
• Intracapsular Fractures
o Fractures which occur within the joint capsule – femoral neck fractures
• Extracapsular Fractures
o Fractures which occur outside the joint capsule
§ Intertrochanteric
§ Subtrochanteric

Greater
Femoral Head
Trochanter
Extracapsular Fracture

Intracapsular
Intertrochanteric
Fracture
Fracture

Lesser
Subtrochanteric Trochanter
Fracture

Femoral Shaft

• Risk Factors
o Osteoporosis/osteopenia
o Diabetes mellitus
o Recurrent falls
o Tobacco and alcohol use
o Caucasian

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• Presentation
o History
§ Young Patient: RTA/High Energy Trauma
§ Elderly Patient: Fall
o Symptoms: pain and inability to weight bear on the affected limb
o Examination: Painful, shortened, externally rotated lower limb

• Imaging
o X-Rays: AP Pelvis, AP Hip, cross table lateral, full length femur
o CT/MRI: if x-rays negative but physical exam consistent with fracture

• Classification
o Intracapsular Fractures
§ Garden Classification
• Garden I: Undisplaced, Incomplete fracture; Head has tilted into the valgus position
• Garden II: Undisplaced, complete fracture
• Garden III: Incompletely displaced complete fracture
• Garden IV: Completely displaced complete fracture

Garden I Garden II Garden III Garden IV

• Treatment
o Non-Operative
§ In non-ambulatory patients or patients with high risk of perioperative mortality
§ Non-weightbearing (NWB) with early out of bed to chair
o Operative
§ Intracapsular Fracture
• Dynamic Hip Screw
• Hemiarthroplasty
• Total Hip Arthroplasty
§ Extracapsular Fracture
• Dynamic Hip Screw
• Intramedullary nail

• Complications
o Osteoarthritis
o Avascular necrosis of femoral head
o Non-union
o Mortality
o Wound infection
o Haematoma

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Tibial Plateau Fracture
• Associated with soft tissue injuries
o Meniscal tear
o ACL Injury

• Bimodal distribution
o Males in 40s – high energy trauma
o Females in 70s – Falls

• Presentation
o History: high energy trauma in young; low-energy falls in elderly
o Symptoms: pain, inability to weight bear, deformity
o Examination:
§ pain, swelling, tenderness, deformity
§ Assess for ligamentous and meniscal integrity
§ Neurovascular exam

• Imaging
o X-Rays: AP, Lateral, Oblique
o CT: identifies comminution and articular depression

• Treatment
o Non-Operative
§ Hinged knee brace
o Operative
§ External fixation
§ ORIF

• Complications
o Osteoarthritis
o Compartment syndrome
o Vascular Injury

Tibial Fracture
• Most common long bone fracture
• Low energy injury – torsional injury – spiral fracture
• High energy injury – wedge/short oblique fracture – severe soft tissue injury
• Associated with soft tissue injuries, compartment syndrome, bone loss, ipsilateral skeletal injury e.g. tibial
plateau/posterior malleolus

• Presentation
o History: torsional injury; high energy trauma
o Symptoms: pain, inability to weight bear, deformity
o Examination
§ Pain, swelling, tenderness, deformity
§ Check compartments ? compartment syndrome – palpate, pain, passive motion of toes
§ Neurovascular exam
• Nerves: deep peroneal nerve, superficial peroneal nerve, sural nerve, tibial nerve,
saphenous nerve
• Pulses: dorsalis pedis, posterior tibial

• Imaging
o X-Rays: AP, Lateral, full length tibia; AP, lateral, oblique of ipsilateral knee and ankle
o CT: if intra-articular fracture extension or joint involvement
• Treatment

316
 o Non-Operative
§ Closed reduction, cast immobilisation
o Operative
§ External fixation
§ Intramedullary nail
§ Percutaneous locking plate

• Complications
o Osteoarthritis
o Nonunion
o Malunion
o Malrotation
o Compartment syndrome
o Nerve injury

Ankle Fractures
• Multiple injury patterns – isolated medial malleolus fracture, isolated lateral malleolus fracture, isolated
posterior malleolus fracture, bimalleolar fractures, trimalleolar fracture

• Presentation
o History: Fall from height (axial loading) or foot inversion (torsional injury)
o Symptoms: pain, swelling, deformity, inability to weight-bear
o Examination
§ Pain, swelling, tenderness, deformity
§ Neurovascular exam
§
• Imaging
o X-Rays: AP, Lateral, Mortise, External rotation stress, proximal tibia
o CT: further evaluate fracture

• Classification
o Danis-Weber; based on the level of the fibular fracture – the more proximal the injury the greater
the risk of instability and syndesmosis disruption
§ A: Below the level of the syndesmosis
§ B: At the level of the syndesmosis
§ C: Above the level of the syndesmosis
o Lauge-Hansen: based on foot position and force of applied stress
§ Supination-Adduction
§ Supination-External Rotation
§ Pronation-Abduction
§ Pronation-External Rotation

• Treatment
o Non-Operative
§ Short leg walking boot
o Operative
§ Open reduction internal fixation

• Complications
o Wound infections
o Deep infections
o Nonunion
o Malunion
o Stiffness
o Osteoarthritis

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Compartment Syndrome
• Muscle groups of limbs are divided into compartments formed by fascial membranes
• Compartment syndrome results from increased pressure within a compartment, leading to compromised
circulation.
• Can occur acutely post trauma or can be chronic, most often seen in athletes presenting with insidious pain

• Risk Factors (Acute Compartment Syndrome)

o Trauma: crush injury, long bone fracture
o Bleeding, haematoma
o Burn injury (especially circumferential burn)
o Prolonged extremity ischaemia with reperfusion
o Intravenous extravasation injury
o High pressure injection

• Clinical Features
o Pain – out of proportion to injury
o Tense firm compartment
o Pain exacerbated by passive stretch
o Compartment specific neurovascular findings
o Compartment pressure within 30mmHg of diastolic BP

• Initial Treatment
o Relieve external pressure e.g. remove or bivalve cast; escharotomy for circumferential burns
o Normalise perfusion to the extremity e.g. reduce fractures, fluid resuscitation
o Measure compartment pressures
§ Handheld manometer
§ 18 Gauge needle attached to pressure transducer can be used

• Fasciotomy
o Indicated if high clinical suspicion or compartment pressure within 30mmHg of diastolic pressure
o Early fasciotomy (< 4 hours of symptom onset) can save the extremity
o Contraindicated if there is established late compartment syndrome
§ Tissue damage is irreversible 4 -8 hours post increased compartment pressure
§ Fasciotomy in established compartment syndrome (>6 hours after onset) is associated with
increases rates of infection and amputation
o Leg: Four compartment fasciotomy using a one or two incision approach
o Forearm: Volar incision and dorsal incision

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Pelvic Fractures
• Pelvic fractures, with the exception of pubic rami and insufficiency fractures, are as a result of high energy
trauma e.g. RTA
• Mortality from pelvic fractures is high – up to 15% in closed fractures and up to 50% in open fractures,
usually secondary to haemorrhage from the venous plexus.
• Can be associated with thoracic and intra-abdominal injuries.

• Presentation
o History: High energy blunt trauma; fall in elderly
o Symptoms: pain, inability to weight bear
o Examination
§ External bleeding
§ Ecchymosis – flank/perineal/scrotal
§ Blood at penile meatus
§ Vaginal bleeding
§ Assess position of iliac crests and legs - ?leg length discrepancy
§ Palpate bony landmarks – iliac crests, greater trochanters, sacrum, sacroiliac joints, pubic
symphysis
§ Assess ROM
§ Neurovascular exam – lumbosacral plexus – rectal exam to assess sphincter tone and
perirectal sensation

• Imaging
o X-Ray: AP Inlet, Outlet
o CT: gold standard – contrast enhanced CT; allows identification of concomitant injuries; identifies
arterial bleeding and retroperitoneal haemorrhage
o Retrograde cystourethrogram: recommended if blood at urethral meatus, high riding prostate or
haematuria

• Treatment
o Initial management as per ATLS Guidelines
§ Resuscitation
• Packed Red Blood Cells:Fresh Frozen Plasma:Platelets 1:1:1
§ Pelvic binder/bedsheet at level of greater trochanters
§ Do not “spring” the pelvis as risks disturbing any pre-formed clots.
§ Open Fracture: tetanus, IV antibiotics
§ External fixation – if emergent laparotomy required
§ Angiography and embolisation
o Non-Operative
§ Protected weight bearing
o Operative
§ ORIF
§ Anterior subcutaneous pelvic fixator
§ Diverting colostomy

• Complications
o Urogenital injuries
o Neurological injuries
o Chronic instability
o DVT/PE
o Infection

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Back Pain
• Low back pain affects approximately 50-80% of the population at some stage in their life
• It is the second most common cause of presentation to doctor following RTI

• Aetiology
o Muscle strain
o Lumbar disc herniation
o Lumbar disc stenosis
o Discogenic back pain

• Risk Factors
o Obesity
o Smoking
o Lifting
o Prolonged sitting

• Red Flags

• Night pain
• Associated Symptoms
o Bilateral lower limb symptoms
o Sphincter disturbance – urinary/faecal retention/incontinence
o Lower limb weakness
o Altered perineal/perianal sensation
• Trauma
• Systemic symptoms - ? Infection – IVDU, presenting with fever/chills
• Previous history of cancer ?metastasis

• Treatment is dictated by cause of pain

• Important to outrule metastatic disease, AAA, Cauda Equina syndrome, spinal cord compression

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Cauda Equina Syndrome
• Compression of the nerve roots in the thecal sac of the lumbar spine
• Usually due to acute lumbar disc herniation – usually L4/5
• M>F

• Aetiology
o Space occupying lesion in lumbrosacral canal
§ Disc herniation
§ Tumours
§ Trauma
§ Spinal stenosis
o Iatrogenic
§ Spinal manipulation
§ Epidural fat graft
§ Excessive dural retraction

• Presentation
o Symptoms
§ Back pain
§ Leg pain, progressive weakness
§ Saddle anaesthesia – acute onset
§ Impotence
§ Bladder dysfunction
§ Bowel dysfunction (rare)
o Examination
§ NB - ASIA Score (American Spinal cord Injury Association)
§ Inspection: leg muscle atrophy with insidious presentations e.g. spinal stenosis
§ Palpation – lower back tenderness not a distinguishing feature; bladder may be palpable in
case of urinary retention
§ Neurovascular exam
• Bilateral/unilateral lower extremity weakness or sensory disturbances
• Decreased rectal tone
• Decreased/absent lower extremity reflexes
• Reduced/absent sensation to pinprick in perianal/perineal/posterior thigh regions
§ Provocative tests
• Bulbocavernosus reflex – diminished/absent
• Anal wink – diminished absent

o Imaging
§ X-Rays: AP, Lateral - ? burst fractures
§ MRI: study of choice; evaluates neurologic compression – must be done urgently if cauda
equina syndrome suspected
§ CT Myelography: if MRI contraindicated e.g. pacemaker, MRI incompatible implants

o Treatment
§ Urgent surgical decompression within 48 hours

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Osteoarthritis
• Most common type of arthritis.
• Degenerative disease which results in progressive loss of the articular cartilage.
• Knee most commonly affected

• Risk Factors
o Trauma to joint
o Occupation
o Obesity
o Female sex
o Increased age
o Hip dysplasia

• Presentation
o Symptoms
§ Joint pain
§ Stiffness
§ Restricted range of motion
o Examination
§ Joint line tenderness
§ Reduced range of motion
§ Joint effusion
§ Antalgic gait

• Imaging
o X-Rays
§ Joint space narrowing
§ Subchondral sclerosis
§ Subchondral cysts
§ Osteophyte formation

• Treatment
o Non-Operative
§ NSAIDs – first line treatment for symptomatic OA
§ Physiotherapy
§ Weight loss
§ Corticosteroid joint injections

o Operative
§ Knee
• High tibial osteotomy: younger patients with medial unicompartmental OA
• Unicompartmental arthroplasty – isolated unicompartmental disease
• Total knee arthroplasty (TKA) – advanced disease refractory to conservative
measures
o Distal Femur and proximal tibia are replaced with a prosthesis
§ Hip
• Arthroscopic debridement – degenerative labral tears
• Femoral head resection – pathological hip lesions
• Hip resurfacing – young, active, male patients with OA
• Total hip arthroplasty (THA) – end stage, symptomatic, severe OA; preferred
treatment in those >50

322
Septic Arthritis
• Causes irreversible cartilage destruction in the involved joint
• Important to diagnose early as extensive cartilage damage occurs within hours
• Risk of sepsis
• Most commonly affects the knee (~50%)
o Knee>Hip>Shoulder>Elbow>Ankle>Sternoclavicular joint
• Staphylococcus aureus is most common pathogen in all patients

• Risk Factors
o Recent joint surgery
o Age >80
o Comorbidities: diabetes, RA, HIV, cirrhosis
o Endocarditis
o History of crystal arthropathy
o IVDU

• Three Aetiologies of Bacterial Seeding

o Bacteraemia
o Direct inoculation – trauma/surgery
o Direct spread – adjacent osteomyelitis/wound

• Presentation
o Symptoms
§ Pain in affected joint
§ Fever (60% of cases)
o Examination
§ Erythema
§ Effusion
§ Warm and tender
§ Inability to weight bear
§ Cannot tolerate passive range of motion
• Imaging
o X-Rays: AP, Lateral
o US: Assesses for joint effusion; can guide aspiration
o MRI: detects bone involvement e.g. osteomyelitis

• Investigations
o WCC, ESR, CRP
o Joint Fluid Aspirate
§ Gold standard – allows specific antibiotic treatment
§ Gram stain
§ Cell count with differential
§ Culture
§ Glucose level
§ Crystal analysis
o Saline load test
§ Determines if wound communicates with joint

• Treatment
o IV Antibiotics
o Irrigation and drainage of joint
o Monitor treatment with WCC, ESR and CRP levels

323
• Complications
o Osteoarthritis
o Osteomyelitis
o Fibrous ankylosis

324
References

• UpToDate: General Principles of Acute Fracture Management

• UpToDate: General principles of fracture management: Bone healing and fracture description
• Bailey & Love’s Short Practice of Surgery: Extremity Trauma
• Radiopaedia.org
• Standards for the Management of Open Fractures
https://oxfordmedicine.com/fileasset/9780198849360_Book.pdf
• Orthobullets https://www.orthobullets.com
• UpToDate: Shoulder Dislocation and Reduction
• UpToDate: Acute Compartment Syndrome of the Extremities
• ASIA Score https://asia-spinalinjury.org/wp-content/uploads/2019/04/ASIA-ISCOS-IntlWorksheet_2019.pdf

325
15. Transplant

• Ms Laoise Coady, Mr Adam Daly, Mr Joseph McLoughlin, Professor David G Healy

• General Principles
• Liver Transplant
• Cardiac Transplant
• Lung Transplant
• Kidney Transplant
• Pancreas Transplant

326
Transplant

• The process of transferring an organ of part of an organ (graft) from a donor to a recipient.
o Allograft: Organ or tissue transplanted from one individual to another
o Autograft: Organ or tissue transplanted from one point to another of the same individuals body
o Xenograft: Organ or tissue transplanted from one individual to another species
o Orthotopic Graft: Graft placed in its normal anatomical site e.g. liver transplant
o Heterotopic Graft: Graft placed in a site different to that where the organ is normally located e.g.
kidney transplant

Graft Rejection

• Allografts will provoke an immune response which will result in graft rejection unless immunosuppression is
given.
• Manifests as failure of the transplant and is confirmed by histological examination.
• The graft rejection response is triggered due to allelic differences at polymorphic genes which give rise to
histocompatibility antigens

o ABO Blood Group Antigens (ABO)

Recipient A B AB O
Donor
A ü ü
B ü ü
AB ü
O ü ü ü ü

o Human Leukocyte Antigens (HLA)

§ Group of highly polymorphic cell-surface molecules
• The amino acid sequence varies widely between individuals
§ Function as antigen recognition units
§ Most common cause of graft rejection
§ Two types of HLA molecule – Class I and Class II
• Class I: HLA-A, HLA-B, HLA-C
• Class II: HLA-DR, HLA-DP, HLA-DQ

