Surgery Notes

These notes are based on readings from textbook & internet (mainly Medscape) and are meant for revision purposes only. (Not for
sale! Major copyright issue may arise!) They are far from complete and there may be mistakes or inaccurate information. Feel free to
share among any medical student who might find them useful and good luck for final exams!

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Gastro-oesophageal Reflux Disease (GORD)
Definitions  Montreal classification: A condition that develops when the reflux of stomach contents
causes troublesome symptoms and/or complications
 ≥ 2 heartburn per week, adversely affects individual’s wellbeing
 Physiologic reflux - postprandial, short-lived, asymptomatic, rarely during sleep
 Pathological reflux – a/w symptoms or mucosal injury, often including nocturnal episodes
 Reflux esophagitis = patients with GERD symptoms + endoscopic or histopathologic
evidence of oesophageal inflammation
Classification

Clinical  Lower oesophageal sphincter (LES) - zone of high pressure that prevents gastric reflux
Anatomy  Anatomical constriction of oesophagus – cricopharyngeal (15cm), aortic & bronchial (25cm),
diaphragmatic (40cm)
Risk Factors  Obesity
 Alcohol
 Smoking
 Spicy & fatty food
Pathophysiology  LES dysfunction – initially increased number of transient LES relaxations  decreased LES
resting tone  loss of sphincter function
 Hiatus hernia – LES not in the abdomen, do not function properly
 Delayed gastric emptying
Symptoms  Heartburn – burning sensation in the retrosternal area, worse after meal, on lying flat and
bending forward
 Regurgitation – perception of flow of refluxed gastric contents (acid/bitter) into mouth or
hypopharynx
 Dysphagia – d/t reflux oesophagitis or stricture
 Odynophagia – ulcer
 Water brash (hypersalivation)
 Globus sensation (constant perception of lump in the throat)
 Nausea
Extraoesphageal
 Chest pain
 Cough/wheeze – aspiration
 Hoarseness – irritation of vocal cord
 Ear pain – otitis media
 Tooth decay

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DDx  Infectious oesophagitis
 Motility disorder e.g. achalasia
 Oesophageal carcinoma
 Peptic ulcer disease
 Coronary artery disease
Ix  OGDS + biopsy (mandatory) – Look for oesophagitis, Barrett’s oesophagus, carcinoma,
strictures, hiatal hernia
 Oesophageal manometry (mandatory) – determine LES function, persistent symptoms
despite medical Rx, investigation of atypical symptoms e.g. chest pain & asthma
 Ambulatory 24H oesophageal pH monitoring – extent & severity of reflux
 Double contrast barium swallow – visualise mucosal changes, ulcers, delayed gastric
emptying
 ECG, cardiac biomarkers – TRO MI if chest pain
 CXR – if pulmonary symptoms, may have pulmonary fibrosis
Savary-Miller  Grade I – ≥1 non-confluent reddish spots +/- exudate
Classification of  Grade II – erosive and exudative lesions in the distal oesophagus that may be confluent, but
endoscopic not circumferential
appearance on  Grade III – circumferential erosions in the distal oesophagus, covered by haemorrhagic and
OGDS pseudomembranous exudate
 Grade IV – presence of chronic complications: deep ulcers, stenosis, scarring with Barrett's
metaplasia
Mx Lifestyle  Weight loss
 Smoking cessation
 Avoid excessive alcohol (relax sphincter)
 Avoid coffee, chocolate, fatty, spicy food
 Avoid large meals at night
 Small frequent meals
 Avoid bending or straining soon after meal
 Elevate head of bed
Medical  Proton-pump inhibitors (PPI) – omeprazole 20mg od, pantoprazole
 H2 receptor antagonist – ranitidine, cimetidine
 Antacids – aluminium hydroxide, magnesium hydroxide
 Prokinetics – metoclopramide, domperidone
Surgical  Balloon dilatation of stricutures
 Laparoscopic Nissen fundoplication
- Indications
 Inadequate control by medical therapy
 Poor compliance
 Patient’s wish (not to take long term medication)
 Barrett’s oesophagus
 Extraoesophageal manifestations
 Young patients
- Procedure
 Dissection of gastro-oesophageal junction at hiatus
 Tightening the crura
 Wrap gastric fundus around intra-abdominal portion of
oesophagus to recreate a flutter valve
- Complications
 General – bleeding, infection, injury to adjacent structures
 Specific and common – temporary dysphagia, gas-bloat
syndrome, increased flatus
 Specific but rare – slipped wrap: down onto stomach or up into
chest – acute onset chest/upper abdominal pain, dysphagia

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Complications  Reflux oesophagitis
 Barett’s oesophagus
 Oesophageal adeocarcinoma
 Oesophageal stricture

Oesophageal Carcinoma
Clinical
Anatomy

Epidemiology  6th commonest cancer in the world

 Mid-late adulthood
 Poor prognosis
Types Squamous cell carcinoma (SCC) Adenocarcinoma
 Common  Rising trend
 Upper 2/3  Lower 1/3
 RF: Tobacco, alcohol, dietary (hot fluid,  RF: Obesity, GERD, Barett’s, smoking
nitrosamines), betel nut chewing,  Pathophysiology: GERD  Barrett’s
predisposing condition (achalasia, oesophagus  intestinal metaplasia 
oesophageal diverticula & webs, Plummer- dysplasia  CIS  carcinoma
Vinson syndrome, HPV)
 Pathophysiology: Exposure of the
oesophageal mucosa to noxious or toxic
stimuli  dysplasia  carcinoma in situ 
carcinoma
Spread  Direct – aorta, tracheobronchial tree
 Lymphatic – early local LN invasion (situated in lamina propria), mediastinal LN, coeliac &
perihepatic LN (the latter 2 more in ADC)
 Haematogenous – liver, lung, bone, brain
Symptoms  Local effects:
- Dyspepsia
- Progressive dysphagia – solid to liquid
- Odynophagia
- Cough, regurgitation, vomiting
- UGIB
 Adjacent structures:
- Lungs (fistula) – pneumonia
- RLN – hoarseness
- Aorta – massive haemorrhage

