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Andre Tan Surgical Notes PDF
Andre Tan Surgical Notes PDF
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I TRAUMA (MULTI-SPECIALTY APPROACH) 2
II APPROACH TO ABDOMINAL PAIN 10
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4. DISABILITY SECONDARY SURVEY
- Glasgow coma scale When to do secondary survey
Eye Verbal Motor - Primary survey and resuscitation completed
Spontaneous opening 4 Oriented speech 5 Obeys 6 - ABCDEs reassessed
Opens to voice 3 Confused 4 Purposeful 5 - Vital functions returning to normal i.e. no need for active resuscitation at the moment
Opens to pain 2 Inappropriate 3 Withdraws 4
No response 1 Incomprehensible 2 Flexion response 3
No verbal response 1 Extension response 2 1. AMPLE HISTORY
No response 1 - Allergy
- Medications
GCS: 14-15 (minor); 8-13 (moderate); 3-7 (severe) - Past history
- Last meal
- AVPU score: Alert, Verbal stimuli (responds to), Pain stimuli, Unresponsive - Events leading to injury, Environment in which trauma occurred
- Pupillary reactivity
2. COMPLETE HEAD-TO-TOE EXAMINATION
- Call for neurosurgical consult as indicated
Head
- Complete neurological examination
5. EXPOSURE
- GCS or AVPU assessment
- Remove all clothes - Comprehensive examination of eyes and ears for base of skull fractures
- Check everywhere for injuries (log-roll to look at the back) - Caution: unconscious patient; periorbital oedema; occluded auditory canal
- Prevent hypothermia
Maxillofacial
6. ADJUNCTS TO PRIMARY SURVEY - Bony crepitus/deformity
Monitoring - Palpable deformity
- Vital signs – BP, pulse rate, saturation (pulse oximeter) - Comprehensive oral/dental examination
- ECG monitoring - Caution: potential airway obstruction in maxillofacial injury; cribriform plate
- Arterial blood gas fracture with CSF rhinorrhoea do not insert nasogastric tube
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CT SCAN CARDIOTHORACIC TRAUMA
- Only suitable for stable patient as quite long time involved in imaging with only
patient in the room can collapse There are 5 clinical scenarios in chest trauma where bedside procedures are lifesaving:
cardiac tamponade, airway obstruction, flail chest, haemothorax, and pneumothorax.
- Advantages
Able to precisely locate intra-abdominal lesions preoperatively
Able to evaluate retroperitoneum CARDIAC TAMPONADE
Able to identify injuries that can be managed non-operatively - High index of suspicion required
Not invasive - Clinical features
- Disadvantages Chest trauma and hypotension
Expensive Beck’s triad (hypotension, muffled heart sounds, distended neck veins) – only
Time required to transport patient seen in 50% of cases as hypovolaemia may prevent neck vein distension; muffled
Use of contrast heart sounds are least reliable
Pulseless electrical activity
Kussmaul’s signs (increased neck distension during inspiration, pulsus paradoxus)
DIAGNOSTIC PERITONEAL LAVAGE (DPL)
- Involves making a cut in the infraumbilical region and inserting a catheter into the - Diagnostic clues
peritoneal cavity, aspirate, then instillation of saline and re-aspiration Enlarged cardiac shadow in CXR (globular heart – very rarely seen)
Small ECG voltages, electrical alternans (uncommon)
- Positive DPL Pericardial fluid demonstrated on FAST or 2D-echo - definitive
Frank blood (>5ml) or obvious bowel contents aspirated
Lavage fluid seen to exit from chest drain or urinary catheter - Management
RBC >100,000 per mm3, WBC >500, Gram stain positive for bacteria in effluent Aggressive fluid resuscitation – helps maintain cardiac output and buys time
Pericardiocentesis: ECG lead-guided or 2D-echo guided
- Indications:
Any unstable patient with suspicion of abdominal trauma or where clinical exam
is difficult or equivocal AIRWAY OBSTRUCTION
Unexplained hypotension in multiple trauma - Chin lift or jaw thrust
Patient requiring immediate surgery for extra-abdominal injuries - Remove any foreign body manually, suction blood/secretions
- Definitive airway – ETT, cricothyroidotomy, tracheostomy
- Contraindications
Absolute indication for laparotomy already exists
Previous abdominal surgery or infections FLAIL CHEST
Gravid uterus - When 2 or more ribs are fractured at 2 points forming a flail segment that moves
Morbid obesity paradoxically with breathing
Coagulopathy - Results in hypoxaemia mainly due to underlying pulmonary contusion, contributed to
by pain with restricted chest wall movement
- Advantages
Can promptly reveal or exclude the presence of intraperitoneal haemorrhage - Management: ensure adequate oxygenation and ventilation; judicious fluid therapy
Valuable in discovery of potentially lethal bowel perforation (avoid fluid overload); adequate intravenous analgesia
- Consider mechanical ventilation in high risk patients: shock, severe head injury,
- Disadvantages previous pulmonary disease, fracture of >8 ribs, age > 65, >3 associated injuries
Morbidity involved – wound complications (haematoma, infection);
intraperitoneal injury
False negative rate of 2% when there is failure to recover lavage fluid, early
hollow viscus injury, diaphragmatic injuries, injuries to retroperitoneal structures
HAEMOTHORAX (b) Subdural haemorrhage
- Chest tube insertion in the triangle of safety (bound by the lateral border of the Crescent shaped haematoma under the dura (between the dura and the
pectoralis major medially, a line just anterior to the mid-axillary line laterally, and the arachnoid)
upper border of the fifth rib inferiorly) More severe than EDH (usually due to nature of injury that causes SDH to
- Be wary of sudden cessation of chest tube drainage as tube can get blocked by clot occur – associated with higher impact, thus brain has other injuries)
- If blood >1500mls massive haemothorax, call urgent cardiothoracic consult Pathology: underlying brain damage in addition to expanding SOL
Removal of blood does not solve underlying brain damage poorer results
PNEUMOTHORAX (OPEN/TENSION) (c) Traumatic subarachnoid haemorrhage
- Tension pneumothorax is a clinical diagnosis (CXR will only delay treatment, and Usually only small amount of blood conservative treatment sufficient
may cause death) – signs of pneumothorax, hypotension, neck vein distension, severe (d) Intraparenchymal haemorrhage
respiratory distress Any shape, size, location
- Immediate needle thoracotomy in second intercostal space in mid-clavicular line If large haematoma, will require evacuation
- Followed by chest tube insertion
4. Diffuse axonal injury
- Open pneumothorax occurs in a large chest wall defect with equilibration between - Global injury of axons
intrathoracic and atmospheric pressure, producing a “sucking chest wound” - Arises from injury that causes rotational and shearing forces (high impact
- Cover defect with a sterile dressing, taping it down on 3 sides to produce a flutter- injury) – rapid acceleration and deceleration of brain in the intracranial cavity
valve effect, letting air out of the pleural cavity but not back in against relatively fixed points of attachment at the falx and tentorium
- Insert chest tube (not through the wound) - Maximal effects at corpus callosum and brainstem
- If severe, will see punctate haemorrhages at the grey-white border
5. Cerebral oedema (2 types)
NEUROSURGICAL TRAUMA (a) Hypoxic (cellular)
Decreased blood supply (oxygenation) loss of function of Na-K pump as
AIM in management of head injuries is the prevention of secondary brain injury (from ATP decreases increased intracellular sodium cellular swelling
hypotension, hypoxaemia, increased ICP etc) since neuronal death is irreversible.
(b) Interstitial
Breakdown of blood-brain barrier proteins enter interstitial space
PATHOLOGIES: oedema
1. Concussion
- Physiological dysfunction without anatomical or radiological abnormality
- (Physiological dysfunction is the first step towards cell death, but is reversible if PATHOPHYSIOLOGY
no further insult occurs) 1. Monroe-Kellie doctrine
- Usually recovers in 2-3 hours - Intracranial cavity is of fixed volume and its contents (brain, CSF, blood) are
relatively incompressible
2. Contusion - Thus increase in intracranial volume raised ICP
- Small haematoma <1cm
Cerebral perfusion pressure = Mean arterial pressure – Intracranial pressure
3. Intracranial haemorrhage
(a) Extradural haemorrhage - Compensatory mechanisms:
Lens-shaped haematoma outside the dura (between skull and dura) (a) Hyperventilation vasoconstriction of cerebral vessels due to increased
Pathology: expanding space-occupying lesion partial pressure of carbon dioxide decrease in blood volume
20% of patients with EDH are alert and well; underlying brain is minimally (b) CSF pushed into spinal canal (but limited volume available)
damaged, thus drainage gives good results - Removal of any reversible cause of raised ICP will improve cerebral perfusion
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2. Fixed dilated pupil
- Constrictor fibres to the pupil run in the oculomotor nerve, which exits the 3. Moderate head injury
brainstem at the upper midbrain – nerve fibres lie just under the tentorium - All will be CT-scanned at ED NES will operate if any indication to do so
- Uncus of the temporal lobe sits on the tentorium - In ward: as per mild head injury
- In raised ICP, the uncus herniates over the edge of the tentorium,
compressing the fibres of the oculomotor nerve just below 4. Severe head injury
- Thus a fixed dilated pupil occurs on the side of the compression due to - Must scan to look for reversible causes of raised ICP but stabilise patient first
unoppressed sympathetic supply (dilates the pupil)
- Medical methods to lower ICP
3. Cushing’s reflex (a) Intubate and hyperventilate
- A triad of: (b) IV mannitol (must catheterise patient also; do not give if patient is unstable)
(a) Raised ICP - Screen for other life-threatening injuries (likely to be multi-trauma patient)
(b) Hypertension - Achieve haemodynamic stability
(c) Bradycardia (a) Check for long bone fractures
- From Monroe-Kellie doctrine, an increase in mean arterial pressure helps to (b) FAST for bleeding into abdominal cavity
maintain cerebral perfusion pressure when ICP is raised (c) ABG to detect acidosis
- Increase in mean arterial pressure achieved by sympathetic overdrive: (d) Keep monitoring patient and re-investigate where appropriate
(a) Increased heart rate - Operate if reversible cause found
(b) Increased contractility (a) Craniectomy (i.e. bone flap not replaced) or craniotomy (bone flap replaced
(c) Increased vasoconstriction – increased total peripheral resistance after blood evacuated) [Burrhole usually not big enough to drain an acute
(a) and (b) increase cardiac output increased BP; (c) increases BP bleed]
- Baroreceptors detect abnormally raised blood pressure and try to decrease it (b) Evacuate clot
heart rate falls (c) Insert endoventricular drain (EVD) if there is hydrocephalus
- Total sedation after operation, ward in ICU
MANAGEMENT Prevents patient from struggling which will raise ICP
1. Assessment
- 3 important parameters: ABCs, GCS, pupil size 5. Depressed skull fracture
- Glasgow coma scale (see above) – Minor head injury: 14-15; moderate injury: 8- - Can leave alone unless depression is greater than the thickness of the skull bone
13; severe injury: 3-7
6. Compound depressed fracture
2. Minor head injury - There is through-and-through skin laceration over the fracture
- Most common - Always explore to ensure underlying dura is intact, and repair if dura is torn
- Indications for admission: (since meningitis can occur with a torn dura)
Persistent headache and/or vomiting
CSF leak
Neurological deficit
Skull fracture
History of loss of consciousness
Amnesia
- In ward: NBM, IV drip (no dextrose saline!), no sedation, monitor GCS
- If patient deteriorates CT scan, exclude metabolic causes (e.g. hypoglyc), do
septic workup (exclude sepsis)
MUSCULOSKELETAL TRAUMA Wound care
- Swabs of the wounds for culture and sensitivity
GENERAL POINTS - IV antibiotic prophylaxis
- Extremity trauma tends not to be life-threatening - Tetanus toxoid cover
- But occult blood loss can occur in large volumes especially in certain types of - Photograph wound (to prevent re-opening of wound by every doctor that comes to
injuries – pelvic fracture (up to 3L), femoral shaft fracture (up to 2L) see patient)
- Need to have high level of suspicion and treat with urgency - Betadine dressing
- Look out for any tachycardia, early signs of shock - In OT: generous debridement, irrigation (within 4-8 hours, especially in open
- Prepare to resuscitate patient fractures), fracture stabilisation (internal or external fixation depending on Gustilo
classification)
- Leave wound OPEN
ASSESSMENT OF THE EXTREMITY
- Perfusion: colour, pulses, skin temperature, capillary refill
- Deformity MANAGEMENT OF FRACTURES
- Wounds – open or closed injury; abrasion over a fracture is considered open fracture - Recognise fracture and/or dislocation
- Soft tissue assessment - Complete neurovascular examination of the limb involved before reduction
- Abnormal joint mobility – ligamentous injury around the joint; if in the knee, highly - Appropriate X-rays (at least 2 planes)
likely that the popliteal artery is injured as well - Analgesia
- Neurological assessment - Correction of deformity
- Viability of the limb - Temporary immobilisation – backslab, malleable splint
- Neurovascular examination; examine for compartment syndrome
- Circulation chart
THE PULSELESS EXTREMITY
Things to consider
- Is pulselessness due to shock? OPEN FRACTURES
- Arterial or venous compromise? Definition: there is communication between the fracture or fracture haematoma and the
- Is there compartment syndrome (pulselessness is a very late sign) external environment
- Any pre-existing vascular disease?
Gustilo-Andersen classification
Physical examination
Type I <1cm AND clean
- Any limb deformity (can result in kinking of vessels)?
- Any joint instability (dislocation of a joint can result in intimal tear in the major Type II >1cm AND no extensive soft tissue damage, avulsions or flaps
vessel running across it, with thrombosis and occlusion)? Type IIIA Extensive soft tissue damage, avulsions or flaps but adequate soft
- Skin colour/temperature tissue coverage of bone OR
- Post-reduction tibial pulse in knee dislocation – if still absent, do an urgent High-energy trauma cause irregardless of size of wound
angiogram!
Type IIIB Extensive soft tissue loss with periosteal stripping and exposure of
bone.
SOFT TISSUE INJURIES
Massive contamination common
Types
- Open: laceration, abrasion Type IIIC Arterial injury requiring repair
- Crushing
- Degloving: open or closed
- Closed
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- Grade I
Low velocity injury, prognosis similar to closed fracture
Treat with ORIF within 6 hours
- Grade II
Moderate velocity, more trauma
- Grade IIIA
Skin graft usually possible
- Grade IIIB
Skin graft alone often not adequate
Local and free flaps will be necessary
Secondary bone procedures
- Grade IIIC
Neurovascular injuries present in addition to musculoskeletal injuries
Surgery involves:
(a) Generous debridement of the wound with irrigation to decrease bacterial load
(b) Treat any soft-tissue injuries
(c) Stabilise fracture – usually using external fixator
ABDOMINAL PAIN
RHC Epigastric LHC
Thoracic Hepatic Thoracic Others Thoracic Others
Pneumonia Hepatitis (viral, autoimm etc) MI Pancreatitis Pneumonia Subphrenic abscess
Pleural effusion Hepatomegaly Pericarditis Pleural effusion Splenomegaly
Abscess Aortic aneurysm MI Pancreatitis
Biliary
Cholangitis Others Gastrointestinal Gastrointestinal
Cholecystitis Subphrenic abscess Oesophagitis PUD
Gallstone disease Pancreatitis GERD Diverticulitis
PUD PUD Mesenteric ischaemia
Appendicitis Gastric outlet obstructn
CA stomach
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ABDOMINAL MASS
RHC Epigastrium LHC
Liver Gallbladder Liver (see RHC) Stomach Spleen Stomach
Massive Pancreatic/periampullary ca Cancer Massive
Cancer: HCC Acute cholecystitis Pancreas Distension (GOO) Infxns Descending colon
Metastases Hydrops Pseudocyst CML Cancer
Myeloprolftve dz Empyema Tumour Aorta Myelofibrosis Diverticular mass/abscess
Alcoholic liver dz Mirizzi syndrome Aortic aneurysm Faeces
Moderate
Rt ht failure/tricuspid regurg Transverse colon
Above causes
Ascending colon Cancer Retroperitoneal lNpathy Left kidney(see Rt lumbar)
Moderate Portal hypt
Cancer Diverticular mass/abscess Lymphoma
Above causes Lymphoprolftve dz
Diverticular mass/abscess Faeces Teratoma Left adrenal gland
Lymphoprolftve dz (lymphoma, CLL)
Faeces Other malignancies
Haemochromatosis H’lytic anaemia (thal, HS)
Amyloidosis Storage dz (Gaucher’s)
Right adrenal gland
Mild Mild
Above causes Right kidney(see Rt lumbar) Above causes
Infxns: Viral – Hep, IMS Infxns: Viral hep, IMS
Bacterial – abscess Endocarditis
Parasitic – hydatid Autoimm – SLE, RA, PAN
cyst, amoebic abscss Myeloprolftve dz – PRV,
Biliary obstruction essential thrombocytopaenia
Cirrhosis Infiltratn – sarcoid, amyloid
INVESTIGATIONS Supportive
1. Blood investigations:
Diagnostic
- Full blood count – Low Hb (anaemia from chronic blood loss)
1. Barium swallow
High TW (aspiration pneumonia)
- Advantage of barium swallow is that it is less invasive than OGD, especially - Urea, electrolytes, creatinine – electrolyte disturbances from vomiting, poor
when suspecting webs, diverticula in the oesophagus where OGD may cause intake; raised creat and urea in dehydration (creat will be raised more than urea if
perforation; however if patient is at high risk of aspiration, barium swallow is patient has prerenal failure from dehydration)
dangerous.
- Liver function tests – low albumin with nutritional deprivation
- Visualisation of obstructive lesions:
o Shouldering of a stricture (benign strictures form a smoother contour 2. CXR
whereas malignant strictures form a more right-angled contour) - Consolidation (aspiration pneumonia)
o Bird’s beak sign of achalasia
3. 24-hour pH probe monitoring
- If patient complains of reflux symptoms and no signs are seen on OGD (see later
section on Gastro-oesophageal reflux disease)
2. Oesophagogastroduodenoscopy (OGD)
- Advantage is direct visualisation of the lesion and ability to take tissue biopsy
(especially useful in malignancy), may also be therapeutic (stopping bleeding
from a tumour, stenting the lumen, etc)
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CANCER OF THE OESOPHAGUS STAGING
T Tis High-grade dysplasia/carcinoma in-situ
Stage T N M
EPIDEMIOLOGY T1a Tumour invading lamina propria or
muscularis mucosa 0 is 0 0
- Third most common gastrointestinal tract cancer in Singapore
- Male predominance T1b Tumour invading submucosa but does I 1 0 0
- Increasing incidence with age not breach submucosa IIA 2/3 0 0
T2 Tumour invades the muscularis propria IIB 1/2 1 0
T3 Tumour invades adventitia
RISK FACTORS T4 Invasion of surrounding structures
III 3 1 0
- Smoking (100x increased risk for SCC, 10x for adenocarcinoma) 4 any 0
N N1 Regional node involvement (1-3 nodes
- Alcohol (2x increased risk) involved =1a; 4-7=1b; >7=1c) IVA any any 1a
- Obesity (related to reflux, increases adenocarcinoma incidence) M M1a Nonregional lymph node involvement IVB any any 1b
M1b Other distant metastases
- Diet: Hot beverages, preserved foods (nitrosamines), betel nuts; vitamin and mineral
deficiencies (selenium, vitamin E, beta-carotene)
PRESENTATION
- Tylosis (autosomal dominant disorder with keratosis of palms and soles
Usually of insidious onset, with earliest symptoms being non-specific e.g. retrosternal
- Barrett’s oesophagus (intestinal metaplasia of oesophageal mucosa due to reflux; discomfort, “indigestion”, and most patients already have advanced disease when they
increased risk of cancer due to metaplasia-dysplasia-carcinoma sequence; risk is 30- are diagnosed – 75% have lymph node involvement at time of diagnosis.
40x higher than in individual without Barrett’s, and is about 1% per year)
1. Dysphagia
- Achalasia (2-8% incidence of SCC) - Present in 80% of patients – most common presentation
- Caustic injury (ca occurs at site of scar/stricture, mostly middle third of oesophagus) - Pain develops late and is usually due to extra-oesophageal involvement
- Plummer-Vinson (or Paterson-Brown-Kelly) syndrome – Post-cricoid oesophageal 2. Weight loss
web and iron deficiency anaemia. (10% develop cancer in upper third of oesophagus) 3. Regurgitation
4. Anaemia (with or without malaena/frank haematemesis – bleeding is usually occult)
PATHOLOGY 5. Vocal cord paralysis (left more than right)
- 70% squamous cell carcinoma, 30% adenocarcinoma 6. Aspiration pneumonia
- SCC can arise anywhere in the oesophagus while adenocarcinoma occurs in lower 7. Tracheo-oesophageal or broncho-oesophageal fistula
third and gastro-oesophageal junction (related to reflux and Barrett’s oesophagus)
- Overall: 10% of cancers occur in the upper third, 60% in the middle third, 30% in the INVESTIGATIONS
lower third
Diagnosis
- Three growth patterns: 1. Barium swallow
Fungating (60%) - 92% accuracy in showing mucosal irregularity and annular constrictions but not
Ulcerative (25%) able to diagnose malignancy with confidence
Infiltrative (15%)
- Tumour spread: direct extension into surrounding structures, vascular invasion, 2. Oesophagogastroduodenoscopy
lymphatic spread - Allows biopsy of the lesion confirmatory histological diagnosis
- Common sites of metastases: liver, lung, bone Staging
1. Endoscopic ultrasound
- If endoscope can pass around the lesion, the EUS is good for T staging, and also
to identify enlarged regional lymph nodes
2. Chest X-ray - Endoluminal surgery – for early lesions; no attempt to remove any LNs (usually no
- Presence of any lung metastases LN involvement)
- Aspiration pneumonia
- Pleural and/or pericardial effusion - Oesophagectomy
- Tracheal deviation or extrinsic compression of tracheobronchial system (i) Ivor-Lewis
- Widened superior mediastinum in an upper oesophagus tumour Two-stage procedure involving gastric mobilisation (first stage, done through
- Raised hemidiaphragm with phrenic nerve involvement upper midline abdominal incision), oesophagectomy and gastro-oesophageal
anastomosis in the chest (second stage, through right thoracotomy incision)
3. CT scan or MRI of the thorax with extension to include liver and adrenals
- Can be used for T, N, and M staging (ii) Trans-hiatal
Done via two incisions – one in the abdomen and one in the neck
4. Bronchoscopy Blunt oesophagectomy, gastric mobilisation, and gastro-oesophageal
- Exclude bronchial involvement especially in tumours involving upper two-thirds anastomosis in the neck
of oesophagus Less morbidity than Ivor-Lewis as the chest is not opened, but controversial
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Chemotherapy GASTRO-OESOPHAGEAL REFLUX DISEASE (GORD)
- Current regimen: 5-Fluorouracil and cisplatin
- Addition of chemotherapy to external beam radiation for unresectable cancers shown EPIDEMIOLOGY
to have improved survival compared to EBRT alone Incidence in Singapore not known
- Chemotherapy given preoperatively and postoperatively improves survival Increasing prevalence, more common in males than females
PRESENTATION
- Heartburn: retrosternal pyrosis
- Acid brash: reflux of sour gastric juices into back of mouth i.e. regurgitation
- These symptoms occur usually after food, particularly a heavy meal, and are
aggravated by lying flat (posturally related)
- Long-standing disease can lead to dysphagia due to stricture formation; dysphagia
can also result from an underlying oesophageal motility disorder; odynophagia
suggests oesophagitis with ulceration
- Reflux can also lead to pulmonary symptoms: chronic cough, chest infections - Can detect motility disorders that cause reflux, and also pick up oesophageal
(aspiration) ulceration and stricturing resulting from reflux
- Other symptoms: globus (feeling of a lump at the throat), chest pain (can mimic - Can sometimes see reflux of barium contrast into oesophagus
anginal pain with radiation to neck, jaw, arm), nausea, water brash (hypersalivation in 5. Manometry
response to reflux) - No value in reflux except for detecting motility disorder
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UPPER BLEEDING GIT AND ITS CAUSES 3. Aetiological clues
Gastric ulcer/gastritis/erosions
APPROACH TO BLEEDING UPPER GIT - Any history of dyspepsia, gastric ulcer (any OGD done in the past showing these
problems? On any “gastric” medications?)
CAUSES - Any drugs that may predispose – NSAIDs, antiplatelets, steroids, anticoagulants,
1. Peptic ulcer disease (bleeding peptic ulcer) TCM
2. Gastro-oesophageal varices Varices
3. Gastritis, gastric erosions - Any history of chronic liver disease
4. Mallory-Weiss tear Mallory-Weiss tear
5. Gastric malignancy - Binge-drinking with subsequent severe retching and vomiting leading to
6. Rare causes: AV malformation (Dieulafoy lesion), aortoenteric fistula haemetemesis
Malignancy
HISTORY (if patient is stable) - Recent constitutional symptoms e.g. LOA, LOW, malaise
1. Nature of bleeding - Early satiety
- Dyspepsia
Haematemesis
- Can be fresh red blood as in variceal bleeding, Mallory-Weiss tear, AV 4. Complications
malformation - Symptoms of anaemia: postural giddiness, shortness of breath, lethargy,
- Coffee grounds vomitus is altered blood (due to gastric acid) and can come from decreased effort tolerance, palpitations, chest pain
gastric ulcer, gastritis/erosions, or variceal blood that has entered the stomach - May even be having AMI if it’s an old patient with history of IHD
Malaena
5. Comorbidities
- Altered blood; malaena indicates bleeding from the upper GIT i.e. above the
ligament of Treitz - Elderly patient (>60) high risk
- Other comorbidities: liver disease, renal disease, IHD high risk
- Different types of malaena:
(a) Fresh malaena – jet black with sheen, tarry, non-particulate (almost liquid
in consistency) PHYSICAL EXAMINATION
(b) Stale malaena – black-grey, dull, mixed with normal stool, occasionally 1. Vitals!
particulate - Blood pressure, heart rate stable? Any postural hypotension? (Tachycardia is an
(c) Iron stool – greenish hue on rubbing between gloved fingers, particulate. early sign of shock)
- If gloved finger is stirred in a cup of water, malaena will “dissolve” completely - Patient’s conscious level – confused?
with no sedimentation and turn the water black, but iron stool will sedimentate - Compare current vitals with vitals in ambulance, ED – is there a worsening trend?
and turn the water green
2. General inspection
Frank PR bleeding - Pallor
- Very brisk upper GI bleed can present as frank PR bleeding as blood passes - Cold clammy peripheries impending shock
down so fast it doesn’t get altered - Stigmata of chronic liver disease
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5. IV somatostatin/octreotide If bleeding is not remediable by endoscopic intervention:
- Not given in ulcer bleed; mode of action is as a splanchnic vasoconstrictor which - Insert Sengstaken-Blakemore tube (only temporary) and repeat endoscopy 10-12
decreases portal blood flow and hence portal pressures decreased variceal hours later
bleeding
- Also acts indirectly to inhibit secretion of gut hormones that increase portal - Radiologically guided insertion of transjugular intrahepatic porto-systemic shunt
blood flow (TIPSS)
PRESENTATION
1. Incidentally detected on OGD
PEPTIC ULCER DISEASE
2. Symptoms of dyspepsia
EPIDEMIOLOGY (a) Ulcer-like dyspepsia: pain in the upper abdomen is the predominant symptom
- Incidence about 100 per 100,000 per year (b) Dysmotility-like dyspepsia: non-painful discomfort in the upper abdomen,
- 68% of patients are over 60 years of age associated with upper abdominal fullness, early satiety, bloating, belching,
- Overall mortality is 7-10%, unchanged for last 2 decades – mostly due to ulcer nausea
bleeding especially in elderly with significant comorbidities (c) Unspecified dyspepsia
- Pain is usually worse with food in a gastric ulcer, while it is relieved by food in a
MAIN AETIOLOGICAL FACTORS duodenal ulcer
H. pylori 3. Bleed
- 60% of population are positive for H. pylori by age 21 - As above, presenting with haematemesis (coffee-grounds vomitus) or malaena
- About 10-20% of infected patients develop an ulcer
- Accounts for 90-95% of duodenal ulcers, and 50% of gastric ulcers 4. Perforation
- Patient presents with sudden generalised abdominal pain that is aggravated by
NSAIDs even the slightest movements
- Accounts for most of the rest of ulcer disease not caused by H. pylori - Board-like rigidity, guarding will be present on examination (signs of peritonism)
- 30% of patients on NSAIDs will get an ulcer, of which one-fifth will have a clinically - Erect CXR will show air under diaphragm
significant ulcer i.e. symptomatic, bleeding
Other factors ENDOSCOPY (OGD)
- Cigarette smoking - The most important and valuable investigation
- Alcohol
- Steroids and anticoagulants do not increase the risk of ulcer formation, but increase - Roles of endoscopy:
the risk of bleeding in an existent ulcer (a) Diagnosis
Confirmation of ulcer disease
PATHOGENESIS Location of ulcer
- An imbalance between mucosal protective mechanisms against acid, and aggressive Biopsy to rule out malignancy (usually 6 bites)
forces that damage the gastric mucosa Biopsy of antral tissue for CLO (Campylobacter-like organism) test for H.