• Types of Graft Rejection

o Hyperacute Rejection
§ Immediate graft destruction (minutes to hours)
§ Caused by ABO or preformed anti-HLA antibodies (from previous blood
transfusion/transplant/pregnancy)
§ Characterised by interstitial haemorrhage and intravascular thrombosis

o Acute Rejection
§ Usually occurs within first six months
§ May be antibody mediated, cell mediated or both
§ Characterised by mononuclear cell (Cytotoxic T-Cells, B-Cells, natural killer (NK) cells)
infiltration of the graft
§ Usually reversible with additional immunosuppressive therapy

o Chronic Rejection
§ Usually occurs after first six months
§ Most common cause of graft failure
§ Pathophysiology not fully understood – alloantibodies are major cause
§ Functional deterioration of the graft over months/years resulting in complete graft failure

327
Causes of Allograft Dysfunction
• Early
o Primary non-function – irreversible ischaemic damage
o Delayed function – reversible ischaemic injury
o Hyperacute/Acute rejection
o Arterial or venous thrombosis of graft vessels
o Drug toxicity
o Infection
o Mechanical obstruction e.g. ureter/bile duct

• Late
o Chronic rejection
o Arterial stenosis
o Recurrence of original disease in the graft, e.g. hepatitis C, glomerulonephritis
o Mechanical obstruction e.g. ureter/bile duct

Immunosuppression
• Immunosuppressive agents work to prevent rejection by acting at different stages during T-Cell activation
• Immunosuppressive regimens should be designed to provide sufficient levels of immunosuppression to
protect the graft from rejection without exposing the patient to side effects
• Most regimens include steroids, a calcineurin inhibitor e.g. tacrolimus and an anti-proliferative agent e.g.
azathioprine

• Side Effects
o Infection
§ Risk of opportunistic infection – viral/bacterial/fungal
§ Risk of reactivation of latent infections e.g. CMV, HSV
§ Highest risk in first six months
§ Chemoprophylaxis should be used in high risk patients
§ Patient should be vaccinated annually
o Malignancy
§ Most cancers are more common after transplant
§ High risk of squamous cell carcinoma of skin
§ Transplant recipients, especially children, are at risk of lymphoproliferative disease

Evaluation of Potential Recipients for Organ Transplantation

• Multidisciplinary team evaluation including relevant surgeon and physician
• Must exclude malignancy and systemic sepsis
• Determine presence of any comorbid disease
• Determine patient’s ability to cope psychologically with transplant
• Determine patient’s likelihood to comply with immunosuppression
• Optimise recipient condition pre-transplant
• Ideal Candidate
o Ability to endure surgery and immunosuppression
o History of compliance to medical recommendations and therapies
o Understanding of potential morbidity and mortality

Donors
• Donation after Cardiac Death (DCD)
o Five categories – Maastricht Classification
1. Dead on arrival at hospital
2. Resuscitation attempted without success
3. “Awaiting cardiac arrest” after withdrawal of care
4. Cardiac arrest while brain dead
5. Cardiac arrest and unsuccessful resuscitation in hospital

328
 o Categories 1, 2 and 5 are considered uncontrolled DCD donors as the warm ischaemia time in these
donors is usually longer and less predictable than that of donors in category 3 and 4.

• Donation after Brain Death (DBD)

o Brain death occurs when severe brain injury e.g. trauma/stroke results in irreversible loss of
consciousness and irreversible loss of ability to ventilate
o The patient will have suffered major brain damage of known aetiology, be unconscious and require
ventilatory support
o Tests to confirm brain death should be performed on two separate occasions by two separate
experienced clinicians. At least one clinician must be a consultant and neither clinician should have
any affiliation to the transplant team.

Clinical Testing for Brainstem Death

Absence of motor response
Absence of cranial nerve reflexes
Absence of spontaneous respiration
Absence of motor response to painful stimuli
applied to the head and face coupled with the
absence of motor response within the cranial
nerve distribution to stimulation of any somatic
area
Pupillary Reflex
Corneal Reflex
Pharyngeal (gag) and tracheal (cough) reflex
Oculovestibular (caloric) reflex
The patient should be pre-ventilated with 100%
Oxygen for a minimum of 5 minutes. The
ventilator is then disconnected for ten minutes
to confirm absence of respiratory effort. During
this time the arterial PCO2 level should be >8kPa
(60mmHg) to ensure adequate respiratory
stimulation. O2 is delivered via endotracheal
catheter at 6L/min to prevent hypoxia during
the apnoeic period.

329
Liver Transplant

• Indications
o Cirrhosis
§ Chronic liver failure secondary to alcoholic liver disease, viral liver disease, primary biliary
cirrhosis, non-alcoholic steatohepatitis, sclerosing cholangitis
§ Paediatric transplant (10-15% of all transplants) – Biliary atresia is most common indication
o Acute fulminant liver failure
§ Accounts for ~10% of transplants
§ Viral or drug induced e.g. Paracetamol overdose
o Metabolic liver disease
§ Wilson’s Disease, Oxalosis, Familial Amyloid Polyneuropathy
o Primary hepatic malignancy
§ Common in patients with cirrhosis, particularly virally induced
§ Best treated with transplant as field changes in cirrhotic liver may predispose to further
malignancies

• Surgical Technique
o Transverse abdominal incision with midline extension (Reverse L)
o Diseased liver mobilised and hepatectomy performed
§ Common bile duct divided
§ Hepatic artery divided
§ Inferior vena cava clamped and divided above and below the liver
§ Portal vein clamped and divided
o Occlusion of vena cava and portal vein will lead to a reduction in cardiac output, therefore
venovenous bypass is necessary
§ Bypass circuit delivers blood from IVC +/- portal vein back to the heart via a cannula inserted
into the jugular vein
o Donor liver is placed in position
§ Supra and infrahepatic caval anastomoses
§ Portal vein and hepatic artery anastomoses
§ Biliary duct to duct anastomoses

• Complications
o Haemorrhage
§ Meticulous haemostasis and correction of coagulopathy necessary to minimise risk
o Hepatic Artery Thrombosis
§ Spontaneous or secondary to acute rejection
§ Most common in children and adults with primary sclerosing cholangitis
o Portal Vein Thrombosis
§ Rare
§ Presents with features of portal hypertension
o Biliary leaks

• Outcomes
o Depends on underlying disease
§ Transplant for acute liver failure – higher risk of mortality in early post-transplant period
secondary to multiorgan failure
§ Transplant for primary hepatic malignancy – excellent early outcome, however recurrent
malignancy limits long term survival
§ Transplant for viral hepatitis – graft failure due to recurrent disease may occur, however
antiviral therapy can decrease this risk

330
Cardiac Transplant

• Cardiac transplantation is the treatment of choice for many patients with end-stage heart failure (HF) who
remain symptomatic despite optimal medical therapy.
• Given the extremely limited supply of suitable donor hearts, the patients expected to gain maximum benefit
from heart transplantation must be identified.

• Indications
o NYHA class of III or IV despite maximized medical and resynchronization therapy
o Recurrent life-threatening left ventricular arrhythmias despite an implantable cardiac defibrillator,
antiarrhythmic therapy, or catheter-based ablation.
o End-stage congenital HF with no evidence of pulmonary hypertension.
o Refractory angina without potential medical or surgical therapeutic options.
o Cardiogenic shock requiring continuous intravenous inotropic therapy.
o Refractory cardiogenic shock requiring intra-aortic balloon pump counter pulsation or left ventricular
assist device (LVAD).

• Absolute Contraindications
o Systemic Illness with life expectancy <2 years despite heart transplantation
o Irreversible pulmonary hypertension
o Active substance abuse (including tobacco)
o Multiple demonstrations of inability to comply with drug therapy

• Relative Contraindications
o Age > 70
o Obesity
o Poorly controlled diabetes.

• Prognosis Following Heart Transplant

o Median Survival for adult heart transplant recipients is 11 years.
o Primary Causes of Death Post Heart Transplant
§ Graft Failure
• Typically within 30 days of transplant
§ Opportunistic Infections
• Due to immunosuppression, leading cause of mortality between 6 – 12 months post-
transplant
§ Acute Allograft Rejection
• Cellular and antibody-mediated rejection typically within the first 3 years following
transplantation.
§ Cardiac Allograft Vasculopathy
• One of the top three causes of death beyond the first year post-transplantation.
§ Lymphoma and other malignancies
• Most frequent cause of death beginning at five years post-cardiac transplantation

331
Left Ventricular Assist Device (LVAD)
• This is an implantable long-term mechanical circulatory support device that is used in patients with advanced
heart failure. It is used in two main circumstances.
o Bridge to Transplant
§ In this scenario the device is implanted in rapidly deteriorating patients who are awaiting
transplantation.
§ The device aims to provide time for an organ to become available.
o Destination Therapy
§ The LVAD device is implanted in patients with refectory heart failure who are not candidates
for transplantation.
§ The device aims to support their cardiac function for the duration of their lifetime.

332
Lung Transplant

• Lung transplantation should be considered for patients with advanced lung disease whose clinical status has
progressively declined despite maximal medical or surgical therapy. Candidates are usually symptomatic
during activities of daily living and have a limited life expectancy over the next two years

• Indications
o Advanced chronic obstructive pulmonary disease (COPD)
o Interstitial lung disease (ILD)
o Cystic fibrosis (CF)
o Emphysema due to alpha-1 antitrypsin deficiency
o Pulmonary arterial hypertension (PAH)

• Absolute Contraindications
o Uncontrolled or untreatable pulmonary or extrapulmonary infection
o Active Mycobacterium tuberculosis infection
o Malignancy in the last two years
o Significant dysfunction of other vital organs
o Un-correctable bleeding diathesis
o Class II or III obesity: body mass index (BMI) ≥35 kg/m2
o Active tobacco smoking / drug or alcohol dependency
o Unresolved psychosocial problems or noncompliance with medical therapy

• Transplant Options
o Single lung transplant
§ Single lung transplants are typically performed through an anterior or posterior
thoracotomy.
o Double lung transplant
o Combined heart and lung transplant
§ Double lung or heart lung transplants are usually performed through a larger clamshell
incision.
o The choice of which transplant type is performed is based on multiple factors including the reason
for transplantation, age of recipient and availability of organs.
o Patients with cystic fibrosis tends to receive a double lung transplantation.
o The Lung Allocation Score is used to aid in order of priority on the waiting list.
§ Higher scores represent higher urgency and greater potential transplant benefit.
§ Calculated from a recipients clinical and physiological characteristics.

• Prognosis Post Lung Transplant

o Median survival for all adult lung transplant recipients is 6.5 years.
o Double lung transplant has a higher median survival compared to single lung transplant (7.6 versus
4.7 years, respectively) however it is felt that this is largely due to the typically younger recipients
receiving a double lung transplant.
o Lung transplantation offers significant benefit in terms of quality of life improvement. Following
recovery 80% report no activity limitations.

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Kidney Transplant

• Treatment of choice for those with end-stage kidney disease (ESKD)

• Successful kidney transplant reduces mortality risk and improves quality of life in the majority of patients in
comparison to maintenance dialysis
• Transplant is also more cost-effective than dialysis
• Donor organ can be from a living donor, a donation after circulatory death (DCD) donor or a donation after
brain death (DBD) donor

• Causes of End-Stage Kidney Disease

o Diabetic nephropathy
o Glomerulonephritis
o Renal vascular disease
o Hypertensive nephrosclerosis
o Pyelonephritis
o Polycystic kidney disease
o Analgesic nephropathy
o Obstructive uropathy
o Systemic lupus erythematosus

• Surgical Technique
o The transplanted kidney is placed retroperitoneally in the iliac fossa
o The native kidney is left in situ
§ Native nephrectomy is only required prior to transplantation in the case of intractable renal
sepsis or large polycystic kidneys which invade the iliac fossae
o The donor renal artery is anastomosed to the external or internal iliac arteries
o The donor renal vein is anastomosed to the external iliac vein
o The donor ureter is kept short and anastomosed to the bladder by direct implantation into the dome
of the bladder

• Complications
o Causes of Graft Dysfunction – common problem early in post-operative period
§ Acute tubular necrosis
• Can result in delayed graft function and need for dialysis post-transplant
• Usually resolves within the first four weeks post-transplant
§ Arterial/Venous thrombosis
§ Urinary leak/obstruction
§ Calcineurin inhibitor toxicity
§ Hyperacute rejection

o Late onset dysfunction

§ Develops >1 month post-transplant
• Acute/chronic rejection
• Ureteric obstruction (lymphocoele, ureteric stricture)
• Recurrent disease
• UTI

• Outcomes
o Graft survival is >90% after 1 year and >80% after 5 years (Deceased Donor)
o For living donors, graft survival is approximately 95% at 1 year and 85% at 5 years

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Pancreas

• Successful pancreas transplant results in the restoration of normal control of glucose metabolism thus
obviating the need for insulin therapy in patients with Diabetes Mellitus.
• Improved control of blood glucose levels in diabetics reduces progression of complications associated with
diabetes such as peripheral vascular disease, retinopathy and nephropathy
• For the majority of diabetic patients, the additional risks, which go hand in hand with transplant from both
the procedure itself and future need for immunosuppression, are only justifiable when kidney
transplantation for end stage renal disease from diabetic nephropathy is undertaken too.
• Pancreas transplant is usually performed as part of a simultaneous pancreas and kidney transplant (SPK)
• Some patients who have already undergone successful kidney transplantation will receive a pancreas
transplant – pancreas-after-kidney transplantation (PAK)
• In some cases, pancreas transplantation alone is justified when used to treat life-threatening complications
of diabetes such as hypoglycaemic unawareness.
• Transplantation of Isolated Pancreatic Islets
o Evolving technology
o Avoids major surgery
o Pancreatic islets for transplantation are obtained by injecting collagenase into the pancreatic duct
and mechanically disrupting the pancreas
o The islets are purified and delivered into the recipient liver by injection into the portal vein
o Options to use xenograft islet cells
o Studies evaluating alternative sources of islet cells are ongoing

Simultaneous Pancreas-Kidney (SPK) Transplant

• Diabetic renal disease is a significant cause of end stage renal disease (ESRD).
• Renal transplantation can improve survival of those with diabetes and ESRD, however the diabetic state is
associated with poor patient and graft outcomes.
• Pancreas transplantation
o Form of endocrine replacement therapy
o Developed to achieve normoglycaemia and insulin independence.
• Combined pancreas and kidney transplantation can render patient free of both insulin and dialysis.
o Prevents further diabetic complications
o Occasional reversal of established disease

• Indications
• Type 1 Diabetes Mellitus
o Common chronic disease of childhood caused by insulin deficiency secondary to autoimmune
destruction of pancreatic b-cells
o Can result in severe long term complications if not treated
§ These complications are attributed to hyperglycaemia secondary to poor insulin
secretion
• Microvascular Complications
• Retinopathy/Neuropathy/Nephropathy
• Macrovascular Complications
• Cerebrovascular/Coronary/Peripheral Vascular System
• End Stage Renal Disease
• Microalbuminuria Proteinuria Nephropathy ESRD
• Tight glycaemic control slows the progression and reduces risk of micro and macrovascular
complications

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• Assessment for Transplant
• SPK Procedure is usually reserved for patients with T1DM
o Confirmed by low/absent levels of C-Peptide
o Significant nephropathy/ESRD
o Hypoglycaemic unawareness
o Recurrent hospitalisation from DKA
o Progressive retinopathy/enteropathy/neuropathy
• Daily insulin requirement
• Fasting serum C-Peptide levels
• HbA1C
o Determine type of diabetes
o Determine severity of insulin resistance

• Surgical Technique
o The whole pancreas together with a segment of duodenum is transplanted.
o The graft is placed intraperitoneally in the pelvis through a midline incision
o The pancreas graft is usually placed on the right while the kidney graft is placed on the left.
o The donor vessels from the pancreas are anastomosed to the recipient iliac vessels
o The donor duodenum is anastomosed to the small bowel (enteric drainage) or bladder (urinary
drainage) to allow for drainage of exocrine secretions
§ Urinary drainage is advantageous in that urinary amylase can be monitored to assess for
graft rejection
§ However, due to complications associated with urinary drainage 20% of patients will require
conversion to enteric drainage
o The pancreas graft will function immediately after revascularisation, however, supplementary insulin
may be required initially

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• Complications
o Vascular thrombosis of graft (5%)
o Graft pancreatitis – common but usually mild
o Wound infection (10%)
o Duodenal anastomotic leaks
§ Can result in intrabdominal sepsis or bowel adhesions
o Bladder anastomosis complications
§ Anastomotic leaks
§ Cystitis – due to effects of pancreatic enzymes
§ Urethritis/Urethral stricture
§ Reflux Pancreatitis
§ UTI
§ Metabolic acidosis secondary to loss of bicarbonate in urine
§ Haematuria
o Acute rejection occurs in 10-20% of cases
§ Responds to treatment with steroids if detected early
o Acute rejection of the renal graft may herald subsequent pancreas rejection, however, kidney or
pancreas rejection can occur in isolation.