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  Distant metastasis:
- Liver – jaundice
- Lungs – SOB
- Brain – altered behaviour, focal neurological signs
- Bone – back pain
 General
- LOA
- LOW
Signs  Normal except spread to LN/ distant mets
 LN – supraclavicular (Virchow’s)
 Hepatomegaly
 Lung crepitations/ pleural effusion
DDx  Oesophageal motility disorders – achalasia
 Oesophageal strictures
 Bronchogenic carcinoma (compression on oesophagus)
Ix  Blood
- FBC – Hb
- LFT – liver mets
 Imaging
- OGDS + biopsy
- EUS – depth of tumour penetration (T) and enlarged local lymph nodes (N) – patients
without distant mets and planned for surgery
- CT TA – distant mets to lungs, liver
- PET – occult LN & bone mets
- Laparoscopy – staging regional LN
- Thoracoscopy – staging regional LN
- Bronchoscopy – invasion of trachea & bronchi
- Barium swallow (rarely) – studying the distal anatomy in obstructive tumors that are
inaccessible by endoscopy
 Assess fitness for surgery
- FBC, RP, LFT, coagulation profile
- Cardiovascular risk assessment – FPG, FPL, ECG, ECHO, cardiopulmonary exercise
testing
- Fitness for thoracotomy – spirometry, ABG
TNM staging
(AJCC)

Mx Principles  Potentially curative vs palliative

 Stage I – Consider endoscopic therapy (eg, mucosal resection or submucosal

dissection), particularly for Tis and T1aN0 by EUS; consider initial surgery for
T1b and any N
 Stages II-III – Consideration for neoadjuvant chemoradiation followed by
surgery (trimodality therapy)

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  Stage IV – Chemotherapy, symptomatic, supportive care (palliative)

Indications for surgery:

 Dx suggests candidate for surgery
 High-grade dysplasia in Barrett esophagus that cannot be adequately
treated endoscopically

Contraindications for surgery:

 Metastasis to N2 (celiac, cervical, supraclavicular) nodes or solid organs
(liver, lungs)
 Invasion of adjacent structures (RLN, tracheobronchial tree, aorta,
pericardium)
 Severe comorbid (cardiovascular disease, respiratory disease)
 Impaired cardiac or respiratory function
Surgical  Endoscopic mucosal resection - experimental approach for T1a disease or
high-grade dysplasia (limited to certain centers and performed only under
protocol)
 Lesion above carina  3-stage oesophagectomy (McKeown operation)
- 1: right thoracotomy in L lateral position to mobilize tumour &
oesophagus
- 2: laparotomy in supine position to mobilize stomach & fashion it into a
conduit
- 3: neck incision to deliver oesophagus & tumour. Gastric conduit
anastomosed to cervical oesophagus
 Lesion below carina  2-stage Ivor-Lewis operation
- 1: open abdomen, mobilize stomach & fashion into conduit
- 2: L lateral, open right chest, mobilize oesophagus, excise tumour and
LN, anastomose gastric conduit to proximal oesophagus remnant (Roux-
en-Y if not possible)
- Benefit of 3-field lymphadenectomy (cervical, thoracic, abdominal)
controversial
 Transhiatal
- Avoid thoracotomy by mobilising oesophagus & tumour by blunt
dissection from below via diaphragmatic hiatus & above via neck
incision, anastomosis via the neck
- Disadvantage: Safety margin may be insufficient for potential cure,
adequate lymphadenectomy impossible in the chest, risk of damaging
azygos vein causing massive haemorrhage
 Laparoscopic approach increasingly used
Chemo-  Mainly neoadjuvant
radiotherapy - Reduce tumour bulk, increase curative resection rate, eliminate/delay
distant metastases
- Radiotherapy (approximately 45 Gy, local effect) and chemotherapy
(distant effect) with cisplatin and 5-fluorouracil
 Chemotherapy
- Alkylating (cisplatin), antimetabolite (5-FU), anthracycline (epirubicin),
and antimicrotubular (Paclitaxel) agents
- SCC mainly cisplatin-based
- ADC similar to gastric ca regime
Palliative  Chemotherapy
(mainly to  Radiotherapy
relieve  Argon plasma tissue coagulation
dysphagia)  Laser therapy
 Stenting – food has to be liquefied, take fizzy drinks after food to cleanse
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Consent  Indication/benefits
 How is it done
- above
 Complications in 40%
Early
- Respiratory (15-20%) - atelectasis, pleural effusion, and pneumonia
- Cardiac (15-20%) - cardiac arrhythmias and myocardial infarction
- Septic (10%) - infection, anastomotic leak, pneumonia
- Anastomotic leakage  mediastinitis, lung abscess, oesophago-pleural fistula.
Anastomosis placed in neck/upper chest (cervical) region because an intrathoracic leak
(lower) can cause severe sepsis & death
- Injury to RLN – hoarseness
Late
- Anastomotic stricture
- Dysphagia, early satiety, reflux (antacid)
Prevention  Smoking cessation
 Reduce alcohol intake
 High fibre & vitamin diet
 Treatment of GERD/Barrett’s oesophagus
- GERD – fundoplication
- Barrett’s – endoscopic ablation using radiofrequency ablation, photodynamic therapy
or cryotherapy