- Aggressive forces: gastric activity and pepsin activity pylori
- Protective mechanisms: mucus secretion, bicarbonate secretion into mucus, robust
mucosal blood flow to remove protons, epithelial regenerative capacity,
prostaglandin secretion by mucosa to maintain blood flow
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(b) Prognostication of bleeding risk (in UBGIT) SURGICAL MANAGEMENT
Forrest classification (or endoscopic stigmata of recent haemorrhage – ESRH)
DUODENAL ULCER
Forrest grade Bleeding risk Indications for surgery:
1a Spurting (arterial) 90% 1. Persistent bleeding (e.g. erosion of a posterior duodenal ulcer into gastroduodenal
1b Non-spurting, ooze (venous) 20% artery)
2a Non-bleeding ulcer with visible vessel 40% 2. Perforation
2b Non-bleeding ulcer with adherent clot 20%
2c Ulcer with haematin-covered base (flat spot) 10% 3. Gastric outlet obstruction (patient presents with vomiting of undigested food not
3 Ulcer with clean base 5% long after meal, succussion splash, air-fluid levels on AXR; characteristic
electrolyte abn of hypokalaemic hypochloraemic metabolic alkalosis with
paradoxical aciduria)
(c) Endotherapy (in UBGIT)
Injection with adrenaline (1:10,000) or absolute alcohol 4. Failure of medical management (ulcer does not heal)
Thermal coagulation (heater probe) Surgery:
Haemostatic clipping (endoclip) 1. Oversewing the bleeding vessel
Argon plasma coagulation 2. Vagotomy with gastric drainage procedures
- Rationale for vagotomy is to eliminate direct cholinergic stimulation to gastric
CONSERVATIVE MANAGEMENT secretion; parietal cells also become less responsive to histamine and gastrin, and
vagal stimulus for gastrin release is abolished
1. Gastroprotection
- Vagotomy can be truncal, selective, or highly selective
(a) Standard dose proton pump inhibitor - Drainage procedures usually done with vagotomy as gastric emptying is
20mg OM decreased with denervation gastrojejunostomy or pyloroplasty
Promotes ulcer healing even with ongoing NSAID use
3. Antrectomy with truncal vagotomy
(b) Double dose famotidine
4. Gastrectomy
40mg BD
Inferior to omeprazole as famotidine only promotes ulcer healing if NSAIDs 5. Omental patch repair is sufficient for small perforated ulcer
are stopped; ulcers will not heal with ongoing NSAID therapy Perforated ulcer: IV fluids, IV antibiotics, PPI, surgery (patch repair)
2. H. pylori eradication
First line triple therapy: omeprazole 20mg BD, amoxicillin 1g BD, GASTRIC ULCER
clarithromycin 500mg BD for 7 days Indications for surgery
In penicillin-allergic patients, substitute amoxicillin with metronidazole 400mg 1. Failure to heal after 3 months of conservative therapy
BD 2. Dysplasia or carcinoma
Document eradication by endoscopy with CLO test, urea breath test or stool 3. Recurrence
serology testing 4. Perforation, persistent bleeding
Treatment failure occurs in up to 20% - treat with quadruple therapy: colloidal Surgery
bismuth subcitrate 120mg QDS, tetracycline 500mg QDS, metronidazole 400mg 1. Oversewing the bleeding vessel
BD, omeprazole 20mg BD for 7 days 2. Gastrectomy
3. If prepyloric ulcer, can treat similar to duodenal ulcer
Re-scope in 6 weeks to document ulcer healing
If ulcer still present, biopsy ulcer again (exclude malignancy for gastric ulcer) and also
do antral biopsy for CLO test (to confirm eradication of H. pylori)
GASTRIC CARCINOMA 5. H. pylori infection
- 3-6X increased risk of gastric cancer
EPIDEMIOLOGY
- Fourth most common cancer in males, sixth most common in females in Singapore HISTOLOGY
- Female to male ratio 2:1
- Incidence 10-18 per 100,000 per year Adenocarcinomas
- Incidence increases steeply after 50 years old - Make up 90-95% of stomach tumours
- Lauren classification:
RISK FACTORS (a) Intestinal type (most common overall) – occurs in high risk population, distal
1. Environmental third of the stomach, in older men; associated with erbB2 and erbB3 receptor
- Diet: preserved foods (nitrosamines), smoked foods, polycyclic hydrocarbons stimulation
- Smoking (b) Diffuse type – occurs in low risk population, proximal third and cardio-
- Alcohol oesophageal junction, in younger and female patients; more aggressive, present
- Occupational exposure: asbestos, heavy metals, rubber later, worse prognosis; associated with K-sam oncogene
- Low socioeconomic status - Early gastric cancer
2. Genetic Confined to mucosa and submucosa
- Blood type A Good survival and prognosis regardless of size, lymph node status, histological
- HNPCC – Lynch syndrome II grade
- P53 mutation
Non-adenocarcinoma
- Germline mutation of e-cadherin
- Family history of gastric cancer - Make up less than 10% of stomach tumours
- Types: SCC, neuroendocrine tumour, leiomyosarcoma, GIST, primary gastric non-
Hodgkin’s lymphoma (MALT, linitis plastica)
PRECURSOR CONDITIONS
1. Partial gastrectomy for benign disease with Bilroth II reconstruction
- Usually occurs >15 years after surgery MORPHOLOGY
- Due to chronic exposure of gastric mucosa to biliary, pancreatic and intestinal Borrmann’s classification:
secretions at the anastomotic zone - Type I (3%): Nonulcerated, polypoid, growing intraluminally
2. Gastric polyps - Type II (18%): Ulcerated, circumscribed with sharp margins
- Highest risk in inflammatory polyps: 75-90% - Type III (16%): Ulcerated, margin not sharply circumscribed
- 10-20% risk in adenomatous polyps especially in large polyps (>2cm) or those - Type IV (63%): Diffuse, infiltrating, may be ulcerated; may diffuse entire stomach
with villous histology (linitis plastica)
- Also increased risk of adenocarcinoma elsewhere in the stomach
3. Chronic atrophic gastritis LOCATION
- Hypertrophic gastritis (Menetrier’s disease) – inflammatory disease of gastric - 30% in pyloric channel or antrum
epithelium, up to 10% risk of malignant change - 20% in body
- Pernicious anaemia – autoantibodies to parietal cells with achlorhydria, 2-10% - 37% in cardia
risk of gastric cancer
- 12% in entire stomach
4. Peptic ulcer disease
- <1% risk of malignant change
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SPREAD 6. CT scan – good for T and N staging
- Direct extension to neighbouring organs 7. Staging laparoscopy prior to operation – picks up small peritoneal metastases that
- Lymphatic spread are occult on CT scanning (up to one-fifth of patients whose disease was thought to
(a) Regional nodes be resectable) change in stage of disease
(b) Supraclavicular nodes (Virchow’s node)
(c) Umbilical (Sister Joseph’s node) STAGING
- Haematogenous spread – liver, lung, bone, brain
Tis Carcinoma in situ N0 No regional LN
- Peritoneal seeding to omentum, parietal peritoneum, ovaries (Krukenberg’s tumour), T1 Tumour limited to mucosa and submucosa N1 1-6 regional LN involved
or cul-de-sac (Blumer’s shelf) T2 Tumour invades muscularis mucosa N2 7-15 regional LN involved
T3 Tumour penetrates serosa N3 >15 regional LN involved
PRESENTATION T4 Tumour invades adjacent structures
Very non-specific symptoms and signs:
- Abdominal pain 60% CURATIVE TREATMENT
- Weight loss 50%
- Nausea/vomiting 40% SURGERY
- Anaemia 40%
Principles of surgery:
- Palpable mass 30%
- Wide resection of the tumour to negative margins (at least 6cm margins)
- Haematemesis/malaena 25%
- En-bloc excision of regional lymph nodes
- Early satiety 17%
- Choice between total gastrectomy and subtotal gastrectomy
- Metastatic symptoms late (bony tenderness, neurological deficits, etc)
Subtotal gastrectomy leaves a small portion of proximal stomach – easier to
New onset dyspepsia at age>35 years old should cause concern anastomose to jejunum than oesophagus since oesophagus does not have serosa
(higher risk of leak)
COMPLICATIONS Subtotal gastrectomy is associated with less morbidity, better functional outcome
(some residual reservoir function preserved)
- Bleeding Total gastrectomy is the resection of choice for proximal tumours (fundus, cardia,
- Gastric outlet obstruction vomiting (dehydration, hypokalaemic metabolic body) as well as diffuse-type tumours and cardio-oesophageal junction tumours
alkalosis, aspiration)
- Perforation - Reconstruction
- Malnutrition Bilroth I (end-to-end gastroduodenostomy) – rarely done as it is difficult to
mobilise duodenum up to anastomose with residual stomach
INVESTIGATIONS Bilroth II/Polya (gastrojejunostomy) – no protection against biliary reflux into
stomach
Diagnosis by OGD – best for visualisation and biopsy (usually an ulcer with heaped- Roux-en-Y – to prevent biliary reflux; but involves 2 anastomoses, higher
up edges) chance of leak
Supportive/staging investigations Oesophagojejunostomy (after total gastrectomy)
1. FBC – low Hb
Complications of gastrectomy:
2. U/E/Cr – if vomiting, low potassium, low chloride, alkalosis
Early
3. LFTs – albumin as a marker of nutritional status (alb<35 is poor); liver mets
1. Bleeding
4. CXR – lung mets 2. Infection
5. Endoscopic ultrasound – gold standard for T staging and good for N staging 3. Anastomotic leak
Late PALLIATIVE THERAPY
1. Early satiety - For palliation of symptoms such as pain, bleeding, obstruction
2. Retained antrum syndrome - Endoscopic laser ablation for obstruction
- Not enough antrum removed leads to increased acidity in residual stomach, with - Embolisation for bleeding
formation of marginal ulcers on the jejunal side of the anastomosis - Surgical options: subtotal gastrectomy (6-15% mortality), total gastrectomy (20-40%),
gastrojejunostomy for obstruction
3. Intestinal hurry - External beam radiotherapy for pain, low-level ongoing bleeding (not for heavy
- Inadequate reservoir function leads to poor digestion may have phytobezoar bleeding as it takes weeks to cause fibrosis)
formation
4. Dumping syndromes PROGNOSIS
- Early dumping syndrome: due to increased osmotic load in bowel occurring
half to one hour after meal, resulting in flushing, palpitations, dizziness, nausea; - Stage I 90% 5-year survival
treat by eating small frequent meals with low carbo and high protein/fat - Stage II 70%
- Late dumping syndrome: reactive hyperinsulinaemia with hypoglycaemia; treat - Stage III 40%
by eating more carbohydrates - Stage IV 0%
5. Biliary/intestinal reflux into stomach
- Leads to symptoms of dyspepsia
6. Afferent limb syndrome
- Occurs in Bilroth II/Polya reconstruction
- Mechanical obstruction of the afferent jejunal loop due to kinking, anastomotic
narrowing, or adhesions postprandial epigastric pain with non-bilious
vomiting
- Can be decreased by doing Roux-en-Y surgery (but may still occur)
7. Nutritional deficiency
- Iron deficiency – mixed picture
(a) Loss of intrinsic factor B12 deficiency
(b) Decreased conversion of iron from Fe3+ to Fe2+ by gastric acid decreased
iron absorption in terminal ileum
- Need to supplement with B12 injections and iron supplements
CHEMOTHERAPY/RADIOTHERAPY
Adjuvant therapy
5-fluorouracil with chemotherapy
5-fluorouracil with epirubicin for advanced disease
Neoadjuvant therapy
- 5-FU and cisplatin can be used to downstage unresectable, locally advanced disease
with a significant increase in resectability (61% 79%)
- For resectable disease: preoperative 5-FU, cisplatin, doxorubicin, methotrexate,
followed by intraperitoneal 5-FU improved resection rates, response rates, median
survival
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COLORECTAL DISEASES
2. Defects in DNA mismatch repair
- Involved in 10-15% of sporadic cases
COLORECTAL CARCINOMA
- Like the APC pathway, there is accumulation of mutations, but due to a different
EPIDEMIOLOGY mechanism, and without clearly identifiable morphologic correlates i.e. no
Commonest cancer in Singapore men, number 2 cancer in Singapore women adenomas
Peak incidence at 60-70 years of age - Due to mutations in one of the five DNA repair genes (MSH2, MSH6, MLH1,
PMS1, PMS2) of which MSH2 and MLH1 are the most commonly involved in
PATHOLOGY sporadic colorectal carcinomas
- Almost all tumours are adenocarcinomas - Loss of DNA mismatch repair results in microsatellite instability which affects
- 90% of tumours are sporadic coding or promoter regions of genes involved in cell growth such as the BAX
- 8% arise in association with hereditary non-polyposis colon carcinoma (HNPCC) and gene and the type II TGF-β receptor
1% in association with familial adenomatous polyposis (APC) - Tumours that arise from this pathway have a better prognosis than tumours that
- 1% arise in association with long-standing ulcerative colitis (>10 years) arise from the APC pathway
PATHOGENESIS SITE:
There are 2 pathways for cancer development in the colorectal mucosa: - 25% in caecum and ascending colon
- 25% in transverse colon
1. APC pathway (adenoma-carcinoma sequence) - 25% in descending colon and proximal sigmoid
- Accounts for 80% of sporadic colorectal carcinomas - 25% in distal sigmoid and rectum
- Characterised by chromosomal instability - Most are left-sided though there is an increasing incidence of right-sided tumours
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B) High-risk factors INVESTIGATIONS
Positive Family history Aims
- 1 or more 1st deg relative with CC at age <40 - Diagnose colorectal cancer
- 2 or more 1st/2nd deg same side relative with CC at any age - Stage the cancer
- Personal or family history of breast, ovarian cancer - Investigate for complications of cancer
FAP history
I. DIAGNOSIS
Amsterdam Criteria for Hereditary Non-Polyposis Colorectal Ca (HNPCC) – (a) Colonoscopy – first-line investigation
[3, 2, 2, 1] - Can visualise lesion and have an idea of which part of the colon it is in
- 3 or more family members from the same side with CRC, - Can take biopsies of the lesion
- At least 2 of which must be first-degree relatives
- Enables detection of synchronous lesions – synchronous polyps in 30%,
- 2 successive generations
synchronous cancer in 3-5%
- 1 of the CC must occur prior to age 50
- Enables therapeutic procedures e.g. polypectomy, stenting of obstructed colon
- FAP is excluded
Family history alone considered high-risk; FAP and HNPCC considered very (b) Double-contrast barium enema (barium + air)
high-risk - Not adequate for diagnostic purposes, may miss small lesions
- Classically can see an apple core lesion with barium enema
C) Other risk factors
(c) Carcinoembryonic antigen level (CEA)
- Low fibre diet
- Obesity - A tumour marker for colorectal carcinoma – >90% of tumours produce CEA
- Red meat - Measured pre-operatively as a baseline level – if the CEA is raised pre-op and
- Ulcerative colitis falls to within normal range post-op, it is likely tumour has been totally removed
- Follow-up after surgery with CEA levels to detect tumour recurrence
D) Complications - Causes of false positive raised CEA: smoking, pregnancy, bronchitis, cholangitis
- Haemorrhage (usually occult) anaemia and cancers of the stomach, lung, breast, pancreas, cervix, bladder and kidney
- Obstruction (left sided lesion)
- Perforation II. STAGING
- Fistula – colovesical fistula causing faecuria, pneumaturia, recurrent UTI
- Infection – abscesses, peritonitis (a) CT scan of the abdomen and pelvis
- Local T staging
- Staging of regional and no-regional lymph note involvement
PHYSICAL EXAM
- Metastases to the liver
1. Abdominal mass
2. Mass on DRE – hard, non-tender, polypoid, irregular, contact bleeding (b) Endoscopic ultrasound, or transrectal ultrasound for rectal tumour
- Very good for T staging to determine depth of involvement by tumour
3. Complications, Metastases - Can also assess local lymph node status
- Cachexia
- Anaemia (c) CXR + CT scan of the chest
- Jaundice, hepatomegaly
- Lungs (d) MRI of the tumour
- Brain - Superior to CT for delineating fat planes in T staging especially in rectal cancer
- Bone tenderness
(e) Bone scan if appropriate
- Cervical lymphadenopathy – Virchow’s node
III. COMPLICATIONS While segmental resection (excision of only the segment of colon containing the
(a) FBC for low Hb, together with iron studies tumour) is sufficient for primary tumour removal, a wider resection is often
required to achieve sufficient lymphadenectomy
(b) Urea, electrolytes and creatinine in patient with obstruction – may be vomiting,
may have third space losses (intraluminal) with fluid and electrolyte abnormatlities; Adequate clearance of the draining lymphatics involves excision of the vascular
creatinine may be elevated due to pre-renal failure arcades supplying the segment of involved colon back to their origin (from the
SMA or IMA) as lymphatics follow the arteries generally
(c) Liver function tests for derangements caused by metastasis (though these
changes will only occur late) – raised bilirubin, ALP - Obstructed left sided carcinoma
(d) If patient presented with symptoms of intestinal obstruction – erect and supine No difference shown for doing a staged procedure (i.e. tumour removed with
AXR can help in diagnosis and location of obstruction proximal end of colon brought out as a colostomy) as compared to creating a
primary anastomosis
(e) Erect CXR in perforated tumour to detect air under diaphragm
On-table bowel decompression is equivalent to irrigation for clearance of faecal
material
DUKE’S STAGING Segmental colectomy for the tumour with intraoperative decompression is
Stg Description 5yr surv comparable to subtotal/total colectomy without decompression with regard to
A Tumor confined to bowel wall with no extension into extrarectal/ 75% bowel function and rates of complications
extracolic tissue, no LN mets
- Site of surgery for colonic carcinoma
B Invades past muscularis propria into extrarectal/ extracolic tissue, 55%
no LN
C LN mets present
C1: only nearby nodes involved (paracolic LNs) C1:40%
C2: continuous string of LN involved up to proximal resection C2:20%
(LN at base of mesentery)
D Distant mets/ extensive local mets such that surgically incurable poor
TREATMENT
SURGERY
Pre-operative measures
- Bowel prep
Modification of diet – 3 days low residue diet, NBM day before operation)
Bowel clearance with polyethylene glycol
- Prophylactic antibiotics
ampi/ genta/ metronidazole at induction of anesthesia
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Tumour site Surgery Structures involved - Reconstruction
- Caecum Right - Excision of caecum and ascending colon Formation of a straight coloanal anastomosis in anterior resections is associated
- Ascending colon hemicolectomy - Division of ileocolic and right colic arteries, and with poor function due to the lack of reservoir function
the right branch of the middle colic artery
- Hepatic flexure Extended right - Excision of caecum, ascending colon, and Creation of a colonic J-pouch using the proximal end of colon (the end of the
- Transverse colon hemicolectomy proximal transverse colon colon is folded back on itself to form a J, and the two limbs opened and stitched
near the hepatic - Division of ileocolic and right colic arteries, and together to form a pouch, the apex of the J being anastomosed to the anus) is
flexure the middle colic artery at its origin associated with improved post-operative function
- Mid-transverse Transverse - Excision of transverse colon Coloplasty is another alternative that is equivalent to colonic J-pouch (the distal
colon colectomy - Division of middle colic artery colon is cut longitudinally but sewn transversely, widening the diameter at that
- Transverse colon Left segmental - Excision of distal transverse colon and proximal segment to form a small pouch), done when there is difficulty creating the
near splenic colectomy descending colon colonic J-pouch
flexure - Division of supplying vessels – left branch of
middle colic artery, left colic artery - Mesorectal excision
- Descending colon Left - Excision of descending colon
Proximal rectal tumours – 5cm distal margin of mesorectal excision
hemicolectomy - Division of left colic and inferior mesenteric
arteries Mid-rectal tumours – wide mesorectal excision of at least 4cm distal to the
- Sigmoid colon Sigmoid - Excision of sigmoid colon tumour
colectomy - Division of inferior mesenteric artery and/or Lower rectum tumours – total mesorectal excision required (complete excision
sigmoid branches of the intact visceral mesorectal tissue to the level of the levators)
- Extended resections
Principles of surgery for rectal carcinomas For locally advanced, adherent tumours (T4), multivisceral resection of organs
involved (pelvic exenteration) is associated with improved local control and
- En-bloc resection with adequate margins overall survival compared with standard resection, though high morbidity of 25-
For rectal tumours a margin of 5 cm proximally and 2 cm distally is adequate (as 50% is associated
it has been found that lymphatic spread of rectal tumours is predominantly in the Consider neoadjuvant chemoradiotherapy prior to surgery to downstage disease
proximal direction)
Radial margins are also important as there is a zone of downward spread within - Stoma creation
the mesorectum (peritoneal investment of the upper rectum) – for upper rectal A defunctioning loop ileostomy (or loop colostomy) is usually created during an
tumours, mesorectal excision of 5 cm distal to the distal margin of the tumour is anterior resection as the manipulation of the colon deep within the pelvic cavity
adequate (see Mesorectal excision below) causes increased risk of an anastomotic leak
- Sphincter-sparing versus loss of sphincter A defunctioning stoma does not protect against anastomotic leak, but mitigates
against disastrous complications should a leak occur
The anal sphincter can be spared if the distal margin is >2cm above the level of
the sphincter complex, usually taken to be at the level of the dentate line (which - Neoadjuvant chemoradiotherapy
is 5cm above the anal verge) i.e. distal margin of the tumour must be >7cm from
the anal verge Neoadjuvant therapy with radiotherapy in combination with 5-fluorouracil can
downstage tumour significantly ability to preserve sphincter, ability to resect
Sphincter-sparing surgery involves a low anterior resection previously unresectable tumour, etc
If the tumour is so low that it cannot be resected without removing the sphincter
complex, then an abdominoperineal resection is performed where the entire anus
and sphincter complex is dissected, with the creation of an end colostomy
- Surgical treatment according to stage Surgery for metastases
- Isolated liver metastases (synchronous or metachronous) may be resected with
Stage of disease Treatment
survival benefit; neoadjuvant chemotherapy can be given to downstage the
T1 Involvement of submucosa, but no Local excision (AR or APR)
metastases if they are initially resectable
penetration through muscularis propria
- Lung metastases usually indicate systemic dissemination of disease, but in the rare
T2 Invasion into, but not penetration a) Local excision + adjuvant setting that there is an isolated lung secondary, resection can provide survival benefit
through, muscularis propria Chemo/RT OR
b) radical resection Surgery for recurrence
T3 Penetration through muscularis propria Neoadjuvant chemo / RT before - Loco-regional recurrence, if detected early with adequate resection, can confer
into subserosa (if present), or pericolic radical resection survival benefit
fat, but not into peritoneal cavity or
other organs RADIOTHERAPY
T4 Invasion of other organs or - Role as neoadjuvant therapy in rectal cancer to downstage tumour
involvement of free peritoneal cavity - Post-operative adjuvant therapy in stage II or III rectal cancer
CHEMOTHERAPY
Operative complications Adjuvant therapy
Immediate (<24h) Damage to other organs e.g. ureters - Colon cancer: 5-FU + folinic acid (leucovorin) for 6 months, or 5-FU + levamisole
for 12 months in Duke’s C cancer (node positive); not recommended in Duke’s B or
Early (<30 days) Wound infection less
Bleeding
- Rectal cancer: post-operative adjuvant therapy in combination with radiotherapy in
Abscess
stage II or III disease (5-FU based regimen used)
Anastomosis breakdown/leak
Early stoma complications Palliative therapy
Late (>30 days) Diarrhoea - 5-FU in combination with folinic acid is first-line therapy
Impotence (damage of pelvic nerves) - Alternatives for first-line therapy: Raltitrexed when 5-FU is not tolerated;
Adhesions (I/O) capecitabine or UFT (uracil combined with tegafur) plus folinic acid
Anastomotic stricture
Late stoma complications
FOLLOW UP
- Follow-up visits 3-monthly for the first 2 years, then 6-monthly for the next three
years, and subsequently yearly, measure CEA at each visit
Surgery for palliation - Yearly colonoscopy
- Resection of primary for palliation of symptoms such as bleeding, perforation, - CXR and liver ultrasound to detect metastases (recommended frequency not known)
obstruction or pain
- Resection of asymptomatic primary is controversial, but may confer survival benefit
in a select group of patients where metastatic tumour burden is restricted to one side
and liver involvement is not extensive
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STOMA PRINCIPLES Stoma Complications
STAGING
TERMS
- Hinchey classification of acute diverticulitis – need for surgery is reflected by
- Diverticulosis coli – presence of acquired pseudodiverticula
degree of infective complications
- Diverticular disease – symptomatic diverticulosis coli
- Diverticulitis – inflammation of diverticula Stage 1 Pericolonic / - ABx, NBM, IV fluids
Mesenteric abscess - Consider 1 stage surgery after acute episode –
resection of affected bowel segment with primary
EPIDEMIOLOGY anastomosis
- Increases with age Stage 2 Pelvic / retroperitoneal - Percutaneous drainage
- 10-30% of diverticulosis coli are symptomatic abscess - Elective 1 stage surgery
- Risk factors – dietary fibre & genetics Stage 3 Purulent peritonitis - 2 stage operation – Hartmann’s procedure (partial
- Site – majority are in the sigmoid colon (dec. diameter, inc. pressure) Stage 4 Faecal peritonitis colectomy + diverting end colostomy & rectal
stump formation) + secondary re-anastomosis 3
months later
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Presentation Clinical features Investigations Differentials Management
Acute - LIF pain – colicky, progressing to - FBC – leucocytosis - Acute salpingitis Conservative
Diverticulitis constant, relieved by defecation - ↑ ESR - Acute appendicitis - Bed rest
- LIF tenderness - AXR – ileus, air-fluid level w/in an abscess - GE - NBM, IV fluid
- Palpable LIF mass - Barium enema - Irritable bowel syndrome - Broad-spectrum antibiotics –
- Nausea - ± CT or U/S: thickened bowel wall, pericolic fat augmentin or metronidazole or
- Pyrexia inflammation, extraluminal gas & contrast, abscess, ciprofloxacin
- Increase pulse rate free fluid & gas - Antispasmodics
- Laparoscopy – if diagnosis is in doubt
- CT scan w triple contrast is gold std for diagnosis After acute phase has settled
Contrast: IV for vascular lesions, oral for small - Ba enema &/or Colonoscopy –
bowels, enema for large bowels confirm dx & exclude CA colon
Features – diverticula, mesenteric fat infiltration,
concentric bowel thickening, pelvic abscess
Chronic - Recurrent LIF pain - Rigid sigmoidoscopy – oedematous mucosa & - CA colon – may coexist. Hard Conservative – see above
Diverticulitis - Irregular bowel habits – constipation rigidity of rectosigmoid junction to differentiate – therefore,
Surgical
& bouts of diarrhoea - Flexible sigmoidoscopy – diverticular orifices ALWAYS exclude CA colon
Indications:
- Passage of mucus PR - Barium enema – ‘saw-tooth’ appearance, e.g. histology after bowel
- Severe / recurrent attacks of
diverticula, strictures resection
diverticulitis
- Colonoscopy – exclude differentials (i.e. Ca colon) - Ischaemic colitis
- Possible CA colon
- Radiation colitis
- Segmental resection of affected
- Colonic endometriosis
colon + anastomosis
Generalised - Acute onset abdominal pain – severe - FBC – ↑ TW, ↑Hb (dehydration) - Other causes of peritonitis – Mgmt as for acute abdomen
peritonitis / & continuous - U/E/Cr – dehydration & ARF perforated PUD, appendicitis - Resuscitate
perforation - Abdominal guarding & rigidity - CXR – free gas under diaphragm etc - Surgical
- Vomiting Peritoneal toilet
- Tachycardia Resection of affected segment
- Pyrexia End sigmoid colostomy
(Hartmann’s procedure)
Advice to patients:
- 70% of patients will not have recurrence after first attack
- Advise high fibre diet & to drink lots of fluid
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SURGICAL LIVER PROBLEMS - Segment I is the caudate lobe
- Segments II to VIII are named clockwise, while facing the patient, starting from
ANATOMY OF THE LIVER the upper right corner (i.e. the upper left segment of liver) – see picture
- The liver is divided into two lobes, right and left - Segment IV can be further divided into IVa and IVb, where IVa is the superior
subsegment and IVb is the inferior subsegment
- The anatomical division of the liver lobes is demarcated by the falciform ligament
- The functional division (more practical in surgery) is demarcated by the plane of the - The liver has two blood supplies – portal vein (formed from the joining of the splenic
gallbladder and inferior vena cava (also by the plane in which the middle hepatic vein and superior mesenteric vein) and hepatic artery (a branch of the coeliac trunk)
vein runs) - Drainage is via the three hepatic veins into the inferior vena cava
HEPATOCELLULAR CARCINOMA
EPIDEMIOLOGY
- The liver can be further divided into 8 functional segments (Couinaud segments) that - Incidence in Singapore is 18 per 100,000 per year in males, and 4.6 per 100,000 in
each have their own vascular inflow, outflow, and biliary drainage, independent of females
the other segments - Third most cancer among males, overall fourth most common cancer
- The segments are divided by one transverse plane and three sagittal planes as shown - More common in men, with a ratio of 3:1
in the picture - Peak age of onset: 30-40 years old
- The transverse plane is at the level of the main branches of the portal vein, and - Primary cancers of the liver are mainly hepatocellular carcinomas (85%), with a
divides the liver into an upper half and a lower half small proportion of intrahepatic cholangiocarcinoma (6%)
- The sagittal planes are formed by the three main hepatic veins (right, middle and left)
AETIOLOGY AND RISK FACTORS 6. Other manifestations
- Hepatitis B infection (high HBV DNA load, HBeAg positivity increase the risk) - Budd-Chiari syndrome (occlusion of portal vein, resulting in portal hypertension)
- Hepatitis C infection - Pyrexia (central tumour necrosis)
- Cirrhosis (of which cirrhosis resulting from hep B, hep C and haemochromatosis are - Paraneoplastic syndromes – hypoglycaemia (high metabolic demands of tumour),
associated with the highest risk) erythrocytosis (tumour produces erythropoietin), hypercalcaemia, watery
- Aflatoxin ingestion diarrhoea, etc.