• Outcomes
o SPK Transplantation 1 year survival >95%

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16. Radiology

• Dr Kevin Quinlan

• Introduction
o Radiation Protection
o Requesting a Radiological Examination
o Contrast Agents
o Radiologic Terminology

• Imaging modalities with sample cases

o Radiography (X-ray)
o Breast Imaging
o Fluoroscopy
o Computed tomography (CT)
o Nuclear Medicine
o Interventional Radiology (IR)
o Ultrasound
o Magnetic Resonance Imaging (MRI)

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Radiation Protection

Terminology
(not important, but may explain some terms used in this chapter)
• Gray (Gy): Joule per kilogram of tissue. Absorbed dose (energy per unit mass of body tissue) uses Gray.
• Sievert (Sv): Joule per kilogram of tissue. Equivalent dose (absorbed dose in an organ multiplied by a
radiation weighting factor) uses Sievert to avoid confusion with absorbed dose. In the low doses used in
diagnostic radiology, absorbed dose = equivalent dose.
• Effective dose (mSv, or J/kg): the ionising radiation dose related to overall risk and includes the different
effects of radiation type and tissue sensitivity.

Effects of ionising radiation (from radiographs, computed tomography, fluoroscopy, interventional radiology, nuclear
medicine) can be divided into stochastic and deterministic effects:
• Stochastic effects
o Occur by chance and can occur at any dose.
o Probability of occurrence increases with dose.
o Examples:
§ Cancer (see Appendix A).
§ Hereditary effects (negligible effects in the low doses used in radiology, 0-100 mSv).
• Deterministic effects
o Direct effect of radiation only above a known threshold dose.
o Deterministic effects should never be seen diagnostic radiology, but can occur with doses used in
interventional radiology (and interventional cardiology). But rest assured, the use of radiation
protection in reality means that interventionalists rarely reach strict dose limits.
o Severity of effect increases with dose.
o Examples:
§ Cataract (> 0.15 - 1 Gy).
§ Skin burn (> 2 Gy).
§ Sterility (> 2.5 Gy).
§ Hair loss (> 3 Gy).

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 Radiation-induced sarcoma in a patient who had radiotherapy for left breast cancer 10 years prior, and presented
with an axillary mass (yellow arrows) adjacent to the breast prosthesis (orange arrows). Subsequent ultrasound-
guided biopsy revealed angiosarcoma, which was presumed to be radiation-induced, given the time interval since
radiation and this tumour developed within the radiation field.

The three principles of radiation protection regarding patients, public and staff:

1. Justification: Exposing a patient to radiation should only occur if the benefit to the patient’s care outweighs
the risks involved (which includes the risks of not performing the diagnostic test). What impact the
requested will have on a patient’s management? Could alternative imaging modalities that do not involve
ionising radiation be considered, e.g. ultrasound or MRI?

2. Optimisation: In obtaining a diagnostic image, the dose should be kept “As Low As Reasonably Achievable”
(ALARA principle). National DRLs (diagnostic reference levels) exist for each exam to compare a centre’s
performance with other hospitals & optimise protocols.

3. Dose limitation: Only apply to staff and members of public. There is no dose limit for patients.

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Special Considerations

• Children have a higher cell turnover and a longer life expectancy. Thus, when exposed to ionising radiation,
children are at 2-3 times higher risk of developing cancer during their lifetime. Childhood leukaemia is an
extra consideration when exposing children to ionising radiation. Significant attention is paid to optimising
techniques to reduce doses and to seeking alternative non-ionising diagnostic imaging techniques.

• Pregnant women: For the same reasons, the foetus is highly sensitive to the harmful effects of ionising
radiation. For your interest only, the below are the potential foetal effects of radiation:
o Stochastic effects to the foetus:
§ The baseline childhood cancer incidence (1:500) is increased by 1:10,000 with a foetal dose of
1 mGy, while a dose of 25 mGy doubles the risk of childhood cancer.
§ The risk of hereditary effects are negligible at low doses used in diagnostic radiology.
o Deterministic effects to the foetus depend on gestational age and include:
§ 0 – 3 weeks: Implantation failure or embryo death (“All or nothing” effect).
§ 3 – 8 weeks: Organ malformation at 100 mGy (i.e. 3 pelvic CTs or 20 conventional X-ray
studies), foetal death at 500 mGy.
§ 8 – 25 weeks: Decreased IQ (up to 30 IQ points reduction per 1 mSv) and growth retardation.
§ > 25 weeks: Lower risk period.

• Women of childbearing age (12 – 55 years old):

o 10-day rule: Ionising radiation examinations are only carried out during the first 10 days of the
menstrual cycle. Applies to doses > 10 mGy to the foetus (e.g. CT abdomen/pelvis should be
scheduled within 10 days post LMP).
o 28-day rule: Ionising radiation examinations could be undertaken within 28 days following LMP. If a
patient is overdue menstruation and the patient cannot be certain that she is not pregnant, then
one must consider postponing the examination.
o Clinical waiver can be applied in urgent situations or if not appropriate (peri-adolescence, post-
menopausal, post-hysterectomy).

• Radiosensitive organs: Include the gonads, breasts, thyroid gland and eyes especially. Eye, breast and
gonadal shields can be used for patients. Staff personal protective equipment (e.g. interventional radiology)
include lead glasses, lead aprons and thyroid shields.

• Staff Protection
o Time: reduce time spent in areas with high exposure to ionising radiation; avoid long exposures and
unnecessary repetitive exposures.
o Distance: increasing distance to the source (patient) is the most effective method to reduce staff
dose; doubling one’s distance can reduce one’s dose x4 (inverse square law).
o Shielding: personal protective equipment, including lead glasses, thyroid shields, lead aprons;
dosimeters; lead shields around patient; room design and materials.

N.B.

Referring clinician must (legal requirement per national and European Union regulations):
• Enquire about pregnancy status of the patient.
o A urinary pregnancy test does not outrule pregnancy, as they are not reliable in early pregnancy
or after 16 weeks gestation.
• Ensure that the exam is justified.
• Provide the practitioner with all relevant information as part of the examination request.

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Nuclear Medical Imaging Safety
• Uses ionising radiation. PET/CT uses relatively high radiation doses. As the patient is injected with a
radionucleotide, the patient becomes the radiation source. Thus, there are additional radiation safety
concerns.

Fluoroscopy and Interventional Radiology

• Uses ionising radiation. Safety measures include radiation safety and those that are specific to the
procedure. Some fluoroscopic procedures can use low radiation doses, while others use relatively high
radiation doses equivalent to CT. Interventional radiology procedures can use very high radiation doses.

Magnetic Resonance Imaging (MRI) Safety

• MRI does not use ionising radiation and is safe when the essential precautions are taken. Ferromagnetic
metal objects will propel towards the magnetic field at high speed and can cause life-threatening injuries,
e.g. intracranial aneurysmal clip or a metallic foreign body. This is why an MRI safety questionnaire is
essential to avoid dangerous movement of metallic objects, heating of metallic objects or pacemaker /
neurostimulator malfunction.

Ultrasound Safety
• Generally regarded as very safe. Ionising radiation is not used in ultrasound. Heating of objects can occur
with high-power ultrasound machines, which is more of a concern in foetal imaging.

When requesting a radiological examination:

• Ensure it is the correct patient.

• Provide adequate clinical information:
o History & exam findings.
o Relevant investigations.
o Top differential diagnoses.
o Detail the relevance of the requested investigation to the patient’s management.
• Include relevant background regarding:
o Prior allergy.
o Risk factors for contrast induced nephropathy (low eGFR), nephrogenic systemic fibrosis (low
eGFR), lactic acidosis (metformin and low eGFR), thyrotoxicosis,.
o Contraindications: pregnancy, breastfeeding, metallic implants in MRI.
o Risk group status and mode of transport.

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 Radiation dose to patients from common imaging examinations, ACR, RSNA, RadiologyInfo.org, 2015.
https://radltd.com/about/radiation-safety/

The average annual natural background radiation dose = 3.4 mSv (1 year).
A return flight from Dublin – Rome = 0.027 mSv (2 days).
The average lifetime cancer incidence in adults = 1:3.
The average cancer incidence in children = 1:500.

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Contrast Agents
• Contrast media is administered to highlight structures not evident or clearly characterised on non-contrast
imaging.
• Contrast agents vary depending on imaging modalities (CT, fluoroscopy, MRI, ultrasound).
• Route of administration depends on the organ of interest.
• Intravenous contrast is the most common route and the scan can be timed depending on organs / vessels of
interest (arterial, delayed arterial, portal venous, nephrographic, urographic, delayed).
• Oral contrast can help distinguish the gastrointestinal lumen from other structures (e.g. abdominopelvic
abscess).
• Depending on the investigation, contrast can be administered to the rectum, bladder, vagina, biliary tree,
abnormal collection, joint spaces or intrathecally.
• Intravenous iodinated contrast are the most commonly used. X-rays cannot penetrate dense iodine
molecules and thus, areas of highly concentrated iodinated contrast appear bright.

Acute Contrast Reactions

• Anaphylaxis (angioedema, laryngospasm, stridor, O2 desaturation, hypotension).
• Urticaria.
• Bronchospasm.
• Facial or laryngeal oedema.
• Vasovagal reaction (hypotension & bradycardia).
• Hypotension with tachycardia.
• Pulmonary oedema.
• Contrast extravasation.
o Can be avoided with using an appropriately sized IV cannula with high flow intravenous contrast:
20-gauge for most IV contrast; 18-gauge for angiographic phases, which have to administered
quickly and require higher flow rates.
• Thyrotoxicosis in patients with uncontrolled hyperthyroidism (if using iodinated contrast).

Normal physiological reactions include flushing, nausea, syncope, headache or mild self-limiting hypertension.

Enteric Contrast Media

• Oral / rectal agents, often used in fluoroscopy.
• Barium sulphate use in barium swallow / enema in patients with perforated viscous who develop
mediastinal / peritoneal extravasation can cause mediastinitis / peritonitis, which is associated with high
(80%) mortality.
• Water soluble iodinated contrast agents, like Gastrografin, are used in patients with a suspected perforation.
However, if Gastrografin is aspirated into the lungs, this can result in severe pulmonary oedema. Use of
agents with further decreases in osmolarity, like Niopam, can be used if the benefits outweigh the risks, in
patients with risk of aspiration. However, the lower the osmolarity, the less dense appearing contrast will be.

Gadolinium based contrast agents in MRI

• Appear bright on T1-weighted imaging.
• Adverse reactions are rare.
• Intracranial gadolinium accumulation, which has been found in patients that undergo multiple studies, has
an unknown clinical significance.
• Nephrogenic systemic fibrosis is extremely rare but severe, debilitating and often fatal condition that
primarily involves the skin and subcutaneous tissues, but can also involve the lungs, liver, heart and skeletal
muscle.
• Therefore, for patients with an eGFR < 25: consider non-contrast or other imaging modalities; post-contrast
dialysis; as low a dose as possible; avoid repeated doses within 1 week.

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 Radiologic Terminology

How to describe dark / grey / bright objects:

• Radiographs (x-rays):
o Density.
o Lucency (dark) or opacification (bright).
o The following appear progressively less radio-lucent (dark) or more radio-opaque (bright):
§ Air (dark, or radio-lucent) < fat < water / soft tissue < calcium < bone < metal (bright, or
radio-opaque)

• Computed Tomography (CT):

o Attenuation.
o Hypoattenuating (dark), isoattenuating (same grey level as surrounding muscle) or hyperattenuating
(bright).
o Hounsfield units (HU) are the standard numerical measurement of attenuation relative to water: (air -
1000 HU; fat -50 HU; water 0 HU; muscle 50 HU; haemorrhage 60-110 HU; bone 700-3000 HU).

• Nuclear Medical Imaging:

o Uptake / metabolic activity.
o High or low uptake / metabolic activity.

• Ultrasound:
o Echogenicity.
o Hypoechoic (dark), isoechoic (same grey level as surrounding muscle), hyperechoic (bright).
o Sound waves generated from the ultrasound probe can be transmitted, reflected, refracted or
absorbed as they pass through the patient.

• Magnetic Resonance imaging (MRI):

o Signal intensity.
o Hypointense (dark), isointense (same grey level as surrounding muscle), hyperintense (bright).
o Fluid appears dark on T1-weighted imaging and bright on T2-weighted imaging.
§ T1- and T2-weighted imaging are the most commonly used sequences and represent specific
times after a radiofrequency pulse is sent from the MRI machine into the patient.
§ T1 (longitudinal relaxation time) is the time constant for excited, spinning protons in a
material in the patient to return to equilibrium by realigning with the external magnetic field.
§ T2 (transverse relaxation time) is the time constant for excited, spinning protons in a material
in the patient to return to equilibrium by going out of phase with each other.

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Radiographs

Chest Radiograph

Normal PA chest radiograph.

• The chest radiograph is the commonly performed procedure in general radiology (30 – 50% of cases).
• Various views / techniques:
o PA (postero-anterior)
§ The standard chest radiograph (if not possible, then an AP chest radiograph is performed).
§ Projection minimizes cardiomediastinal magnification.
• PA (postero-anterior) means that the direction of the x-ray beam through the
patient goes from back to front. The patient stands with their back to the x-ray tube
while hugging the detector in front in order to remove the scapulae from partially
obscuring the lung field (see Figure 1).
§ Erect.
§ Full suspended inspiration (to maximise lung field).
§ +/- Expiratory radiograph:
• Pneumothorax, which will appear relatively larger in comparison to the inspiratory
radiograph (see Figure 1). Small pneumathoraces may not be visible on an
inspiratory film.
• Inhaled foreign body, which will cause persistent expansion of the obstructed lung
despite expiration.

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 Pneumothorax in an inspiratory (left) versus expiratory (right) chest radiograph. Both images
display 500 ml in the pleural space. During inspiration, there is 2500 ml in the lung, and a
17% pneumothorax is displayed. During expiration, there is 1500 ml in the lung and a 25%
pneumothorax is displayed – note that at the apex, the pleural line is displaced more
inferiorly than on the inspiratory view, and the mediastinum is now displaced away – a
tension pneumothorax.

o AP (antero-posterior)
§ Standard portable chest radiograph for bedbound or immobile patients, e.g. ill patients in
the intensive care unit.
• Detector is placed behind the patient back with the x-ray tube in front.
§ Pitfalls:
• Projection results in cardiomediastinal magnification, so the cardiomediastinal
silhouette cannot be accurately analysed.
• Scapulae (not retracted like in PA view) can partially obscure the lung field.
• Often supine / semi-erect: pathology often obscured due to raised diaphragms,
reduced lung volumes and cardiomediastinal magnification.
• Skin folds can be mistaken for a pneumothorax.

PA versus AP chest radiograph.

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 o Rarely performed chest radiograph views:
§ Lateral
• Rarely performed now with availability of CT.
• Can help identify retrocardiac lesion and clarify location of lesion (e.g. a skin lesion
or nipple) seen on PA.
§ Decubitus (highlight pleural effusion).
§ Lordotic (see lung apices).