Peptic Ulcer Disease (PUD)

Definition  Disruption of the mucosal integrity of the stomach/duodenum or both, caused by local
inflammation or decreased mucosal resistance or hyperacidity
Clinical
Anatomy

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Epidemiology  Very common in developed countries – 10%
 Incidence of duodenal ulcer decreased, gastric ulcer constant
Aetiology/ Risk  H. pylori infection
Factors  NSAIDs
 Smoking
 Alcohol
 Stress/anxiety
 Spicy/fatty food
 Gastrinoma: Zollinger-Ellison syndrome (rare)
Pathophysiology  Normal: balance btwn acid secretion & mucosal defense
- Mucus impermeable to acid & pepsin
- Bicarbonate buffers effect of acid
- Prostaglandin E increases production of mucus & bicarbonate
- Ion pumps remove excess H+
 H. pylori (Gram –ve microaerophilic spiral bacterium)  urease  alkalinize
microenvironment  thrives in highly acidic stomach  causes mucosal inflammation 
effect of gastric acid & pepsin on mucosa  ulcer
 Duodenal ulcer: H. pylori  impaired bicarbonate secretion + increased gastric acid
production  gastric metaplasia  duodenitis  duodenal ulcer
 NSAIDs  inhibits PGE secretion  reduced mucus & bicarbonate secretion
 Extension through submucosal & muscular layers  deep ulceration  repair with scarring
& distortion  narrowing of gastric outlet  pyloric stenosis
 Deep ulceration  perforation (anterior)  peritonitis
 Deep ulceration  erosion of major blood vessel (posterior)  UGIB
 Sites of ulceration: (From commonest)
- First part of duodenum
- Gastric antrum along the lesser curve
- Lower end of oesophagus
- Meckel’s diverticulum with ectopic gastric mucosa
- Jejunal site of gastrojejunal anastomosis
Clinical features Duodenal ulcer (more common) Gastric ulcer
Epigastric pain –  Pain before meal & middle of  Pain aggravated by eating
gnawing, burning night, relieved by food & milk
 Pain radiating to the back
suggests posterior penetrating
ulcer causing pancreatitis
Other GI  Dyspepsia  Dyspepsia
symptoms  Heartburn, chest discomfort less  Heartburn, chest discomfort
common common
 Malaena>haemaemesis  Haematemesis >malaena

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  Bloating, nausea, vomiting
several hours after meal
suggest GOO
LOW  Well-built  Ill-built
Complications  Anterior ulcer – perforation  Gastric outlet obstruction
 Posterior ulcer – bleeding  Perforation
 Usually not a/w malignancy  Bleeding
 Gastric carcinoma
Classification

DDx  Functional dyspepsia

 Crohn’s disease
 Zollinger-Ellison syndrome
 GERD
 Cholecystitis/ascending cholangitis
 Oesophagitis/oesophageal rupture
 ACS
Ix  Laboratory
- H. pylori test
 Endoscopic biopsy – rapid urease test (CLOtest), histopathology & culture
 Stool antigen test
 Serology (IgG)
 Urea breath test
- FBC – anaemia
- Iron studies
- LFT amylase– TRO hepatobiliary & pancreatic causes
- Serum gastrin – if suspect Zollinger-Ellison syndrome
 Imaging
- OGDS + biopsy – direct visualisation, detect H. pylori, malignancy
 Gastric ulcer (benign) – well-defined, punched out, smooth base with whitish
fibrinoid exudate, surrounding mucosa shows radiating folds
 Duodenal ulcer - well-demarcated break in the mucosa that may extend into
the muscularis propria
- Erect CXR – air under diaphragm when perforation suspected
- Barium meal – GOO, perforation (largely replaced by OGDS)
- Angiography – massive UGIB in which OGDS cannot be performed
Mx Conservative  Avoid aggravating food
 Reduce alcohol intake
Medical  Triple therapy (2/52) – standard
- Omeprazole (Prilosec): 20 mg PO bid
- Clarithromycin (Biaxin): 500 mg PO bid
- Amoxicillin (Amoxil): 1 g PO bid or
- Metronidazole (Flagyl): 500 mg PO bid
 Quadruple therapy if triple therapy fails
- PPI, standard dose, or ranitidine 150 mg, PO bid
- Bismuth 525 mg PO qid
- Metronidazole 500 mg PO qid
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 - Tetracycline 500 mg PO qid
 Maintenance therapy with PPI/H2-receptor antagonists in patients with
recurrent, refractory, or complicated ulcers
 Discontinue NSAIDs, change to selective COX-2 inhibitor or cover with PPI
 Other: cytoprotective – misoprotol, sucralfate
Surgical  See perforated ulcer

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Upper GI Bleed
Definition  Bleeding in the GIT proximal to ligament of Treitz
Variceal Non-variceal
Clinical  Splenic vein + SMA  portal vein  L & R  Blood supply of oesophagus
Anatomy - Upper 1/3 by inferior thyroid artery
- Middle 1/3 by branches from descending thoracic aorta
- Lower 1/3 by left gastric artery

 Blood supply of stomach

Sites of portosystemic shunt
 Oesophageal veins (P) & azygous veins (S)  oesophageal varices
 Paraumbilical veins (P) & abdominal epigastric veins (S)  caput
medusae
 Superior rectal veins (P) & inferior rectal veins (S)  haemorrhoids
 Colic veins (P) & retroperitoneal veins (S)
- Coeliac trunk originates from aorta at L1 and trifucates into
common hepatic artery (CHA), left gastric artery (LGA) and
splenic artery
- LGA supplies the lesser curvature of the stomach and gives an
ascending branch to the oesophagus
- CHA runs on the superior border of pancreas and gives off
gastroduodenal artery (GDA) which runs behind D1. CHA
continues as hepatic artery proper