PATHOLOGY INVESTIGATIONS
- Pathogenesis involves a chronic inflammatory process or ongoing hepatocellular DIAGNOSIS
damage with high cellular regeneration, which leads to increased rates of genetic Biopsy is usually not performed due to risk of tumour seeding (1-2% risk) along the
mutation in the cells and accumulation of these mutations leading to carcinoma needle track – diagnosis is based on clinical, biochemical and radiological tests
formation
- Two histological subtypes: WHO criteria for HCC:
Nonfibrolamellar – associated with hep B and cirrhosis (a) Risk factors for HCC e.g. hep B/C carrier
Fibrolamellar – associated with younger patients, more common in females, no (b) Characteristic CT findings (of a hypervascular lesion)
association with hep B or cirrhosis, 70% resectable, good prognosis
(c) Raised AFP (>400)
- Metastasises to lymph nodes, bones, lungs and adrenals
1. Alpha-foetoprotein (AFP)
PRESENTATION - Elevated in 80% of hepatocellular carcinoma
1. Asymptomatic
- During screening (ultrasound) for chronic hepatitis B carrier 2. Triphasic CT scan is the gold standard investigation
- Investigations for liver cirrhosis - Triphasic CT involves scanning the liver at three different times after
- Incidentally found on imaging of the abdomen intravenous contrast:
2. Local symptoms (a) Arterial phase – aorta lights up as contrast fills arteries; IVC and portal
- Upper abdominal pain vein are dark
- Hepatomegaly found on examination (b) Portal venous phase – contrast enters portal system so portal vein is as
- Obstructive jaundice due to invasion of intrahepatic biliary tree, compression of bright as the aorta
a major duct (c) Delayed phase – contrast drains out, so none of the vessels in the liver are
lighted up
3. Liver decompensation (on top of underlying cirrhosis)
- Characteristic feature of HCC is enhancement in the arterial phase (as HCCs
- Worsening liver function
have a rich arterial supply derived from the hepatic arterial system) with rapid
- Ascites
contrast washout in the portal venous phase (hypodense)
- Variceal bleeding
- Encephalopathy - In a patient with hepatitis B/C and raised AFP, a liver lesion that is not a
haemangioma on imaging should be considered HCC until proven otherwise
4. Tumour rupture
- CT can also look for nodal involvement, and metastases to the adrenals
- Abdominal pain (peritonitis)
- Shock
3. Dynamic MRI scan of the liver
5. Metastases - Adjunct investigation done when CT findings are equivocal
- Bone pain - Images liver in greater detail, can be used to exclude benign conditions
- Dyspnoea
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4. Hepatic angiogram with lipiodol and post-lipiodol CT scan 4. Residual liver function post-operatively
- Lipiodol will be retained in HCC even after many days as the HCC does not - Dependent on tumour size and how much of the liver it takes up, because tumour
contain Kupffer cells to ingest lipiodol is non-functional
- Hepatic angiogram may reveal abnormal blood vessels within the HCC - A large tumour taking up most of the liver segments being resected translates to
- CT scan of the liver weeks after lipiodol ingestion will pick up the areas of smaller amount of functional liver tissue being resected, while a small tumour
tumour (where the pre-lipiodol CT may not have demonstrated the tumour means that more functional tissue is removed with the same resection margins
clearly) 5. Degree of portal hypertension
5. If indicated, investigations to look for GI primary - Resection of the liver results in worsened portal hypertension since the effective
portal venous capillary bed has decreased increased resistance to flow
- CEA, CA 19-9, endoscopy
6. Location of tumour
STAGING (looking for metastases) - Has to be located in a suitable location for resection
1. Lung – chest X-ray, CT thorax
Hepatectomy
2. Adrenals – CT abdomen
- Problem in patients with cirrhosis is that there is already a “field-change” effect in
3. Bone – bone scan if clinically indicated the liver, thus a new tumour can still develop in the remnant liver
- Requires a fine balance between adequate resection margins and preservation of
TREATMENT sufficient functional liver to prevent liver failure
- Good immediate and short-term results, but not long term (<30% 5-year survival)
SURGERY
due to occurrence of new primaries in the cirrhotic liver
- The only curative treatment for HCC is surgical removal of the tumour
- Only about 10-20% of patients with HCC will have disease amenable to surgery Transplantation
- 2 surgical possibilities: - Milan criteria for transplantation (>75% 5-year survival if followed)
(a) Resection of tumour (partial hepatectomy) (a) Single tumour 5cm or smaller, or 3 or less tumours none larger than 3cm
(b) Liver transplantation (b) No evidence of gross vascular invasion
(c) No regional nodal or distant metastasis
Factors affecting resectability: - Problems with availability of donor organ – the disease might have progressed past
1. Stage of disease being suitable for transplant by the time donor organ is available
- Metastatic disease is not suitable for resection Possibility of “bridging therapy” such as radiofrequency ablation to shrink
- Multicentric disease affecting both lobes is a contraindication to hepatectomy disease and prevent progression until donor liver is available
2. General fitness for operation - In hepatitis B carriers, there is a risk for reinfection of the donor liver (high risk
factors are HBeAg positivity, high HBV DNA levels) – can be aggressively treated
3. Liver function pre-operatively with anti-viral drugs 2 months before transplant and anti-HBV immunoglobulin long-
- Cirrhotic patients have higher risk of post-operative mortality (4-14%) compared term after transplant
to non-cirrhotic patients (0-4%) due to complications such as liver failure,
bleeding and infection PALLIATIVE THERAPY
- If patient has cirrhosis, assess the Child’s status Child’s C and most of Child’s Loco-regional ablation
B will not be fit for operation; only Child’s A and good Child’s B (a) Radiofrequency ablation – best results for locoregional strategies
- Use of indocyanin green (ICG) – the percentage of ICG remaining in the liver (b) Percutaneous ethanol injection
after 15 minutes indicates the level of liver function. If >15% remains after 15 (c) Cryotherapy
minutes, the patient cannot tolerate major liver resection (>3 segments removed)
Intra-arterial therapy TRIPHASIC CT
(a) Transarterial chemoembolisation - Hypodense on arterial phase (as metastases are usually hypovascular compared to
(b) Transarterial embolisation hypervascular HCC)
(c) Radioactive isotopes – Yttrium-90 - Increasing contrast uptake on portal venous and delayed phases
PRESENTATION
LIVER METASTASES 1. Usually small and asymptomatic, found incidentally
2. Mass effects compressing on surrounding organs
- Still more common than primary liver tumour for malignancy occurring in the liver 3. Pain from liver capsule stretch
- Primaries: Colorectal, gastric, pancreatic, urogenital, breast, lung 4. Rupture (<1%)
5. Kassabach-Merritt syndrome for large haemangiomas – consumptive coagulopathy,
thrombocytopaenia
PRESENTATION DEPENDS ON SITE OF METASTASIS 6. Heart failure from large arteriovenous shunt
Mets to liver parenchyma Mets to porta hepatis LN
Hx - Incidentally found on follow up - Symptoms of obstructive jaundice DIAGNOSIS
(for cancer) Yellow sclera - Radiological
- Hard mass Tea-coloured urine Characteristic features on triphasic CT – slow enhancement of the rims on arterial
- Heaviness Pale stools and portal venous phase, brightest in the delayed phase
- Pain from rupture - DO NOT BIOPSY
P/E - Hard, irregular nodular hepatomeg - Jaundice early, progressive
- Jaundice is a late sign - Hepatomegaly may not be present TREATMENT
Invx - Both obstructive and transaminitis - Obstructive picture in early stages - Only for symptomatic or complicated lesions
picture - Possible role for prophylactic surgery in large, lateral, inferior lesions since there is
higher risk for rupture
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SIMPLE LIVER CYSTS HEPATIC ABSCESS
EPIDEMIOLOGY 2 types depending on aetiology: pyogenic or amoebic
- 50% of cysts are single
- Prevalence 1-3% PYOGENIC ABSCESS
- 9:1 female predominance for symptomatic cysts
- More common than amoebic abscess locally
PATHOGENESIS - Causative organisms: Klebsiella pneumoniae, Enterococcus, Enterobacter, E. coli,
- Congenital malformation when an aberrant bile duct loses communication with the Staph aureus
rest of the biliary tree and becomes progressively dilated (fluid within the cyst is not
bilious) - Routes of infection:
- No solid component and not septated (mixed cysts with septations are suggestive of (a) Ascending infection from biliary system (ascending cholangitis)
malignancy)
(b) Intra-abdominal source through portal vein – acute appendicitis, diverticulitis,
- [Cysts that communicate with the biliary system are called choledochal cysts]
inflammatory bowel disease, pancreatitis, pelvic abscess
PRESENTATION – WITH COMPLICATIONS (c) Contiguous spread – from gallbladder empyema
- Bleeding (d) Haematogenous spread in sepsis e.g. infective endocarditis
- Rupture (e) External inoculation – iatrogenic, traumatic
- Mass effect
- Torsion - Presentation: Spiking fever with chills, rigors. 50% of patients have jaundice, and
- Compression of inferior vena cava one-third have hepatomegaly
- Fistulation into duodenum
- Cholestasis due to compression of CBD - Investigations:
- Portal hypertension FBC, U/E/Cr
- Carcinoma (rare) Blood cultures
Melioidosis serology
TREATMENT (IF SYMPTOMATIC) Tumour markers: AFP, CA 19-9, CEA (may resemble tumour on imaging)
- Aspiration Stool ova, cysts and parasites
- Ethanol sclerotherapy (painful)
Ultrasound
- Fenestration (open or laparoscopic)
- Excision/resection CT scan to exclude liver tumour (KIV endoscopy to rule out GI malignancy)
If any aspiration done, aspirates for histology, stains, cultures
- Imaging: Irregular lesion with central area of necrosis, air-fluid levels, may be
multiloculated. Rim-enhancing appearance on triphasic CT scan.
- Treatment
1. Antibiotics
Empirical antibiotics – Ampicillin/Gentamicin/Metronidazole
Change to definitive antibiotics when blood c/s results return
Total duration of 6 weeks – first 2 weeks intravenous, next 4 weeks oral
2. Drainage
Drainage if >3cm – open drainage or percutaneous aspiration
AMOEBIC ABSCESS
- Causative organism: Entamoeba histolytica (infects the gut, forming ulcers in the
colon, then spreads to the liver through the portal vein)
- Transmission is faecal-oral
- Presentation
Usually single abscess
No sepsis, jaundice
Hepatomegaly often present
Complications: rupture into pleural/peritoneal spaces
- Treatment:
Metronidazole
Aspiration if amoebic serology inconclusive; pregnancy (metronidazole
contraindicated); suspicion of secondary infection; severe symptoms from
distension or fever; impending rupture
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PANCREATIC DISEASES
- Gallstones are thought to cause acute pancreatitis due to obstruction of the
ACUTE PANCREATITIS pancreatic duct causing interstitial oedema which impairs blood flow to the
pancreatic cells ischaemic cellular injury predisposition to enzyme activation
DEFINITION
- The mechanisms in which alcohol cause pancreatitis are not known, though it is
An acute inflammatory process of the pancreas with variable involvement of regional believed alcohol itself results in injury to pancreatic cells through generation of free
tissues or remote organ systems radicals during its metabolism, and may sensitise the pancreas to injury by other
agents
EPIDEMIOLOGY
Incidence is difficult to measure accurately as many patients with mild pancreatitis may
ATLANTA CLASSIFICATION (FOR SEVERITY)
not be diagnosed. Patients with acute pancreatitis make up 7-10% of those presenting
with abdominal pain. 1. Mild acute pancreatitis
- Interstitial oedema
CAUSES (I GET SMASHED) - Minimal organ dysfunction
- Uneventful recovery
1. Idiopathic
2. Gallstones 2. Severe acute pancreatitis (any 1 of the following)
3. Ethanol - Pancreatic or peripancreatic necrosis
4. Trauma - Associated with organ failure
5. Steroids - May be associated with local complications
6. Mumps and other infections (VZV also)
7. Autoimmune – SLE, PAN
8. Scorpion toxin PRESENTATION
9. Hypercalcaemia, hypertriglyceridaemia, hypothermia - Symptoms (generally non-specific):
10. ERCP Abdominal pain (most consistent, in >90% of patients) – constant epigastric
11. Drugs (SAND: Sulphonamides, azathioprine, NSAIDs, diuretics) pain, classically radiating to the back (in 50%), maximal intensity within several
12. Rare causes: Cystic fibrosis, cancer of the head of the pancreas, severe blunt trauma, hours of onset; usually occurs after a heavy meal; alleviated by sitting up, worse
pancreas divisum on movement
Gallstones and alcohol are the most common causes (>90% of acute pancreatitis) Nausea and vomiting
Anorexia
PATHOPHYSIOLOGY
- Signs (also non-specific)
- The final common pathway of pancreatitis involves inappropriate activation of
Epigastric tenderness (less than one third have signs of peritonism)
proenzymes stored within zymogen granules in the pancreatic cell – trypsin is
implicated in this mechanism as it activates most of the proenzymes secreted by the Tachycardia, low grade fever
pancreas when they are secreted into the duodenum Abdominal distension with diminished or absent bowel sounds (paralytic ileus)
- The activated lytic enzymes destroy the pancreatic acinar cells resulting in release of Ecchymoses: flank (Grey-Turner’s sign) or umbilical (Cullen’s) – formed by
potent cytokines that attract neutrophils and macrophages, which themselves secrete blood-stained peritoneal fluid tracking to the flank or umbilicus; suggest severe
pro-inflammatory cytokines haemorrhagic pancreatitis associated with profound fluid loss (third-spacing)
- The cytokine cascade amplifies the local inflammatory response and also results in
a systemic inflammatory response (resulting in systemic complications of acute
pancreatitis such as ARDS and multiorgan dysfunction)
MANAGEMENT STRATEGY 3. Urinary diastase
- Similar function to serum lipase, used when serum amylase is equivocally raised
Diagnosis or normal, as urinary diastase will be elevated for a longer time after onset of
symptoms
DIAGNOSTIC 6. CT scan
1. Serum amylase
- Not the first investigation of choice unless considering pathologies other than
pancreatitis, since CT may worsen pancreatitis
- Serum amylase is raised within 12 hours of onset of acute pancreatitis, usually
more than 1000 or 3 times normal - Value of CT is at a later point in the disease time course to look for
complications such as fluid collections; IV contrast needs to be given to detect
- High sensitivity and moderate specificity (specificity increased when cut-off necrosis
taken at 3 times normal upper limit)
- Returns to normal level 48 to 72 hours after onset – not useful in late diagnosis PROGNOSTIC / SUPPORTIVE / LOOKING FOR AETIOLOGY
- Other causes of elevated serum amylase: 1. FBC (TW for Ranson, Glasgow; haematocrit for Ranson)
GI sources - Ischaemic bowel (can cause elevated amylase in the thousands) 2. U/E/Cr (urea and glucose for Ranson and Glasgow)
- Cholecystitis, cholangitis
- Peptic ulcer disease 3. LFTs (AST for Ranson and Glasgow; albumin for Glasgow; obstructive picture in
- Kidney stone gallstone pancreatitis)
- Ectopic pregnancy 4. Lactate dehydrogenase (for Ranson and Glasgow)
- Intestinal obstruction, perforation
5. ABG (PaO2 for Ranson and Glasgow; base excess for Ranson)
Non-GI - Salivary gland injury or inflammation
sources - Macroamylasaemia
6. Ca/Mg/PO4 with albumin (hypercalcaemia – aetiology)
- Impaired clearance due to chronic renal failure
7. Fasting lipids (hyperlipidaemia – aetiology)
2. Serum lipase
- Rises within 8 hours of onset of symptoms and returns to normal after 7-10 days 8. ECG (rule out AMI as a cause of epigstric pain)
- Thus more useful in late diagnosis of acute pancreatitis
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SEVERITY STRATIFICATION III. Glasgow/Imrie score
ASSOCIATIONS
- Cigarette smoking (most clearly established – 2-5X increased risk) INVESTIGATIONS
- Industrial carcinogens – benzidine, betanaphthylamine DIAGNOSTIC
- Lower socioeconomic class 1. CA 19-9
- Diabetes mellitus - Not a screening test for pancreatic cancer as it can be false positive
- Chronic pancreatitis - Can act as a prognostic marker: high CA 19-9 levels usually associated with
- Genetic factors (mutations in K-ras gene, p16 gene) unresectable disease with poorer prognosis
- Familial cancer syndromes e.g. Peutz-Jeghers - Can be used as a marker for tumour recurrence during post-op follow-up
2. CT scan
PATHOLOGY - Better sensitivity (85-90%) and equal specificity (90-95%) in diagnosing
- Most common histology is ductal adenocarcinoma (90% of tumours) pancreatic cancer
- Anatomic distribution: 75% in the head, 20% in the body, 5% in the tail - Features: Mass lesion within pancreas, bile and pancreatic duct dilatation in head
- Distinct category of tumours collectively called periampullary tumour: of pancreas tumours (double duct sign)
- Any evidence of extra-pancreatic spread: Involvement of regional lymph nodes,
Malignant cells arise from one of a few cells:
liver metastases, ascites
(a) Duodenal epithelium (best outcome out of all three)
(b) Biliary ductular epithelium 3. MRI pancreas with MRCP – MRI pancreas is not superior to CT scan; MRCP is
(c) Ampullary ductular epithelium useful in delineating biliary system anatomy especially if the system is not
The periampullary tumours have better tumour biology than pancreatic adenoca obstructed and there are no therapeutic indications for ERCP (since there are
Prognosis is also better as they present earlier with obstructive jaundice considerable risks with ERCP)
4. ERCP with stenting to relieve obstruction (in cholangitis) - Complications of Whipple’s operation
Mortality rate is 2-7%, with a morbidity rate of up to 20-30% (mostly mild
5. Endoscopic ultrasound + FNA biopsy
complications)
- Can be used to stage tumour and nodal involvement
- FNA with EUS guidance is preferred to transcutaneous biopsy as there is less Intraoperative/early complications
risk of tumour seeding (a) Injury to other organs – liver, kidney, bowel
(b) Bleeding
STAGING (c) Infection sepsis
1. CT/MRI of the abdomen – T, N stage; metastasis to the liver (d) Pancreatitis
2. Endoscopic ultrasound – T, N stage (e) Pancreatic anastomotic leak (5-20%)
(f) Biliary anastomotic breakdown
3. Lungs – CXR + CT thorax (g) Fistulation, pseudocyst formation may occur due to anastomotic leaks
4. Bones – bone scan when suspicion is high
Late
5. Staging laparoscopy – for peritoneal metastases, just before definitive operation (a) Long-term exocrine insufficiency resulting in malabsorption and
for a resectable tumour (since CT/MRI may miss small peritoneal deposits) if no steatorrhoea
peritoneal disease found, continue with surgery, otherwise, close up and abort (b) Gastric stasis with pylorus-preserving Whipple’s
surgery (c) Diarrhoea resulting from autonomic nerve injury during lymph node
dissection
TREATMENT (d) Endocrine insufficiency DM
SURGERY
Palliative surgery
Curative resection
- Improves chances of survival Surgical bypass of obstruction
- However, recurrence rates after surgery are high – 5 year survival only 10 to 30% - Triple bypass involving anastomosis between
- Only about 15-20% of patients will have resectable disease at presentation – usually (a) Stomach and jejunum (gastrojejunostomy)
in periampullary or head of pancreas tumours; tumours of the body and tail present (b) Biliary system and jejunum (choledocho-/hepatico-/cholecysto-jejunostomy)
too late to be resectable (c) Jejunum and jejunum, to prevent reflux of food into biliary tree – essentially a
- Resectable disease: Roux-en-Y loop (jejunojejunostomy)
No metastases (lung, liver, bone, peritoneum)
Patent superior mesenteric vein and portal vein NON-SURGICAL PALLIATIVE MEASURES
Definable tissue plane between tumour and superior mesenteric artery as well as 1. Endoscopic stenting
coeliac axis - Stenting of obstructed biliary duct
- Stenting of obstructed duodenum
- Whipple’s operation
Pancreaticoduodenectomy for head of pancreas or periampullary tumour 2. Coeliac plexus block for pain
Usually preceded by a staging laparoscopy to confirm absence of peritoneal 3. Palliative chemotherapy/radiotherapy/chemoradiotherapy
metastases - Not shown to provide good outcomes
Removal of the head of the pancreas, duodenum, proximal 15cm of jejunum,
common bile duct, gallbladder, and distal part of the stomach
Common hepatic duct and pancreas are then anastomosed to the jejunum, 45-
60cm proximal to the gastrojejunostomy
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DISEASES OF THE BILIARY SYSTEM 2. Aetiology – benign or malignant
- Recurrent spikes of similar jaundice that resolve on their own with time suggest
APPROACH TO OBSTRUCTIVE JAUNDICE benign obstruction e.g. stones, strictures
- A young patient with painful jaundice usually benign cause
CAUSES - Previous history of gallstone disease or biliary colic symptoms
Intraluminal Benign - Previous history of surgery to the biliary tract or ERCP
- Gallstones - Malignancy is suggested if the patient is old, jaundice is of new onset and
- Parasitic infections (recurrent pyogenic cholangitis) progressively worsening, and there is no associated pain (i.e. painless
Mural Benign progressive jaundice)
- Post-instrumentation strictures (ERCP, operation) - Constitutional symptoms: loss of appetite, loss of weight, malaise
- Strictures from other causes (gallstones, chronic pancreatitis) - Metastatic symptoms: bone pain, neck lump, dyspnoea, etc
- Primary sclerosing cholangitis - Pain is a late symptom of pancreatic cancer and tends to be constant and
- Choledochal cyst relentless compared to biliary colic which subsides after a few hours
Malignant 3. Complications
- Cholangiocarcinoma (distal)
- Symptoms of cholangitis: fever, chills, rigors with RHC pain and jaundice
Extramural Benign - Fat malabsorption: steatorrhoea, fat-soluble vitamin deficiency (A, D, E, K) –
- Mirizzi syndrome especially coagulopathy (very unlikely in acute setting)
Malignant - Liver decompensation: encephalopathy
- Head of pancreas cancer - Pruritus as a result of bile salt retention
- Periampullary cancer
- Metastases to the porta hepatis PHYSICAL EXAMINATION
1. Vitals: Is patient haemodynamically stable? Any fever?
HISTORY 2. General inspection: Jaundice. Pallor? Any abdominal distension, leg swelling?
1. Confirm obstructive jaundice 3. Peripheries: Stigmata of chronic liver disease? Scratch marks? Conjunctival pallor?
- Confirm jaundice – patient’s sclera are yellow 4. Abdomen
- Establish obstructive jaundice – tea-coloured urine, pale stools - Any scars of abdominal surgery?