How to interpret a chest radiograph (WOT IF; ABCDES):

NB: Compare with prior chest radiograph for interval change or new pathology.

W Which patient: Ensure correct patient; note age, gender.

O Orientation / labels: L / R, erect (assume erect if not labelled), PA/AP, expiration.
T Technical quality: Exposure (should just about see thoracic vertebrae).
Rotation (clavicles relative to spinous processes).
I Inspiration: 6 ribs anteriorly (9-10 ribs posteriorly) to visualise lung bases.
F Findings (ABCDES):
o Airway Trachea (central/narrow), carina splayed, bronchi narrow/elevated.
o Breasts & bones Mastectomy, neoplastic disease, fractured rib, dislocated shoulder.
o Cardiovascular Heart, retrocardiac, mediastinum, hilum, pulmonary vasculature.
o Diaphragm Elevated, depressed, flattened, subdiaphragmatic free air, effusion.
o Examine lungs Radio-lucency/opacity, volume, pathologic patterns. Compare zones
(upper, mid, lower). Examine edges & apices for pneumothorax.
S. Soft tissues Surgical emphysema.

We can go into more detail on these items later…

Anatomy:
• Right apex
• Right clavicle
• Right scapula
• Trachea
• Aortic arch
• Carina
• Right main
bronchus

• Right hilum
• Left atrium
• Right pulmonary
artery
• Right atrium
• Left ventricle
• Right
cardiophrenic
angle
• Right ventricle
• Right
hemidiaphragm
• Right costophrenic
angle
• Gastric bubble Normal PA chest radiograph.
Annotations by Dr. Kevin Quinlan.

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How to interpret a chest radiograph (WOT IF):
W Which patient: Ensure correct patient; note age, gender.
O Orientation / labels: L / R, erect (assume erect if not labelled), PA/AP, expiration.
T Technical quality: Exposure (should just about see thoracic vertebrae).
Rotation (clavicles relative to spinous processes).

Assessing rotation in a frontal chest radiograph.

I Inspiration: 6 ribs anteriorly (or 9-10 ribs posteriorly) to visualise lung bases.

PA chest radiograph: normally 6 anterior ribs seen.

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F Findings (ABCDES):
A. Airway
• Trachea
o Central
§ Pulled by: lobar collapse, fibrosis, lobectomy.
§ Pushed by: mediastinal mass, tension pneumothorax, large pleural effusion,
diaphragmatic hernia or rupture.
o Narrowed: goitre, mediastinal mass.

• Carina
o Splayed (normal carinal approximately angle 60o) by subcarinal lymphadenopathy, left
atrial enlargement.

• Bronchi
o Narrowed.
o Elevated / depressed: lobar collapse, lobectomy, fibrosis.

B. Breasts & bones

• Mastectomy (if you don’t notice it) results in the ipsilateral lung appearing more lucent and the
contralateral lung base appearing relatively opacified.
o Recurrent disease signs include: lung metastases; interstitial disease (lymphangitis
carcinomatosis); pleural effusion; lymphadenopathy; bone metastases.

Normal right breast tissue can be mistaken for right lung pathology in setting of a left mastectomy.

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• Bones:
o Neoplasm (lytic lesions are lucent, sclerotic lesions are opaque).
o Rib fracture (sensitivity < 20%), so look for pneumothorax, haemothorax, lung contusion.
o Shoulder dislocation.

Right glenohumeral dislocation.

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C. Cardiovascular
• Heart:
o Normal heart size < 50% of cardiothoracic ratio – on PA view only – cardiomediastinal
contour cannot be adequately assessed on AP view.

Top: Normal cardiothoracic ratio < 50%.

o Sternotomy wires, stents, CABG surgical clips, valve replacement, pacemaker / ICD.
o Calcifications: valves, arteries, fibrosis, old infarct.

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 • Mediastinum:
o Thoracic aortic aneurysm.
o Hilar enlargement due to lymphadenopathy / dilated vasculature.
o Aortopulmonary window obliteration due to lymphadenopathy.

Bihilar lymphadenopathy in patient with sarcoidosis: abnormally convex hila (which are usually concave –
concave and apparently enlarged hila can be seen on rotated chest radiographs).

• Pulmonary vasculature:
o Generalised increase in vascular markings: left-to-right shunt.
o Focally / unilaterally decreased lung markings: Watermark’s sign in PE.
o Large central pulmonary arteries: pulmonary hypertension (chronic lung disease).
o Upper lobe pulmonary vein dilatation due to CCF (early sign).

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• Retrocardiac: lung nodule / mass; hiatus hernia.

Hiatus hernia (red arrows).

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D. Diaphragm
• Elevated right / left hemidiaphragm (right normally higher than left by < 2.5 cm): volume loss
(lobar collapse, lobectomy, pneumonectomy); pleural effusion; diaphragmatic hernia; phrenic
nerve palsy (tumour, surgery).
• Depressed / flattened diaphragms: hyperinflation (asthma, COPD, cystic fibrosis).
• Subdiaphragmatic free air due to perforation (patient must be sitting erect for 20 minutes).

Pneumoperitoneum (subdiaphragmatic free air).

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 • Blunted costophrenic angles due to pleural effusion.

Large left-sided pleural effusion (white-out of the left hemithorax with a meniscus sign) with mass effect causing
mediastinal shift (contralateral deviation of the trachea and cardiac silhouette).

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 Hydropneumothorax: right-sided pleural effusion with an absent meniscus.

E. Examine lungs
• Radio-lucency/opacity:
o One lung appears too dark: rotation, (ipsilateral) mastectomy, pneumothorax, large
bulla, pulmonary embolus.
§ Both lungs appear too dark: overexposed radiograph (with clearly visualised
vertebral bodies); COPD (with hyperinflation, flattened diaphragms, +/- bullae).

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Tension pneumothorax – radiographic features:
• Large volume of air (hyperlucency) in the pleural space.
• Collapse of that lung – the radio-opaque pleural line can be visible.
• Flattening of the ipsilateral hemidiaphragm.
• Contralateral tracheal and cardiomediastinal deviation.

Requires urgent needle decompression.

Tension pneumothorax: large volume of air in the right pleural space, lung collapse, flattening and
depression of the ipsilateral hemidiaphragm, mediastinal shift with contralateral deviation of trachea
and cardiomediastinal silhouette. Prompt needle decompression warranted.

o One lung appears too bright: (contralateral) mastectomy, pleural effusion, lobar
collapse, consolidation, pleural / pulmonary mass.
§ Both lungs appear too bright: underexposed radiograph, pulmonary oedema,
pulmonary fibrosis, military infiltrates (TB, metastases).

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 • Heart failure:
A. Alveoli are fluid-filled: air space opacification.
B. Kerley ‘B’ lines due to interstitial oedema.
C. Cardiomegaly: increased cardiothoracic ratio.
D. Dilated hilar vasculature: enlarged pulmonary veins.
E. Effusion: usually bilateral but often unilateral
pleural effusion.

Pulmonary oedema with diffuse alveolar opacification, Kerley ‘B’ lines,

cardiomegaly, dilated pulmonary veins with upper lobe venous diversion.

• Volume:
o Increased unilateral lung volume: tension pneumothorax, large effusion, expanded lobe
(e.g. Klebsiella pneumonia).
o Decreased unilateral lung volume: lobar collapse, lobectomy/pneumonectomy, fibrosis,
diaphragmatic paralysis/rupture.

• Apices and edges for pneumothorax, rib fracture, pleural effusion.

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• Common pathologic patterns:
o Alveolar consolidation.

Alveolar consolidation: air bronchograms in left lower lobe and lingular

pneumonia.

§ Characteristics:
• Focal / multifocal / patchy / diffuse.
• Homogenous / amorphous.
• Well- / ill-defined.
• Air bronchograms.
• No volume loss.
• Absent silhouette → lobe involved:
A. R hemidiaphragm → R lower lobe.
B. R heart border → R middle lobe.
C. L hemidiaphragm → L lower lobe.
D. L heart border → Lingula.
E. None → upper lobes / apical
segments of lower lobes.

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 § Aetiology: pneumonia, pulmonary oedema, pulmonary haemorrhage, aspiration,
neoplasm, chronic infiltrates (cryptogenic organising pneumonia, alveolar
proteinosis, eosinophilic pneumonia).

NB: A repeat chest radiograph in 6 weeks is advised post antibiotics to ensure resolution of lobar pneumonia.
o Failure of consolidation to resolve may indicate an underlying malignancy.
o Next step: urgent referral to respiratory physician (Rapid Access Lung Clinic) with an urgent CT thorax is
warranted.

o Atelectasis (collapse - complete / partial of lung / lobe).

§ Lobar opacification
§ Volume loss: fissure displacement → elevated hemidiaphragm → mediastinal /
tracheal displacement → compensatory hyperinflation of contralateral lung.

Left lower lobar collapse - ‘sail’ sign.

NB: An urgent bronchoscopy or CT thorax is advised in the setting of lobar collapse to investigate the possibility of
an endobronchial mass.

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 Right upper lobe collapse in a 70 year old male who presented with haemoptysis.
Left: Chest radiograph displays an opacity in the medial aspect of the right upper zone that represents the collapsed
upper right lobe, which has migrated upwards and medially as a result. There are further features of volume loss in
the right hemithorax; mildly elevated right hemidiaphragm; tracheal deviation to the right; the upper right ribs
appear closer together than on the left. Also, the remaining right lung is relatively lucent compared to the left (it has
expanded to try to fill the space left by the collapsed upper lobe).
Middle: The horizontal fissure (dashed line) in the middle zoomed image, has migrated upwards and medially as well.
Right: Subsequent CT demonstrated a neoplasm at the right hilum (white arrows), which has occluded the right upper
lobe bronchus (yellow arrow), resulting in the lobar collapse. The displaced horizontal fissure dashed (white arrows).
Bronchoscopic biopsy confirmed that this was a primary bronchogenic neoplasm.

o Nodules (< 3 cm) / masses (> 3 cm).

§ Solitary: lung cancer, granuloma, hamartoma, metastasis.
§ Multiple: metastases, granulomas, rheumatoid nodule, sarcoidosis.

o Cavities / cysts.
§ Cyst: thin (< 3 mm) / thick (> 3 mm) wall.
§ Cavity: air versus air/fluid containing; often inside a consolidation area, mass,
nodule.

o Calcification / ossification.
§ Nodule / diffuse.

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 Metastatic osteosarcoma: numerous very dense and calcified lung masses.
o Interstitial lung disease (ILD).
§ Characteristics:
• Opacifications: reticular (linear) / nodular / reticulonodular.
• Septal lines, e.g.: Kerley B lines.
• Honeycombing.

S. Soft tissues
• Surgical emphysema: trauma (look for pneumothorax & pneumomediastinum), surgery, chest
drain, asthma.

Surgical emphysema with a left apical pneumothorax (arrow).

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Confirmation of nasogastric tube insertion
• 1st line: nasogastric tube (NGT) aspirate pH (safe to feed if pH < 5, per SVUH guidelines).
• 2nd line: chest radiograph (if no NGT aspirate obtained, if aspirate pH > 5, per SVUH guidelines).
o Acceptable NGT position if tip not seen: vertical course through mediastinum, bisects
the carina, passes below the diaphragm, curls toward left upper quadrant.

In each of these patients a nasogastric tube aspirate pH analysis (first line test) either could not be obtained or the pH
measured > 5, so the patients were sent for a chest radiograph (second line test).
Top left (image via Dr. Kevin Quinlan): Satisfactorily sited nasogastric tube (NGT seen below the diaphragm), safe for
use.
Top right: Satisfactorily sited nasogastric tube (NGT), endotracheal tube (ETT), right internal jugular and right
subclavian central venous lines (RIJV and RSCV lines). This patient had acute respiratory distress syndrome (ARDS) due
to severe acute pancreatitis, as evidenced by: extensive bilateral alveolar infiltrates with air bronchograms (double
yellow arrows) and bilateral pleural effusions (*). A normal heart size (even allowing for AP projection), absence of
Kerley B lines and prominent perihilar ‘batwing’ pulmonary vasculature with the presence of air bronchograms favour
ARDS over pulmonary oedema.
Bottom left and right: Malpositioned nasogastric tube coiled in the oesophagus (left) and right main bronchus (right),
unsafe for use due to the risk of aspiration and must be re-sited.

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Abdominal Radiograph (PFA, plain film abdomen)

Normal abdominal radiograph.

Far left: liver and spleen. Middle left: kidneys. Middle right: psoas muscles. Far right: colon.
Images via Dr. David Murphy, Approach to PFA Interpretation via http://www.svuhradiology.ie/tutorials/

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• Indications for an abdominal radiograph:
o Suspected bowel obstruction.
o Perforation (with an erect CXR).
o Abdominal mass.
o Ingested foreign body.
o Toxic megacolon.
o Follow-up of renal tract calculi.
• The following are not indications and result in unnecessary radiation exposure:
o Vague abdominal pain.
o Constipation.
o Uncomplicated appendicitis.
o Gastroenteritis.
o Haematemesis.
• Always look at the indication.
• Always compare to prior radiograph.

• How to interpret an abdominal radiograph:

1. Bowel gas pattern.
§ The 3-6-9 rule for the upper limit of normal of bowel diameter.
• Small bowel < 3 cm.
• Large bowel < 6 cm.
• Caecum < 9 cm.
§ How to distinguish small from large bowel (can be often too difficult to tell):
• Small bowel: valvulae conniventes (that form complete radio-opaque lines across
the lumen), centrally located.
• Large bowel: haustra (that form incomplete radio-opaque lines across the lumen),
peripherally located.
2. Soft tissues (organomegaly, ascites – it is difficult to distinguish soft tissue from fluid on a
radiograph).
3. Bones.
4. Calcification (calculi, vascular, calcified lymph nodes, phleboliths).
5. Surgical hardware and medical devices (surgical clips).

Top: small bowel with valvulae conniventes. Bottom: large bowel with haustra.
Images via Dr. David Murphy, Approach to PFA Interpretation via
http://www.svuhradiology.ie/tutorials/

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 Small bowel obstruction secondary to a stricture. 60 year old male with acute abdominal pain,
distension and vomiting. Left: abdominal radiograph displaying small bowel obstruction, as evidenced
by multiple air filled dilated loops of centrally located bowel with valvulae conniventes. Differential
air-fluid levels can also be another sign of mechanical bowel obstruction. Upper right: coronal CT
confirmed small bowel obstruction. Bottom right: axial CT displays zone of transition (arrow).
Subsequently diagnosed with an ileal stricture due to Crohn’s disease. Images via Dr. David Murphy,
Approach to PFA Interpretation via http://www.svuhradiology.ie/tutorials/

Large bowel obstruction with perforation. 72 year old man with sudden onset severe abdominal pain.
Left: Large bowel obstruction, as evidenced by multiple air filled dilated loops of peripherally located
bowel with haustra – note a generalised central lucency, with intraabdominal air underneath the liver
and outlining the falciform ligament. Right: close up of right upper quadrant in same image – Rigler’s
sign (arrows), which is very sensitive for detecting perforated bowel and describes lucency on either
side of the bowel wall, thus clearly delineating it. This patient was subsequently diagnosed with a
perforated colonic tumour. Images via Dr. David Murphy, Approach to PFA Interpretation via
http://www.svuhradiology.ie/tutorials/
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 Sigmoid volvulus. 83 year old woman with acute abdominal pain and distension. Left: abdominal radiograph
displaying a dilated loop of large bowel, centred in the pelvis with an inverted “U” configuration and its axis
pointed toward the right upper quadrant – this is the coffee bean sign, typical in sigmoid volvulus; dilated loops
of large bowel also in the left upper quadrant; incidental note of an EVAR stent. Right: coronal CT displays the
whirlpool sign, which is a swirling appearance of the mesentery, around which the sigmoid colon twisted
(arrows). Images via Dr. David Murphy, Approach to PFA Interpretation via
http://www.svuhradiology.ie/tutorials/

Ischaemic bowel. 70 year old woman with severe acute abdominal pain. Pneumatosis, gas bubbles in the
bowel wall (arrows) is a sign of ischaemic bowel. Also note generalised lucency with positive Rigler’s sign in
right upper quadrant and subdiaphragmatic free air, consistent with perforation.
Images via Dr. David Murphy, Approach to PFA Interpretation via http://www.svuhradiology.ie/tutorials/
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Musculoskeletal Radiographs

In MSK radiography, especially trauma, at least 2 views are required, usually perpendicular to each other as (e.g. AP
and lateral) as fractures are often only seen in only one projection.