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 - Right gastric artery (RGA) is a branch of CHA and runs along the
lesser curvature to join the LGA
- GDA gives of posterior superior pancreaticoduodenal artery
(PSPDA) and continues to branch into right gastroepiploic artery
and ASPDA. The RGEA runs along the greater curvature
- Splenic artery runs on the superior border of pancreatic body
and tail and gives off the LGEA which runs along the greater
curvature and joins the RGEA

 Blood supply of the duodenum

- Gastroduodenal artery (from CHA) which gives off a branch of

supraduodenal artery and then divides into ASPDA and PSPDA
- Superior mesenteric artery which gives rise to AIPDA and PIPDA
Epidemiology  6.4% UGIB in Malaysia  Bleeding PUD commonest cause
 Cirrhosis  80% stop spontaneously, 20% may have persistent/recurrent bleed
- Present in 60% decompensated & 30% compensated cirrhosis at  10% mortality
time of diagnosis
- 30% will bleed
- Major cause of death – 30-50% within 6/52 (1st bleed)

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Aetiology  Risk factors for oesophageal varices bleed  Commonest: PUD (64% of all UGIB), acute erosive gastritis - NSAIDs,
- Severity of liver dysfunction steroids, alcohol (16.5%), oesophagitis, oesophageal ca, gastric ca
- Size (large) of varices (malignancy 3.6%)
- Presence of endoscopic wale signs  Oesophagus – GERD, oesophagitis, oesophageal ulcer, oesophageal
- HPVG >12mmHg ca, Mallory-Weiss tear
- Previous bleed (70% recurrent haemorrhage)  Stomach – gastric ulcer, erosive gastritis, haemorrhagic gastritis,
gastric polyp, gastric ca, gastric lymphoma, leiomyoma, hereditary
haemorrhagic telangiectasia, angiodysplasia, Dieulafoy lesion (large
tortuous arteriole in submucosa)
 Duodenum – duodenal ulcer, duodenal erosion, duodenal polyps,
ampullary Ca, Ca pancreas, haemobilia, AVM, aorto-duodenal fistula
 Small bowel – stomal ulcer, diverticulum (inc Meckel’s), tumour,
AVM
Risk factors  Cirrhosis from  H. pylori
- Alcoholic liver disease  NSAIDs
- Chronic hepatitis B, C  Aspirin
Pathophysiology  Normal hepatic venous pressure gradient (HPVG) <5mmHg, >10mmHg  PUD – amount of bleeding depends on size of vessel. Posterior
 risk of developing varices duodenal ulcer can erode the gastroduodenal artery causing massive
 Portal HPT  portosystemic collaterals inc gastro-oesophageal varices bleeding
 Majority bleeding are from oesophageal varices, 20-30% from gastric  Gastritis, oesophagitis – erosion of BV
varices, but mortality is higher with the latter  Mallory-Weiss syndrome – acute GOJ tear - severe vomiting/retching
 Boerrhaave’s syndrome – full thickness tear
 Oesophageal/ gastric carcinoma – ulcerative stage
Classification Japanese classification of oesophageal varices Forest Classification for Bleeding Peptic Ulcer
 Grade 1 – small straight varices not disappearing with insufflations
 Grade 2 – medium varices occupying 1/3 lumen
 Grage 3 – large varices occupying >1/3 lumen

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 GOV I – continuation of oesophageal varices, extend 2-5cm along lesser
curvature Major – Ia, b, IIa, b
 GOV II – extend towards fundus of stomach
 IGV I – fundus of stomach Rockall Score for Prognosis
 IGV II – ectopic, anywhere

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 <3 = good prognosis (3.5-5.3% re-bleeding risk, 0-0.2% mortality)
>8 = bad prognosis (41% re-bleeding risk, 41% mortality)

Clinical features  Haematemesis – fresh blood or coffee ground (gastric acid breaks down Hb into haematin)
 Malaena – black, tarry, sticky, loose, malodorous stool (degradation of blood in intestine)
 Rarely haematochezia – life-threatening massive bleeding
 Iron deficiency anaemia (chronic) – SOB, palpitations, postural hypotension, lethargy
 Positive FOB
 Ask for risk factors of bleeding (above)
 Examine for stigmata of CLD & features of portal hypertension (caput medusae, ascites, splenomegaly), cutaneous & buccal telangiectasia (Osler-
Weber-Rendu syndrome)
Ix  Blood - Coagulation profile
- FBC – Hb (anaemia), HCT, WCC, Plt - ABG
- RP – Urea (blood meal, dehydration), Cr, electrolyte inbalance - GXM
- LFT – albumin (liver function), bilirubin, AST, ALT (liver disease),  Imaging
GGT (alcohol), ALP - OGDS (urgent)
Mx Oesophageal Varices PUD Bleed

1. Aggressive resuscitation to restore haemodynamic stability
 A: May consider intubation to protect airway if severe uncontrollable
bleeding, encephalopathic, inability to maintain O2 saturation
adequately and to prevent aspiration
 B: O2
1. Aggressive resuscitation to restore haemodynamic stability
 A: May consider intubation to protect airway if drowsy, comatose,
continuing vomiting/haematemesis (risk of aspiration)
 B: O2