- Exclude pre-hepatic and hepatic jaundice (more importantly hepatic jaundice - Generalised distension? (ascites could be due to malnutrition, peritoneal
since it can also cause tea-coloured urine) malignancy, or obstruction of portal vein by cancer)
Symptoms suggestive of viral hepatitis: prodrome of fever, malaise, - Hepatomegaly? (Could be due to metastatic disease, or primary liver pathology)
arthralgia, myalgia, nausea/vomiting, etc. - Enlarged gallbladder? (Recall Courvoisier’s law – if the gallbladder is palpable
Risk factors for viral hepatitis: travel history, ingestion of seafood, family in a person with painless obstructive jaundice, the cause is unlikely to be stones)
history of hepatitis (esp mother, siblings), blood transfusions, drug - Splenomegaly? (Portal hypertension – think prehepatic, hepatic, posthepatic)
abuse/needle sharing, needlestick injuries, sexual contact
5. DRE: Pale stools?
Alcohol intake
Drug history: any TCM intake recently, any new medications taken 6. Cervical and supraclavicular lymph nodes
History of chronic liver disease 7. Bony tenderness
8. Respiratory examination
INVESTIGATIONS (guided by clinical suspicion after Hx and P/E) STONE COMPOSITION AND PATHOPHYSIOLOGY
Bloods Cholesterol stones
1. FBC – any infection, anaemia - More common in older patients (peak at 40-50 years)
2. U/E/Cr - Cholesterol stones are hard and faceted
3. LFT – bilirubin raised, more direct bilirubin than indirect in obstructive jaundice; - Cholesterol stones results from disruption in the solubility equilibrium of bile
ALP and GGT should be raised more than AST and ALT in an obstructive picture - Risk factors for cholesterol stones formation:
4. PT/PTT – any prolonged PTT from vitamin K malabsorption, liver dysfunction 1. Increased cholesterol secretion in bile
5. Tumour markers – CA 19-9, CEA (cholangioca and pancreatic ca) Obesity
Hyperlipidaemia
Imaging
Increased oestrogens: female, pregnancy, exogenous administration
- Ultrasound versus CT
2. Decreased emptying of the gallbladder
Both useful in demonstrating dilated biliary system and site of obstruction as Gallbladder malignancy is an important cause to exclude
well as the cause of obstruction Truncal vagotomy
Ultrasound is sufficient if malignancy is unlikely, but CT is preferred if there is a Spinal cord injury
suspicion of malignancy as it can define the tumour better and also have a
staging function at the same time to determine involvement of nodes and other Pigment stones
organs - More common in younger patients
- Pigment stones are soft stones and crumble easily
MANAGEMENT - Can be divided into black pigment stones and brown pigment stones
The patient is managed as for the causative aetiology (see relevant sections)
- Black pigment stones are composed of mostly calcium salts and bilirubin –
predisposing factors include increased secretion of bilirubin into bile (e.g. chronic
haemolysis, chronic liver disease, TPN), decreased bilirubin solubilisers, and
gallbladder stasis
GALLSTONE DISEASE - Brown stones are composed of calcium salts, bilirubin, and more cholesterol than
black pigment stones; they form in the biliary ducts due to infection with bacterial
DEFINITION
degradation of biliary lipids, the degradation products of which then precipitate
Gallstone is a generic term for any kind of stone (cholesterol, pigment) in any part of
the biliary system (gallbladder, cystic duct, hepatic duct, common bile duct, etc)
Biliary sludge
- Microlithiasis suspended in bile; a milieu that predisposes to stone formation
EPIDEMIOLOGY - Can be visualised on the ultrasound scan as layering in the biliary tree
- Exact incidence in Singapore not known
- Sludge is a pre-stone condition, but not all sludge becomes stones
- In the West: overall 10-15%; 20% in women and 10% in men
- 20% of biliary sludge will disappear, 60% recur, and 10% form stones
- Consistent 2:1 female to male ratio
- Typical picture (the F’s): Fat, female, forty, fertile, flatulent
CLINICAL COURSE
NORMAL PHYSIOLOGY OF BILE Asymptomatic
- Normal bile contains bile salts (primary and secondary), phospholipids, cholesterol, - 80-95% of patients will have asymptomatic gallstones
protein, and bilirubin - Risk of symptom occurrence is 1 to 2% per year, of which the greatest risk is
- Bile salts and phospholipids are amphiphatic and help to solubilise cholesterol within the first 5 years of diagnosis – 10% at 5 yrs, 15% at 10 yrs, 18% at 15-20 yrs
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- Of those who develop symptoms, 7-10% will have moderate symptoms, and 3-5% INVESTIGATIONS FOR GALLSTONE DISEASE
severe; the rest will have minor symptoms
1. Plain abdominal X-ray
- Thus the majority of patients do not require removal of the stones or the
gallbladder expectant management - Pickup rate for gallstones is less than 10% since most stones are radiolucent
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- Definitive treatment – laparoscopic cholecystectomy - Patient is usually toxic, requiring urgent surgery
Timing of cholecystectomy
- Dependent on several factors: 3. Gangrene and perforation
Severity of illness - Localised perforation abscess that is confined by the omentum
Response to resuscitation and antibiotic therapy - Free perforation generalised peritonitis and sepsis, requiring emergency
Logistical considerations (availability of OT, surgeon etc) laparotomy
- Possibilities available: 4. Cholecystenteric fistula
i. Emergency (immediate; in very sick patients who are not doing well/not - Most commonly occurs in duodenum, then colon, and stomach; after repeated
responding to treatment) attacks of cholecystitis
ii. Early (within few days of onset) - Usually asymptomatic
iii. Delayed/interval (after 6-8 weeks) - On AXR, aerobilia is seen in 40% of cases
Early Delayed - Symptomatic fistulas should be treated with cholecystectomy and fistula closure
Advantages Advantages
- Everything done in one admission - Lower risks 5. Gallstone ileus
- Easier to operate as the gallbladder is - Better laparoscopic success - Stones causing cholecystenteric fistula pass into the enteric lumen causing
oedematous intermittent bouts of small bowel obstruction
- Accounts for 1-2% of IO overall
Disadvantages Disadvantages - Most common site of obstruction is terminal ileum
- Ongoing inflammation higher risk - Fibrosis difficulty mobilising - Small stones (<2-3cm) usually pass spontaneously without problems
of bleeding gallbladder - Mortality is 10-15%, mostly in elderly patients in whom gallstone ileus is more
- Higher risk of injuring some other - Need for another admission common
structure due to difficulty in - Chance of recurrence during the time
- Small bowel enterotomy proximal to the point of obstruction is usually required
visualisation
to remove the stone
- Higher conversion rate to open chole
- Increased risks of post-op infection - Immediate cholecystectomy not warranted as <4% of patients will have further
symptoms
Early surgery has been found to be more beneficial than delayed surgery
PRESENTATION
- Painless jaundice (painful if there is cholangitis)
RECURRENT PYOGENIC CHOLANGITIS
- Acholic stools BACKGROUND
- Pruritus Cholangiohepatitis, or recurrent pyogenic cholangitis (RPC), is characterized by:
- Advanced signs and symptoms: - Recurrent bacterial cholangitis
Abdominal pain - Intrahepatic pigment stones
Fatigue, malaise - Intrahepatic biliary obstruction.
Weight loss
Hepatomegaly
PATHOPHYSIOLOGY
Helminthic infxn (eg Ascaris lumbricoides, Clonorchis sinensis) epithelial damage
DIAGNOSIS predispose to seeding of coliforms into biliary system stone formation
- CA 19-9 >100μl/ml (good sensitivity of 89%, specificity 86%) recurrent cholangitis
- Contrast CT
- PTC (2 functions: 1) roadmapping for surgery; 2) drainage of obstructed system if
ERCP cannot drain) HISTORY:
- A history of recurrent attacks of cholangitis – typical hx:
1-2 episodes of fevers, jaundice, and RUQ abdominal pain per year
CURATIVE TREATMENT Hx of prev biliary surgery, endoscopic procedures, or percutaneous biliary
- Surgery is the only chance of long-term cure drainage procedures.
- Only 25% of tumours are resectable
- Complications of pyogenic cholangitis
- Contraindications to surgery cirrhosis with portal hypertension
Bilateral or multifocal intrahepatic disease cholangiocarcinoma
Invasion of portal vein trunk or hepatic artery
Bilateral involvement of hepatic arterial or portal venous branches
PHYSICAL EXAMINATION
Unilateral hepatic vascular invasion with contralateral ductal spread
No specific physical findings are evident in RPC. Dx based on history.
Distant metastases
DIFFERENTIALS
PROGNOSIS FOR RESECTABLE DISEASE (5-year survival) Primary Sclerosing Cholangitis
- Intrahepatic: 35-45%
- Distal 35-45%
- Perihilar 10-30% (worse prognosis due to early lymphatic spread) INVESTIGATIONS
For diagnosis
PALLIATION For Complications
- Endoscopic/percutaneous transhepatic biliary stenting Bloods
- Bilateral drainage for hilar cholangiocarcinoma - FBC
- If after opening up and finding that tumour is not resectable, can perform surgical - LFT with ALP>ALT, AST
bypass - Prothrombin time: N/ (if prolonged cholestasis causes fat malabsorption and
vitamin K deficiency)
Impt to exclude – correct with parenteral Vit K before invasive procedures
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- Blood C/S: bacteremia – results help guide antibiotic choice.
- Ova and parasites: RPC freq a/w Clonorchis infxn – look for it and treat when present.
Radiology
- U/S HBS
segmental biliary dilatation
hepatolithiasis
liver abscesses
helps determine choice of supplemental axial imaging techniques.
- ERCP or PTC – imaging modality of choice for delineating the biliary tree.
- CT scan
centrally dilated bile ducts with peripheral tapering
bile duct stones
pyogenic liver abscesses.
TREATMENT PRINCIPLES:
- Treat current infection
- Biliary drainage
- Management of other complications e.g. dehydration etc
Surgical
- Usual surgical approach includes:
Initial biliary decompression – ERCP sphincterotomy / stent placement
Definitive biliary drainage procedure – e.g. Roux-en-Y choledochojejunostomy
PROGNOSIS
- Death occurs in approximately 15-20% of patients over 5-6 years.
DISEASES OF THE BREAST Level II: posterior to pectoralis minor
Level III: medial to pectoralis minor, extending up to apex of axilla
ANATOMY 2. Internal mammary nodes
- The breast is a modified sweat gland that lies in the subcutaneous tissue of the Account for about 20% of drainage from the ipsilateral breast – upper and
anterior chest wall between the superficial and deep layers of the superficial fascia lower inner quadrants
- The base of each breast extends from the lateral border of the sternum to the mid- About 4 nodes per side, with one node in each of the first three interspaces
axillary line, from the second to the sixth rib and one in the fifth or sixth interspace
- The axillary tail pierces the deep fascia and enters the axilla 3. Interpectoral (Rotter’s nodes) – between pec major and pec minor muscles
- Each mammary gland consists of 15-20 lobules that are drained by lactiferous ducts
that open separately on the nipple
PRESENTATION OF BREAST DISEASE
- Fibrous septa (Cooper’s ligaments) interdigitate the mammary parenchyma and
extend from the posterior capsule of the breast to the superficial layer of fascia within 1. Breast lump (painful vs painless)
the dermis, and provide structural support to the breast (involvement of these 2. Pain with no lump (cyclical vs non-cyclical)
ligaments by malignancy causes dimpling of the overlying skin) 3. Nipple changes or discharge
HISTORY
1. History of lump
- Site of the lump? Single or multiple?
- When was it first noticed? Why was it noticed (pain, self-examination, etc)?
- Duration since first noticed
- Lymphatic drainage: - Painful or painless?
1. Axillary nodes – 75% of ipsilateral breast drains to the axillary nodes - Overlying skin changes noted: erythema, warmth, dimpling, swelling? Any
1. 40-50 nodes in total, in 5 groups: Anterior, posterior, medial, lateral, general asymmetry of the breasts noticed?
apical - Any increase in size from first noticed to now?
2. Drain secondarily into supraclavicular and jugular nodes - Any changes in the nipple e.g. retraction
3. Anatomic division into levels I, II and III by the pectoralis minor - Nipple discharge? If present, what is the colour and consistency?
muscle: - Any other lumps elsewhere – other breast? Axilla? Neck?
Level I: lateral to pectoralis minor
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2. Oestrogen exposure history and other risk factors for cancer Palpation
- Age of menarche (early menarche <12 years old increased risk) - Patient should be lying down at 45 degrees to the horizontal with her hand tucked
- Whether married, and if married, how many children (nulliparity) behind her head – this splays the breast out so it can be palpated properly
- Age at which first child was born (>30 years old) - Start with the normal side first!
- Whether patient breastfed her children, and if so, for how long after birth - Ask for any pain before starting to palpate
- Is patient currently postmenopausal? If so, how old was she when she became - Use one hand to retract and stabilise the breast and palpate with the other
menopausal? (>55 years old)
- Palpate in a systematic manner e.g. quadrant by quadrant from centre outwards
- Use of hormonal replacement therapy and/or oral contraceptive pills
- Be thorough and examine the entire breast including the axillary tail
- Family history of breast cancer or ovarian cancer (BRCA gene) especially if
cancer occurs in first degree relative below the age of 40, or in bilateral breasts - When the lump is located, check with the patient whether this is the same lump she
- Previous breast cancer that has been treated detected on her own
- Previous biopsy of the breast showing atypical ductal hyperplasia or LCIS - Characterise the lump:
- Exposure to ionising radiation Site (which quadrant)
Tender or non-tender
- Alcohol intake, especially before age of 30
Warmth of overlying skin
3. Systemic review Size
- Loss of appetite, loss of weight Shape
- Fever (infective cause) Surface (smooth or nodular/irregular)
- Bone pain (metastasis) Consistency (soft, firm, or hard)
Fluctuance
PHYSICAL EXAMINATION Margins (regular and smooth, or irregular and ill-defined)
Preliminaries Fixation to the skin – try to pick up the skin above the lump
- Introduce yourself to the patient, ask for permission to examine the breast Fixation to underlying muscle – ask patient to press her hands against her hips to
contract the pectoralis major muscle, then try to move the lump in 2
- Always have a chaperone to accompany you if you are male
perpendicular directions, then ask patient to relax and try to move the lump again
- Expose patient adequately from the waist up with exposure of axillae
- Good lighting - Don’t be happy just finding one lump, still examine carefully for other lumps
(multiple lumps are unlikely to be malignant, usually fibroadenoma or fibroadenosis)
- Position the patient at 45 degrees or sitting position if a bed is not available
- If the patient complains of nipple discharge and none is visible, ask patient if she can
Inspection show you the discharge by expressing it herself (NEVER squeeze the nipple
- Start off with patient’s hands relaxed at her sides – look for any asymmetry in the yourself!); if patient cannot do it, then ask the chaperone to help
breast contours, any obvious skin changes (peau d’orange, erythema, puckering)
- Look for any scars of previous operation, or procedure e.g. punch biopsy Axillary lymph nodes
- Then ask patient to raise her arms (to accentuate any tethering to the skin which - Palpate the normal side first
shows up as dimpling) - Rest the patient’s right forearm on your right forearm and use your left hand to
- Ask the patient to push her hands against her hips to contract the pectoralis major palpate the right axilla (vice versa for the left side)
muscles – this may reveal a previously unnoticeable lump - Palpate gently, slowly, and systematically, covering the major groups of nodes:
- Look for nipple changes (7 D’s): anterior, posterior, medial, lateral, and apical
Discolouration Depression (retraction) Destruction - If any lymph nodes are found to be enlarged, note the number of lymph nodes, their
Discharge Deviation (Duplication – unlikely) site, size, tenderness, consistency (firm, hard, matted), mobility
Displacement
To complete the examination - Stellate lesion is a localised distortion of the breast parenchyma without
- Examine the cervical lymph nodes especially the supraclavicular nodes perceptible mass lesion – high chance of it being malignant
- Examine the lungs for any pleural effusion - Causes: Invasive cancer, radial scar (a benign lesion), fat necrosis,
- Percuss the spine for bony tenderness abscess, etc
- Examine the abdomen looking for hepatomegaly (d) Architectural disortion
- Look at the axilla on the MLO view for any enlarged lymph nodes
FINDINGS FOR THE COMMON BREAST LUMPS - BI-RADS (Breast Imaging Reporting and Data System) classification
Type of lump Age Pain Surface Consistency Mobility Category 0: Need additional imaging evaluation
Cyst 30-55 Occ Smooth Soft to hard Not fixed Category 1: Negative (nothing to comment on, 0.05% risk still present)
Nodularity 20-55 Occ Indistinct Mixed, Not fixed Category 2: Benign
fluctuant Category 3: Probably benign, short-term follow-up suggested (<0.2% risk)
Fibroadenoma 15-25 No Smooth, bosselated Rubbery Very mobile
Category 4: Suspicious, biopsy should be considered (25-74% risk)
Cancer 35+ No Irregular Stony hard May be tethered or
fixed
Category 5: Highly suggestive of malignancy (75-99% risk)
Category 6: Known malignancy
INVESTIGATIONS 2. Ultrasound
- Usually used as the first investigation in young patients (<35 years old) or
“The evaluation of a breast lump is via the TRIPLE ASSESSMENT – (i) Clinical
pregnant, lactating patients
examination; (ii) Imaging; and (iii) Histology.”
- Can be used to guide interventional procedures such as biopsy, localisation of a
Imaging lump preoperatively, drainage of abscess, aspiration of cyst
1. Mammography - Evaluates consistency (solid vs cystic), margins
- Most sensitive of the proven breast imaging modalities - Localisation of lesion seen in only one mammographic projection
- Usually performed in older women (>40 years old) as the breast tissue in - Evaluation of a palpable mass with a negative mammogram
younger women is denser, more difficult to pick up abnormalities on - Evaluation of mass in mammographically-difficult areas e.g. chest wall, axilla
mammogram - Pitalls: Operator dependent, non-standardised techniques, poor resolution,
- Normally, 2 views are done: craniocaudal (CC) and mediolateral oblique (MLO) “partially blind” to microcalcifications
- Additional specialised views: magnification and coned compression; done on - Features of malignancy:
request to help magnify areas of abnormality or help visualise breast better Markedly hypoechoeic + thick echogenic halo
- Abnormal features: Irregular edges
Hypoechoeic shadowing
(a) Neo-density or asymmetric density
Taller than it is wide (fir-tree appearance)
(b) Microcalcifications High central vascularity
- Calcifications <0.5mm in size (if >0.5mm macrocalcifications)
- Sole feature of 33% of cancers detected on mammography 3. MRI of the breast
- Causes: DCIS, invasive cancer, fibrocystic disease, papilloma - Rarely used due to high cost, but provides good soft tissue definition
- Features of malignancy: pleomorphic microcals, heterogeneous - Indications:
appearance, closely grouped or arranged in a linear pattern (ductal Positive axillary lymph node but mammogram and ultrasound negative
distribution), underlying density Suspicion of multifocal or bilateral malignancy (esp ILC which has a high
- Benign microcals are punctate, and may have a “tea-cup” appearance incidence of multifocality/bilaterality)
(c) Spiculated mass or stellate lesion Assessment of response to neoadjuvant chemotherapy
- 95% of spiculated masses on mammography are due to malignancy When planning for breast conservation surgery
Screening in high-risk patient?
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Histology APPROACH TO NIPPLE DISCHARGE
- Options available:
CAUSES
(a) Fine needle aspiration cytology
(b) Core biopsy (Trucut) Colour of discharge Cause
(c) Incisional biopsy Red or pink (blood + serum) Ductal papilloma
(d) Excisional biopsy Ductal carcinoma
Clear yellow (serous) Ductal papilloma
- Mostly a choice between FNAC and core biopsy
Duct ectasia (= periductal mastitis)
FNAC is less invasive, less painful, smaller wound, does not require any local Cyst
anaesthetic, but only cells are obtained with no histology cannot differentiate Ductal carcinoma
between in-situ cancer and invasive cancer, requires skilled cytopathologist Green, brown, black (cell debris) Duct ectasia
Core biopsy is more invasive, requires local anaesthetic, will result in a larger Purulent, foul-smelling Mastitis/abscess
wound, more painful, risk of complications higher (because biopsy needle is a Thin, white fluid (milk) Galactorrhoea/lactation
spring-loaded firing mechanism, improper angling may result in puncture of the
lung or heart), but can obtain tissue specimen, can stain for ER/PR status better HISTORY:
diagnostic value 1. Is the discharge true?
- Can be guided by clinical palpation (if there is a palpable mass) or radiologic - Exclude other conditions that can cause discharge but not from the nipple e.g.
guidance if the mass is small or there is no palpable mass more accurate but still eczema, Paget’s, etc
not 100% 2. Is the discharge significant?
Ultrasound guidance - Spontaneous discharge or discharge only on pressing (spontaneous is sig)
Stereotactic guidance (stereotactic mammotome) - Intermittent or persistent (persistent is sig)
- Relation to breastfeeding (significant if >1yr after stopping breastfeeding)
MANAGEMENT 3. Is the discharge worrisome?
- If triple assessment suggests benign disease (i.e. all three aspects suggest benign - Unilateral or bilateral (unilateral more worrisome)
nature of lump), follow patient up with physical examination for a year (q3-6mths) to - Discharge from multiple ducts or single duct (single duct more worrisome)
make sure the lump is stable or regresses - Nature of discharge (bloody more worrisome)
- If all three aspects of triple assessment suggest malignancy further staging and - Age of the patient (more worrisome in older patient >60)
treatment 4. Is it troubling the patient?
- If one or two out of three aspects suggest malignancy further workup, may require
excisional biopsy PHYSICAL EXAMINATION (as described above)
INVESTIGATION
1. Discharge for cytology to detect malignant cells
2. Mammography/ultrasound of both breasts to detect any underlying malignancy
3. Histology of lesion if found on imaging
4. Ductography
MANAGEMENT
- If malignancy found, manage malignancy
- Microdochectomy for intraductal papilloma
- Antibiotics for mastitis/abscess + incision and drainage for abscess
- Conservative management for most other pathologies unless discharge persists and is
troubling patient microdochectomy of offending duct
BREAST CANCER Lobular LCIS ILC
- Malignant cells arise from terminal - 5-10% of invasive cancers
EPIDEMIOLOGY duct lobular unit (like DCIS) but do - 10-20% multicentric and/or bilat
- Most common cancer in females in Singapore not distort lobular architecture - Cells morphologically similar to
- Age-standardised incidence 55 per 100,000 in 2002; incidence is half that of the West - Usually does not form palpable cells of LCIS: monomorphic, bland
- Bimodal age distribution, one peak at 45-55 years and another in older women (>75) mass and not detected by mammo, round nuclei
- Gender ratio is about 100-150:1 incidentally detected - Cells invade individually into
- 60-80% multicentric and bilateral stroma (due to loss of E-cadherin, a
RISK FACTORS - Not premalignant, but a marker for cell-adhesion molecule)
1. Age (increases with increasing age with two peaks as mentioned) increased risk of invasive disease in - Similar prognosis to IDC
2. Family history (breast or ovarian cancer, especially if first degree relative, young both breasts (7-10x increased risk)
- If ca develops, will be IDC usually,
onset <40 years old, bilateral cancer in relative affected)
occurs >15 years after diagnosis
3. Genetic predisposition (BRCA1 on 17q, Li-Fraumeni syndrome involving p53
mutation) Others Specialised types
4. Previous breast cancer - Medullary, colloid (mucinous),
5. Alcohol consumption tubular, papillary
6. Oral contraceptive usage - Better prognosis than IDC
7. Hormonal replacement therapy Inflammatory carcinoma
8. Previous biopsy showing atypical ductal hyperplasia or lobular carcinoma in-situ - Presents as erythematous. enlarged,
9. High oestrogen exposure (early menarche <12y/o, nulliparity, late childbearing with swollen breast w/o palpable mass
first child at >30y/o, late menopause >55y/o) - Histologically not specialised
10. Ionising radiation to breast - Diffuse invasion of breast
parenchyma by ca cells blocking
numerous dermal lymphatic spaces
PATHOLOGY swelling
- WHO classification divides breast cancers into epithelial and non-epithelial tumours. - No histo features of inflammation
- Non-epithelial tumours arise from supporting stroma (e.g. angiosarcoma, malignant - Very poor prognosis, rapidly fatal
phyllodes tumour, primary sarcomas) and are very uncommon
- Epithelial tumours arise from cells lining the ducts or lobules, and can be further
divided into invasive and non-invasive based on invasion of the basement membrane PRESENTATION
Non-invasive Invasive - Most patients present with self-detected lump in the breast (more than one-third of
patients), other presentations include painful lumpiness, pain alone, discharge, nipple
Ductal DCIS IDC retraction
- Malignant cells arise from terminal - 70-80% of invasive breast cancer
duct lobular unit, cause distortion - Includes all cancers that cannot be - In patients presenting late, there may be overlying skin changes e.g. peau d’orange,
of lobules, but do not invade BM subclassified into a specialised type tethering (means mass is still mobile but overlying skin will be indented when
- Non-palpable, detected on mammo “no special type” moving the lump), fixation (means the mass is not mobile), even fungation
as microcals - Poorer prognosis than a carcinoma - May have symptoms of metastatic spread e.g. bone pain (metastases from breast
- 35% multicentric, occult invasive of specialised type cancer spread to lung, liver, lymph nodes, bone, brain)
ca in 10-20% - Two-thirds express ER/PR, one- - Increasing number of patients with abnormalities detected on mammographic
- Progress to ca within 10 yrs, ~30% third overexpress C-erbB2 screening but with no palpable lump
risk; considered pre-malignant
- Good prognosis if treated
DIAGNOSIS – BY TRIPLE ASSESSMENT (see above)
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STAGING Survival
- Investigations: Stage I: 90% (70% in 10 years)
(i) Chest X-ray (for lung metastases) Stage II: 60% (40-50%)
(ii) CT chest Stage III: 30% (20-30%)
(iii) CT abdomen Stage IV: 10% (<2%)
(iv) Bone scan
THERAPEUTIC OPTIONS
T stage N stage M stage
Tis: Carcinoma in-situ, Paget’s N1: Mobile ipsilat axillary nodes M1: distant mets Options can be divided into aims of control:
with no tumour N2: Fixed/matted ipsilat axillary nodes (a) Locoregional control:
T1: <2cm Surgery
N3: N3a – Ipsilat infraclav nodes
T1a – 0.1 to 0.5 cm N3b – Ipsilat int mammary nodes
Radiotherapy
T1b – 0.5 to 1.0 cm N3c – Ipsilat supraclav nodes (b) Systemic control:
T1c – 1.0 to 2.0 cm Chemotherapy
T2: 2 to 5 cm Hormonal therapy
T3: >5cm Targeted therapy
T4: T4a – Chest wall involvmt
T4b – Skin involvmt Surgery
T4c – Both 4a and 4b 1. Wide excision (breast-conserving surgery)
T4d – Inflammatory ca - Removal of tumour with clear margins, while achieving good cosmetic result
- Criteria:
Stage 0 Stage I Stage II Stage III Stage IV Tumour <5cm in size, no skin or chest wall involvement (i.e. T2 or less)
Tis Only one tumour, not multiple (unless in the same quadrant)
T1N0 T2N0, T3N0 No metastatic disease
T0N1, T1N1, T2N1 T3 N1 Appropriate tumour size-to-breast ratio (to achieve good cosmetic result)
T0N2, T1N2, T2N2, T3N2
Patient must agree to post-operative radiotherapy
Any T, N3
T4, any N - Overall survival at 25 years for WEAC comparable to SMAC
M1 - Slightly higher local recurrence rates for WEAC (1% per year, 4% in 5 years)
Aaaaa – Stage Xb (e.g. IIb, IIIb) - Higher risk in younger patients as cancer tends to be more aggressive
2. Simple mastectomy
PROGNOSIS
- Removal of breast tissue, nipple-areolar complex, and overlying skin
Prognostic factors: - Lower rates of local recurrence
1. Stage of disease – tumour size, lymph node involvement [Major prognostic factor]
2. Histological grade of tumour 3. Axillary clearance
3. Lymphovascular invasion - Performed for all invasive carcinoma (WEAC or SMAC)
4. Age (younger patient higher chance of recurrence, progress of disease) - Not required for DCIS (because theoretically cancer cells are confined to the
5. C-erbB2/Her-2 positivity indicates more aggressive tumour worse breast)
6. ER/PR positivity is good – more of a “predictive factor” because it predicts - Complications: numbness/pain along inner aspect of arm, shoulder stiffness,
response to treatment with tamoxifen; also means tumour is less undifferentiated lymphoedema
7. p53 mutation
- Sentinel lymph node biopsy is a new modality of treatment Radiotherapy
Principle: the sentinel lymph node, being the first lymph node draining the 1. Adjuvant
breast, is representative of the rest of the axilla; if the SLN is negative for - Usually done after breast-conserving surgery
tumour cells, then the rest of the axillary nodes should be negative as well - Regimen consists of 25 to 30 cycles in total, 1 cycle per day from Monday to
Use of blue dye (isosulphan blue, methylene blue) or radioactive isotope (Tc- Friday over five to six weeks
99 sulphur colloid or colloidal albumin) injected in the area of the breast just 2. Palliative
before surgery concentrates in the first lymph node (sentinel node) that
drains the breast Chemotherapy
During the op, look for the SLN by colour, or using a Geiger-Muller counter 1. Neoadjuvant
to detect the node with highest radioactivity - Given in locally advanced cancer to shrink the tumour before surgical resection
Send node for frozen section - 20% of tumours achieve complete clinical response (cCR) i.e. tumour is no
If negative, do not clear axilla; if positive, perform axillary clearance longer palpable
- Of these tumours, a further 20% will achieve complete pathological response
False negative rate 8% (quite good)
(cPR) i.e. no more tumour cells
No difference in axillary recurrence between full axillary clearance versus - Need to place a clip into the tumour before starting neoadjuvant therapy to guide
only sentinel node biopsy surgery in case the tumour “disappears”
SLN biopsy is now standard of care in many hospitals in SG
2. Adjuvant
4. Palliative surgery - Given in all locally advanced cancers after resection, and in some early breast
- Palliative mastectomy for symptoms (bleeding, fungating, infected tumour) cancers depending on stage (see below)
- Surgery at other sites: Fixation of pathological fractures, decompression of - Premenopausal patients tend to have better response to chemotherapy than
spinal cord compression, surgical excision of brain metastases hormonal therapy (and vice versa for postmenopausal patients)
- Main active agents are the anthracyclines (e.g. doxorubicin, epirubicin) and the
5. Breast reconstruction taxanes (e.g. paclitaxel, docetaxel)
- Safe, can be done during breast surgery or at a later time - Common regimens: AC (anthracycline, cyclophosphamide), FAC (5-FU,
- No delay in subsequent treatment and no increase in rates of relapse anthracycline, cyclophosphamide), CMF (cyclophos, methotrexate, 5-FU)
- Options:
3. Palliative
(i) Prosthesis
- Anthracyclines and taxanes are the mainstay
(ii) Muscle flap from rectus abdominis or latissimus dorsi
- Helps to reduce load of disease to alleviate symptoms, increase survival
Complications of surgery
Hormonal therapy
Early Haemorrhage (POD1)
Wound Infection (POD3) - Used in adjuvant setting
Seroma formation (accumulation of serum) in 50% - For hormone receptor-positive disease
Flap ischemia - Preferred for postmenopausal women as response to hormonal therapy is better than
Late Cosmetic deformity to chemotherapy
Complications of Axillary Clearance: - Mostly used as adjuvant therapy but can also be used as palliative treatment
- Lymphoedema – RT is contraindicated with AC as it worsens oedema Classes
- Cellulitis – even in minor trauma, due to lymphoedema. Need to clean even
(a) Selective oestrogen receptor modulators (SERMs)
minor wounds with antiseptic solution + prophylactic ABx vs staphstrep - Tamoxifen 50% reduction in recurrence, 25% reduction in mortality
- Shoulder stiffness – require physiotherapy
- Side effects: menopausal symptoms (hot flushes, etc), endometrial cancer (0.1%
- Intercostobrachial nerve transection – numbness over inner aspect of arm.