The importance of 2 views in MSK radiology, in this case a right radial head fracture. Left: lateral view of the right
elbow, which does not demonstrate a fracture despite the presence of a right elbow effusion, which causes elevation
of the anterior and posterior fat pads (radio-lucent area in the juxtacortical soft tissue just anterior and posterior to
the supracondylar right humerus). In practice, an elbow effusion without direct evidence of a fracture is presumed to
be due to a fracture of the radial head. Right: AP view of the right elbow demonstrates the mildly displaced intra-
articular fracture of the head of the left radius (arrow). Images via Dr. Rory O’Donohoe, Approach to fracture
interpretation for medical students via http://www.svuhradiology.ie/tutorials/

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Fracture Interpretation

1. Fracture Detection
• Separated bone fragments result in a radio-lucent (dark) line.
• Overlapping bone fragments result in a radio-opaque (bright) line.

Left: transverse fracture of the waist of the right scaphoid with radio-lucent line due to separated bone
fragments. Right: displaced fracture of the diaphysis of the left radius, with a radio-opaque line due to
overlapping bone fragments. Images via Dr. Rory O’Donohoe, Approach to fracture interpretation for medical
students via http://www.svuhradiology.ie/tutorials/

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2. Pitfalls
• Accessory ossicles (normal variant).
• Physis (growth plates).
• Clinical correlation with site of tenderness.

Top two images: normal left shoulder radiograph in a 15 year old with posttraumatic left shoulder pain. The
physis (growth plate) of the left humeral head could be confused for a fracture. There are two radio-lucent
lines through the left proximal humerus as the growth plate runs obliquely through the plane of the
radiograph. Another clue is the age of the patient and the presence of growth plates in the left acromion and
coracoid process.
Bottom two images: Weber B fracture and an os subfibulare (normal variant accessory ossiscle) in a 28 year
old male with a traumatic sports related injury. Bottom left: AP view of the left ankle. Bottom right: lateral
view of the left ankle. There is an oblique and intra-articular fracture through the distal left fibula at the level
of the syndesmosis, with overlying soft tissue swelling, consistent with a Weber B fracture. Inferiorly to the
left lateral malleolus, there is a bone fragment that is well corticated (clearly defined cortex all the way
around it), consistent with a an accessory ossicle. Images via Dr. Rory O’Donohoe, Approach to fracture
interpretation for medical students via http://www.svuhradiology.ie/tutorials/

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3. Anatomical Location
• Long bones, e.g.: femoral epiphysis, metaphysis, diaphysis.
• Short bones, e.g.: proximal / mid / distal phalanx.
• Intra-articular (involves articular surface and associated with poorer prognosis and secondary
osteoarthritis).
§ Alignment (may determine management):
• Dislocated (articular surfaces not in contact).
• Subluxed (articular surfaces partially in contact).

Right sided Maisonneuve fracture, which is a combination fracture involving an unstable ankle fracture and
proximal fibula, usually due to pronation-external rotation injuries. The unstable right ankle fracture involves
the talus with subluxation (articular surfaces partially in contact).
Image via Dr. Rory O’Donohoe, Approach to fracture interpretation for medical students via
http://www.svuhradiology.ie/tutorials/

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4. Fracture Description
• Comminuted = more than two fracture fragments.
§ May determine surgical / conservative (cast) management.
• Transverse / oblique / spiral.
• Alignment (may determine management):
§ Displacement (of the distal fragment).
§ Angulation (of the distal fragment).
• Lastly, these are more clinical descriptions and are often difficult to determine on a radiograph:
§ Simple = only involve bone.
§ Compound = break skin surface (prone to infection).

Top: completely displaced comminuted (three fragments) fracture at the junction of the middle and lateral
thirds of the right clavicle in a 27 year old with a sports-related right shoulder injury. Bottom: Colles fracture
in a 70 year old female who fell on an outstretched hand. Dorsally displaced and angulated fracture of the
distal radius (dinner fork deformity). Images via Dr. Rory O’Donohoe, Approach to fracture interpretation for
medical students via http://www.svuhradiology.ie/tutorials/

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Cervical Spine Radiograph
• Cervical spine series in trauma: AP, lateral and open-mouth ‘peg’ view.
• Radiographs are very limited at displaying the C7-T1 vertebrae due to obscuring shoulder tissue at that
level. Swimmers view can help to an extent.
• Cervical spine injuries can be subtle on radiographs, so one should have a low threshold for ordering a CT if
a cervical vertebral injury is suspected and/or an MRI if a spinal cord injury is suspected.
• When assessing for fractures, look at the vertebral alignment, vertebral body height, cortical margins and
overlying paravertebral soft tissue.

High impact mechanism of impact (road traffic accident): book a CT.

Neurological deficit: book an MRI (usually after a CT in trauma cases).

Jefferson fracture in a young male who suffered a head injury in a road traffic accident. The AP and lateral views (not
shown) were normal in this case. Although Jefferson fractures rarely result in a spinal cord injury, Jefferson fractures
can result in instability and are often associated with other potentially unstable vertebral fractures or vertebral artery
injury (as in this case).
(a) Open-mouth view demonstrates that the lateral margins of the lateral masses of C1 (labelled ‘C1’) subtly extend
beyond the margins of the lateral masses of C2. There is asymmetric widening of the gap between the odontoid
process of C2 and the medial edges of the C1 lateral masses (dashed line).
(b) Coronal CT image displays the abnormal overhang of the C1 lateral masses.
(c) Axial CT image demonstrates the Jefferson fracture, as evidenced by three separate fracture (arrows) – two in the
anterior arch and one in the posterior arch of C1, while the lateral masses are displaced laterally. Also note that the
posterior arch fracture extends into the right lateral mass of C1 and has disrupted the right transverse foramen for
the vertebral artery (intact on the left). A CT angiography is required to assess for vertebral artery injury, which can
result in stroke or death.

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 C2 fracture in a 58 year old female who fell off a wall.
Left: Lateral cervical spine radiograph displays abnormal thickening of the prevertebral soft tissues anterior to the
upper cervical spine (orange arrows; the normal thickness of the prevertebral soft tissues from C1 to C4 < 50% of the
AP dimension of the adjacent vertebral body). The anterior margin of C2 does not align normally with the body of C3
below (white arrow), but the underlying fracture here is not seen on the radiograph.
Middle and right: The fracture is at the junctions of both pedicles and the vertebral body of C2, which is a form of a
‘hangman’s fracture’ (yellow arrow).

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Thoracic Spine Radiograph

74 year old female with thoracic back pain after a fall. Anterior wedge compression fracture of the T7
vertebral body, with approximately 50% loss of height and associated kyphosis. Comparison with prior
radiograph is essential in determining chronicity of the fracture. CT is required in assessing the complications
of acute vertebral fractures: involvement of posterior vertebral elements; stable or unstable fracture;
retropulsion into spinal canal. If there is significant or symptomatic (distal neurologic symptoms/signs)
retropulsion into the spinal canal, an urgent MRI is required to investigate for spinal cord compression.

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Arthritis

1. Osteoarthritis
• The cardinal features (LOSS) commonly occur at weight-bearing joints, usually at the hips, knees and 1st
carpometacarpal joints (can be mono- or oligo-articular):
L Loss of joint space.
O Osteophytes - periarticular.
S Subchondral sclerosis.
S Subchondral cyst formation.
• Usually involves the:
o 1st metacarpophalangeal (MCP) joint.
o Distal interphalangeal (DIP) joint – especially of the index finger.

Severe osteoarthritis of the right hip, as evidenced by joint space loss, marked sclerosis on both sides of the joint and
very large subchondral cysts – but there is no osteophytosis.

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2. Rheumatoid Arthritis (RA)
• Multisystem inflammatory disorder.
• Bilateral, symmetrical and polyarticular arthropathy, involving:
§ Joint space loss.
§ Periarticular loss of bone density.
§ Periarticular erosions.
• Hands - usually involves the:
§ Metacarpal-phalangeal (MCP) joints, with associated ulnar deviation (resulting in Z-thumb
deformity at the 1st MCP).
§ Proximal inter-phalangeal (PIP) joints. Advanced changes include:
• Boutonniere’s deformity: fixed flexion of the PIP joint with normal extension of the distal
inter-phalangeal (DIP) joint.
• Swan neck deformity: hyperextension of the PIP joint with fixed flexion of the DIP joint.
§ Carpal joints.
§ Sparing of the distal inter-phalangeal (DIP) joints.

Frontal radiograph of the right hand in a 67 year old female with rheumatoid arthritis. Note the destructive changes
at the wrist, MCP and PIP joints, while the DIP joints are normal. If the DIP joints are involved in a case that looks like
rheumatoid arthritis, think of psoriatic arthritis.

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3. Gout
• Monoarticular arthropathy involving joint or soft tissue deposition of monosodium urate crystals.
• Features:
§ Preponderance for the 1st metatarsophalangeal (MTP) joint – i.e., the big toe.
§ Juxta-articular erosions (as opposed to periarticular erosions in RA).
§ Gouty tophi seen as increased density in the overlying tissues of affected joints.

Left foot frontal radiograph in a 76 year old male with severe gout. Note the extensive destruction and erosions at all
of the MTP joints, with surrounding chronic gouty tophi, as evidenced by soft tissue swelling and calcification.

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Breast Imaging

Breast Cancer Screening

• Mammogram every 2 years for women aged between 50 – 69 years old.

Mammogram
• Radiographic x-ray image of the breast, which is compressed between the x-ray machine and flat x-ray
detection plate.
• Excellent detection of microcalcifications within breast tumours.
• For middle-aged and older women, in whom glandular tissue density is decreased.
o Difficult to interpret in females under 35 years old.
• Stereotactic biopsy, which is performed via mammographic guidance in two different planes for lesions that
are not visible on ultrasound.

Ultrasound Breast
• Usually for females under 35 years old, due to the increased density of glandular tissue in this age group.
• Can further characterise suspicious lesions seen with mammography, especially in distinguishing fluid-filled
cysts (usually benign) versus solid masses (which may require further investigation).
• Ultrasound-guided biopsy.

MRI Breast
• Staging: helps determine the extent of breast cancer.
• High false positive rate, so not primarily used as a screening tool (otherwise, higher rates of unnecessary
subsequent tests / biopsies).
o Can be used for breast cancer screening in some women with high risk of breast cancer, in
conjunction with mammography.

Sentinel Lymph Node

• Mapping for biopsy and surgery
• Radioactive coloured dye (usually blue) is injected (by the surgeon) into the area near the breast tumour and
then spreads to the regional lymph nodes. During mastectomy/lumpectomy, the surgeon can use a device to
detect radionucleotide uptake in the visually stained regional lymph nodes. The first node that displays
uptake is called the sentinel lymph node. The sentinel lymph node, and sometimes other regional lymph
nodes, can be surgically excised and sent for pathologic analysis.
• Positive sentinel lymph node biopsy suggests regional lymph node involvement and can aid decision
regarding axillary clearance.

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 Metastatic breast cancer in a patient who presented with a left breast lump.
(a) Mammogram displays an irregular mass (arrows) in the left breast, suspicious for a carcinoma. Subsequent
ultrasound guided biopsy confirmed this. The patient then underwent staging CT.
(b) Staging CT demonstrates the left breast mass (arrow).
(c) Enlarged left axillary lymph node (arrow).
(d) Multiple rounded nodules in both lungs, in keeping with metastases.

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Fluoroscopy

• Involves dynamic real-time moveable low dose x-ray tube units, almost always using iodinated contrast.
• Largely superseded by CT nowadays.

Common fluoroscopic studies include:

• Video swallow to investigate aspiration or unsafe swallow.
• Barium swallow (see below) for pharyngeal pouch, dysphagia, oesophageal reflux or a gastro-oesophageal
junctional neoplasm.
• Gastrografin swallow to investigate oesophageal perforation or post-operative anastomotic leak.
o Gastrografin is used as barium mediastinitis or peritonitis carries a high mortality (80%).
o Gastrografin is not used in video or barium swallow studies, as aspiration of Gastrografin can cause
acute pulmonary oedema and chemical pneumonitis.
• Small bowel follow through to investigate for inflammatory bowel disease.
• Cystogram / urethrogram to investigate for post-operative anastomotic leak.
• Fluoroscopic procedures include lumbar punctures, nerve root blocks, therapeutic joint injections.

Barium Swallow

Bird’s beak sign in oesophageal achalasia. Barium swallow in a 32-year-old female who presented with progressive
dysphagia. Note the dilated oesophagus tapers abruptly at its distal end at the level of the gastro-oesophageal
sphincter – this is the bird’s beak sign, a classic sign on barium swallow in achalasia (arrow). The differential for this
sign is malignancy, so endoscopic correlation is advised. A large proportion of patients with achalasia have a normal
barium swallow.

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Small Bowel Follow Through

Crohn’s disease on a small bowel follow through, as evidenced by severe stricturing of a long segment of the terminal
ileum (arrows), also known as the ‘string sign of Kantor’. Another typical sign seen here is the ‘creeping fat’ sign: the
affected bowel loop appears to be separated from the normal small bowel, which is a typical feature of longstanding
Crohn’s disease, due to a large amount of fat around the affected terminal ileum.

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Computed Tomography (CT)

• The major workhorse of the Radiology Department.

• A doughnut-shaped x-ray tube / detector configuration that rotates around the patient who is moved along
a gantry through the CT scanner.
• See above regarding contrast and general description of terms.

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Brain

Acute ischaemic stroke:

Immediate investigation of acute ischaemic stroke includes:

1. Non-contrast CT brain to exclude haemorrhage and assess stroke size / chronicity. Then…
2. CT angiogram intracranial (three phases with delayed imaging to assess collaterals with a view to potential
thrombectomy).
3. CT angiogram aortic arch and carotids.

‘Time is brain’: the ischaemic penumbra, around the infarcted area, will become infarcted if there is a delay in
treatment. Thus, the infarct will be larger and the morbidity / mortality significantly worse.

Stroke is a radiologic emergency case. Stroke cases are usually performed straight after the patient who is
currently in the CT scanner. Please bear in mind that a regular non-contrast CT brain may be performed in turn
and thus not for a few hours.

So, if your patient on the ward develops symptoms of an ischaemic stroke, it is advisable to urgently seek senior
help, quickly perform a focused clinical assessment to calculate NIHSS and inquire regarding contraindications to
thrombolysis or thrombectomy and book the above. Ask yourself whether the above test is required if there is a
contraindication. If there is a contraindication (e.g. outside the thrombectomy window), then consider booking an
urgent (rather than emergent) non-contrast CT brain.

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Acute Ischaemic Stroke

Top left: Acute left-sided stroke. Area of low attenuation with loss of grey-white matter differentiation and sulcal
effacement, which is due to cytotoxic oedema (yellow outline).
Top right: Subacute (> 24 hours) right MCA territory infarct in a different patient. Area of lower attenuation with
grey-white matter de-differentiation, including the lentiform nuclei (yellow outline). Mass effect from cytotoxic
oedema including midline shift and effacement of the sulci and right lateral ventricle.
Bottom two images: Dense MCA sign (arrow in left image) with corresponding occlusion of the left MCA on CT
angiogram (arrow in right image) in a different patient. This patient presented with a 2 hour history of right-sided
hemiplegia, NIHSS 12, ASPECTS 8 and received thrombolysis and mechanical thrombectomy.