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 C: 2 large bore IV brannula/ central venous access, bloods, GXM,  C: 2 large bore IV brannula/ central venous access, bloods, GXM, IV
cautious transfusion of packed RBC to keep Hb around 8g/dL/ HCT 24% crystalloids (Hartmann’s or normal saline)
(Overtransfusion can increase portal pressure & exacerbate bleeding), - Indications of blood transfusion:
correct coagulopathy  SBP <110 mmHg
 Monitor vital signs closely, monitor for continuous bleeding  PR >110 bpm
 Postural hypotension
2. Pharmacological Rx  Hb <8 g/dL
 Start IV vasoactive drug as early as possible to reduce blood flow &  Angina/CVD with Hb <10 g/dL
pressure within varices  Monitor vital signs closely, monitor for continuous bleeding
- Terlipressin (synthetic vasopressin analogue): 2mg bolus and 1mg
every 6 hours x 2-5/7 2. Pharmacological Rx
- Somatostatin: 250mcg bolus, then 250mcg/hour infusion x 5/7  Proton pump inhibitor (PPI)
- Octreotide (somatostatin analogue): 50mcg bolus, then - pH control to allow blood coagulation & platelet aggregation
50mcg/hour x 5/7 - High dose IV: IV Omeprazole 80mg stat followed by infusion of
 Antibiotic prophylaxis – reduce rate of infection, SBP, re-bleeding. 8mg hourly for 72H
- IV 3rd gen cephalosporin (ceftriaxone 1g daily) or x 1/52
- PO fluoroquinolones (norfloxacin 400mg bd, ciprofloxacin 500mg 3. Endoscopic Therapy
bd) x 1/52  Various modalities
- Thermal – heater probe, electrocoagulation, argon plasma
3. Surgical Rx coagulation
 OGDS a.s.a.p. If unavailable  consider balloon tamponade & send to - Injection – adrenaline, procoagulants (fibrin glue, human
tertiary centre thrombin), sclerosants (can cause perforation, fatal gastric
 Control of bleeding – endoscopic variceal ligation (EVL) recommended, necrosis)
use endoscopic sclerotherapy if EVL difficult - Mechanical – clips
- EVL – more effective, fewer complications, more difficult to - Combination
perform  Adrenaline – prolonged vasoconstriction, platelet aggregation,
- Sclerotherapy – easier to perform, more complications (ulceration, tamponade effect. Safe. S/E: tachycardia
stricture)  Fibrin – little tissue damage
 Persistent bleeding – repeat OGDS, TIPS, Sx, consider balloon
tamponade 4. Surgical Rx
- TIPS – effective but high morbidity & mortality  Surgery if decided upon should be performed early rather than late
- Sx – oesophageal transection +/- devascularisation, portosystemic to avoid an unfavorable outcome especially in the hypotensive
shunts, liver transplantation. High mortality elderly patient
- Balloon tamponade – effective but high re-bleeding rate,  Types
complications e.g. ulceration, perforation, aspiration pneumonia. - Local - under-running/ over-sewing or excision of ulcer
Only as temporary bridge for max 24H - Radical surgery - gastric resection or vagotomy
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  Interventional radiology (embolization) is an effective alternative
Gastric Varices
 GOV I  Rx as oesophageal varices
 GOV II & IGV  inject with cyanoacrylate (tissue adhesive)
 Persistent bleed  TIPS, Sx, consider balloon tamponade
Prevention Primary prophylaxis (preventing 1st bleed) Follow-up
 Non-selective beta-blocker e.g. propranolol to reduce splanchnic blood  Discharge with PPI
flow  Gastric ulcers should be re-endoscoped in 6 weeks to assess healing
 Screening endoscopy at time of dx of cirrhosis & every 2 years in and rule out malignancy
patients not known to have varices  Helicobacter pylori eradication for all H. pylori positive ulcers
 NSAIDs - consider COX-2 inhibitors, or least damaging NSAID + PPI
Secondary prophylaxis
 Non-selective beta-blockers/EVL/both
 TIPS/shunt Sx if non-compliant/refractory to above

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18
Gastric Carcinoma
Epidemiology  4th commonest cancer
 2nd commonest cause of cancer death
 Higher in Asian (Japan) and South American countries
Aetiology/ Risk  Diet – high salted meat/fish, high nitrate, salted/smoked
Factors  Environmental – poor drinking water, radiation, occupation – coal, rubber, asbestos
 Medical – H. pylori, prior gastric Sx, gastric atrophy, pernicious anaemia, adenomatous
polyps, gastrinoma
 Family history
Symptoms  Asymptomatic
 Anaemia
 Malaena, haematemesis
 Palpable epigastric mass
 LOA, LOW
 GOO
 Symptoms of complications
Signs  General – nutritional status, anaemia, jaundice
 Palpable epigastric mass
 LN – supraclavicular (Virchow’s), left axillary (Irish)
 Hepatomegaly
 Ascites
 Pleural effusion
 DRE – nodule in rectovesical pouch (Bloomer’s shelf), ovaries (Krukenberg)
 GOO - Visible peristalsis, succession splash
 Sister Mary Joseph nodule (umbilical nodule)
Complications  GOO – visible peristalsis, succession splash
 Distant mets
- Direct
- Lymphatics - coeliac, supraclavicular
- Haematogenous – liver, lung, bone
- Transcoelomic – krukenberg tumour of the ovary, umbilical nodules (Sister Mary Joseph
nodule)
 Transverse colon fistula – faeculent vomiting
 Intestinal obstruction
 DVT
Classification  Microscopic
- Adenocarcinoma (90-95%)
- Lymphoma
- Gastrointestinal stromal tumour (GIST)
- Carcinoid tumours
- Squamous cell carcinoma
 Macroscopic
- Superficial
- Polypoid
- Ulcerative
- Scirrhous (diffuse linitis plastica) – leather bottle like