per year), deep vein thrombosis
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(b) Aromatase inhibitors
- Lanastrazole, letrozole, exemestase Adjuvant therapy usually involves chemotherapy if tolerable and/or hormonal
- Inhibit peripheral conversion of testosterone and androstenedione to oestradiol therapy if ER/PR positive
- Only suitable for post-menopausal patients as use of these agents will cause In general: In premenopausal pt chemotherapy + hormonal
overactivity of the HPA axis in premenopausal women In postmenopausal pt hormonal + chemotherapy
- Side effects: musculoskeletal pain, osteoporosis
3. Locally advanced breast cancer
Targeted therapy - T3 or T4 (tumour >5cm or skin/chest wall involvement), N2 or N3 (fixed lymph
node involvement or supraclavicular node involvement)
- Main agent is Herceptin (trastuzumab) which targets Her-2-neu a.k.a. C-erbB2
- Surgical resection dependent on size of tumour and resectability (if tumour is too
receptor (a type of epidermal growth factor receptor [EGFR] that is overexpressed in
large, the skin defect will be very large inoperable)
18-20% of cancers)
- Systemic therapy:
- Used in C-erbB2 positive tumours, early or late stage
Neoadjuvant therapy to downstage inoperable tumour (in addition, it helps by
- Side effects of Herceptin: cardiomyopathy, pulmonary toxicity, infusion reactions,
predicting the tumour response to chemotherapy before resection)
febrile neutropaenia
Adjuvant therapy after resection – chemotherapy or hormonal (as above)
- Other agents include Avastin (or bevacizumab, targets vascular endothelial growth
factor [VEGF] receptor, used in advanced cancer); Lapatinib (targets Her-1 and Her- 4. Advanced breast cancer
2, used in advanced cancers) - Distant metastases
- Minimal locoregional therapy except for palliative purposes
- Systemic therapy is the mainstay of treatment – chemotherapy or hormonal
TREATMENT BY TUMOUR STAGE therapy
Tumour can be divided into in-situ cancer, early breast cancer, locally advanced breast
cancer, or advanced breast cancer. FOLLOW-UP
1. DCIS - 3-monthly for first 2 years
- Wide excision without axillary clearance - 6-monthly for the next 3 years (i.e. third to fifth years)
- Usually no adjuvant therapy - Yearly for another 5 years (to tenth year)
- Some patients given hormonal therapy to reduce recurrence at surgical site; - At each visit – ask about symptoms and do clinical examination
tamoxifen reduces overall breast cancer risk by 50% (in contralateral breast as - Repeat mammo of same breast 1yr postop; then 2-yrly bilateral mammo subsequently
well) – strictly not adjuvant therapy
BREAST SCREENING
2. Early breast cancer
- T2 or less (<5cm), N1 or less (no nodes or non-fixed nodes) Normal risk, 40-49 YO Annual mammogram
- Locoregional therapy: SMAC, or WEAC with postop radiotherapy asymptomatic 50-64 YO Biannual mammogram (by invitation)
- Adjuvant therapy >65 YO Optional 2 yrly mammogram
Purpose of adjuvant therapy is to destroy systemic micrometastases
Likelihood of patient having micromets is deduced from T and N stage (major Increased risk Start screening 5 yrs before Monthly BSE
prognostic factors): onset of breast dz in 6 mthly CBE & U/S breast
Chemo Intermediate No chemo youngest family member Annual mammography
T >20mm, N stage >1 11mm < T < 20mm, N=0 T <10mm, N=0
HRT therapy 40-49 YO Annual mammogram
Look at histological grade
50-65 YO Biannual mammogram up to 5 yrs after cessation of
(minor prognostic factor); if
high grade chemo HRT
PAGET’S DISEASE OF THE NIPPLE
- Presents as erythema and eczematous change of the nipple (not the areola) with
crusting exudates, may develop into erosions and ulcerations
- Often associated with intraductal carcinoma (DCIS) or invasive carcinoma just
beneath the nipple
- Malignant cells invade across the epithelial-epidermal junction and enter the
epidermis of the nipple, breaking the normal epidermal barrier thus allowing fluid to
be extruded onto the nipple
- Examination and investigations should be targeted towards detecting an underlying
tumour – may find a palpable mass and/or mammographic abnormalities
- Punch biopsy of the nipple may be required
- Prognosis of the underlying cancer is not altered by the presence of Paget’s disease of
the nipple
- Treatment should be planned according to the underlying cancer if found
- If no palpable mass or mammographic abnormality is detected, wide excision is an
adequate treatment
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APPROACH TO NECK MASSES MASSES BY LOCATION
Midline
NECK MASSES 1. Submental lymph node
2. Thyroglossal cyst
ANATOMY 3. Thyroid nodule in the isthmus
- The neck is composed of two triangles on each side – anterior and posterior 4. Sublingual dermoid cyst
triangles 5. Plunging ranula (retention cyst of the sublingual)
- The anterior triangle is bounded by the lower border of the mandible superiorly, the 6. Rarely, hyoid pathology e.g. bursa
midline anteriorly, and the anterior border of the sternocleidomastoid posteriorly
- The posterior triangle is bounded by the posterior border of the sternocleidomastoid Anterior triangle
anteriorly, the anterior border of the trapezius posteriorly, and the clavicle inferiorly 1. Lymph node – along anterior border of sternocleidomastoid (levels II, III, IV)
2. Thyroid nodule
3. Submandibular gland mass (see later section on Salivary gland swellings)
4. Branchial cyst + fistula
5. Chemodectoma (carotid body tumour)
6. Carotid aneurysm
7. Pharyngeal pouch
8. Laryngocoele (rare; an air-filled, compressible structure seen in glass-blowers)
Posterior triangle
1. Lymph node – level V and supraclavicular lymph node groups
2. Cystic hygroma
3. Cervical rib
4. Brachial plexus neuroma/schwannoma
- Masses in the neck region can be subdivided according to the triangle they occur in Thyroglossal cyst
as there are pathologies peculiar to each triangle Epidemiology:
- Locations: (i) Midline Equal in males and females. Occurs mostly in children and adolescents but up to one-
(ii) Anterior triangle third occur in patients older than 20 years.
(iii) Posterior triangle
Pathology:
- In general, enlarged lymph nodes are the most common cause of a lump in the neck, A cystic expansion of the remnant thyroglossal tract (the embryological origin of the
regardless of location (see section on Lymph node enlargement) thyroid gland which descends from the foramen caecum on the tongue).
Features: Plunging ranula
Smooth, rounded, cystic lump. 75% are in the midline while 25% are slightly to the left Pathology:
or right. Usually asymptomatic but may become infected with sinus formation and A pseudocyst associated with the sublingual glands and submandibular ducts. Ranulas
seropurulent discharge (occurs with incision or rupture of cyst) can be congenital or acquired after oral trauma. A large ranula can present as a neck
mass if it extends through the mylohyoid musculature of the floor of the mouth – termed
Histology:
Cyst with columnar or squamous epithelial lining which may be ciliated. The cyst may a “plunging” ranula.
also contain thyroid and lymphoid tissue. If malignancy occurs (carcinoma of the Treatment:
thyroglossal duct), it is usually a papillary carcinoma (~90%). - Complete resection if possible, often in continuity with the associated sublingual
gland (but often difficult due to close association with the lingual nerve and
Treatment:
Sistrunk procedure – resection of the cyst and mid-portion of the hyoid bone in submandibular duct).
continuity and resection of a core of tissue from the hyoid upwards towards the foramen - If complete resection not possible, marsupialisation and suturing of the pseudocyst
caecum. wall to the oral mucosa may be effective.
Complications:
Pharyngeal pouch (also called Zenker’s diverticulum) - Cystic hygroma seen on prenatal ultrasound in the first trimester suggests
Pathology: chromosomal abnormality (50% of foetuses, usually trisomy 21) or other structural
A herniation of the pharyngeal mucosa (pulsion diverticulum) through its muscular coat abnormalities (33% of foetuses with no chromosomal abnormality, usually congenital
at the weakest point – Killian’s dehiscence – between the cricopharyngeus muscle and heart anomalies)
the lower inferior constrictor muscles. - May obstruct delivery
- Compressive problems after delivery – respiratory, swallowing
Management: CERVICAL LYMPHADENOPATHY
- Radiological investigations e.g. CXR, CT to delineate extent of cyst
- Non-surgical treatment – aspiration and injection of sclerosant (usually unsuccessful) ANATOMY:
- Surgical excision – partial (to alleviate symptoms) or complete
Cervical rib
Features:
- Usually more symptoms than signs as it causes thoracic outlet syndrome
- A hard mass in the posterior triangle at the root of the neck
- Symptoms/signs:
o Arterial: pallor, gangrene or necrosis of the tips of the fingers
o Venous: oedema, cyanosis
o Neurological: complaints of radicular symptoms (pain, paraesthesia), wasting of
the small muscles of the hand
- Adson’s test can be done – ask patient to extend neck and rotate it towards side of
symptoms radial pulse will be diminished, occasionally with reproduction of
radicular symptoms in the limb
- Diagnosis by CXR
Neuroma/Schwannoma
Features:
- Slow growing tumour arising from peripheral neural structures of the neck e.g.
brachial plexus, cervical plexus, vagus nerve, phrenic nerve, etc.
- Fusiform, is mobile in plane perpendicular to axis of nerve but not parallel
- Usually benign
- May be Tinnel’s positive – tap on the mass for any paraesthesia occurring in
distribution of the nerve Levels
There are six levels of lymph nodes in the neck, and different structures drain to
- DO NOT PERFORM FNA – excruciatingly painful
different groups of nodes:
Level Ia – submental
Ib – submandibular
II – long internal jugular vein from skull base to bifurcation of carotids
(includes jugulodigastric nodes)
III – along internal jugular vein from carotid bifurcation to omohyoid
IV – along internal jugular vein from omohyoid to clavicle
Va – Posterior triangle
Vb – Supraclavicular
VI – Tracheo-oesophageal groove (not palpable)
VII – Superior mediastinum
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Drainage: PHYSICAL EXAMINATION
- Oral cavity and oropharynx levels I – III Inspection
- Thyroid and larynx levels II – VI - Location
- Nasopharynx II – V (usually upper neck – level II and high level V) - Any overlying skin changes e.g. erythema, discharging sinus (multiple lymph node
enlargement with discharging sinuses can be TB or actinomycosis; sulphur granules
CAUSES: seen in actinomycosis)
Can be divided into three main groups: infective, inflammatory, and neoplastic
Palpate from behind, one side at a time – start at submental, then submandibular,
Infective Viral
preauricular, postauricular, along anterior border of sternocleidomastoid,
Epstein-Barr virus, cytomegalovirus (infectious mononucleosis); HIV
supraclavicular, posterior triangle, lastly occipital. Use pulps of the fingers in a gentle
Bacteria
rolling movement.
Streptococcus, Staphylococcus, Klebsiella (from intraoral pathology
e.g. dental abscess, tonsillitis) - Tenderness to palpation
Tuberculosis - Consistency – hard, matted nodes are more suspicious for malignancy
Parasitic - Fixation to overlying skin or underlying structures
Toxoplasma
To complete the examination:
Fungi
Actinomycosis - Complete examination of the face and scalp for any primary site of infection or
neoplasia
Neoplastic Metastatic Head and neck primary
Nasopharyngeal carcinoma - Formal ear, nose, throat examination especially looking at the post-nasal space for
Oral cavity, oropharynx, larynx, hypopharynx, nasopharyngeal carcinoma (NPC being the most common cancer causing enlarged
thyroid, etc. cervical lymph nodes)
Other primary sites (4B’s) - Examination of the thyroid gland
Bowel (stomach, colon), breast, bronchus (lung), - Examination of lymphoreticular system – other lymph node groups, liver, spleen
balls (testicular) - Full respiratory and abdominal examination especially if supraclavicular lymph node
Primary - lymphoma found
Inflammatory SLE - Breast examination in female patient
Kikuchi’s (necrotising lymphadenitis occurring in young females,
presenting as painful cervical lymphadenopathy) INVESTIGATIONS:
Sarcoidosis - Fine needle aspiration provides most definitive results (though there is still the
possibility of false positive and false negative results)
HISTORY - Radiological investigation e.g. ultrasound, CT – to assess nature of lump, extent,
- The lump itself – onset, duration, rate of growth, any pain, associated symptoms, other enlarged nodes that are not clinically palpable, and can be used to visualise
lumps elsewhere primary tumour if present
- Constitutional symptoms
o Fever, malaise, arthralgia, myalgia (viral prodrome); MANAGEMENT:
o Night sweats, low-grade fever (TB, B symptoms of lymphoma); - According to FNAC results
o Loss of appetite, loss of weight (chronic infection, malignancy) - Malignant – work up for primary if present (e.g. squamous cell carcinoma – look for
- Local symptoms – intra-oral diseases e.g. tooth decay, oral/tongue ulcer, tonsillitis oral cavity, skin, ENT, lung malignancy; adenocarcinoma – look for breast, GI tract
- Past medical history – cancer, TB (contact? Diagnosed? treated or untreated?) malignancy) and treat as appropriate
- Social history: travel and contact history, sexual history for HIV - Infective/Inflammatory – treat underlying condition
SALIVARY GLAND SWELLINGS - Histology: predominantly serous acini, many ducts (other glands have few ducts)
ANATOMY: Submandibular gland
Parotid gland
- Consists of a large superficial part and a small deep part that are continuous with one
another around the free posterior border of the mylohyoid
- The deep part of the gland is closely associated with the lingual nerve (with the
- Surrounded by tough fibrous capsule – the parotid sheath (thus mumps is painful as
attached submandibular ganglion) above it, and the hypoglossal nerve and
the gland swells within a tight envelope)
submandibular duct below it – surgery may injure these nerves
- Sandwiched between the posterior border of the ramus of the mandible and the
- Nerve supply: parasympathetic secretomotor supply from lingual nerve carrying
mastoid process
postganglionic fibres from the submandibular ganglion (preganglionic fibres in
- Important structures that pass through the gland in order from lateral to medial: superior salivary nucleus)
(i) Facial nerve and its branches
(ii) Retromandibular vein (formed as the maxillary veins drain into the superficial - Submandibular duct (of Wharton) arises from the superficial part of the gland, runs
temporal vein) forwards deep to mylohyoid and drains into the oral cavity at the sublingual papilla
(iii) External carotid artery (branching into its two terminal branches, the just adjacent to the frenulum
superficial temporal and maxillary arteries) - Histology: mixed serous and mucous acini, few ducts
- Nerve supply:
(i) Parasympathetic secretomotor supply from auriculotemporal nerve carrying Sublingual gland
postganglionic fibres from the otic ganglion (preganglionic fibres from inferior - A small almond-shaped gland sitting just under the mucosa of the floor of the oral
salivary nucleus); cavity
(ii) Somatic sensory supply of the gland from auriculotemporal nerve; sensory - Each gland has 15 or so ducts, half of which drain into the submandibular duct, the
supply of the capsule from the great auricular nerve. rest draining directly into the oral cavity
- Parotid duct (of Stensen) runs 5cm across the masseter (surface marking: along the - Nerve supply is similar to the submandibular gland
line joining the intertragic notch to the midpoint of the philtrum), drains into the - Histology: almost solely mucous acini, few ducts
mouth opposite to the upper second molar tooth
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HISTORY - Palpate the gland openings for stones.
- About the lump: onset, duration, progress, associated symptoms e.g. pain - Bimanual palpation of the submandibular gland
- If pain is present, is it precipitated by food ingestion? (suggestive of sialolithiasis) - Facial nerve examination
- Symptoms of infection e.g. fever, malaise; if considering mumps, ask about testicular
pain and swelling (orchitis), abdominal pain (pancreatitis) Suspicious features of malignancy:
- Any noticed asymmetry of the face – incomplete closure of the eye on one side, - Hyperaemic hot skin over lump
drooping corner of the mouth, drooling - Pain
- Fixation to underlying structures or skin
- Does the patient have symptoms of xerostomia (e.g. cannot eat a piece of biscuit or
bread without water), xerophthalmia - Hard consistency
- Irregular surface or ill-defined border
- History of connective tissue disease e.g. rheumatoid arthritis, SLE - Facial nerve involvement
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Features: Mucoepidermoid ca is the most common malignant tumour in the parotid, while
- Slow-growing, painless swelling occurring in the lower pole of the parotid adenoid cystic ca is the most common in the submandibular, sublingual and minor
- Irregular and lobulated surface, texture of cartilage (slightly harder than Warthin’s) salivary glands
- Does not invade or metastasise
- Chance of malignant transformation if left for 10-15 years (1-6% risk) Malignant pleomorphic adenoma
- If not completely excised, can recur (recurrence rate of 2%) - Usually occurs in pre-existing pleomorphic adenoma, rarely de novo
- Worst prognosis of any salivary gland tumour
Diagnosis by clinical, FNAC, + MRI - 30-70% recurrence and metastasis rate
Treatment – surgical excision
- Parotid: Superficial parotidectomy for superficial tumour; if tumour is deep or large, Treatment of salivary gland cancers
total parotidectomy with preservation of the facial nerve Parotid:
- Submandibular: Total gland excision together with adjacent connective tissue, - Total parotidectomy with sacrifice of facial nerve if tumour has infiltrated it (may be
sparing lingual and hypoglossal nerves grafted with great auricular nerve)
- Radical neck dissection if neck nodes positive
- Postoperative radiotherapy
Warthin’s tumour
Epidemiology: Submandibular:
- Only occurs in the parotid gland (10% of parotid tumours) - Radical excision of gland with lymphatic clearance of submandibular triangle
- More common in males than females (4:1) - Radical neck dissection if neck nodes positive
- Occurs in older patients (>50 years) - Postoperative radiotherapy
- Related to cigarette smoking
COMPLICATIONS OF PAROTIDECTOMY
Histology:
Also called papillary cystadenoma lymphomatosum or just adenolymphoma. Consists Immediate (within 24 hrs)
of cleftlike or cystic spaces lined by two-tiered epithelium, containing mucin, 1. Intraoperative facial nerve transection – lower motor neurone palsy (in surgery to
surrounded by a stroma of well-developed lymphoid tissue with germinal centres. the submandibular gland, damage to the hypoglossal and/or lingual nerves can
occur intraoperatively)
Features: 2. Reactionary haemorrhage
- Slowly enlarging, soft to firm cystic fluctuant swelling in parotid tail
- Invariably benign with no risk of malignant change Early (1 to 30 days)
1. Wound infection
Diagnosis by clinical, FNA + MRI
2. Skin flap necrosis
Treatment 3. Temporary facial weakness (neuropraxia of facial nerve)
- Can be left alone if absolutely certain that the entire mass is composed of only 4. Salivary fistula
Warthin’s tumour cells, since there is no malignant potential 5. Division of great auricular nerve loss of sensation over pinna
- Superficial parotidectomy if causing trouble to patient 6. Trismus (inability to open mouth due to spasm of masseter)
Treatment Surgical resection Surgical resection Palliative therapy for Chemotherapy and/or
- Hemithyroidectomy for selected low-risk patients (see below) - Aggressive resection – total thyroidectomy with compressive effects radiotherapy depending
- Total thyroidectomy for the majority level VI node clearance - Chemotherapy to shrink on type of lymphoma
- LN clearance: tracheo-oesophageal nodes cleared, and neck dissection if - Sampling of cervical and mediastinal nodes and tumour
neck nodes are positive modified dissection where positive - Surgical debulking
- For suspicious lesion – hemithyroidectomy with histology, KIV TT - Tracheostomy
No good adjuvant therapy
Adjuvant therapy Follow-up
- Radioactive iodine at ablative levels to ablate remnant thyroid and any
- Thyroxine replacement (not for TSH suppression but
cancer tissue (only for total thyroidectomy)
to maintain euthyroid state)
- External radiotherapy (only shown to have good results in pts with locally
- Serum calcitonin and CEA six mths after surgery (if
advanced follicular ca)
normal, considered cured – 5% 5yr recurrence)
TSH suppression – give L-thyroxine to suppress TSH levels to <0.005U/L - High calcitonin – screen for residual or metastatic
disease, treat surgically, with RT or chemo as
Follow-up
appropriate
- Check TSH levels
- Thyroglobulin as a tumour marker of recurrence
- Radioactive iodine scan to detect recurrence, followed by ablation
5yr survival 95% in low-risk pts, 88% in intermediate-risk pts, 50% in high-risk pts 60-70% Median survival <6mths Dependent on histo, stage,
Slightly worse for follicular ca treatment, etc.
Differentiated thyroid cancer Disadvantages of TT:
- Papillary and follicular cancers are considered differentiated thyroid cancer (as - Risk of bilateral recurrent laryngeal nerve injury and permanent hypoparathyroidism
opposed to anaplastic – undifferentiated – thyroid cancer) - Very low incidence of cancer recurrence in residual thyroid – microfoci probably not
- Prognosis is excellent clinically significant
- Limited thyroidectomy may spare patient from having to be on lifelong thyroid
RISK STRATIFICATION: hormone replacement
- Risk factors can be divided into patient factors and disease factors Thus, risk stratification helps to guide the extent of surgical resection in differentiated
- Patient factors: Age – >45 years old is high risk; Gender – male is high risk thyroid cancer according to the patient’s disease.
- Tumour factors:
Size – nodule >4cm has higher risk Lymph node clearance
Histology – tall cell variant of papillary ca and Hurthle cell variant of follicular ca - Tracheo-oesophageal groove (level VI) node clearance usually done
are considered unfavourable - Radical neck dissection or modified radical neck if:
Extrathyroidal extension into surrounding structures – worse (i) Tracheo-oesophageal groove nodes histologically positive for cancer
Lymph node or distant metastases – worse (ii) Clinically positive nodes in the neck – palpable or enlarged on ultrasound
- Various score systems have been formulated to stratify risk:
AMES – Age, Metastases, Extent, Size Radical neck dissection
AGES – Age, Grade (Histological), Extent, Size) – rarely used as histological - The removal, en-bloc, of the entire ipsilateral lymphatic structures of the neck, from
grading is not commonly performed the mandible superiorly to the clavicle inferiorly, from the infrahyoid muscles
MACIS – Metastasis, Age, Completeness of resection, Invasion, Size medially to the anterior border of the trapezius laterally
- Patients can be divided into three groups: - Classic radical neck dissection (Crile’s) – internal jugular vein, sternocleido-
(i) Low risk – low risk patient and low risk disease (i.e. no high risk features) mastoid muscle, and accessory nerve are resected. Structures not resected: carotid
(ii) Intermediate risk – low risk patient with high risk disease, or high risk patient arteries, vagus nerve, hypoglossal nerve, brachial plexus, phrenic nerve
with low risk disease
- Modified radical neck
(iii) High risk – high risk patient and high risk disease
(i) Type I: one of the three structures not removed, usually accessory nerve
- Risk helps to guide treatment – low risk patients can undergo hemithyroidectomy (ii) Type II: two of the structures not removed – accessory and IJV
without ablative radioiodine therapy post-op, while high risk patients undergo total (iii) Type III: all of the three structures not removed
thyroidectomy with post-op ablative RAI treatment; treatment in intermediate risk (iv) Extended radical neck dissection: resection of lymph nodes and/or structures
patients is tailored to the disease, but usually is similar to that in high risk patients not included in the classic neck dissection
- 5 year survival is also prognosticated by the risk: low risk patients have a survival - Complications of radical neck dissection:
of 95-98%, intermediate risk patients 88%, and high risk patients 50% (i) Injury to nerves – vagus (vocal cord paralysis), cervical sympathetic chain
(Horner’s), mandibular branch of facial (lower lip weakness)
TOTAL THYROIDECTOMY VERSUS HEMITHYROIDECTOMY (ii) Haematoma bring back to OT to find source of bleeding and stop it
Advantages of TT: (iii) Salivary fistula (usually when pt has received RT to the neck, and if the upper
- Evidence for microfoci of disease and multicentricity of cancer – removal of the GI tract was opened during the surgery) – infection can result
entire thyroid decreases risk of recurrence (iv) Wound infection – risk factors: previous irradiation, if upper aerodigestive tract
- Ability to use adjuvant radioiodine to ablate any residual cancer tissue after surgery is opened during surgery with salivary contamination, salivary fistula
- Ability to use radioiodine to detect recurrent disease (normal thyroid picks up iodine (v) Carotid blowout – risk factors: infection, irradiation resus, apply constant
better than cancer cells, thus the presence of the thyroid gland will decrease the pressure all the way to the OT!
ability of RAI to pick up recurrent cancer) and as treatment for recurrence (vi) Poor healing – usually in irradiated skin; weakest point is the junction of the
- Ability to use serum thyroglobulin as a cancer marker for recurrence trifurcate incision
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Multiple endocrine neoplasia PART IV: SURGERY IN BENIGN THYROID DISEASE
A group of inherited diseases resulting in proliferative lesions (hyperplasia, adenomas, Indications for surgery:
carcinomas) of multiple endocrine organs. 1. Cannot be treated medically - failed medical therapy or unsuitable for medical tx
2. Cancer
FEATURES:
3. Compression on neighbouring structures
- Tumours occur at younger age than sporadic cancers
4. Cosmesis
- Multiple endocrine organs involved, either synchronously or metachronously
5. Compliance/cost problems – with long-term medical therapy (but patient may still
- Multifocal tumours in each organ involved
require long-term therapy after op if he/she becomes hypothyroid or is still
- Tumour usually preceded by asymptomatic stage of endocrine hyperplasia
hyperthyroid)
- More aggressive and higher chance of recurrence compared to sporadic type of
6. Child-bearing (not a very strong indication since medical therapy can still be given,
tumours in the same organs
but not RAI)
MEN 1
- Autosomal dominant inheritance Types of surgery available:
- Gene involved is the tumour suppressor gene MEN1 located on chromosome 11q13 1. Hemithyroidectomy – removal of one lobe of the gland, including the isthmus and
where mutations cause loss of function of the gene the pyramidal lobe; usually for suspicious thyroid nodules
- Three P’s: 2. Total thyroidectomy – entire gland removed completely; usually done in MNG
Parathyroid (95%) – hyperparathyroidism from hyperplasia of parathyroid glands 3. Subtotal thyroidectomy
Pancreas (>40%) – aggressive metastatic tumours (e.g. gastrinoma, insulinoma), - Conventional subtotal thyroidectomy – leave a thumb-sized amount (about 4-6g)
leading cause of death in MEN 1 patients of remaining thyroid tissue on both sides
Pituitary (>30%) – most commonly prolactin-secreting macroadenoma; some have - Harley-Dunhill subtotal thyroidectomy – leave a thumb-sized amount only on
growth hormone-secreting tumours one side with removal of the rest of the gland
MEN 2
Total versus subtotal thyroidectomy (for hyperfunctioning thyroid disease)
- Autosomal dominant inheritance
- Gene involved is RET protooncogene at 10q11.2 where activating mutations occur - Result of total thyroidectomy is always hypothyroidism, thus the patient will require
- Two distinct groups of disorders: life-long thyroid replacement and follow-up problems with compliance, cost,
inconvenience
1. MEN 2a (Sipple syndrome)
Medullary carcinoma of the thyroid (almost all) - Results of subtotal thyroidectomy (at 5 years):
Phaeochromocytoma (50%, of which less than 10% are malignant) o 60-70% euthyroid (do not require medication but still have to be followed up
Parathyroid hyperplasia and hyperparathyroidism (30%) closely)
o 16-20% hypothyroid (usually becomes evident within 1 year of surgery)
2. MEN 2b (William syndrome) o 8-10% hyperthyroid (percentage increases proportionately with time failure of
Thyroid and adrenal involvement like MEN 2a, but no hyperparathyroidism surgical therapy)
Neurocutaneous manifestations: ganglioneuromas on oral mucosa, lips eyelids
Other features: Marfanoid habitus, SCFE, delayed puberty Difficulty in managing post-operatively and in the long term as patients need
close monitoring (better off to just replace everyone after TT?), but weigh this
against the benefits of not requiring any medication (for which there is a good chance)
Complications of thyroid surgery: (Mostly H’s, one I and one T) LATE (MORE THAN 30 DAYS)
IMMEDIATE (<24HRS) 1. Hypothyroidism
1. Haemorrhage with haematoma formation 2. Hyperthyroidism (failed treatment)
- Haematoma forms in the paratracheal region, mostly below the strap muscles 3. Permanent hypoparathyroidism
can result in compression of airway if not released (patient can die!)