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Haemorrhagic Transformation in Acute Stroke

Top two images: Left-sided occipital infarct with subsequent haemorrhagic transformation (top right image).
Bottom left: Chronic right MCA infarct in a different patient. Area of very low attenuation with associated cerebral
volume loss and prominence of the local ventricles and sulci.
Bottom right: Haemorrhagic stroke in a different patient with hypertension with a large area of attenuation centred
on the left basal ganglia and a rim of low attenuation and grey-white matter de-differentiation. There is resultant
mass effect with effaced sulci and left lateral ventricle. There is also a small haemorrhage in the right basal ganglia
(arrow).

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Intracranial Haemorrhage
• Acute haemorrhage: bright or hyperattenuating on CT.
• Oedema: dark or hypoattenuating on CT.
o Cytotoxic oedema (e.g. stroke): involves grey and white matter, so you get grey and white matter
de-differentiation (cannot distinguish between cortical grey matter, which is usually isoattenuating,
and white matter, which is relatively hypoattenuating).
o Vasogenic oedema suggests more sinister underlying pathology (e.g. around tumour / abscess /
haemorrhage): only involves white matter, so no grey-white matter de-differentiation.
• Mass effect (look for asymmetry): effacement of sulci, ventricles, midline shift and herniation (subfalcine,
uncal or tonsillar herniation).
• Hydrocephalus (especially in subarachnoid haemorrhage or those with intraventricular extension).
• Traumatic associations: skull fracture, pneumocephaly (intracranial air, often if fracture through a nasal
sinus).
• MRI brain can help identify microhaemorrhage (which can occur after an acute ischaemic stroke) or an
underlying neoplasm not seen on CT.
• Intracranial haemorrhage can be subdivided into:
o Extradural haemorrhage (EDH).
o Subdural haemorrhage (SDH).
o Subarachnoid haemorrhage (SAH).
o Intracerebral haemorrhage (ICH).

Extradural Haemorrhage (EDH, also known as epidural haemorrhage)

• 90% are associated with an overlying skull fracture and one particular site of weakness is the pterion, with
injury to the middle meningeal artery.
• Biconvex ‘lens’ shape that does not cross skull suture lines, as the dural attachments at skull sutures limit
extension of the blood that lies between the inner table of the skull and the dura.
• As the haematoma expands, mass effect with midline shift and herniation occurs.

Extradural haematoma in patient who had a traumatic head injury with loss of consciousness and a lucid
interval. There is mass effect with effacement of right cerebral sulci, right lateral ventricle and midline shift.
There is also a scalp haematoma and skull fracture (seen on bone windows).

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Subdural Haemorrhage (SDH)
• Crescentic ‘moon’ shape (not limited by skull sutures) on CT.
• Classically in patients who have generalised cerebral atrophy (e.g. elderly / alcoholics), who have a higher
risk of shearing of the bridging veins in the subdural space.
o As the underlying brain is often atrophic, the haematoma needs to be large to result in midline shift.
• Often (relatively) asymptomatic and patients can present with acute, subacute or chronic SDH. There can
also be acute on chronic SDH.
o Acute (< 1 week): hyperattenuating, bright relative to adjacent grey matter.
o Subacute (1 week – 1 month): isoattenuating, similar to normal blood or adjacent grey matter
(difficult to see).
o Chronic (> 1 month: hypoattenuating, dark relative to adjacent grey matter and similar to
cerebrospinal fluid; indolent clinical presentation.

Left: acute subdural haemorrhage. Crescent shaped haematoma overlying the right cerebral hemisphere and
extending along the right tentorium (small arrow). Note the midline shift and effacement of the sulci of the right
cerebrum and right lateral ventricle.
Middle: subacute bilateral subdural haemorrhage can be difficult to detect as they are of similar attenuation to
adjacent grey matter.
Right: chronic bilateral subdural haemorrhage are hypoattenuating relative to adjacent grey matter.

Subarachnoid haemorrhage (SAH):

• All suspected cases of SAH with a normal non-contrast CT brain should undergo lumbar puncture looking for
xanthochromia (unless contraindicated).
• Angiogram (CT first, then MRI or conventional angiogram in IR) should be performed in the setting of an
atraumatic SAH in order to investigate for a treatable aneurysm.
o Neurointerventional radiologic techniques include insertion of coils or gelfoam into the aneurysm.
o Neurosurgical clipping of an aneurysm is an alternative.

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Subarachnoid Haemorrhage (SAH)
• Can be due to trauma or intracranial aneurysmal rupture.
o Traumatic
§ Subtle, linear and small volume haemorrhage in the sulci (between the gyri).
o Atraumatic
§ Usually due to a ruptured aneurysm (older patients) or arteriovenous malformation
(younger patients): thunderclap headache.
§ Star sign: 5-pointed star shaped linear area of hyperattenuation as blood accumulates at the
circle of Willis with extension along the both anterior, middle and posterior cerebral arteries.

Top left: traumatic acute subarachnoid haemorrhage, as evidenced by the linear hyperattenuation along several sulci
(arrows). There is also a subdural haemorrhage along the right tentorium between the right occipital lobe and
cerebellum (small arrow) and a scalp haematoma (star).
Top right (different patient)t: classic 5-pointed star appearance of an acute SAH. There is also acute hydrocephalus
(as evidenced by dilatation of the temporal horns of the lateral ventricles and of the 4th ventricle).
Bottom left: circle of Willis.
Bottom right: 3-dimensional reconstruction of a CT intracranial angiogram displaying an aneurysm of the anterior
communicating artery (large arrow).

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Intracerebral Haemorrhage (ICH)
• Following head trauma, the common sites for ICH include the inferior aspects of the frontal lobes and the
anterior aspects of the temporal lobes.
• Contre-coup contusion injuries occur at the opposite side of the brain to the traumatic site.
• Large ICH can rupture and extend into the subarachnoid space or ventricles.

Top: multiple ICH contusions of various sizes in the inferior aspects of both frontal lobes.
Bottom: superiorly, the patient also had a fracture of the frontal bones with depression of the skull fragment and
pneumocephaly (air in the cranial vault).

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Brain Abscess

Pre- and post-contrast CT (left and right respectively) in a patient with an area of extensive vasogenic oedema
centred around a ring-enhancing mass in the left frontal lobe with mass effect and midline shift. This patient was an
intravenous drug abuser and this turned out to be an abscess.

CT Brain with Contrast: Brain Metastases

• The most common sources of brain metastases in adults: breast, lung, renal cell cancers, melanoma.

Bilateral cerebral metastases in a patient with widespread metastatic breast cancer. Peripherally located enhancing
intracranial lesions are typical of brain metastases, which tend to develop at the junction between grey and white
matter (where there is a rich blood supply). Most brain metastases are found in the cerebral hemispheres, while10-
15% occur in the cerebellum (brainstem metastases are rare).
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Thorax

CT pulmonary angiogram: pulmonary embolus (PE)

Investigation of suspected pulmonary embolus:

• Other differential diagnoses can be investigated quickly:

o Palpate chest wall: costochondritis, fibromyalgia, rib fracture.
o Chest radiograph: pneumonia, pneumothorax, rib fracture.
o Acute coronary syndrome: electrocardiogram, serum troponin.
• Well’s score.
o 3 points: clinical signs & symptoms of PE; PE is the #1 diagnosis or equally likely.
o 1 – 1.5 points: tachycardia > 100 bpm; immobilisation > 3 days or prior surgery < 4 weeks; prior
PE / DVT; haemoptysis; malignancy < last 6 months or palliative.
• Serum D-dimer.
o Used for its good negative predictive value – if it is normal, then pulmonary embolus is unlikely.
o Useful if Well’s score = 1 – 2.
o Not indicated if Well’s score = 0, consider investigating other differentials
o Not useful if Well’s score ³ 3, just book a CT pulmonary angiogram.
o Non-specific: will be raised if inflammatory markers are raised or in active cancer.
• CT pulmonary angiogram is indicated if a Well’s score requires a D-dimer that turns out positive and another
differential is not obvious (e.g. pneumonia on chest radiograph).
• Consider right heart strain as a complication in a large / central PE (ECG changes, troponin leak,
haemodynamic instability): does the patient require an emergency CTPA with a view to catheter angiography
and intravascular thrombolysis in the interventional radiology department?
o Right heart strain features on CTPA include: right ventricular enlargement, flattening/bowing of
the interventricular septum, reflux of contrast into the hepatic veins.

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 Pulmonary embolism (PE) with Hampton’s Hump. A 31-year-old male presented with acute onset left-sided chest
pain. Chest radiograph revealed a wedge-shaped area of opacification in the periphery of the left lung base (blue
arrow, yellow dashed lines). CT pulmonary angiogram (CT PA) demonstrates multiple filling defects in the pulmonary
arteries bilaterally (yellow arrows), including a large thrombus in the left lower lobe pulmonary artery (single yellow
arrow) and a wedge-shaped area of opacification, consistent with a pulmonary infarct (dashed yellow line), which
correlates with the finding on the chest radiograph (Hampton’s Hump). In most cases, a PE will not cause an infarct
due to collateral blood supply. However, it is important to consider that large, central or bilateral PE can cause right
heart strain (right ventricle swells, left ventricle compresses to due bowing of the intraventricular septum), which can
cause ECG changes, troponin I leak, hypotension and haemodynamic instability.

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CT Aortogram: Aortic Dissection

Thoracic aortic dissection with haemopericardium. 60-year-old male presented with severe acute onset chest pain on
a background of hypertension. Chest radiograph demonstrated cardiomegaly only. CT angiogram of the aorta
demonstrated Stanford type A aortic dissection, involving the ascending aorta, the aorta and the descending thoracic
aorta. The dissection flap (orange arrows) separates the true lumen from the false lumen. The dissected aorta
ruptured into the pericardium, causing haemopericardium (haemorrhagic pericardial effusion, yellow arrows), which
explains the cardiomegaly seen on the chest radiograph. Stanford type A thoracic aortic dissections involve the
ascending aorta, are more common and are associated with mortality, unless treated surgically. Stanford type B
dissections involve the descending thoracic aorta (distal to the left subclavian artery) and are typically treated
medically with antihypertensive agents. CT angiogram can also help in demonstrating complications of aortic
dissection: haemopericardium; occlusion of the coronary arteries or branches of the aorta.

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Abdomen

Acute Appendicitis
• In right iliac fossa pain, ultrasound is a good first line imaging modality (no ionising radiation) if acute
uncomplicated appendicitis is suspected.
• This is especially true for females as the pelvis can be assessed.
• Ultrasound has a high sensitivity in the detection of acute appendicitis in slim patients, but this decreases in
obese patients.
• Complications of appendicitis can be visualised on CT: perforation, abscess formation, portal vein
thrombosis, liver abscess formation.

Acute appendicitis.
Top images: Longitudinal (left image) and transverse (central and right images) views show a blind-ending tubular
structure in the right iliac fossa, consistent with an appendix, which is dilated. Subsequent laparoscopic
appendicectomy confirmed acute appendicitis.

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 Bottom image: Coronal CT image displays the appendix (arrows), which is dilated and there is local haziness (‘fat
stranding’), indicating an inflammation.

Appendix abscess. There is a large fluid-filled abscess (arrows) in the right iliac fossa, caused by perforated
appendicitis. The abscess was subsequently drained percutaneously in Interventional Radiology.

Acute Diverticulitis on CT Abdomen and Pelvis

Acute diverticulitis in a 60-year-old female who presented with fever and left iliac fossa pain. CT abdomen and pelvis
was performed.
Left: axial image displaying oedematous mural thickening of the descending colon (dashed yellow lines) with
surrounding fat stranding suggestive of inflammation. Focal colonic wall thickening is most often due to diverticulitis,
infectious colitis, ischaemic colitis, inflammatory bowel disease or colorectal cancer.
Right: multiple gas filled diverticulae with one fluid-filled diverticulum (yellow arrow), around which the inflammatory
fat stranding is centred, in keeping with acute diverticulitis.
Complications seen on CT include: perforation, abscess (which can be drained via Interventional Radiology),
strictures, fistula (best seen on MRI, but CT can demonstrate secondary findings, e.g. air or oral contrast in the
bladder lumen due to a colovesical fistula). .
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CT Renal Stone / Kidneys Ureters Bladder (KUB): Urinary Tract Calculus

Ureteric calculus on CT KUB, which is a non-contrast study, performed at a lower radiation dose than a CT abdomen
and pelvis. There is left-sided hydronephrosis (yellow arrow, left image), due to a calculus in the proximal left ureter
(white arrow, right image).

Small Bowel Obstruction on CT

Small bowel obstruction due to a paraumbilical hernia.

CT demonstrates moderately dilated small bowel (valvulae conniventes) in the left of the abdomen. There is a focal
zone of transition to normal calibre small bowel at the small bowel containing paraumbilical hernia in the midline
(arrow). The cause is most likely due to the hernia. However, adhesions are not visible on CT and when no other
reason for obstruction is identified in a patient with known prior abdominal surgery, adhesions are usually the cause.

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Large Bowel Obstruction on CT

Large bowel obstruction due to colorectal cancer.

Left: Abdominal radiograph shows dilated large bowel in the left abdomen, measuring up to 7.5 cm (normally £ 6
cm). There is no small bowel dilatation. There is a soft tissue density that narrows the descending colonic lumen
(arrows).
Right: Coronal view of a CT abdomen and pelvis, which confirms the presence of a circumferential lesion in the
descending colon (arrows), suspicious for colon cancer. Also note the multiple hypoattenuating liver lesions.
Subsequent histologic sampling confirmed metastatic colorectal adenocarcinoma.

Perforated Duodenal Ulcer

Perforated duodenal ulcer in a 43 year old male, who presented with acute abdominal pain. Chest radiograph (not
shown) displayed free air under the diaphragm.
Left: Axial CT shows pneumoperitoneum anterior to the liver (yellow arrow), with some free fluid (white arrow).
Middle and magnified right: Coronal image demonstrates a defect (arrow) in the wall of the duodenum (D).
Subsequent surgery confirms a perforated peptic ulcer.

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CT Pancreas

Acute pancreatitis complicated by pancreatic necrosis and pseudocyst formation.

Left: CT pancreas in a patient with a rising inflammatory markers 7 days after a diagnosis of acute gallstone
pancreatitis. There is pancreatic necrosis, as evidenced by a large and irregularly shaped area of hypoattenuation
(yellow arrows) between the normal attenuating pancreatic head (H) and lateral aspect of the pancreatic body (B).
Right: This patient represents 6 weeks later with upper abdominal pain and nausea. This follow-up CT displays a
thick-walled pseudocyst (orange arrows) extending from the site of previous necrosis into the lesser sac. This
pseudocyst causes mass effect on the stomach (*), which is compressed by the anterior aspect of the pseudocyst.
Calcified gallstones are also noted in the gallbladder.

Ruptured Abdominal Aortic Aneurysm (AAA) on CT Aortogram

Ruptured AAA. CT aortogram (note the contrast in the aorta) displays a large abdominal aortic aneurysm. There is a
defect in the wall of the aneurysm (yellow arrow) and contrast is leaking out of the lumen. There is also extensive
abnormal high attenuation in both sides of the retroperitoneum (red arrows on both images), representing
haemorrhage.

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Ischaemic Colitis on CT Mesenteric Angiogram

• Raised serum lactate that does not decrease despite fluid resuscitation is an indicator of ischaemia.
• CT mesenteric angiograms display contrast in the mesenteric arteries to identify potential clots in mesenteric
ischaemia or active extravasation in the setting of an active gastrointestinal bleed.
• Ischaemic colitis is more common in patients over 60 years old and atherosclerosis.
• Precipitating events include hypoperfusion (due to heart failure or hypotension as a result of sepsis /
hypovolaemia) or arterial emboli (atrial fibrillation). Most cases are transient, reversible and involve the left
colon (inferior mesenteric arterial territory from the splenic flexure to the upper rectum).
• Severe cases can display pneumatosis, portal venous gas or occluded mesenteric arteries.