19
  Lauren Classification
Intestinal Type Diffuse Type
- Well-differentiated - Poorly-differentiated
- Slow growing - Aggressive
- Tend to form glands - Scatter throughout stomach
- Men>women - M=F
- Older - Younger
- Environmental - Familial
- Gastric atrophy, intestinal - Blood group A
metaplasia
- Microsatellite instability, APC gene - Decreased E-cadherin
mutations
- Haematogenous spread - Lymphatic spread
 Japanese classification of early gastric carcinoma

 Borrmann classification of advanced gastric carcinoma

Ix  Bloods
- FBC – anaemia
- LFT – liver mets, low albumin (poor nutrition)
- CEA – raised in 45-50%
- CA 19-9 – raised in 20%
 Imaging
- OGDS + biopsy
- Double-contrast barium studies – in obstructive cases
- CT TAP
- EUS – pre-op assessment of local disease
Staging  T
- T1a – mucosa
- T1b – submucosa
- T2 – muscularis propria
20
 - T3 – subserosa
- T4a – contiguous/beyond serosa
- T4b – invades adjacent structure
 N
- N0 - No regional lymph node metastasis
- N1 - 1–2 regional lymph nodes
- N2 - 3–6
- N3 - 7 or more
- N3a - 7–15
- N3b - 16 or more
 M
- M0 – no distant metastasis
- M1 – distant metastasis
Mx Principles  Tis/T1 – endoscopic mucosal resection/complete surgical resection
 IB-IIIC – neoadjuvant chemoradiotherapy + surgical resection +/- post-op
chemotherapy
 Metastatic – palliative
Non-surgical  Neoadjuvant chemotherapy (epirubicin, cisplatin, and 5-fluorouracil)
- Downstaging of disease to increase resectability
- Decrease micrometastatic disease burden prior to surgery
- Allow patient tolerability prior to surgery
- Determine chemotherapy sensitivity
- Reduce the rate of local and distant recurrences
 Adjuvant chemotherapy/radiotherapy/chemo-radiotherapy
Surgical  Total gastrectomy (if required for negative margins)
- 5-cm surgical margin proximally and distally to the primary lesion
(extensive lymphatic network around the stomach and the propensity to
extend microscopically)
- Lymph node dissection
 D1 (perigastric lymph nodes)
 D2 (hepatic, left gastric, celiac, and splenic arteries, as well as
those in the splenic hilum)
 Oesophagogastrectomy for tumours of the cardia and gastroesophageal
junction
 Subtotal gastrectomy for tumours of the distal stomach
Palliative  Radiotherapy provides relief from bleeding, obstruction, and pain
 Surgical procedures e.g. wide local excision, partial gastrectomy, total
gastrectomy, simple laparotomy, gastrointestinal anastomosis, and bypass
to allow intake of food and alleviate pain
 Platinum-based chemotherapy
 Novel therapy – trastuzumab for HER2 +ve, bevacizumab being evaluated
Prognosis  Poor prognostic features
- Depth of invasion
- Regional LN involvement
- Linitis plastica

Billroth 1 & 2

21
Approach to Obstructive Jaundice
Enterohepatic Circulation

 RBC break down  Haem  Bilirubin  bound to albumin (insoluble)  liver  conjugated with glucuronic
acid (soluble)  excreted into bile  bowel  bacteria action  urobilinogen (colourless) + urobilin
(brown)  urobilinogen reabsorbed into liver & re-excreted in bile, some escapes into circulation & excreted
in urine (yellow)
 Bile acid (salt) synthesized in liver from cholesterol-based precursors  excreted into bile  duodenum 
facilitate lipid digestion & absorption  95% reabsorbed in distal ileum  portal vein  liver  re-excreted
in bile

Obstructive Jaundice

 Conjugated bilirubin  blood  raised plasma bilirubin

 Conjugated bilirubin excreted in urine  dark urine
 Less urobilin to darken the stool  pale stool
 Less bile acid in the bowel  defective fat absorption  fatty stool
 Raised bile acid in the blood  deposit in skin  pruritus
 Malabsorption of fat soluble vitamin ADEK
 Vitamin K deficiency  decreased hepatic synthesis of clotting factors II, VII, IX, X  bleeding risk

Causes of Obstructive Jaundice

CBD stones
(common)
Painful
Mirizzi Syndrome
(Rare)

Intra-lumen Ascaris

Obstructive
Cholangio-
Jaundice
carcinoma

Peri-ampullary
carcinoma

Intra-mural GB carcinoma
Painless

PSC

Stricture

Ca head of
pancreas
(common)
Extra-mural
Portal LN
enlargement

22
Causes

Stone Common bile - Biliary colic

duct stone - Jaundice – progressive, fluctuant or intermittent depending on impaction
of stone/s
Mirizzi’s - Gallstone impacted in Hartmann’s pouch causing inflammation of GB
syndrome which then fuses with CBD causing obstruction
Tumour Ca head of - Painless jaundice, persistent/progressive
pancreas - Gall bladder may become palpable (Courvoisier’s law)
- May invade D2
Periampullary - Ca of ampulla, distal bile duct or duodenum
carcinoma - Similar features to Ca head of pancreas
Other - LN metastases in porta hepatis
malignant - Primary cholangiocarcinoma
tumour - Carcinoma of gall bladder
Wall Benign - Surgical damage/inflammation by stone
stricture of - Similar features to Ca head of pancreas
CBD
Intrahepatic/ - Primary cholangiocarcinoma
hilar bile duct - Primary sclerosing cholangitis (PSC)
obstruction
Other Intrahepatic - Viral hepatitis
cholestasis - Systemic sepsis
- Drugs – chlorpromazine, OCP, chlorpropamide interfere with bile excretion
from hepatocytes
- Widespread hepatic lymphoma (rare)
Pancreatitis - CBD obstructed by inflammatory swelling (acute) or fibrosis (chronic)