- Cut the subcuticular stitches and also the stitches holding the strap muscles 4. Hypertrophic scarring or keloid formation – ask patient if he/she has keloids
opposed to let the blood drain out
2. Hoarseness or airway compromise from recurrent laryngeal nerve injury
- Risk of nerve injury is <1%
- Unilateral nerve injury for hemithyroidectomy, bilateral nerve injury for total or
subtotal thyroidectomy
- If bilateral nerve palsy resulting in compromised airway, will require
tracheostomy
3. Hyperthyroidism
- Resection of gland can release large amounts of stored thyroid hormone into
bloodstream
- May result in thyroid storm (see Management of thyroid storm)
4. Tracheomalacia
- Floppiness of trachea resulting from chronic compression e.g. by large goitre
- Requires intubation to secure airway
Acute Chronic
Critical Non-critical.
- External iliac artery continues as the femoral artery after crossing the inguinal Asymptomatic Claudicants.
ligament (surface landmark: the mid-inguinal point i.e. midway between the pubic
symphysis and the anterior superior iliac spine)
- The femoral artery then divides into the superficial femoral and the profunda femoris
(or deep femoral) arteries about 4cm below the inguinal ligament ACUTE LIMB ISCHAEMIA
- The profunda femoris supplies the compartments of the thigh via two main branches, Acute limb ischemia is defined as a sudden decrease in limb perfusion that causes a
the medial and lateral circumflex femoral arteries potential threat to limb viability (manifested by ischemic rest pain, ischemic ulcers,
- The superficial femoral runs distally and passes through the adductor hiatus to reach and/or gangrene) in patients who present within two weeks of the acute event (if >2
the popliteal fossa, where it changes its name to become the popliteal artery weeks, it is considered chronic ischaemia).
- The popliteal artery divides into the anterior tibial artery and the posterior tibial The decrease in perfusion is usually due to sudden occlusion of a feeding arterial vessel,
(also called tibioperoneal trunk by some), and the posterior tibial will give off the and this may be in a setting of already narrowed vessel lumen (acute on chronic
peroneal artery ischaemia) or in a normal lumen.
CAUSES:
4. Dissecting aortic aneurysm
1. Arterial embolism - As the blood dissects between the intima and media of the aorta, it can cause
- Most common cause of acute limb ischaemia (60-80% of the time) occlusion of the aortic branches at their origins
- The most likely source of embolus is the heart (80%), of which 70% is due to
atrial fibrillation, 20% to AMI with left ventricular mural thrombus, and a small PATHOPHYSIOLOGY
proportion to prosthetic heart valves
In order of sensitivity to ischaemia, the tissues affected are nerves (most sensitive),
- Non-cardiac emboli arise from other arteries where there are atherosclerotic muscle, skin, and bone (least sensitive); thus early signs of ischaemia involve pain and
plaques or an aneurysm (the embolic material may be thrombus or part of a numbness, and muscle paralysis as well as skin changes occur later. The lower limb can
plaque, but atheroemboli are less likely to cause complete arterial occlusion) survive about 6 to 8 hours in an ischaemic state before injury becomes irreversible.
- Most common sites where emboli lodge:
Bifurcation of the femoral artery (most common site) PRESENTATION
Trifurcation of the popliteal artery (next most common site in the lower limb)
The classic 6 P’s of acute limb ischaemia: Pain, Paraesthesia, Pallor, Pulselessness,
Aortic bifurcation
Paralysis, Perishingly cold
External and internal iliacs
Arm (about 20% of emboli) Pain
- Emboli usually cause lower limb ischaemia mostly - Develops acutely
- After emboli obstructs the vessel, thrombus can propagate distally (due to stasis - Starts off in a distal part of the extremity and then progresses proximally, increasing
of blood) and proximally (due to turbulence of incoming blood hitting embolus) in severity with time
by derangements in the Virchow’s triad - Further progress leads to decrease in pain as the nerves die off from ischaemia
- Important to ask for any previous claudication pain (10% of claudicants can develop
2. Acute thrombosis
acute ischaemia due to thrombosis of the stenosed vessel)
- Thrombosis of a previously stenotic but patent artery (atherosclerotic vessel)
- Less common cause of acute limb ischaemia Paraesthesia
- When thrombotic occlusion of a vessel does occur, the resulting ischaemia is - Starts off with paraesthesia (develops relatively early in the course of ischaemia) and
usually less severe than in an embolic occlusion, because collaterals have had develops to complete loss of sensation
time to form around the chronically stenosed vessel
Pallor
- Other less common causes of acute thrombosis include the arteritides (usually
- Assess skin colour, temperature, and capillary refill
affecting medium-sized arteries), ergotism, and hypercoagulable states (notably
antiphospholipid syndrome). - The limb may still be slightly pink though pale, but in severe ischaemia it can be
marble-white (especially in embolus where there are no collaterals)
3. Arterial trauma - Other colours:
- Increasing incidence of acute arterial occlusion due to endovascular diagnostic Mottling/Marbling (patches of blue on white): deoxygenation of stagnated blood;
or interventional procedures surrounding areas of pallor are due to vasoconstriction
- Trauma can cause development of an arteriovenous fistula that shunts blood Duskiness: due to deoxygenation of stagnated blood; if there is fixed staining (i.e.
away from the limb does not blanch on pressure) then the limb is non-viable
- Fracture or dislocations can stretch an artery and cause an intimal tear while the Black: gangrene
media and adventitia layers are intact (because they contain elastin and can - The disclouration usually affects a large part of the distal limb e.g. the toes, foot;
stretch) a thrombus forms at the site of the tear where underlying rarely does it only affect one toe (more in chronic ischaemia)
thrombogenic collagen is exposed - The site of arterial occlusion is usually one joint above the line of demarcation
- Compartment syndrome can result from trauma as well between normal and ischaemic tissue
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Pulselessness EARLY ANTICOAGULATION
- If able to feel one good pulse (PT or DP), quite unlikely that the limb is ischaemic, - Important to start anticoagulation with heparin if the suspicion of acute limb
but still possible ischaemia is high
- If unable to feel, assess with a handheld Doppler the arterial and venous flow in the - Give IV heparin bolus 3000-5000 units
limb – there can still be flow without a palpable pulse - Follow with IV heparin infusion at 1000 units/hour
- Also feel the pulses on the other limbs – gives a clue as to whether the cause is - Ideal PTT is 2 to 2.5 times normal
embolic or thrombotic (see below)
INVESTIGATIONS
Paralysis
- Pre-operative investigations
- Total paralysis occurs late and usually indicates that the limb is non-viable
- Can assess viability of muscle by making a cut – viable muscle will be shiny and - FBC, U/E/Cr, PT/PTT, GXM
twitches in response to flicking, while dead muscle will be dull and will not twitch - CXR and ECG if patient is older than 40 yrs old
- Dangerous to save dead muscle as reperfusion can cause circulation of toxic - If suspecting an AMI with mural thrombus, do cardiac enzymes
metabolites in the muscle - Angiogram can be done in patients with viable limb, but in patients with threatened
limb there is no time for angiogram may do on-table angiography
CLASSIFICATION OF SEVERITY (SVS/ISCVS) [Angiography is useful in confirming an occlusion, the cause – thrombotic or
Three categories: viable, threatened and non-viable embolic – and also pinpointing the level of occlusion and the anatomy]
(i) Viable: No immediate threat of tissue loss
(ii) Threatened: Salvageable if revascularised promptly DEFINITIVE TREATMENT OPTIONS
(iii) Non-viable: Limb cannot be salvaged and has to be amputated, no emergency to
Surgical Endovascular
operate. Patient may require revascularisation to allow lower amputation or help
- Embolectomy - Thrombolysis
the amputation to heal
- Endarterectomy - Angioplasty
Viable Threatened Non-viable - Bypass grafting - Stenting
Pain Mild Severe Variable - Fasciotomy
Capillary refill Intact Delayed Absent (fixed stain) - Primary amputation
Motor deficit None Partial Complete
Sensory deficit None Partial Complete In general, embolectomy is done for embolic occlusion, while thrombolysis is done for
Arterial Doppler Audible Inaudible Inaudible thrombotic occlusion.
Venous Doppler Audible Audible Inaudible
Treatment Urgent work-up Emergency surgery Amputation Embolectomy
- Can be done under LA but still require anaesthetist to monitor patient as he may be
quite sick (e.g. AMI), and hyperkalaemia with cardiac arrhythmia can occur after
DIFFERENTIATING BETWEEN EMBOLIC AND THROMBOTIC CAUSE
reperfusion
Embolic Thrombotic - Involves clamping of the involved artery and making an arterotomy
Identifiable source Present – AF, recent AMI Less common
Claudication hx Negative Positive - A Fogarty balloon catheter is inserted into the artery until distal to the clot, then the
Physical findings Contralat pulses present Contralat pulses diminished balloon is inflated to trawl the clot out of the artery
White limb (no blood) Dusky limb (collaterals still - Check for forward-bleeding and back-bleeding of the vessel (i.e. free spontaneous
supplying limb) flow from proximal and distal ends of the artery when unclamped)
Angiography Minimal atherosclerosis, Diffuse atherosclerosis, - Flush with heparinised saline
sharp cut-off, few collaterals irregular cut-off, well-
developed collaterals - Check foot – warm foot with good pulse indicates reperfusion
- Important to monitor ECG for any arrhythmias! CHRONIC LIMB ISCHAEMIA
- Closure of arterotomy with meticulous haemostasis as patient is on heparin Chronic limb ischaemia can be divided into critical and non-critical limb ischaemia,
- Post-op: patient monitored in high-dependency; look out for reperfusion injury and non-critical ischaemia further subdivided into that which causes symptoms (usually
The reperfused muscles become oedematous, increasing pressure in the claudication) and that which is asymptomatic.
compartments of the leg, like compartment syndrome
Patient complains of calf pain Most common cause is atherosclerosis with gradually developing diffuse stenosis of
the peripheral arteries resulting in diminished blood supply to the lower limb
Unable to dorsiflex ankle as the anterior compartment is affected first (imbalance between supply and demand). Multiple collaterals form to bypass the
Requires three compartment fasciotomy to release pressure obstructed vessels as a compensatory mechanism
- Need to convert to full warfarin anticoagulation, uptitrating dose until INR 2-2.5
before stopping heparin (patient at risk of further embolic events) CRITICAL LIMB ISCHAEMIA
- Discharge patient to anticoagulation clinic for follow-up with warfarin advice Critical limb ischaemia is defined as decrease in limb perfusion that causes a
potential threat to limb viability (manifested by ischemic rest pain, ischemic ulcers,
Thrombolysis and/or gangrene) in patients who present more than two weeks after the acute event
- Angiogram done before thrombolysis to locate occlusion (the converse of the definition of acute limb ischaemia).
- Thrombolysis catheter inserted into the clot, and the thrombolytic agent is infused
FEATURES:
- Patient will be in high-dependency with thrombolytic infusion for 6 hours (~1000-
1. Rest pain requiring regular opioid analgesia (e.g. codeine) lasting >2 weeks
4000 units per minute)
AND/OR
- After 6 hours, redo angiogram to check for residual clot; if some clot remains, adjust
2. Gangrene or ulcers over the toes or feet
catheter into the clot and infuse for 6 more hours
AND
- After complete lysis of the clot, can do angioplasty
3. Objective indication of poor vascular supply to the lower limbs
- Takes much longer than embolectomy (a) Ankle brachial pressure index <0.5
- Thrombolysis may be preferred for embolism in a diseased artery, since it may be (b) Toe pressure <30 mmHg
difficult to trawl out the clot in a diffusely stenosed vessel – the clot may get caught
I. Rest pain
on a proximal stenosed segment
- Severe pain in the distal portion of the lower limb (usually toes, foot but may
involve more proximal areas if disease is severe) occurring at rest
Results:
- Pain is aggravated or precipitated by lifting the limb, relieved by dependency of
- Embolectomy has a 20% mortality, almost full success rate
- Thrombolysis has a 10% mortality, only 35% successful the limb – many patients sleep with the leg hanging over the side of the bed to
relieve the pain
- So severe as to disturb sleep at night
- Not easily controllable with analgesia – requires opioids to control pain
II. Ischaemic ulcers
- Usually arise from minor traumatic wounds with poor healing
- Often painful
- Most often occur on the tips of the toes, bunion area, over the metatarsal heads
(ball of the foot), lateral malleolus (as opposed to venous ulcers that occur over
the medial malleolus)
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- Usually deep, dry, punctate (unlike venous ulcers that tend to be superficial, moist, NEUROGENIC CLAUDICATION
diffuse) - Vascular intermittent claudication needs to be differentiated from neurogenic
- May become infected resulting in cellulitis, even abscess formation, and spread to claudication which can also present as pain in the lower limb on exertion
involve the underlying bone and joints osteomyelitis, septic arthritis - The characteristic of neurogenic claudication is “park bench to park bench” where
the patient has to sit down and flex the spine to relieve the pain (pain results from
III. Gangrene
compression of the cord and spinal nerves in spinal stenosis; extension of the spine
- Cyanotic, anaesthetic tissue associated with or progressing to necrosis
further narrows the spinal canal while flexion widens it)
- Occurs when arterial blood supply falls below that which is necessary to meet
minimal metabolic requirements - “Claudication distance” of neurogenic claudication is more variable
- Either dry or wet: - Pulses will be absent/diminished in vascular but not in neurogenic claudication
DRY – hard, dry texture. Often has a clear demarcation between viable and
necrotic tissue. Occurs in patients with atherosclerotic disease. Safe and can be TAKING A HISTORY OF CHRONIC LIMB ISCHAEMIA
allowed to autoamputate after demarcation with precautions against infection. 1. Claudication
WET – moist, swollen, frequently blistered. Often occurs in diabetics with - Which part of the lower limb does the pain occur in
decreased sensation and unrecognised trauma. An emergency requiring surgical - Nature of the pain
debridement or amputation. - Radiation
- Severity
NON-CRITICAL LIMB ISCHAEMIA WITH CLAUDICATION - Aggravating factors – exertion
- Relieving factors – rest (just standing is sufficient)
Intermittent claudication is defined as a reproducible discomfort of a defined group - Associated symptoms e.g. impotence in LeRiche’s
of muscles that is induced by exercise and relieved with rest. Usually described as the
- When did pain first start
patient as a cramping, aching pain in the muscle group on exertion such as walking, and
- Progress since first noticed until currently (worsening pain, increasing areas of
alleviated on stopping (patient does not have to sit down for pain to go away) – “shop
lower limb affected, pain on less exertion, development of rest pain)
window to shop window”.
- Current claudication distance
- Usually affects the superficial femoral near to the adductor hiatus, or the popliteal - How has symptoms affected lifestyle e.g. impaired mobility
artery calf pain
2. Any rest pain
- Foot claudication results from involvement of the tibial and peroneal arteries, but
- Site, nature, severity
rarely do patients with claudication due to atherosclerosis get foot pain alone (more
common in Buerger’s) - Aggravating factors – raising the limb
- Relieving factors – putting limb in a dependent position
- Thigh claudication results in common femoral artery or aortoiliac disease
- Able to relieve with normal analgesics? Or require opioid analgesia?
- LeRiche’s syndrome arises from occlusion of the aortoiliacs, and is composed of a - How long has rest pain lasted for requiring opioid analgesia (if more than 2
classical tetrad of buttock claudication, impotence in men, absent femoral pulses (and weeks, considered a feature of critical limb ischaemia)
distal pulses), and occasionally presence of aortoiliac bruits.
3. Any ulcer or gangrene in the lower limb?
- Important to determine the “claudication distance” – within a short period of time
the distance is usually fairly constant, but can shorten as the disease progresses - Ask about onset of ulcer/gangrene
- Progress (stable, or increasing in size, getting worse)
CAUSES OF VASCULAR CLAUDICATION - If ulcer, any preceding trauma? Ill-fitting shoes? Altered sensation in the foot?
- Most commonly atherosclerotic disease Does patient take care to protect foot? Pain? Redness/swelling/warmth in
surrounding skin? Purulent/foul-smelling discharge from the ulcer?
- Other less common causes: ergot toxicity, Takayasu’s arteritis, Buerger’s disease
(thromboangiitis obliterans), vasospasm
- If gangrene, is it wet or dry? Redness/swelling/warmth in surrounding skin? Any Neuropathic ulcers form at areas such as the ball of the foot and the heel
feeling in the toe involved? Any sensory changes in the other normal toes, foot, - Size, shape
limb?
- Edges (punched out – arterial; sloping – venous)
- Any systemic signs of infection – fever, chills, rigors, malaise
- Base
4. Risk factors (“Arteropath”) Depth of the ulcer (can see underlying tendon? Down to bone?)
- Diabetes mellitus – take a full diabetic history including other complications Appearance of the base – Necrotic? Granulating (beefy-red)? Sloughy?
- Hyperlipidaemia Any discharge – pus, blood?
- Heart disease
- Surrounding skin
- Stroke
Erythema (cellulitis) – there may be an underlying abscess (confirm on
- Smoking
palpation)
- Family history
Blistering, purplish colour (possibility of necrotising fasciitis)
5. Drug history
5. Presence of gangrene
- Aspirin intake
- Wet (infected) or dry (not infected)
- Any allergies to contrast (for angiography)
- Extent of gangrene (level of demarcation)
- Ergots
6. (If the patient has diabetes, may see deformities – Charcot’s joint)
6. Social history
- Premorbid function and current function Feel
- Social support and home condition (need to climb stairs?)
1. Warmth of the skin
- Use the dorsum of the fingers of both hands to simultaneously run up the
PHYSICAL EXAMINATION patient’s feet to the shins and thighs bilaterally
Examine the patient’s lower limbs in a warm room, with the patient exposed optimally - Compare the temperature on both sides (note if one side is cooler)
(from the thighs to the feet, wearing underwear). Patient is supine with the bed flat. - If one limb feels cool, feel for the level where the skin becomes warm
2. Capillary refill
Look - Press hard on a toe for a few seconds, then release
1. Colour of the lower limb - Normal capillary refill should be 2 seconds or less
- White (pallor); pink (normal); blue/dusky (cyanosed); mottled - If a toe is blue, check for blanchability (fixed staining = dead toe)
2. Trophic changes 3. Palpating the ulcer if present
- Loss of hair - Any surrounding tenderness (infection)
- Dry, shiny skin - Bogginess of surrounding tissue (may have abscess formation)
- Nail changes - See if any discharge from the ulcer when palpating
- Wasting
4. Pulses
3. Presence of any diabetic dermopathy - Feel the distal pulses and work your way proximally
4. Presence of ulcer - Posterior tibial pulse: one-third of the way down a line joining the medial
- Look carefully at the entire lower limb, including the heels (ask patient to flex at malleolus to the heel
the knee so you can look at the heel) and between the toes - Dorsalis pedis pulse: one third of the way down a line joining the midpoint of
- Site of the ulcer the two malleoli to the cleft between the first and second toes
Venous ulcers form at the medial malleolus - Popliteal pulse: Ask patient to bend the knee ~60-90 degrees, then palpate
Arterial ulcers are more distal, usually between the toes, and at pressure deeply in the popliteal fossa with the fingers of one hand pressing the fingers of
points such as the lateral malleolus; the other [If the pulse is very well felt, suspect a popliteal aneurysm]
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- Femoral pulse: Midpoint of the line joining the pubic symphysis to the anterior This ankle pressure is then divided by the brachial pressure (the higher of the
superior iliac spine (mid-inguinal point), just below the inguinal ligament two brachial pressures for both upper limbs) to get the ankle-brachial
pressure index
- Grading of pulses: 2+ is normal; 1+ is diminished (but may be normal for
popliteal); negative if not felt label on a stick-figure diagram - Interpreting the values
Normal ABPI is greater than 0.9 (can be more than 1.0 as ankle pressures
Move tend to be higher than brachial; if >1.3, suggests non-compressible calcified
1. Buerger’s test vessel)
- Do one side at a time ABPI between 0.5 to 0.9 – occlusion, often associated with claudication
- Holding the heel of the foot, with the patient’s lower limb straightened, slowly ABPI <0.5: Critical ischaemia
lift the entire lower limb, looking at the colour of the toes - Accuracy of the index
- Stop when the toes become pale (white) ABPI below 0.9 has 95% sensitivity and 100% specificity for detecting
- Estimate the angle the lower limb makes with the horizontal – this is the angiogram-positive peripheral arterial disease and is associated with >50%
Buerger’s angle stenosis in one or more major vessels
Normal lower limb can be raised to 90 degrees without turning white; if the - Exercise treadmill testing
Buerger’s angle is less than 20 degrees, this indicates severe ischaemia Measure ABPI before and after patient exercises on a treadmill
- There may be venous guttering of the lower limb at this angle as well If the ABPI falls by >0.2 claudication
- If the patient is lying near the side of the bed, tell the patient that you’re going to
put his leg over the edge of the bed before gently abducting the hip and then 2. Duplex ultrasound
letting the leg drop over the edge of the bed - Non-invasive test, good alternative to angiogram
- Look at the leg for reactive hyperaemia (the leg turns purple-red) - Duplex (means two modalities) = 2D ultrasound (like the normal kind) plus
Doppler ultrasound (measures flow and waveforms)
Complete the exam - Normal arterial flow waveform should be triphasic; biphasic and monophasic
- Examine the rest of the pulses waves are abnormal
- Offer to auscultate over the femoral and popliteal arteries for bruits - Can define anatomy of occlusions and also look for relatively good arteries
- Examine the abdomen for any abdominal aortic aneurysm distally for “landing zone” of bypass graft
- Measure the ankle-brachial pressure index (ABPI)
3. Angiogram (arteriogram)
- Invasive and associated with risks of bleeding from arterial puncture,
INVESTIGATIONS dissection/damage to artery with worsening ischaemia
1. Ankle-brachial pressure index - Usually only done if planning intervention e.g. angioplasty, stenting
- How the ankle-brachial pressure index is done - Preparing for angiogram:
Brachial pressure is measured with a blood pressure cuff around the arm and Take informed consent from patient
a Doppler probe at the brachial artery – cuff is inflated until the arterial Ask about contrast allergy, asthma, renal disease, metformin
signal is obliterated, then slowly deflated until the signal just starts being Investigations: FBC (platelets impt), PT/PTT, creatinine
detected, at which the pressure is recorded - Angiogram with digital subtraction – the images of the underlying bone are
Ankle pressures are measured in a similar manner, with the cuff around the removed so as to better visualise the arteries (if the bones are visible, then it is a
calf and the Doppler at the dorsalis pedis and posterior tibial arteries – one normal angiogram, without digital subtraction)
reading for each artery
The ankle pressure to be used for each leg is the higher of the two taken
ASSESSMENT OF SEVERITY 1. Angioplasty
The three L’s of peripheral arterial disease: Stenting usually not done for lower limbs except in aortoiliacs (since stent
(i) Life – does disease threaten life (e.g. sepsis; other complications of atherosclerosis needs to be placed in a vessel which is relatively fixed and won’t be
e.g. stroke, AMI;) or will intervention cause risks kinked/bent by movement)
(ii) Limb – will patient lose the limb Angioplasty only effective for focal stenotic lesions and better for large
(iii) Lifestyle – is the lifestyle of the patient severely handicapped, does it require vessels
intervention Problem with angioplasty is that it is not long-lasting – restenosis can occur
New method: subintimal angioplasty – if lumen is so occluded that guide
Fontaine system
wire cannot pass through, the guidewire is threaded into the subintimal space
Stage I: Asymptomatic
to create a dissection around the occluded segment, and this space is then
Stage IIa: Mild claudication
angioplastied to create a channel parallel to the actual lumen for blood to
Stage IIb: Moderate to severe claudication
flow through
Stage III: Ischaemic rest pain
Stage IV: Ulceration or gangrene
2. Bypass grafting
Consider bypass when lesions cannot be treated by angioplasty i.e. lesion
TREATMENT OF CLAUDICATION extends for long distance through the vessel and/or no lumen for guide wire
Conservative to pass through (complete occlusion)
- Smoking cessation Needs a good “landing zone” for graft distally – if vessel is diffusely
- Exercise training diseased, difficult to perform bypass
Exercise at least half to one hour every day
Walk until pain comes, rest 2-3 minutes, walk again TREATMENT OF CRITICAL LIMB ISCHAEMIA
Keep a walk diary recording daily claudication distance in paces
Will stimulate collateral formation symptoms get better Need to revascularise – see interventions above
- Podiatrist to teach foot care
- Assessment of cardiovascular risk factors and treatment to optimise control – AMPUTATION
cardiologist Indications (3 D’s)
- Teach patient about symptoms of critical ischaemia, to return to ED if such 1. Dead
symptoms arise Necrotic tissue
- Antiplatelets e.g. aspirin 2. Dangerous
Gangrene, ascending sepsis
- ?Use of Vasteral (methoxyphylline)
3. Damn nuisance
- Monitor regularly with measurement of ABPI Non-functional limb; bad smell; pain; constant need to dress wound
Intervention (endovascular or surgical) - Level of amputation depends on vascularity of the limb and the indication (e.g. if
- At least 6 months of conservative treatment first infected, need to amputate above level of infection)
- Monitor claudication distance and ABPI – intervene if deteriorating despite - As far as possible try to preserve function of the lower limb
conservative management - May require revascularisation interventions before amputation to ensure good healing,
- If parameters improve but then plateau, discuss with patient about whether he can or to enable lower amputation
accept the level of symptoms, and the risks of intervention weigh risks against - Do not simply amputate without ensuring good vascular supply to the surgical site,
benefits otherwise the wound will not heal
- Usually do angioplasty rather than bypass as it is less invasive, though may not be as
effective in treating the symptoms
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ABDOMINAL AORTIC ANEURYSM
PHYSICAL EXAMINATION
EPIDEMIOLOGY - Ensure vitals stable
More common in men than in women (4:1 ratio) - Visible pulsation over abdomen
Predominantly in older patients (>60 years old) - Pulsations and mass in epigastric region felt on deep palpation
Other risk factors: smoking, hypertension, strong family history (Marfan, Ehler-Danlos) - Mass is expansile – when fingers of both hands are placed at the edges on either side
of the mass, the fingers are pushed upwards and outwards
PATHOLOGY - Auscultate for bruit over the mass
- An aneurysm is a localised abnormal dilatation of a blood vessel wall or the heart - Check the other arteries – femoral, popliteal – for any aneurysm, and listen for bruits
- True aneurysms are bound by all layers of the blood vessel wall, while a false - Look at the lower limbs for any gangrene, infection, etc
aneurysm is a breach in the blood vessel wall leading to an extravascular haematoma
that freely communicates with the intravascular space INVESTIGATIONS
- Atherosclerosis is the most common aetiological factor – plaque formation results in Mostly imaging to delineate aneurysm CT Scan
destruction of the tunica media (and the elastin fibres in it) arterial wall thinning
and loss of elastic recoil dilatation MANAGEMENT
- Other causes: cystic medial degeneration (in Marfan), trauma, infection (mycotic) Dependent upon clinical context – is patient asymptomatic, symptomatic but not yet
- Location: usually infrarenal (95% of cases), may extend to involve common iliac ruptured, or ruptured?