Ischaemic colitis in a 75-year-old male who presented with acute onset abdominal pain, diarrhoea and rectal
bleeding and a rising serum lactate.
Left: Axial slice contrast enhanced CT demonstrates normally enhancing wall of the ascending colon (white arrows),
but there is mural hypo-enhancement of the descending colon (yellow arrow). There is atherosclerotic disease with
calcified iliac arteries (red arrows).
Middle: Adjacent to the hypoenhancing descending colon, there is local fat stranding suggestive of inflammation
(orange arrows).
Right: coronal slice of illustrates the mural enhancement differences between the ascending colon (AC), splenic
flexure (SF), and the descending colon (DC).

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Nuclear Medical Imaging
• The patient becomes the radiation source (which is a radiation protection issue for staff and the general
public).
• Radiopharmaceuticals are injected, inhaled or ingested, taken up by the target organs and emit gamma-rays,
which are detected by gamma cameras, displaying anatomical and physiologic information.
o The most common radiopharmaceutical is technetium 99m (Tc99m), which can be tagged to a
pharmaceutical that is taken up by the target organ / pathology.
• Studies can be planar, 3-dimensional, static or dynamic (radionucleotide metabolism over time).
• Common examples of radionucleotide imaging include (see table below):
o Planar imaging, which can be static or dynamic (physiologic information over time).
§ Gamma camera is static.
§ Scintigraphy: bone / thyroid / cardiac / renal / sentinel node / dopamine.
o Single photon emission computed tomography (SPECT), e.g. Sestamibi scan.
§ Gamma camera rotates around the patient.
§ Can be combined with CT for hybrid SPECT-CT.
o Positron emission tomography (PET).
§ Most common PET radiopharmaceutical is fluorine-18 tagged to fluoro-deoxy-glucose (18F-
FDG), which is taken up by cells with glucose metabolism: brain, myocardium, brown fat,
skeletal muscle, cancer, inflammation.

Anatomical Location Imaging Modality Indication

Global PET Neoplasm
SPECT
WBC (white blood cell) scan PUO (pyrexia of unknown origin),
osteomyelitis
Bones Bone scan Neoplasm, fracture, infection,
arthritis
Brain PET Alzheimer’s disease
SPECT DAT (dopamine active transporter) scan Parkinson’s disease
Thyroid Thyroid scintigraphy Hyper- / hypo-thyroidism
Thyroid cancer
Parathyroid Sestamibi scan Parathyroid adenoma
Heart Myocardial perfusion scan Coronary artery disease, cardiac
function
Lungs V/Q (ventilation / perfusion) SPECT scan Pulmonary embolus
Stomach Gastric emptying scan Delayed gastric emptying
Hepatobiliary HIDA (hepatobiliary iminodiacetic acid) scan Gallbladder function
Biliary obstruction / atresia / leak /
fistula, cholecystitis, liver transplant
work-up
Abdominal RBC (red blood cell) scan Occult GI bleed
Renal Renal scintigraphy Renal function, renal transplant,
urinary reflux
Neuroendocrine Octreotide (somatostatin receptor) Neuroendocrine tumour (e.g.:
scintigraphy neuroblastoma, medullary thyroid
MIBG (iodine-123 meta-iodobenzylguanidine) carcinoma, small cell and carcinoid
scan lung tumour, phaeochromocytoma,
Gallium PET paraganglioma, pancreatic islet cell
tumour)
Lymphatics Lymphoscintigraphy Lymphoedema

Table of common nuclear medical imaging modalities, by Dr. Kevin Quinlan.

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Below are some examples of common nuclear imaging modalities…
Static Planar Imaging: Tc99m Bone Scan

Bone scan in patient with bone metastases due to metastatic breast cancer.
Left: sagittal view of a CT (bone windows shown) displays multiple sclerotic lesions in the vertebrae, sacrum and
pubic bone.
Right: Corresponding increased uptake on the Tc99m bone scan.

Dynamic Planar Imaging: Tc-99m Sestamibi Parathyroid Scan

Patient with symptomatic primary hyperparathyroidism due to a left lower parathyroid adenoma.
Left: Tc-99m Sestamibi scan displays increased uptake (all four tiles) with delayed washout (fourth tile, taken 2 hours
after radionucleotide administration), consistent with a left inferior parathyroid adenoma. The patient is sent for
ultrasound for anatomical localisation of this lesion in advance of surgical resection.
Right: Targeted ultrasound displays the parathyroid adenoma, which is the well-defined hypoechoic (dark) lesion just
anterior (i.e. above on this page) to the ‘pt’ label, which highlights the parathyroid gland. The left internal jugular
vein (l IJV) and left common carotid artery (CCA) are labelled and skin overlying the lesion is marked to aid
subsequent surgical resection.
Images via Dr. Stephen Skehan, Cases, www.nuclearmedicine.ie/Cases

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3-Dimensional Imaging: PET/CT (PET = positron emission tomography)

FDG-PET/CT in a patient with lung cancer.

Left: Avid tracer uptake in the left upper zone, with normal uptake in the heart, kidneys and bladder.
Right: Fused PET/CT localises the area of increased uptake to the left upper lobe. No abnormal uptake elsewhere
indicates that there is no metastatic disease.
Images via Dr. Stephen Skehan, Cases, www.nuclearmedicine.ie/Cases

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Interventional Radiology (IR)

• Burgeoning field in recent years.

• Real-time imaging for image-guided procedures by radiologists.
• Usually involves ultrasound-guided needle access to a superficial structure (vessel), followed by a guidewire
which is advanced under low dose fluoroscopic guidance to the target area. The needle is removed, a
catheter is advanced under fluoroscopic guidance to the target area and the guidewire is removed.
• Machines in IR can also acquire radiographs, digital subtraction angiograms and CT images.
• Most procedures are minimally invasive and performed with local anaesthetic, sometimes sedation or even
general anaesthetic, depending on the procedure.

Vascular IR
• Endovascular aneurysm repair (EVAR)
• Peripheral arterial angioplasty and stenting
• Thrombectomy and thrombolysis for acute limb ischaemia
• Venous thrombolysis
• IVC filter insertion
• Portacath insertion
• Peripherally inserted central catheter (PICC)
• Embolization for haemoptysis, GI haemorrhage, and haemorrhage from hepatic, splenic, renal
and pelvic trauma
• Transjugular Intrahepatic Portosystemic Shunt (TIPS)
• Uterine fibroid embolization

Non-Vascular IR
• Abscess drainage
• Percutaneous gastrostomy
• Percutaneous biliary drainage and biliary stent insertion
• Percutaneous nephrostomy
• Ureteric stent insertion
• Image-guided biopsy

Interventional Radiological Oncology

• Transcatheter arterial chemoembolization (TACE) for HCC
• Embolization of hypervascular metastases (e.g. RCC)
• Radiofrequency ablation (RFA) for HCC, liver metastases, RCC, lung cancer and lung metastases

Musculoskeletal Intervention
• Bone biopsy (spine and extremities)
• Transforaminal nerve root block
• Percutaneous vertebroplasty

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Peripherally Inserted Central Venous Catheter (PICC)

Peripherally inserted central catheter (PICC) in a patient who requires 2 weeks of IV antibiotics in a patient an acute
exacerbation of cystic fibrosis. PICCs can be used for £ 6 weeks in patients that require a prolonged course of IV
antibiotics and/or total parenteral nutrition (TPN). The PICC is inserted over a guidewire through an upper limb vein,
commonly the basilic or brachial vein, which is punctured with an ultrasound-guided needle. The catheter is
appropriately sized and advanced under fluoroscopic guidance to be located in the distal SVC or right atrium (arrow).

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Non-Tunnelled Central Venous Catheter: Vascath

Dialysis catheter: Vascath, which is used for short-term (£ 4 weeks) haemodialysis. Under combined ultrasound and
fluoroscopic guidance, they are inserted into the internal jugular vein.
Left: Vascath, which is a triple lumen central venous catheter. The two larger lumens (blue and red) are for inflow and
outflow dialysis exchange. The third lumen is for IV therapy.
Right: Chest radiograph showing a right-sided Vascath.

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Tunnelled Central Venous Catheter: Hickman Catheter

Hickman catheters are for long term use, usually chemotherapy. A tunnel in the anterior chest wall is created,
through which the catheter is passed, then advanced into the internal jugular vein. The characteristic feature of a
tunnelled central venous catheter is the cuff (arrow in images on left and right), which promotes tissue ingrowth,
thereby limiting the risk of line dislodgement and infection.

408
Tunnelled Central Venous Catheter: Portacath

Portacaths can be left in situ indefinitely and are typically used for long-term chemotherapy or in poorly controlled
cystic fibrosis patients who require frequent long-term IV antibiotic regimens.
Left: After ultrasound-guided access to the internal jugular vein, a guide wire is advanced via SVC to the right atrium.
A tunnel is created in the chest wall, through which the catheter is threaded and then advanced over the guidewire to
the right atrium.
Right: The port which is positioned subcutaneously in the chest wall. Note the radio-opaque letters ‘CT’ on the port
which indicate that the device is compatible with high-pressure pump-driven injections of contrast, typically used in
CT. If a port has flipped, then an aspirate cannot be obtained and a chest radiograph will be performed, displaying
the letters ‘CT’ in a Portacath as backwards, i.e. ‘TƆ’.

409
Ascitic Drain Insertion

Ultrasound-guided ascitic drain insertion in a female with alcohol-related cirrhosis presented with recurrent large
volume ascites and resultant respiratory compromise. The drainage catheter is being advanced deep to the
abdominal wall and into the simple ascitic fluid which appears anechoic (black) on ultrasound (arrow). The
hyperechoic structures below are bowel, which contain gas that appears as a bright reflective on ultrasound.

Liver Biopsy

Ultrasound-guided liver biopsy in a patient with ocular melanoma with a nodule in the right lobe of the liver
suspicious for metastasis, that was first seen on staging CT (not displayed).
Left: Fat-saturated T1 weighted sequence of a contrast-enhanced MRI liver with Primovist shows two probable
metastases in the right lobe of the liver. Primovist is excreted by the liver, which thus enhances - but metastases do
not enhance and appear as hypointense nodules (single white arrows).
Centre: Targeted ultrasound-guided biopsy with the hyperechoic needle (two white arrows) in the largest
hyperechoic lesion in the right lobe of the liver.
Right: Histological samples in a pot of formaldehyde appear black due to melanin. Histological diagnosis of revealed
metastatic malignant melanoma.

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CT-Guided Lung Biopsy

CT-guided lung biopsy in a 73 year old male smoker.

Left: Chest radiograph displays hyperinflated lungs with a large irregularly shaped mass in the left upper zone.
Subsequent CT thorax showed that this mass was suspicious for a primary lung neoplasm but not amenable for
endobronchial biopsy.
Right: CT-guided biopsy needle at the edge of this left upper lobe mass. Histological analysis revealed a primary
squamous cell carcinoma of the lung. CT-guided lung biopsy is a relatively painless procedure that can be performed
with sedation but carries a 15-20% risk of pneumothorax, most of which are small and asymptomatic, but some
require chest drain insertion. Thus, patients are closely monitored and chest radiographs are performed 1 and 3 hours
post lung biopsy.

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Percutaneous Cholecystostomy Tube Insertion

Cholecystostomy tube insertion in a 60 year old female with a several-day history of abdominal pain and fever. She
then presents with an acute abdomen and peritonism on exam, so a CT is performed (rather than an ultrasound, as is
usually the case in this diagnosis).
a) Axial view of a CT demonstrates gallbladder mural thickening and small volume pericholecystic free fluid,
indicating acute cholecystitis.
b) Coronal view of this CT demonstrates a defect in the inferomedial aspect of the gallbladder wall, due to
perforation.
c) Subsequent percutaneous cholecystostomy was performed in the IR suite, which decompresses and drains the
perforated gallbladder until it the patient is suitable for cholecystectomy, which is not safe in an acutely perforated
gallbladder. This procedure is also an option in patients who are unfit for cholecystectomy. Ultrasound guided needle
insertion into the gallbladder provides access for fluoroscopic insertion of a guidewire and pigtail catheter. Contrast is
injected and seen in the gallbladder (GB).

Radiologically-Inserted Gastrostomy (RIG)

Radiologically-inserted gastrostomy (RIG) in a patient with squamous cell carcinoma of the larynx.
a) Firstly, a nasogastric tube is inserted (arrow). An artery clip has been placed on the patient’s epigastrium to mark
an appropriate skin puncture site.
b) The stomach is distended with gas, via the nasogastric tube, so that the stomach wall abuts the abdominal wall. A
needle is then inserted (arrow). Fluoroscopic images demonstrate injection of contrast into the gastric lumen, which
transmits to the gastric fundus (top right of this image), thus confirming satisfactory needle position.
c) A guidewire passes through the needle, followed by the gastrostomy tube, which is held in place in the gastric
lumen by inflating a small balloon at its tip.

412
Percutaneous Nephrostomy

Percutaneous nephrostomy in a patient with renal failure due to obstruction of both ureters in the setting of pelvic
recurrence of inoperable colorectal cancer.
Top left: Coronal view of CT abdomen and pelvis shows severe bilateral hydronephrosis with dilated ureters (arrows).
Ultrasound-guided needle insertion provided access into one of the dilated calyces in the left kidney (not shown).
Top right: Fluoroscopic images show injection of iodinated contrast that confirms the needle was in the left renal
collecting system.
Bottom left: Subsequently, the dilated left renal pelvis was catheterised by a plastic pigtail catheter.
Bottom right: A right-sided nephrostomy was then inserted and urine drained from both catheters into drainage
bags. This patient later returned for ureteric stent insertion, accessed via the existing nephrostomy catheters, which
were removed 24 hours later.

413
IR Lower Limb Angioplasty

Popliteal angioplasty in a patient with severe atherosclerosis of the right popliteal artery, which was displayed with
CT angiogram of the lower limbs (not shown). Conventional angiography and angioplasty was performed in the IR
suite.
a) Catheterisation and contrast injection of the femoral artery confirmed the stenosis burden (yellow arrow).
b) A guide wire was advanced through the stenosed segment, and an angioplasty balloon inflated (white arrow).
c) A metal stent was then inserted at this site (orange arrows).
d) Subsequent digital subtraction angiogram (DSA) demonstrates successful patency of the right popliteal artery.
DSA is an angiographic technique that subtracts bones from the image, increasing visualisation of contrast in the
arteries.

Bronchial Artery Embolization in the Setting of Life-Threatening Haemoptysis

Bronchial artery embolization in a 31 year old male with cystic fibrosis who presented with massive, life-threatening
haemoptysis. CT thoracic aortogram (not displayed) was performed which demonstrated active contrast
extravasation from one of the bronchial arteries (which usually arise directly from the aorta on the left and from one
of the intercostal arteries on the right). Left: Right common femoral artery access provided catheterisation of the
aortic arch (yellow arrows). Digital subtraction angiography displayed the anatomical origins of the bronchial
arteries, one of which was grossly dilated (orange arrow) and presumed to be the source of bleeding. Right:
Subsequent catheterisation, digital subtraction angiography and embolization of this tortuous artery resulted in
resolution of the patient’s haemoptysis.

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Embolization in the Setting of Life-Threatening Gastrointestinal Haemorrhage

• Learning Point: It is important not to give PO contrast when performing a CT mesenteric angiogram when
suspicious for an acute gastrointestinal bleed. PO contrast in the bowel lumen would obscure active contrast
extravasation into the bowel from the arterial supply.

Embolization of superior mesenteric artery haemorrhage in male patient who had a cardiac arrest a few days after a
small bowel resection.
a) CT mesenteric was performed after resuscitation, which demonstrates pneumoperitoneum, with gas locules (G)
adjacent to the resection site, indicating an anastomotic leak. There is a haematoma that contains IV contrast
(arrows), that was not present on the non-contrast acquisition and later demonstrated distal movement in the bowel
lumen due to peristalsis on the delayed acquisition (both not demonstrated). These findings are in keeping with active
contrast extravasation due to a defect in the distal superior mesenteric artery (SMA).
b) There are also some characteristic features of shock, including a slit-like IVC and hyperenhancing adrenal glands
(Ad).
c) In the IR suite, catheterisation of the SMA, via common femoral arterial access, was followed by injection of
contrast, which can be seen as a blush as it extravasates out of the distal SMA branches (red arrows).
d) Subsequent coil embolization of the SMA successfully led to cessation of the contrast extravasation and the
patient stabilised.
Images via Dr. Ronan Ryan, Case Studies, http://www.svuhradiology.ie/case-studies/

415
Inferior Vena Cava (IVC) Filter

IVC filter insertion in a patient with a lower limb DVT who has contra-indication to anti-coagulation due to a recent
haemorrhagic stroke. IVC filter insertion is performed via catheterisation of the IVC via internal jugular venous access.
Left: Contrast venogram then aids in the selection of an appropriate position for the filter, which should below the
renal veins (arrows), as well as ensuring that the IVC is not too big for a standard filter or that there is no significant
normal variant (e.g. a double IVC).
Right: Deployed IVC filter, which can be removed when no longer required.