Approach to Obstructive Jaundice

Hx - Biliary colicky pain

- Dark urine, pale stool
- Previous episodes of obstructive jaundice
- LOA, LOW, non-specific GI disturbance
- Previous biliary tract Sx
- Attacks of acute pancreatitis
- IBD (PSC)
- Drug Hx e.g. OCP
- Blood transfusion, IVDU, tattoos, shellfish ingestion, sexual Hx
- Excess alcohol intake
PE - Scleral icterus, yellow skin discolouration
- Scratch mark
- Stigmata of CLD
 Spider naevi
 Hepatic flap
 Caput medusae
- Palpable abdominal masses
- Palpable gallbladder
- Hepatomegaly
- Splenomegaly
- Ascites
- Stool & urine inspection

23
Ix Blood/ - Urine dipstick – bilirubin
urine - LFT – bilirubin +++, ALP +++, AST +, ALT +
- Coagulation profile
- Hep B/C
- Tumour markers
Imaging - Hepatobiliary U/S
- CT scan
- ERCP/MRCP
- Liver biopsy – percutaneous/laparoscopic
Mx - Aim – relieve obstruction to avoid infection (acute cholangitis), back pressure interfering liver function
- Potentially curable obstructions
 Stones – ERCP, cholecystectomy
 Strictures – stenting, hepaticojejunostomy
 Periampullary tumours - excision
- Incurable tumours – palliative stenting, palliative triple bypass surgery
 Ca head of pancreas
 LN metastases in porta hepatis
 Ca gall bladder
- Terminal disease
 Stenting
 Pruritus - antihistamine & chlorpromazine

24
Gallstone Disorders
Clinical
Anatomy

Types of Composition Pathogenesis Characteristics

gallstones Mixed (75-90%)  Abnormal bile constituents  Multiple stones
Cholesterol +  Bile stasis  Different sizes (generations)
pigments +  Infection  Hard & faceted or soft, irregular
calcium ‘mulberry’-shaped
 Variable colour – yellow-green-
black
 Most radiolucent, 10% radiopaque
Cholesterol  As above  Usually solitary
(10%)  Large, up to 4cm
 Smooth, egg- or barrel-shaped &
 Colour – yellowish
 Radiolucent
Pigment  Excess bilirubin excretion  Multiple
(commoner in - Haemolytic anaemia  0.5-1 cm diameter, uniform size
Asia) - Infections  Friable
- Malaria  Colour – jack-black
- Leukaemias
Calcium  Excess calcium excretion in  Greyish faceted stones
carbonate (rare) bile  Radiopaque
Epidemiology  10% in developed countries (symptomatic/asymptomatic)
Risk factors Cholesterol  Metabolic syndrome – obesity, T2DM, HPT, hyperlipidaemia
stone  Causes of biliary stasis
- Pregnancy (progesterone reduced GB contractility)
- Obstruction
- Defective contractility of GB
- Prolonged TPN
- Rapid weight loss with severe fat & carbohydrate restriction (e.g.
diet, gastric bypass)
- High spinal cord injury
- Trauma (burn)
- Surgery
 Medications
- OCP – increase biliary cholesterol secretion
- Fibrates – increase hepatic cholesterol elimination via bile
- Somatostatin analogue – decrease GB emptying

25
  Ileal resection – reduced bile salt reabsorption
 Hereditary (25%)
 Rare - Deficiency of the biliary transport protein required for lecithin
secretion (low-phospholipid-associated cholelithiasis)
Pigment stones  Increased haem turnover
(black & brown) - Sickle cell anemia
- Hereditary spherocytosis
- Beta-thalassaemia
- Cirrhosis  portal HPT hypersplenism  increased sequestration
 Colonization (stasis)
- Post-surgical biliary strictures
- Choledochal cysts
- Biliary flukes (strictures)
Pathophysiology  Cholesterol stones
- Changes in concentration of bile constituents
 Cholesterol (++) – hyperlipidaemia, clofibrate  supersaturation
 Bile salt (--) – ileal resection (eg. Crohn’s), PBC, cholestyramines, OCP, genetic
 Lecithin (--)
- Biliary stasis
- Infection & inflammation – bacteria forms the organic nidus for stone formation
 Calcium, bilirubin & pigmented stones
- Unconjugated bilirubin (insoluble), tends to form insoluble precipitates with calcium
- Increased haem turnover e.g. in haemolytic anaemia  calcium bilirubinate crystallize
& form stones
- Oxidation causes bilirubin precipitate to take on ‘jet-black’ colour
- Bile is normally sterile but when there is bacterial colonization e.g. strictures, the
bacteria hydrolyze the conjugated bilirubin  unconjugated bilirubin  calcium
biorubinate crystals
- Bacteria also hydrolyze lechitin to release fatty acids  bind calcium  claylike
precipitate (“brown stone”)
 Spectrum
- Asymptomatic
- Biliary colic
- Acute/chronic cholecystitis
- Mucocoele
- Choledocholithiasis – acute panreatitis
- Ascending cholangitis
- Gall bladder empyema
- Cholecysto-duodenal fistula – gallstone ileus
- Gallbladder carcinoma