arteries, rarely beyond
Ruptured AAA
- Size: 3 to 15 cm (normal aorta is 2cm in diameter) - Very high mortality – nearly 100% if frank rupture (will not get to ED in time)
- Shape: Usually fusiform – long dilated segment (versus saccular which is spherical) - Most of the patients who reach the ED (about 50% reach ED alive) have a leaking
- Often contains mural thrombus due to turbulence and stasis AAA with a tamponade effect by the retroperitoneal structures
- High suspicion in unstable hypotensive patient complaining of severe sharp pain
RISK OF RUPTURE radiating to the back; may feel a pulsatile mass in the abdomen
- Small aneurysms <5cm have a 2-3% chance of rupture per year, while aneurysm 1. Stabilise patient – resuscitation with fluid and blood products
larger than 5.5 cm will have a 10% risk of rupture per year
2. Call for vascular surgeon
- 75% of aneurysms 7cm or larger will rupture in 5 years
3. Do not intubate as neuromuscular blocking agents will reduce tamponade effect,
worsening haemorrhage
PRESENTATION 4. Bring to operating theatre for open repair – surgeon’s main task is to quickly
- Most commonly asymptomatic, found incidentally during imaging isolate the aorta and clamp it proximally (can be clamped for about 30 minutes
- Most feared presentation is that of rupture – patient complains of intense abdominal without significant visceral ischaemia)
pain radiating to the back, becomes rapidly hypotensive and goes into shock 5. After clamping the aorta, the AAA is incised, the surrounding haematoma and
- Thromboembolism distally – gangrene of feet (trash feet) mural thrombus within the AAA are cleared out
- Local compression on neighbouring structures e.g. ureter 6. Synthetic graft (Dacron – polytetrafluoroethylene) is placed within the aorta and
- Obstruction of branches from aorta e.g. iliac, renal, mesenteric, vertebral the vessel wall closed up over the graft i.e. the graft forms the lumen of the aorta
7. Most common complication postoperatively is renal insufficiency – can be
reduced by giving frusemide or mannitol pre-operatively before anaesthesia
induction
- Mortality rate of repair operation in this setting is about 50%
Non-ruptured AAA
- Time available for investigation of size of AAA and related anatomy
- Indications for surgery:
(a) Aneurysm > 5.5 cm in largest diameter
(b) Increase in diameter of more than 1cm per year
(c) Symptomatic aneurysm – back pain, tenderness on palpation, distal embolism,
ruptured/leaking aneurysm
- Patient’s fitness for surgery needs to be properly assessed because it is a major
operation – need to optimise cardiovascular function
- Operation is the same except that it is done under elective setting
- Mortality is <5% in the elective setting, serious morbidity ~10%
Endovascular stenting
- An alternative to open repair which is less invasive, can be done under GA
- Mortality ~1%, but serious morbidity rate is similar to open repair: 10%
- Involves deployment of a non-porous stent within the aneurysm to form the lumen of
the aorta – requires adequate “neck” proximally and good landing site distally
- Not as good results as open surgery; need to do an angiogram every 6 months to
check position of the stent (ensure that stent has not migrated)
COMPLICATIONS OF SURGERY
Intraoperative/early
1. Acute myocardial infarction – most patients already have atherosclerotic disease of
coronary vessels and are at risk of AMI (responsible for 50-60% of mortality)
2. Stroke (due to hypotension or embolism)
3. Renal insufficiency
4. Colon ischaemia – occurs in 2-6%
5. Trash foot – embolism of thrombus from the aneurysm
6. Infection of graft
7. Spinal cord ischaemia (quite uncommon)
Late
1. Aortoenteric fisula – frank PR bleeding, torrential
2. Late infection of prosthetic graft material
3. Sexual dysfunction
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PERIPHERAL VENOUS DISEASE - Course of the great saphenous vein:
Arises from the medial end of the dorsal venous arch of the foot
ANATOMY OF THE VENOUS SYSTEM OF THE LOWER LIMB Passes anterior to the medial malleolus
Runs up the leg posteriorly to pass behind the medial surface of the knee
Then runs anteriorly and laterally up the thigh
Pierces the cribriform fascia at the saphenofemoral junction to drain into the
femoral vein
- The superficial system and the deep system communicate through communicating
veins that contain valves which allow only one-way flow of blood from the superficial
vein into the deep vein
1. Venous dilatations
(a) Telangiectasias (spider veins or venous stars – intradermal veins) CEAP CLASSIFICATION OF CHRONIC VENOUS INSUFFICIENCY
(b) Reticular veins (slightly larger intermediate veins)
(c) Varicosities (visible, dilated tortuous superficial veins; formed by main
tributaries of the saphenous veins because these do not have a strong coat of
smooth muscle in their walls, unlike the saphenous veins; they are more
superficial and not bound down to the deep fascia)
(d) Corona phlebectactica (a network of small dilated venules beneath the lateral
and/or medial malleolus with severe venous hypertension)
2. Oedema – pitting: The hallmark of CVI; present in all but the earliest stages
Unilateral oedema worsened by dependency (worse at the end of the day) and better
with recumbency
3. Skin changes
(a) Hyperpigmentation of the skin over medial lower third of the leg (gaiter
area) – due to extravasation with haemosiderin deposits
(b) Atrophie blanche – hypopigmented scars of healed venous ulcers (avascular
and fibrotic skin)
(c) Venous stasis eczema – pruritic, weeping, scaling, with erosions and crusting
(d) Lipodermatosclerosis – a fibrosing panniculitis of the subcutaneous tissue that
results in a firm area of tender, indurated, hyperpigmented skin that is fixed to VARICOSE VEINS
subcutaneous tissue. Varicose veins are dilated, tortuous veins. They can be divided into primary varicose
Results from severe venous hypertension veins, where the cause is unknown (may be related to posture and components and
Starts in the gaiter area and extends circumferentially to surround the leg structure of the vein wall), and secondary varicose veins, which result from proximal
If severe can result in an “inverted champagne bottle” appearance of the venous obstruction, destruction of the valves by thrombosis or an increase in flow and
leg with brawny oedema above and below the area of lipodermatosclerosis pressure caused by an arteriovenous fistula.
(e) Cellulitis
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PATHOPHYSIOLOGY Special tests
- Inherent weakness in the vein wall, leading to dilation and separation of valve cusps TOURNIQUET TEST
so they become incompetent
- This may be aggravated by obstruction to venous return (as above) - Lie the patient down and empty the varicosities
- Tie a tourniquet just below the SFJ
RISK FACTORS - Ask the patient to stand up
- Age - Look for filling up of the varicosities above and below the tourniquet
- Parity - If the veins dilate above but not below the tourniquet, this indicates that the
- Occupation – requiring long periods of standing perforators below the level of the tourniquet are not incompetent and that the SFJ is
- Weight incompetent confirm this by releasing the tourniquet and watching the veins dilate
- Posture – crossing legs all the time
- If the veins below the tourniquet are dilated when the patient stands up, then the
- Increased abdominal pressure – constipation, chronic cough, etc
incompetent perforator is below the level of the tourniquet
- Pelvic tumour or other lesion compressing on the deep veins
- Repeat the test, placing the tourniquet at different sites:
HISTORY (i) Mid thigh (just below the Hunterian perforator
Usually varicose veins do not cause symptoms and problems unless they are related to (ii) Below the knee
(iii) Mid-calf
chronic venous insufficiency
- The incompetent perforator is located between just above the level where the
tourniquet prevents dilation of the veins in the limb on standing
EXAMINATION:
[The alternative is the triple tourniquet test, where three tourniquets are tied with the
Examine patient standing with adequate exposure of the lower limbs patient lying down and then released from the bottom up to locate the site of
Inspection (look all around the limb!) insufficiency]
1. Presence of signs of chronic venous insufficiency (as above)
- Oedema TRENDELENBURG TEST
- Skin changes - The SFJ is occluded (landmark is 2.5 cm below and lateral to the pubic tubercle) with
- Venous ulcers from pressure necrosis from insude the patient lying down
2. Look at course of great saphenous vein and short saphenous vein for varicosities - Get the patient to stand while holding the SFJ occluded
3. Look at the inguinal region for any saphena varix - If varicosities do not fill up, the SFJ is the site of incompetence; if they fill up, there
are other sites of incompetence (the SFJ may or may not be incompetent)
Palpate
1. Feel any dilated varicosities PERTHES’ TEST
2. Palpate along the course of the saphenous veins and their tributaries to feel any - Tie a tourniquet around the calf or thigh and ask patient repeatedly stand on tiptoe
varicosities present (may be more palpable than visible especially in fat legs) and then relax
- In a person with normal deep venous drainage and competent venous valves in the
3. Palpate the inguinal region for a saphena varix (compressible lump that refills
communicating veins the superficial veins should drain into the deep veins
when released)
- If the patient’s varicosities remain enlarged then he or she has obstructed deep
4. Do the cough test to feel for reflux at the saphenofemoral junction (2.5 cm below venous drainage or incompetent valves in the communicating veins
and lateral to the pubic tubercle)
5. Percussion (tap test) – place two hands some distance apart. First percuss the Completing the examination
distal veins to feel the wave of blood flowing orthogradely normal. Then percuss - Auscultate over the varicosities for any bruit (indicate arteriovenous malformation)
the proximal veins – if the distal hand can feel the wave of blood flowing - Examine the abdomen for any mass that may be causing the varicosities
retrogradely then there is valvular incompetence (not a very valuable test)
Use of a handheld Doppler probe to detect incompetence VENOUS ULCERS
- Doppler probe is placed in the popliteal fossa between the two heads of the
gastrocnemius – over small saphenous vein CAUSE – ANY CAUSE OF CHRONIC VENOUS INSUFFICIENCY
- Squeeze the calf to empty the veins – should hear a whoosh as blood flows through 1. Obstruction to venous flow – thrombosis
the small saphenous vein 2. Incompetent valves – varicose veins, deep vein reflux (post-DVT)
- When the calf is relaxed there should not be any sound – a second whoosh indicates 3. Muscle pump failure – stroke, neuromuscular disease
reflux of blood i.e. there is valvular incompetence
INVESTIGATIONS
INVESTIGATIONS
Venous duplex ultrasound 1. Exclude infection of the ulcer and other complications
- Indications: - FBC for raised total white count
Recurrent varicose veins - Swabs of the ulcer for Gram stain and cultures
History of superficial thromobophlebitis - X-ray of the area to exclude underlying gas, bone involvement
History of DVT 2. Venous duplex to map out venous system
Venous eczema 3. Check for peripheral arterial disease by doing ABPI
Haemosiderin staining
4. Biopsy if cannot exclude malignant transformation (Marjolin’s ulcer)
Lipodermatosclerosis
Venous ulceration
- Can delineate deep and superficial venous systems and locate sites of incompetence MANAGEMENT:
- Exclude presence of deep vein thrombosis – stripping is contraindicated Conservative
1. 4 layer compression stockings (change once per week)
MANAGEMENT (a) Non-adherent wound dressing over ulcer (e.g. Menolin) followed by wool
bandage
Conservative
(b) Crepe bandage
1. Lifestyle changes
(c) Blue-line bandage (Elset)
- Decrease amount of time spent standing
- If due to job, change job or ask for change to position that involves less standing (d) Adhesive bandage (Coban)
and walking 2. Analgesia
2. Graduated compression stockings 3. Antibiotics if infected
3. Medications e.g. Daflon 4. Warn patient to avoid trauma to affected area
5. Encourage rest and elevate leg
Surgical 6. Once healed, compression stockings should be fitted and continued for life
Indications:
1. Cosmesis – large unsightly varicosities Surgical
2. Symptoms – pain, discomfort - If ulcer fails to heal
3. Complications – signs of chronic venous insufficiency, venous ulceration - First, exclude malignancy or other causes of ulcer (biopsy)
Available modalities: - Split skin graft can be considered with excision of dead skin and graft attached to
1. Most commonly done: High tie with great saphenous vein stripping, and stab healthy granulation tissue
avulsion of varicosities - Venous surgery for the underlying pathology
2. Ultrasound-guided foam sclerotherapy
3. Endovenous laser therapy (burns vein from within)
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UROLOGICAL DISEASES HISTORY
Post-renal Causes
APPROACH TO HAEMATURIA 1. Which part of urine stream is blood stained?
DEFINITION: - Beginning – urethra distal to UG diaphragm
- End – bladder neck or prostate
- >3 RBC / hpf.
- Throughout – upper urinary tract or upper bladder
- DDx: haemoglobinuria, myoglobinuria, pseudohaematuria (menstruating women),
medications causing discoloration of urine (eg rifampicin, phenytoin) 2. Painful vs painless haematuria
Painful Painless
CAUSES - Tumour - Malignancy – RCC, TCC, Prostate
Pre- Drugs Analgesics (NSAIDs) - Hydronephrosis - Drugs
Renal Anticoagulants - Renal cysts - GN
Cytotoxic/immunosuppressive agents (eg cyclophosphamide) - Ureteric stone / clot - Bleeding diathesis
OCP - Pyelonephritis - ITP / HSP
Penicillin - UTI - Infections – malaria, schistosomiasis
Quinine - Bladder outflow obstruction (e.g. - Exercise
Warfarin
BPH, strictures)
Systemic Bleeding diathesis
Sickle cell disease 3. Frequency + dysuria + haematuria
Metabolic Hypercalciuria - DDx: nephrolithiasis (colicky), malignancy, UTI (women & children), bladder
Hyperuricosuriia outflow obstruction (men e.g. BPH)
Vascular AV malformations 4. Other urological symptoms
Renal artery disease – thromboembolism, dissecting aneurysms, - Storage problem – frequency, urgency, nocturia, incontinence
malignant hypertension - Voiding problem – strangury, hesitancy, dribbling, incomplete emptying etc
Renal vein thrombosis - Others – polyuria, oliguria, urethral discharge
Renal Vasculitis HSP
PAN Pre-renal & Renal Causes
Wegener granulomatosis 5. Associated fever – pyelonephritis, malaria
Glomerular Post-strep GN 6. Screen for pre-renal causes
Post-infectious GN
IgA nephropathy LOW / bone pain / sickness Malignancies, TB, systemic illnesses
Lupus nephritis Rash, arthritis, arthralgia, Autoimmune causes, vasculitis
Other GNs myalgia, fever, oedema
Sore throat, skin infxns, URTI Post-strep / post-infective GN
Tubulo- Polycystic kidney disease
Nephrolithiasis Ongoing URTI or GE IgA nephropathy
interstitial
Malignancy – RCC, metastatic Iatrogenic Drug causes, radiotherapy
dz
Pyelonephritis Travel history Schistosomiasis, malaria
Renal cysts PMHx Renal disease, HPT, diabetic nephropathy,
bleeding diathesis, sickle cell dz
Post- Infxns of ureter, bladder, prostate, urethra – eg schistosomiasis, TB etc
Family history PKD, sickle cell disease, renal dzes (eg
renal Cancers of ureter, bladder (TCC), prostate, urethra Alport syndrome – ask for deafness), hypt,
Nephrolithiasis urolithiasis
Other necessary history 8. Plain KUB
1. Infection - Fever, travel and contact history - Stones, size of kidney
2. Sorethroat - Post-strep/infective GN, IgA nephropathy
9. Ultrasound of the kidneys
3. Autoimmune - Fever, rash, joint pain, oedema - Renal size
4. Malignancy - LOW, bone pain, neuro deficits, SOB, liver function - Presence of any hydronephrosis
5. PMHx - Renal dz, - Renal stones
- systemic dz (DM HPT Bleeding sickle cell)
6. Drug history / Hx of radiation 10. Intravenous urogram (IVU) – see below for more details
- Distortion of renal outline and pelvic calyces by RCC, may have specks of
7. Family history – PKD, renal dz, Sickle cell, HPT
calcification
- Stones (filling defect, proximal dilatation, decreased distal passage of contrast) +
PHYSICAL EXAMINATION hydroureter and/or hydronephrosis
1. Check patient’s vitals- stable? - Filling defect in bladder due to TCC
2. Conjunctival pallor - Increased residual volume in bladder after micturition due to BPH
3. Abdomen – renal mass, palpable bladder/bladder mass 11. Cystoscopy
4. Scrotum – varicocoele on the left (may have RCC of the left kidney with extension - Detection of bladder tumour (IVU may not pick up small tumours <1cm)
of tumour into renal vein, blocking the testicular vein where it drains into the left - Biopsy can be taken at the same time
renal vein)
5. Digital rectal examination – prostate enlargement (BPH versus cancer) KUB FILM
- Margins: Superiorly needs to be above the upper pole of the right kidney (T12),
inferiorly needs to show the pubic symphysis
INVESTIGATIONS
1. Urine dipstick INTRAVENOUS UROGRAM
- Causes of false-positive for blood: haemoglobinuria, beetroot, drugs (rifampicin), - Intravenous contrast used to delineate anatomy of the kidneys and urinary system
metabolic (alkaptonuria, porphyria)
- Various phases:
2. UFEME (i) Control film – plain KUB
- Confirm presence of red blood cells (ii) Nephrogram phase (taken 1 minute after contrast given) – contrast fills
- Casts nephritis kidney parenchyma so the kidneys become more visible, can measure size
- Elevated WBC (pyuria is >5 WBC per hpf), organisms infection (iii) Pyelogram phase (3-5 minutes) – contrast fills calyces and pelvis, can
3. Urine cytology for malignant cells detect dilated calyces/pelvis (hydronephrosis), any filling defects
(iv) Release film (abdominal binder which was placed to slow the flow of
4. Urine phase contrast contrast into the bladder is released) – shows ureters, any hydroureter,
- RBCs – isomorphic or dysmorphic? Dysmorphic RBCs suggest a tubular source, filling defects; bladder – any filling defects, abnormal appearance of the
while isomorphic RBCs suggest post-renal source (ureter, bladder, etc) bladder (fir-tree appearance in neurogenic bladder)
5. Urine culture and sensitivity (v) Post-micturition – any residual urine in bladder after voiding
6. Full blood count - Contraindicated in:
- How low is the Hb? (a) Contrast allergy
- Elevated TW – infection (b) Renal impairment (Cr >200)
(c) Patients on metformin (can cause lactic acidosis; patients need to stop
7. Urea, electrolytes and creatinine metformin 2 days before and after study)
- Any renal impairment and electrolyte abn (renal or pre-renal dz more likely) (d) Patients with asthma (given steroids for 3 days before study)
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RENAL CELL CARCINOMA
INVESTIGATIONS
EPIDEMIOLOGY
- 3% of adult malignancy DIAGNOSTIC
- Most frequent occurring solid lesion within kidney 1. Imaging – CT and/or ultrasound
- 2:1 male predominance - Presumptive diagnosis is made on imaging – a renal parenchymal mass with
- Peak incidence 60-70 years thickened irregular walls and enhancement after contrast injection suggests
malignancy
PATHOLOGY 2. Pathological diagnosis
- Most common primary renal tumour (80-85% of all tumours of the kidney) - Needle biopsy usually not done for resectable lesions due to fears of tumour
- Arise from the renal tubular epithelium seeding
- Three cell types: clear cell carcinoma (70-80%), papillary renal cell carcinoma (10- - In these resectable lesions, a partial or total nephrectomy is often performed, and
15%), and chromophobe renal cell carcinoma (5%) provides the tissue diagnosis post-operatively
- Other renal tumours: TCC of renal pelvis, Wilms’ tumour, lymphoma - In tumours with metastatic disease on presentation, biopsy of the metastatic site
may be easier
RISK FACTORS
STAGING
- Smoking
1. CT scan of the abdomen
- Exposure to cadmium
- Perinephric invasion, adjacent organ invasion
- Family history
- Extension into renal vein, IVC
von-Hippel Lindau syndrome due to mutation of the VHL gene on chromosome
- Lymph node enlargement
3p25 (associated with CNS haemangioblastomas (usually cerebellar), bilateral
- Liver metastases
multicentric retinal angiomas, phaeochromocytomas, etc) clear cell
carcinomas 2. CT scan of the chest
Hereditary papillary RCC (HPRCC) due to mutation of the MET proto-oncogene - For lung metastases
on chromosome 7q31 multifocal bilateral papillary carcinomas
3. Bone scan
- Acquired polycystic kidney disease (secondary to chronic dialysis)
- Only done if patient complains of bone pain and/or alkaline phosphatase is raised
Prognosis DIAGNOSIS
Stage I (T1N0): >90% 5 year survival 1. Urine cytology for malignant cells
Stage II (T2N0): 75-90% 2. Cystoscopy with cell brushings and biopsy
Stage III (T3N0/N1): 60-70% 3. IVU or CT urogram to detect synchronous lesions (3% chance of proximal tumour)
Metastatic disease: <10%
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STAGING o Ileal conduit (a segment of ileum with ureters attached, as a stoma; not
1. CT abdo/pelvis for T, N and M staging continent)
2. Transurethral resection of bladder tumour (TURBT) with histopathology o Neobladder construction using ileum (only if urethra not removed; continent,
better quality of life)
Ta Superficial, does not involve lamina propria o Stoma with pouch construction under abdominal wall (not continent)
Tis Carcinoma in-situ: “flat tumour”
T1 Superficial, involves lamina propria (up to muscularis propria) - Radiotherapy (not as good as surgery)
T2a Superficial involvement of muscularis propria – up to inner half of muscle
T2b Deep involvement of muscularis propria – up to outer half of muscle
T3a Microscopic extension outside bladder (from TURBT specimen) UROLITHIASIS
T3b Macroscopic extension outside bladder
STONE COMPOSITION
T4a Invasion of prostate, vagina, uterus
- Calcium oxalate or calcium phosphate stones – 75%
T4b Invasion of lateral pelvic walls, abdominal wall
- Magnesium ammonium phosphate (struvite) stones – 15%
Generally can be divided into 2 main groups: - Uric acid and cystine stones – 10%
(a) Superficial tumour (70-80% of patients) – Ta, Tis, T1
(b) Muscle-invasive tumour (20-30%) – >T2 PATHOLOGY
- Can occur at any level in the urinary tract, but most commonly in the kidney
- Most important cause of stone formation is increased urine concentration of the
MANAGEMENT DEPENDENT ON STAGE
stone’s constituents, such that they exceed their solubility precipitate as stones
SUPERFICIAL TUMOUR - E.g. hypercalciuria with or without hypercalcaemia, hyperuricuria
- Primary treatment is TURBT of the tumour - Urinary tract infections can also cause stone formation – struvite stones form in
Proteus vulgaris infections as this organism splits urea into ammonium, generating
- Intravesical therapy indicated in patients with high risk of tumour recurrence or alkaline urine
tumour progression (high grade, multiple primary sites, multiple recurrences, tumour - Bacteria can also form nidi for the formation of any kind of stone
size >3cm, primary or coexisting carcinoma in-situ, prostatic urethral involvement)
BCG – 1 instillation per week for 6 weeks
PRESENTATION DEPENDS ON SITE
Mitomycin C – single instillation within 24hrs of TURBT, or weekly/monthly
treatments for up to 2 years Renal stones
- Most often asymptomatic unless the stone gets lodged in the pelviureteric junction
- Follow-up: causing hydronephrosis and subsequent infection pyonephrosis
3-monthly cystoscopy for 1 year - Vague flank pain may occur
6-monthly cystoscopy for next 4 years Urine cytology with every cystoscopy
Yearly cystoscopy thereafter Ureteric stones
- Even small stones can cause severe symptoms as the ureter is narrow
IVU every 2 years
- Classically ureteric colic pain – severe, intermittent loin-to-groin pain
- Haematuria – gross or microscopic
MUSCLE-INVASIVE - Irritative symptoms – frequency, urgency
- Radical cystectomy - Can cause upper urinary tract infection fever, pain
Radical cystoprostatectomy with pelvic lymphadenectomy in male
Anterior exenteration with pelvic lymphadenectomy in female Bladder stones
- May be asymptomatic
Ways of diverting urine output
- Can cause irritative urinary symptoms – frequency, urgency
o Cutaneous ureterostomy (use ureters to create stoma, but easily stenosed due
- Haematuria
to small calibre; not continent)
- If infection is present – dysuria, fever, etc
PHYSICAL EXAMINATION - High fluid intake
- In ureteric colic, symptoms are often out of proportion to signs – no guarding, - Low salt intake
rebound, etc - Restriction of red meat, dairy produce, refined sugars
- If the patient has pyelonephritis, renal punch may be positive - Increase citrus fruit intake
- Otherwise unremarkable examination
SURGICAL INTERVENTION
INVESTIGATIONS Indications:
- Constant pain
1. Urine tests – dipstick, UFEME, urine culture/sensitivity
- Haematuria - Does not pass after one month
- Pyuria, micro-organisms (UTI) - Too large to pass spontaneously
- Obstructs urine flow
2. KUB - Causes urinary tract infection
- May be able to see radio-opaque stone (90% of renal stones are radio-opaque) - Damages renal tissue or causes significant bleeding
- Look at kidney size, any renal stones - Increase in size
- Trace path of ureter along tips of transverse processes, across sacroiliac joint,
and medially into bladder, looking for ureteric stones Types of treatment available:
- Look for bladder stones 1. Percutaneous nephrolithotomy (PCNL)
- Done for renal stones that are too large for ESWL to disintegrate
3. Intravenous urogram - Contraindicated in uncorrected bleeding diathesis, patients unfit for GA
- Can also help to visualise a stone 2. Extracorporeal shock wave lithotripsy (ESWL)
- Can show dilated urinary system secondary to stone obstruction – hydroureter - Calcium oxalate, uric acid and struvite stones fragment easily, but calcium
and/or hydronephrosis phosphate and cystine do not
4. Ultrasound of kidney or bladder - Used for stones below 10mm in size
- Features of stone: echogeneic rim, posterior acoustic shadowing - Used for renal stones and upper ureter stones – not so good for lower system due
to difficulty in access
5. MAG-3 renogram - Contraindicated in pregnancy, untreated UTI, untreated bleeding diathesis, distal
- If pyelonephritis present due to stone obstruction, it is valuable to measure the obstruction that cannot be bypassed with a stent
renal function using the MAG-3 renogram 3. Ureteroscopy with lithotripsy (usually laser lithotripsy, can also be done by
- The renogram gives the differential function of each kidney – in normal pneumatic drill, electrohydraulic means)
individuals the function should be approximately 50% on each side (out of 100% - For stones along the ureter
for both kidneys combined)
- If one kidney has less than 15% of total renal function, it is not worth salvaging 4. Cystolitholapaxy for bladder stone
the kidney 5. Open surgery (pyelolithotomy or ureterolithotomy) – rarely done; only if failed
other management strategies, altered anatomy, performing open surgery for another
TREATMENT reason anyway, non-functioning kidney
CONSERVATIVE Adjuncts:
Stones smaller than 5mm can be treated conservatively as 60% will be passed out; only - Double-J stent (or DJ stent) – inserted to stent the urinary system when worried that
treat if they do not pass out after 4 to 6 weeks, and/or cause symptoms stone fragments after ESWL may cause obstruction e.g. when ESWL used for
- Treatment of any urinary tract infection treatment of a large stone; or if system is obstructed to begin with, may want to stent
- If underlying disease present that causes increased urinary concentration of stone to ensure good drainage after surgery
components e.g. hypercalcaemia treat disease if possible
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Summary of treatment modalities HISTORY
Location Size Treatment Symptoms of ARU:
Renal < 5mm Conservative management unless symptomatic/persistent - Inability to pass urine
5-10mm ESWL - Suprapubic distension with pain (unlike chronic retention of urine which is painless)
10-20mm Either ESWL or PCNL Precipitating factors:
> 20mm PCNL - Symptoms of urinary tract infection: dysuria, frequency, urgency, nocturia,
Upper ureter < 5mm Conservative management unless symptomatic/persistent haematuria
5-10mm ESWL - Constipation
> 10mm URS with lithotripsy - Drugs e.g. cough mixture, antihistamines
- Immobility
Middle ureter/ < 5mm Conservative management unless symptomatic/persistent
Distal ureter > 5mm URS with lithotripsy History suggestive of aetiology:
- Previous history of obstructive symptoms e.g. poor stream, hesitancy, terminal
Bladder < 30mm Cystolitholapaxy dribbling etc BPH
> 30mm Open cystolithotomy (also if there are multiple stones) - Previous history of ureteric colic pain or stones
- Previous urethral instrumentation or STD stricture
- Gross painless haematuria recently TCC, bladder stone
- Lower limb weakness/paralysis, bowel incontinence, back trauma, history of spinal
disease e.g. PID, spinal stenosis neurogenic bladder
APPROACH TO ACUTE RETENTION OF URINE - Constitutional symptoms: LOW, LOA, malaise (any tumour in general)
CAUSES Complications:
- Infection – symptoms of UTI
Mechanical Extraluminal Prostate enlargement (benign/malignant) - Stone disease (if in the bladder, usually asymptomatic)
Faecal impaction - Renal failure (more likely in chronic retention) – vomiting, lethargy, drowsiness
Pelvic tumour
Pregnancy
UV prolapse PHYSICAL EXAMINATION
Intramural Tumour of the bladder neck (TCC) - General condition – sallow appearance, scratch marks, pedal oedema, etc (uraemia)
Urethritis (UTI) - Abdomen
Urethral stricture from STD, prev instrumentation Palpable bladder – tender
Intraluminal Stones Other pelvic masses – fibroid, gravid uterus, ovarian cyst
Blood clot (clot retention in haematuria) Faecal loading
Foreign body Bilateral enlarged kidneys (hydronephrosis)
Non- Cord disease/ Cord compression - Digital rectal examination
mechanical injury Multiple sclerosis Any saddle anaesthesia
Tabes dorsalis Anal tone
Neuropathy Diabetic autonomic neuropathy Prostate enlargement – firm and smooth? Or hard, craggy, irregular, rectal
Drugs Anticholinergics (cough medicine), antihistamines, mucosa not mobile?
anti-depressants, alcohol Stool impaction
Others Prolonged immobility - Neurological examination
Post-anaesthesia LMN paralysis of the lower limbs?