416
Transarterial Chemoembolization (TACE)

Transarterial chemoembolization (TACE) in a patient with Hepatitis C related cirrhosis who developed a
hepatocellular carcinoma (HCC).
a) Arterial phase of a four-phase liver CT displays a hypervascular lesion (arrow). b) Portal venous phase of the four-
phase liver CT shows contrast 'washout’ as the HCC appears hypoattenuating (arrow) relative to the surrounding
liver. c) Using digital subtraction angiography (DSA) in the interventional radiology suite, TACE was performed via
selective catheterisation of the right hepatic artery, so that a microcatheter could be advanced into the branch
supplying the tumour. Due to angiogenesis, the HCC is demonstrated by a ‘blush’ of contrast on this DSA (arrows). d)
IR fluoroscopy equipment can also acquire CT images and can improve live demonstration of the hypervascular HCC
(arrows). e & f) The arterial branch supplying the tumour was then occluded with embolic material, coated with a
chemotherapeutic agent. Note the subsequent reduction in the arterial supply to the tumour.

Transjugular Intrahepatic Portosystemic Shunt (TIPS)

Transjugular intrahepatic portosystemic shunt (TIPS) in a patient with cirrhosis who had presented with life-
threatening haematemesis secondary to gastro-oesophageal varices. Cirrhosis causes portal venous hypertension and
incorrect retrograde flow in the portal venous system with shunting into the gastro-oesophageal veins, causing
varices. TIPS insertion is usually performed via wire-catheterization of one of the hepatic veins from above (via right
internal jugular venous access), while ultrasound is then used to catheterise the portal venous system via liver
parenchyma and to then connect the portal and hepatic venous systems from below with a metallic shunt/stent.
Left: The gastric balloon of a Sengstaken-Blakemore tube is seen in the left upper quadrant, which was inserted
temporarily to control the variceal haemorrhage while the patient awaited a TIPS. The portal vein catheter is seen
and the metallic shunt has been deployed (stent).
Right: Contrast is injected into the portal vein, which then correctly goes through the shunt and into the hepatic veins.

417
Ultrasound

• High frequency sound waves create images based on interaction at different surfaces.
• Advantages:
o Quick, relatively cheap.
o Good soft tissue contrast.
o Good for hepatobiliary, renal, gynaecological, obstetric, thyroid, testicular and rheumatological
pathology.
o Real-time needle visualisation when performing procedures.
o Doppler ultrasound to detect blood flow and velocity.
o Very safe, no ionising radiation.
• Disadvantages:
o Cannot see through air, calcium or bone.
o Can be operator dependent.

Below are some examples of commonly performed ultrasound examinations…

Biliary Ultrasound: Acute Cholecystitis

Acute cholecystitis in a patient who presented with severe right upper quadrant pain, Murphy’s sign positive and a
fever. There are numerous gallbladder calculi, which are hyperechoic with acoustic shadows behind them. There is
gallbladder mural thickening (yellow arrows). Sonographic Murphy’s sign was also positive. Pericholecystic fluid is
another sonographic feature in acute cholecystitis.

Usual Management Pathway of Suspected Choledocholithiasis:

1st) Ultrasound liver.

+/- 2nd) MRCP if no sonographic evidence of choledocholithiasis.

3rd) ERCP (endoscopic retrograde cholangiopancreatography) to confirm choledocholithiasis seen on ultrasound

or MRCP. ERCP can then provide access for mechanical stone retrieval +/- sphincterotomy and stenting of the
common bile duct.

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Cholechodocholithiasis

Cholangitis due to choledocholithiasis in a 60 year old female who presented with right upper quadrant pain and
jaundice.
Top left: Ultrasound shows a hyperechoic structure with an acoustic shadow (S), in keeping with a calculus, in the
distal common bile duct (CBD), which is dilated. However, due to overlying bowel gas in the duodenum, ultrasound
often fails to demonstrate choledocholithiasis, so an MRCP is often required.
Top right: MRCP was then performed to assess for additional calculi, showing a filling defect in the distal CBD (yellow
arrow. The gallbladder (GB) and intrahepatic biliary ducts are also distended but the pancreatic duct (PD) is of normal
calibre.
Bottom left: ERCP subsequently performed. A wire has been advanced into the common bile duct, around and beyond
the impacted calculus (yellow arrow).
Bottom right: After ERCP sphincterotomy, the stone was retrieved and a plastic CBD stent was inserted.

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Deep Venous Thrombosis (DVT)
• Similar to consideration of a CT pulmonary angiogram for suspected pulmonary embolus, a Well’s score and
D-dimer is required to book an ultrasound lower limb venogram.

Deep venous thrombosis (DVT) in the left superficial femoral vein.

Longitudinal (top images) and transverse (bottom images) views of the mid left superficial femoral vein, which does
not compress when pressure is applied with the ultrasound probe (images on the right) due to the presence of
thrombus. The same area is not patent, as displayed with colour doppler ultrasound (top right) – there should be
blood flow, which is often displayed as blue in a vein due to the caudocranial direction of blood flow.

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Carotid Doppler Ultrasound

Right internal carotid artery (ICA) stenosis in a patient who recently had an acute right frontal lobe infarct.
These carotid Doppler ultrasound images display luminal narrowing due to atheromatous plaque in the right ICA
(yellow arrows), with an increased velocity, as evidenced by the raised peak systolic flow (circle around PSV, middle
image). As a reference, the peak systolic velocity is normal in the left ICA (circle around PSV, right image). Velocity
and directional flow (colour) can be assessed with Doppler ultrasound. Velocity increases with severity of stenosis –
however, velocity can be low in near total stenosis or absent in total stenosis.

Thyroid Ultrasound

Thyroid carcinoma in a 27 year old female with a firm right neck lump. Ultrasound of the thyroid displays a
hypoechoic and irregularly-shaped nodule (left image: white arrow) in the lower pole of the right lobe of the thyroid
gland, suspicious for malignancy, in contrast to the normal hyperechoic thyroid tissue (left image: yellow arrows).
There is also an abnormal-appearing lymph node adjacent to the thyroid (right image). Subsequent fine needle
aspiration (FNA) of the thyroid nodule confirmed a papillary carcinoma.

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Pelvic Ultrasound
• Ultrasound is the best initial modality for pelvic pathology. Pelvic ultrasound is performed transabdominally
and transvaginally (if appropriate). A full bladder is required to transmit sound waves in transvaginal
ultrasound. Menstrual cycle affects the endometrial and ovarian appearances.

Polycystic ovarian syndrome (PCOS) in a 23 year old female who presented with amenorrhoea and an elevated serum
testosterone level. Transverse (left) and longitudinal (right) views of the right ovary as part of a pelvic ultrasound
show ovarian enlargement with centrally located hyperechoic stroma (s) and peripherally located multiple small
anechoic follicles (*), often referred to as the ‘string of pearls sign’.

Testicular US
• Testicular torsion is a clinical diagnosis – awaiting radiologic confirmation can lead to delays and testicular
infarct. However, if the diagnosis is uncertain, then an ultrasound can help diagnose orchitis and
epididymitis.
• Testicular lesions are best viewed on ultrasound.

Ultrasound of a testicular tumour in a young male who presented with a left scrotal mass. The patient underwent left
orchidectomy removed and the subsequent histological diagnosis was a germ cell tumour.
Left: Asymptomatic right testis. Normal testes have an ovoid shape and display a homogenous echogenicity.
Right: Symptomatic left testis is enlarged, irregular in shape and has a heterogeneous echogenicity.

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Magnetic Resonance Imaging (MRI)

• Very complex physics involving a cylindrical magnet, radiofrequency coil and receiver and gradient coils to
manipulate the spin of a hydrogen ion (proton) in all matter of the body in order to create an image.
• Advantages of MRI
o No ionising radiation
o Very high soft tissue contrast, so contrast medium is usually not necessary
o Second to none in certain pathological processes
• Disadvantages of MRI
o MRI safety (see above), which includes theoretical teratogenic effects in pregnant patients
o Claustrophobia
o Motion artefact can render a study non-diagnostic
o Long scans (15 minutes minimum versus a few seconds in CT)
o Costly
o Limited availability

• How to tell T1 versus T2 weighted imaging – T2 is a fluid-sensitive sequence.

o World War 2 (WW2): water is white on T2 (however other sequences can look similar to T1 or T2,
but this is a good starting point).
• Common MRI examinations:

Anatomical location MRI examination Indication

Brain MRI brain stroke / haemorrhage Stroke / haemorrhage
MRI brain with gadolinium Further characterisation of brain lesion on CT
MRI angiogram neck / brain Carotid / intracranial artery stenosis
MRI venogram Cerebral venous thrombosis
Extremity MRI shoulder Rotator cuff tear, shoulder instability
MR arthrogram of shoulder/hip Labral tear
MRI knee Cruciate ligament injury
MRI foot with gadolinium Osteomyelitis
Spine MRI spine Cord compression, radiculopathy, ligamentous
injury
Neck MRI neck with gadolinium Neoplasm
Heart MRI cardiac perfusion study Coronary artery disease, cardiomyopathy
Breast MRI breast Local staging of known breast cancer
Liver MRI liver with primovist Liver metastases
MRI liver with gadolinium Hepatocellular carcinoma
Biliary MRCP (no need for gadolinium) Cholechodocholithiasis, primary sclerosing
cholangitis, cholangiocarcinoma
Pancreas MRI pancreas with gadolinium Pancreatic neoplasm
Bowel MRI enterography Inflammatory bowel disease
MRI rectum Local staging of rectal cancer
Renal / adrenal MRI renal / adrenal with Renal / adrenal neoplasm
gadolinium Renal artery stenosis
MRI renal angiogram
Prostate MRI prostate +/- gadolinium Suspected prostate cancer
Pelvis MRI pelvis (female) Further characterisation of ovarian / endometrial
lesion seen on ultrasound

Below are some examples of commonly performed MRI examinations…

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Cord Compression – Radiologic Emergency

Cervical burst fracture resulting in cord compression.

Left, CT cervical spine: Sagittal view displays a vertical fracture, due to severe axial loading, extending through the 6th
cervical (C6) vertebral body, with anterior retropulsion and (critically) posterior retropulsion of the bony fragments
into the spinal canal.
Right, MRI cervical spine: Sagittal fluid sensitive sequence, in this case a STIR (short-tau inversion recovery), displays
abnormal high signal in the cord at the level of C6 due to compression on the spinal cord causing haemorrhage and
oedema. This patient subsequently underwent urgent spinal surgery.

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Cauda Equina – Radiologic Emergency

Cauda equina is an emergency situation requiring spinal MRI and prompt treatment with high-dose intravenous
corticosteroids and surgery (or radiotherapy if there is a neoplastic process). This patient is a 40-year-old female with
acute onset lower limb weakness and decreased sensation with urinary incontinence. After diagnosis of cauda equina
with MRI, this patient subsequently underwent spinal surgical decompression later that day.
c) sagittal T2-weighted MRI (T2 is fluid-sensitive, so CSF, oedema, water and fat appear hyperintense) demonstrates
marrow oedema of the vertebral endplates (white arrow) with loss of disk height, in keeping with degenerative disk
disease at L2-3. There is a large disk extrusion posteriorly into the spinal canal (yellow arrows).
a & b) axial T2-weighted MRI at L2-3 shows the extent of this disk extrusion (yellow dashed line), with complete
displacement of CSF from the spinal canal at this level.
d) what this patients spinal canal should look like on an axial T2-weighted MRI for reference (taken inferiorly in the
same patient).

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ACL Tear

MRI Knee: anterior cruciate ligament (ACL) tear. MRI is excellent in the evaluation of soft tissue structures, especially
regarding joints. Sagittal view in this MRI knee displays a complete tear of the ACL, which has displaced from its
normal femoral attachment and lies horizontally (yellow arrows). The normal posterior cruciate ligament (PCL) is
intact (white arrow).

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Prostate MRI

MRI prostate of a 69 year old man with an elevated PSA. MRI prostate can identify and stage prostate cancer.
A) T2-weighted MRI sequence: There is a 2 cm hypointense area in the peripheral zone (usually hyperintense) at the
apex of the prostate (yellow arrow). The majority of prostate cancer is found in the peripheral zone.
B) Diffusion weighted MRI sequence: This area of bright signal signifies diffusion restriction, typical for prostate
cancer (yellow arrow).
C) Subsequent targeted transrectal ultrasound (TRUS) guided biopsy: This area corresponded to an abnormal
hypoechoic focus, which was biopsied. Histological analysis revealed a high grade adenocarcinoma.
D & E) MRI of a different patient: Locally advanced tumour has replaced the entire prostate gland, invaded anteriorly
into the bladder (single red arrow) and posteriorly into the rectum (single yellow arrow). Due to tumour invasion of
both vesicoureteric junctions, there is bilateral hydroureter (double red arrows). Note the left pelvic sidewall lymph
node metastases (double yellow arrows) and osseous metastases in the ischium (blue arrows).
Case contributed by Dr Ciaran Redmond, Case Studies, http://www.svuhradiology.ie/case-studies/

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Approach to radiology questions in an exam:

• Read question, take time and look at all the images provided
o Clinical primer is often crucial
• Answer clear and concisely (use bullet points
o Avoid acronyms
o Use radiologic terminology specific to that modality

1. Identify the patient and scan details, modality and image plane (coronal, axial, sagittal view)
2. Note the obvious or life-threatening abnormality first, then analyse systematically
3. Bonus points for practical suggestion (refer for different imaging modality, image-guided biopsy or
multidisciplinary team meeting)

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Acknowledgements

• Written by Dr. Kevin Quinlan, Department of Radiology, St. Vincent’s University Hospital, Dublin.
• Supervised by Prof. Eric Heffernan, Department of Radiology, St. Vincent’s University Hospital, Dublin.

• Any image without a specified reference has been supplied by Prof. Eric Heffernan, Department of
Radiology, St. Vincent’s University Hospital, Dublin via www.svuhradiology.ie.

• Special thanks to:

o All of the radiology, radiography and physics staff at the Department of Radiology, St. Vincent’s
University Hospital, Dublin.
o Dr. Stephen Skehan, Department of Radiology, St. Vincent’s University Hospital, Dublin.
o Dr. Ronan Ryan, Department of Radiology, St. Vincent’s University Hospital, Dublin.
o Dr. David Murphy, Department of Radiology, St. Vincent’s University Hospital, Dublin.
o Dr. Rory O’Donohoe, Department of Radiology, St. Vincent’s University Hospital, Dublin.
o Dr Ciaran Redmond, Department of Radiology, St. Vincent’s University Hospital, Dublin.
o SVUH Radiology

• Please check out the below websites to learn more about Radiology and the Department of Radiology, St.
Vincent’s University Hospital, Dublin:
o http://www.svuhradiology.ie/ and https://www.instagram.com/svuhradiology/?hl=en (diagnostic
and interventional radiology for medical students, created by Prof. Eric Heffernan, Department of
Radiology, St. Vincent’s University Hospital, Dublin).
o http://www.nuclearmedicine.ie (nuclear medical imaging for medical students, created by Dr.
Stephen Skehan, Department of Radiology, St. Vincent’s University Hospital, Dublin).

• Another excellent book for further reference:

o Tutorials in diagnostic radiology for medical students, edited by Dr. Ciaran Redmond and Prof.
Michael Lee.

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