Pain Any sensory level present?
IMMEDIATE MANAGEMENT – CATHETERISATION Due to tubular damage from obstruction of drainage of the pelvicalyceal
- Try urethral catheterisation first (impt: urethral catheterisation contraindicated if system, resulting in transient impairment of concentrating function
patient has signs suggestive of urethral injury – blood at urethral meatus, high-riding Can result in hypotension and electrolyte abnormalities (hyponatraemia,
prostate – more relevant in the trauma setting) hypokalaemia, hypovolaemia)
Requires close monitoring of urine output and fluid/electrolyte status with
If urethral catheterization cannot pass into bladder, there are two possibilities: 1) appropriate replacement and resuscitation
enlarged prostate; and 2) urethral stricture
(b) Haemorrhage ex-vacuo
For enlarged prostate, try again with a thicker catheter (stiffer, easier to pass
through) Bladder mucosal disruption with sudden emptying of greatly distended
bladder
For stricture (when you feel the catheter is stuck quite proximally along the Usually self-limiting
penile urethra, it is more likely to be a stricture), try a smaller gauge catheter
Do not push too hard – may cause false passage creation if the obstruction is due 3. Trial-off catheter
to a stricture - Take off catheter and watch patient’s output, as well as perform bladder scan to
measure bladder volume
- If urethral catheterisation fails, perform suprapubic catheterisation - When patient passes urine, can perform uroflow to investigate severity of outlet
Requires distended bladder which pushes the surrounding bowel loops away so obstruction, and also do bladder scan post-micturition to check residual volume
that risk of bowel injury is lower - If patient cannot pass urine and bladder volume >400ml re-catheterise
Local anaesthetic injected 2 fingerbreadths above pubic symphysis
Small incision made in the skin and fascia, and trocar inserted
When a gush of urine is seen, the suprapubic catheter is inserted and secured
BENIGN PROSTATIC HYPERPLASIA (BPH)
INVESTIGATIONS (FOR CAUSES) EPIDEMIOLOGY
1. Full blood count for raised TW (infection)
- Very common problem in men
2. Urea, electrolytes and creatinine for raised creatinine (renal impairment secondary
- Frequency rises with age after the age of 30, reaching 90% in men older than 80
to obstructive nephropathy)
3. Urine dipstick, UFEME and culture/sensitivity for infection
4. PSA – keeping in mind causes of raised PSA (cancer, BPH [usually <40], prostatitis, PATHOLOGY
instrumentation >11days) - Results from proliferation of both the epithelial and stromal components of the
5. KUB for stones, faecal loading prostate with resultant enlargement of the gland
6. Ultrasound of the bladder for stones, tumour, intravesical protrusion of prostate - Commonly occurs in the central zone of the prostate
- Major stimulus for hyperplasia appears to be dihydrotestosterone (produced from
testosterone by the enzyme 5-alpha reductase)
TREATMENT - Age-related increases in oestrogen levels may also contribute to BPH by increasing
1. Treat reversible causes the expression of dihydrotestosterone receptors on prostatic parenchymal cells
- Stop drugs that may have precipitated ARU
- Relieve constipation with fleet enema, lactulose, senna etc
PRESENTATION
- Treat any urinary tract infection if present
- Main result of BPH is obstruction of the prostatic urethra resulting in lower urinary
2. Anticipate complications tract symptoms (LUTS) which can be divided into irritative and obstructive
(a) Post-obstructive diuresis symptoms – obstructive symptoms predominate
Urine output >200ml/hr for 2 hours or more
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Obstructive Irritative I. Watchful waiting
Hesitancy Frequency - Suitable for patients with minimal symptoms, no complications and normal invx
Straining to pass urine Urgency - Monitor patient’s symptoms and clinical course annually
Weak stream Nocturia
Prolonged micturition Dysuria II. Medical treatment
Terminal dribbling Urge incontinence 1. Alpha blockers
Feeling of incomplete voiding - Prazosin, Terazosin, Doxazosin, Alfuzosin
Double voiding (pis-en-deux) - Treatment of symptoms of BPH by acting on the alpha-1 adrenergic receptors
that are abundant in the bladder neck, prostate and urethra
- May progress to the point of acute urinary retention admitted to hospital - Result in decreased outflow resistance and decreased bladder instability
- In the chronic setting, the patient may have chronic urinary retention with high post- - Side effects include postural hypotension, dizziness
void residual volume in the bladder asymptomatic, may have overflow
2. 5-alpha reductase inhibitors
incontinence
- Finasteride, Dutasteride
- Obstruction leads to hypertrophy of the detrusor muscle and trabeculation of the - Treats the disease (not just the symptoms) by inhibiting the conversion of
bladder mucosa as the bladder tries to empty against increased resistance testosterone to dihydrotestosterone by 5-alpha reductase reduced prostate size
- Proven to decrease need for surgery and acute retention rates
PHYSICAL EXAMINATION - Only effective after 6 months, and in prostates >40g
- Palpable tender bladder in ARU (non-tender in chronic retention) - Most common side-effect is sexual dysfunction
- Digital rectal examination: smooth enlarged prostate, rubbery, non-tender
III. Surgery – Transurethral resection of prostate (TURP)
INVESTIGATIONS Indications:
- Creatinine level (renal impairment due to chronic obstruction) - Refractory urinary retention
- Urinary investigations for infection (stasis predisposes to UTI) - Recurrent urinary tract infection
- KUB for bladder stone - Obstructive uropathy
- Ultrasound of kidney and bladder – hydronephrosis, post-void residual volume - Bladder calculi
>100ml, bladder stone - Recurrent gross haematuria
- Uroflow to confirm obstruction to urinary outflow (normal peak flow rate should be Complications of surgery (TURP)
more than 15ml/sec) Early
1. Bleeding
PROBLEMS 2. TUR syndrome
- Acute/chronic urinary retention - Hyponatraemia due to constant irrigation during TURP (glycine used for
- Gross haematuria irrigation – cannot use N/S, as ionic solutions make diathermy non-functional)
- Bladder stones - Irrigation fluid is hypotonic, thus water enters open vasculature during surgery
- Recurrent UTI - Risk increases with prolonged operation and increased pressure of irrigation,
- Renal impairment secondary to outflow obstruction thus op is kept to shorter than one hour, and irrigation pressures <60mmHg
- Co-existence of prostate cancer - Symptoms: Nausea, vomiting, confusion, hypertension, visual disturbances
- Patient usually given spinal anaesthesia during TURP so the surgeon can assess
MANAGEMENT the patient’s mental status during the operation
- Divided into watchful waiting, medical management, and surgical management 3. Perforation of the urethra or bladder dome
- Objectives of treatment: Rapid and sustained relief of symptoms, prevent long-term
Late
complications, improve patient’s quality of life
1. Retrograde ejaculation
PROSTATIC CANCER STAGING
1. Clinical examination (palpable tumour T2)
EPIDEMIOLOGY 2. TRUS biopsy for staging purpose
- Prostate Cancer is the 6th commonest cancer among men in Singapore.
- 5th common cancer in Singapore 3. CT scan of the abdomen and pelvis to assess extent of tumour invasion and nodal
- Peak incidence between 65 and 75 years of age status (regional, non-regional)
4. Bone scan for metastasis
PATHOLOGY
- Adenocarcinoma TREATMENT
- Arise in the outer parts of the prostate 70-80% of the time and are thus palpable on LOCALISED DISEASE
digital rectal examination 1. Radical prostatectomy
- Open, laparoscopic or robot-assisted
RISK FACTORS - Open – retropubic or perineal approaches
- Hormonal – growth of tumour can be inhibited by orchidectomy or administration of 2. Radiotherapy
oestrogens - External beam radiotherapy (EBRT)
- Genetic – racial variations in onset and prevalence, family history - Brachytherapy
- Environmental – industrial chemical exposure, diet containing high animal fat
LOCALLY ADVANCED DISEASE
PRESENTATION 1. Radiotherapy with androgen ablation
- Often asymptomatic, may be incidentally picked up on digital rectal examination or - Castration
due to elevated prostate-specific antigen (PSA) level Surgical
- Can cause local symptoms such as obstruction of the prostatic urethra (uncommon as Medical – LHRH agonist
most cancers arise in peripheral zones) – LUTS, bladder outlet obstruction - Anti-androgen
- Metastatic symptoms – bone pain Non-steroidal e.g. Flutamide
Steroidal – cyproterone acetate
PHYSICAL EXAMINATION - Combined androgen blockade
- Digital rectal examination: Asymmetric area of induration, or frank hard irregular - Oestrogen therapy (diethylstilbestrol)
nodule
- Percuss spine for any bone pain METASTATIC DISEASE
1. Androgen ablation
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APPROACH TO SCROTAL SWELLINGS
ANSWER 4 QUESTIONS:
1. Can you get above the swelling?
2. Can you identify the testis and the epididymis?
3. Is the swelling transilluminable?
4. Is the swelling tender?
Can get Testis not definable Opaque Non tender Chronic haematocoele
above from epididymis Gumma
swelling Tumour
Tender Torsion
Epididymo-orchitis
Acute haematocoele
Transilluminable Hydrocoele
Non-tender TB epididymis
swelling of
epididymis
Tender Epididymoorchitis
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CENTRAL VENOUS PRESSURE LINE INSERTION Technique of IJV cannulation
Place the patient in a supine position, at least 15 degrees head-down to distend the neck
INDICATIONS veins and to reduce the risk of air embolism. Turn the head away from the venepuncture
1. Vascular access site. Cleanse the skin and drape the area. Sterile gloves and a gown should be worn to
2. Total parenteral nutrition avoid catheter-related sepsis.
3. Infusion of irritant drugs
4. Measurement of central venous pressure Procedure
5. Cardiac catheterization 1. Use local anaesthetic to numb the venepuncture site.
6. Pulmonary artery catheterization 2. Introduce the large calibre needle, attached to an empty 10 ml syringe.
7. Transvenous cardiac pacing. 3. Surface mark the internal jugular vein at the centre of the triangle formed by the
two lower heads of the sternocleidomastoid muscle and the clavicle. Palpate the
CONTRAINDICATIONS: carotid artery and ensure that the needle enters the skin lateral to the artery.
1. Do not insert into an infected area. 4. Direct the needle caudally, parallel to the sagittal plane, aiming towards the
2. Avoid infraclavicular approach to subclavian vein if patient has apical emphysema ipsilateral nipple.
or bullae. 5. While needle is advanced, maintain gentle aspiration.
3. Avoid internal jugular vein if carotid aneurysm present on the same side.
4. Bleeding diatheses 6. When vein is entered, flush of blood appears in the syringe. Now, cannulate the
5. Septicaemia vein via the Seldinger technique as described below.
6. Hypercoagulable states 7. Remove syringe, holding needle firmly in place. Occlude needle to prevent air
embolism or bleeding.
ROUTES FOR CENTRAL VENOUS CANNULATION INCLUDE: 8. Advance guide wire, J-shaped end first, into the vessel through the needle.
1. Internal jugular vein 9. Hold guide wire in place and remove needle. Maintain a firm grip on the guide wire
2. Subclavian vein at all times.
3. Femoral vein 10. Use a dilator to enlarge the hole in the vein. Remove the dilator.
4. External jugular vein 11. Thread tip of catheter into the vein through the guidewire. Grasp the catheter near
the skin and advance it into the vein with a slight twisting motion.
CANNULATION OF THE INTERNAL JUGULAR VEIN 12. Advance catheter into final indwelling position. Hold catheter and REMOVE
The internal jugular vein (IJV) is accessible, so cannulation of this vein is associated GUIDEWIRE.
with a lower complication rate than with other approaches. Hence, it is the vessel of 13. Check lumen placement by aspirating through all the pigtails and flushing with
choice for central venous cannulation. saline next.
Anatomy of the IJV 14. Suture the catheter to the skin to keep it in place.
The vein originates at the jugular foramen and runs down the neck, to terminate 15. Apply dressing according to hospital protocol.
behind the sternoclavicular joint, where it joins the subclavian vein. It lies alongside 16. The catheter tip should lie in the superior vena cava above the pericardial reflection.
the carotid artery and vagus nerve within the carotid sheath. The vein is initially Perform check chest X-ray to confirm position and exclude pneumothorax.
posterior to, then lateral and then anterolateral to the carotid artery during its descent
in the neck. The vein lies most superficially in the upper part of the neck. Complications
1. Pneumothorax/haemothorax
Relations of the IJV 2. Air embolism - ensure head-down position.
Anterior: Internal carotid artery and vagus nerve. 3. Arrhythmias – This happens if cathether “irritates” the heart. Avoid passing
Posterior: C1, sympathetic chain, dome of the pleura. On the left side, the IJV lies guidewire too far, observe rhythm on cardiac monitor during insertion.
anterior to the thoracic duct.
Medial: Carotid arteries, cranial nerves IX-XII
4. Carotid artery puncture/cannulation - palpate artery and ensure needle is lateral to it, NASOGASTRIC TUBE
or use ultrasound-guided placement, transduce needle before dilating and passing
central line into vessel, or remove syringe from needle and ensure blood is venous. INDICATIONS
5. Chylothorax- Avoid cannulating the vein on the left side as the thoracic duct lies 1. Diagnostic
there. a) bleeding from the upper gastrointestinal tract, haematemesis
6. Catheter-related sepsis b) pentagastrin studies (rarely done now)
2. Decompresssion
CANNULATION OF THE SUBCLAVIAN VEIN a) intestinal obstruction
The subclavian vein (SVC) may be preferred for central venous access if b) pyloric stenosis
1. Patient has a cervical spine injury c) haematemesis, particularly in patients at risk of hepatic encephalopathy
2. Line is for long-term use e.g. dialysis, feeding. This site may be more comfortable d) therapeutic and prophylactic decompression after major abdominal surgery
for the patient. e) prevention of further soilage after gastric perforation
f) prevention of anastomotic rupture after gastric surgery
Anatomy of the SCV g) prevention of obstruction of the operative field by air in the stomach
The SCV is the continuation of the axillary vein and originates at the lateral border of 3. Nutrition
the first rib. The SCV passes over the first rib anterior to the subclavian artery, to join a) patients with dysphagia
with the internal jugular vein at the medial end of the clavicle. The external jugular b) comatose or weak patients
vein joins the SCV at the midpoint of the clavicle. 4. Lavage
Technique a) poisoning
1. Place the patient in a supine position, head-down. b) gastrointestinal bleeding
2. Turn the head to the contralateral side (if C-spine injury excluded).
3. Adopt full asepsis. CONTRAINDICATIONS
4. Introduce a needle attached to a 10 ml syringe. 1. Base of skull fracture
5. Surface mark the subclavian vein 1 cm below the junction of the middle and medial 2. Oesophageal tear
thirds of the clavicle. Direct the needle medially, slightly cephalad, and posteriorly 3. Severe facial injury
behind the clavicle toward the suprasternal notch.
6. Slowly advance the needle while gently withdrawing the plunger. The cuffed endotracheal and tracheostomy tubes should be deflated prior to nasogastric
7. When a free flow of blood appears, follow the Seldinger approach, as detailed tube insertion.
previously.
8. The catheter tip should lie in the superior vena cava above the pericardial reflection. PRE-PROCEDURE
Perform check chest X-ray to confirm position and exclude pneumothorax. 1. Gather equipment.
2. Don non-sterile gloves.
Complications 3. Explain the procedure to the patient and show equipment.
As listed for internal jugular venous cannulation. The risk of pneumothorax is far 4. If possible, sit patient upright for optimal neck/stomach alignment with the head
greater with this technique. Damage to the subclavian artery may occur; direct pressure forward. Otherwise, prop the patient up at 45 degrees.
cannot be applied to prevent bleeding. 5. Deflate the endotracheal tube or tracheostomy cuff
Ensure that a chest X-ray is ordered, to identify the position of the line and to exclude 6. Determine the size of the nasogastric tube required (usually 14 – 16FG). If
pneumothorax. aspirating, use as large a tube as possible to reduce the risk of blocking during use
or the formation of a false passage during introduction; if feeding, a smaller tube
may be used (eg. 8FG) because it is more comfortable in the long term.
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PROCEDURE PROBLEMS AND COMPLICATIONS
1. Estimate the length of the tube to be inserted: from the bridge of the nose to the 1. Technical
tragus of the ear to the point halfway between the xiphisternum and the navel. Mark a) insertion into the trachea, resulting in choking.
the Mark measured length with a marker or note the distance. b) coiling and reentry into the oesophagus (rare).
2. Examine nostrils for deformity/obstructions (eg. choanal stenosis) to determine best c) trauma to the nose and the pharynx.
side for insertion. Select the largest nostril for inserting the tube. d) dislodgement
e) perforation of the pharynx and oesophagus.
3. Lubricate tube with water. The nose may be lubricated with lignocaine gel.
2. Lung complications
4. Introduce the tube through the nostril, passing the tube along the floor of the nose. a) decreased ventilation
Resistance may be felt as tip reaches the nasopharynx, which is the most b) aspiration pneumonia
uncomfortable part of the procedure. In the operation theatre, when the patient is
under general anaesthesia, the McGill’s forceps may be used to guide the tube down. 3. Loss of fluids and electrolytes, especially sodium, potassium, chloride
and hydrogen ions.
5. Instruct the patient to swallow (you may offer ice chips/water if not contraindicated)
and advance the tube as the patient swallows. Swallowing of small sips of water 4. Dry mouth and parotitis due to fluid loss and mouth breathing.
may enhance passage of tube into esophagus. If patient is uncooperative, bend his 5. Gastrointestinal
head to elicit a swallowing reflex. a) gastric erosions
6. Continue to advance the tube down the oesophagus. There should not be resistance. b) pressure necrosis of the pharynx, oesophagus or the external nares.
If resistance is met, rotate the tube slowly with downward advancement towards the c) traumatic haemorrhage of varices.
closer ear. Do not force the tube down against resistance as this may form a false d) gastroesophageal reflux due to functional incompetence of the lower
passage. oesophageal sphincter.
e) erosions of the oesophagus leading to strictures.
7. Withdraw the tube immediately if changes occur in the patient's respiratory status,
if the tube coils in the mouth, or if the patient begins to cough or turns pretty
colours.
8. Advance the tube until mark is reached (approximately 40cm). Stop.
9. Check for correct placement by attaching a syringe to the free end of the tube and
aspirating a sample of gastric contents to test with litmus, auscultating the
epigastrium while injecting air through the tube, or obtaining an x-ray to verify
placement before instilling any feedings/medications or if you have concerns about
the placement of the tube.
10. Secure the tube with adhesive tape.
11. Re-inflate the endotracheal tube or tracheostomy cuff if necessary.
12. If for suction, remove the syringe from the free end of the tube; connect to suction;
set machine on type of suction and pressure as prescribed.
13. Document the reason for the tube insertion, type & size of tube, the nature and
amount of aspirate, the type of suction and pressure setting if for suction, the nature
and amount of drainage, and the effectiveness of the intervention.
TRACHEOSTOMY 8. Visualise the thyroid isthmus and retract isthmus.
9. Retract cricoid cartilage upwards wth cricoid hook.
INDICATIONS FOR TRACHEOSTOMY
1. Maintenance of airway patency. 10. Incise the trachea between the 2nd and 3rd tracheal rings, making an inverted U-flap
2. Protection of the airway from aspiration. incision.
3. Application of positive pressure to the airway. 11. Insert tracheal dilator through the tracheostoma and remove the cricoid hooks.
4. Facilitation of secretion clearance. 12. Suction of blood and secretions in the lumen.
5. Delivery of high oxygen concentrations. 13. Insert the tracheostomy tube.
14. Remove the obturator and insert the inner cannula.
RELATIVE CONTRAINDICATIONS
15. Dress wound and secure to the neck using sutures and adhesive tape.
1. Evidence of infection in the soft tissues of the neck at the prospective surgical site.
2. Medically uncorrectable bleeding diatheses.
3. Gross distortion of the neck anatomy due to hematoma, tumour, thyromegaly, high COMPLICATIONS
innominate artery or scarring from previous neck surgery. During Procedure
4. Documented or clinically suspected tracheomalacia. 1. Bleeding if damage to the innominate or inferior thyroid artery.
5. Need for positive end-expiratory pressure (PEEP) of more than 15 cm of water. 2. Damage to surrounding structures, eg esophagus, recurrent laryngeal nerve,
6. Patient obesity with short neck that obscures neck landmarks. brachiocephalic vein.
7. Patient age younger than 15 years. 3. Pneumothorax.
4. Pneumomediastinum.
TYPES OF TRACHEOTOMY Immediate post-op
1. Temporary: Portex (cuffed). 1. Surgical emphysema.
2. Permanent: Consist of inner and outer tubes made of stainless steel. 2. Obstruction, eg clot, mucus.
3. Bleeding.
Tracheostomy is more useful in the elective setting compared to endotracheal intubation
4. Dislodgment.
because:
5. Subcutaneous emphysema.
1. Better tolerated.
2. Avoids risk of laryngeal stenosis Late post-op
3. Avoids risk of endotracheal obstruction. 1. Infection .
2. Obstruction, eg dislodgment of tube, crust formation from secretions.
PROCEDURE 3. Tracheo-esophageal fistula.
1. Position the patient. Place rolled towel under the patient’s neck to hyperextend the 4. Tracheal stenosis.
neck for better exposure. 5. Wound breakdown.
2. Clean and drape. Clean the skin of the neck from the chin to the suprasternal notch 6. Scarring.
and laterally to the base of the neck and clavicles. Drape field. 7. Tracheomalacia.
3. Identify anatomical landmarks (thyroid cartilage, cricoid cartilage).
POST-OP CARE
4. Administer local anaethesia. 1. Position patient in a propped up position.
5. Incise skin. In the emergency setting, make a vertical incision 3cm from cricoid 2. Prevent obstruction by suction, saline irrigation, mucolytic agents (mucomyst,
cartilage downwards. In the elective setting, make a tranverse incision 4cm wide, guaifenesin) and humidified air.
3cm above the suprasternal notch. 3. Change Portex tube every 3rd day and remove the inner tube for cleaning everyday.
6. Dissect through the subcutaneous layers and platysma. 4. Unlock the metal tube every night so that the patient can cough it out if it becomes
7. Identify the communicating branch of the anterior jugular vein, clamp and ligate the obstructed.
artery (ignore this in an emergency).
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SENGSTAKEN-BLAKEMORE TUBE (OR MINNESOTA TUBE) URINARY CATHETERISATION
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MATERIALS COMPLICATIONS
1. Iodine & alcohol swabs for skin prep 1. Laceration or puncture of the intrathoracic and/or abdominal organs, all of which
2. Sterile drapes & gloves can be prevented by using the finger technique before inserting the chest tube.
3. Scalpel blade & handle 2. Introduction of pleural infection.
4. Clamp 3. Damage to the intercostals nerve, artery or vein.
5. Silk suture
6. Needle holder 4. Incorrect intrathoracic or extrathoracic tube position.
7. Petrolatum-impregnated gauze 5. Chest tube kinking, clogging or dislodging from the chest wall or disconnection
8. Sterile gauze from the underwater seal apparatus.
9. Tape 6. Persistent pneumothorax
10. Suction apparatus (Pleuravac)/underwater seal apparatus 7. Subcutaneous emphysema, usually at tube site.
11. Chest tube (size 32 to 40 Fr, depending on clinical setting) 8. Recurrence of pneumothorax upon removal of the chest tube.
12. 1% lignocaine with epinephrine, 10 cc syringe, 25- & 22-g needles
9. Lungs fail to expand due to plugged bronchus; bronchoscopy required.
10. Anaphylactic or allergic reaction to surgical preparation or anaesthesia.
PRE-PROCEDURE PATIENT EDUCATION
1. Obtain informed consent
2. Inform the patient of the possibility of major complications and their treatment Recovery from the chest tube insertion and removal is usually complete, with only a
3. Explain the major steps of the procedure, and necessity for repeated chest small scar. The patient will stay in the hospital until the chest tube is removed. While
radiographs the chest tube is in place, the nursing staff will carefully check for possible air leaks,
breathing difficulties, and need for additional oxygen. Frequent deep breathing and
coughing is necessary to help re-expand the lung, assist with drainage, and prevent
PROCEDURE normal fluids from collecting in the lungs.
1. Determine the site of insertion. Locate the triangle of safety; bounded by the lateral
border of the pectoris major, 5th or 6th intercostal space, imaginary vertical line
between the anterior and mid axillary lines.
2. Surgically prepare and drape the chest at the predetermined site of the tube insertion.
3. Locally anaesthetized the skin and rib periosteum.
4. Make a 2-3cm transverse incision at the predetermined site and bluntly dissect
through the subcutaneous tissues, just over the top of the rib.
5. Puncture the parietal pleura with the tip of a clamp and put a gloved finger into the
incision to avoid injury to other organs and to clear any adhesions, clots, etc.
6. Clamp the proximal end of the chest tube and advance the tube into the pleural
space to the desired length.
7. Look for fogging of the chest tube with expiration or listen to air movement.
8. Connect the end of the chest tube to an underwater seal apparatus.
9. Suture the tube in place.
10. Apply a dressing and tape the tube to the chest.
11. Do a chest X ray
12. Obtain arterial blood gas values and/or institute pulse oximetry monitoring as
necessary.