26
Acute Cholecystitis
Definition  Inflammation of the gallbladder that occurs most commonly because of an obstruction of
the cystic duct by gallstones arising from the gallbladder (cholelithiasis)
Aetiology  Calculous - obstruction of the cystic duct  distention of the gallbladder  blood flow and
lymphatic drainage are compromised  mucosal ischemia and necrosis
 Acalculous – biliary stasis, MI, sickle cell disease, salmonella infections, DM, AIDS with
cytomegalovirus, cryptosporidiosis, or microsporidiosis
Symptoms  Pain – RUQ/epigastric, radiating to tip of right shoulder/scapula, colickyconstant
 Nausea, vomiting
 Fever
Signs  Fever, tachycardia
 +/- jaundice
 RUQ/epigastric tenderness, guarding, rebound tenderness
 Murphy’s sign - tenderness and an inspiratory pause elicited during palpation of the RUQ
 Palpable gallbladder (exception of Courvoisier’s) – GB mucocoele, GB empyema
Complications  Gallbladder empyema
 Perforation  subphrenic abscess, generalised peritonitis
 Gangrene
 Cholecysto-duodenal fistula & gallstone ileus
 Emphysematous cholecystitis - gas-producing organisms e.g. E. coli, Clostridia
perfringens, and Klebsiella
 Sepsis
DDx  PUD
 Acute gastritis
 Acute pancreatitis
 AAA
 Acute pyelonephritis
 Appendicitis
 Inferior MI
 Lower lobe pneumonia
 Pregnant lady – pre-eclampsia,
Ix Blood &  FBC – Hb (haemolytic anaemia), WCC (inflammation/infection), Plt (low in
urine sepsis)
 LFT – total bilirubin, direct/indirect bilirubin, ALP, AST, ALT, GGT
 Coagulation profile – fat hence vit K malabsorption  coagulopathy
 Serum amylase – TRO pancreatitis
 RP – Urea, Cr (dehydration, bilirubin deposits at renal tubule causing
hepatorenal syndrome), electrolyte
 UFEME – urobilinogen, TRO pyelonephritis
 UPT – women of childbearing age
Imaging  U/S hepatobiliary – gallstones in GB, pericholecystic fluid, GB wall thickening
 Plain AXR – 10-15% gallstone radiopaque, gas in the gallbladder wall
(emphysematous cholecystitis), free air under diaphragm (PGU), calcified GB
(carcinoma)
 CT abdomen (uncertain cases) – choleystitis (wall thickening (>4 mm),
pericholecystic fluid, subserosal edema, intramural gas, and sloughed
mucosa), complications e.g. gangrene, gas formation, perforation, TRO
other pathology
Mx Supportive  NBM – bowel rest, prep for cholecystectomy
 IV fluid, correct electrolyte abnormalities
 Analgesia – tramadol, mepiridine

27
  IV antibiotics – cefuroxime/gentamicin (Gram –ve), metronidazole
(anaerobe)
 Anti-emetic (metochlopromide)/ NG tube for vomiting
 Plan for immediate/delayed laparoscopic cholecystectomy (4-6 weeks for
inflammation to subside)
Surgical  Laparoscopic cholecystectomy is the standard
 Timing
- Emergency – complicated cases e.g. gangrene, perforation
- Immediate – within 72H admission
- Delayed – 4-6 weeks, after inflammation subside. Risk of further attacks,
pancreatitis
 5% probability of conversion into open cholecystectomy due to technical
difficulties/complications
 Indications
- Symptomatic gallstone disease
- Asymptomatic gallstone disease with high risk of
symptoms/complications
 Contraindications
- High risk of GA
- Morbid obesity
- Late stages of pregnancy
- Uncontrolled major bleeding disorders
- End-stage liver disease with portal HPT & severe coagulopathy
- Signs of GB perforation – abscess, peritonitis, fistula
- Septic shock from cholangitis
- Acute pancreatitis
- Lack of equipment, lack of surgical expertise
- Previous abdominal surgery (adhesions)
- Intra-abdominal malignancy
 Higher risk for jaundiced patient (preferable to relieve any obstruction with
ERCP/stenting prior to cholecystectomy)
- Infection
- Hepatic impairment
- Coagulopathy
- Acute renal failure
- Venous thrombosis
 Procedure
- GA
- Pneumoperitoneum established using automatic gas insufflation
- Subumbilical, upper midline, midclavicular line, anterior axillary line
ports inserted to introduce laparoscope & operating instruments
- Cystic duct & artery identified
- Cystic artery isolated, clipped/ligated & divided
- Identify junction btwn cystic duct & CBD
- Cystic duct clipped/ligated near GB
- Operative cholangiogram performed (if desired, unsure of anatomy)
percutaneously
- Cystic duct divided, GB dissected out of liver bed using
diathermy/ultrasonic coagulation probes
- Secure haemostasis
- GB removed via umbilical port
- Umbilical fascial defect sutured to prevent herniation but others left
unsutured
 Post-op

28
 - Able to walk & tolerate food within 6H
- 80% discharged within 24H
 Complications
- Bleeding
- Infection – including subphrenic abscess
- Injury to common bile duct  biliary peritonitis causing multi-organ
failure; require open Sx & risks long-term bile duct strictures
- Bile leaks through suture lines (biliary peritonitis, high fatality if
infected) – drain should be left in situ for 5 days
- Bowel injury
- Postcholecystectomy syndrome – persistent/recurring abdominal pain &
dyspepsia. ERCP/MRCP TRO stone in CBD/cystic duct, CBD damage

Choledocholithiasis
Definition  Gallstone in the common bile duct
- Primary stones - usually brown pigment stones, which form in the bile ducts
- Secondary stones (85%) - usually cholesterol, which form in the GB but migrate to CBD
- Residual stones - missed at the time of cholecystectomy (evident < 3 yr later)
- Recurrent stones - develop in the ducts > 3 yr after surgery

 Causes of CBD obstruction

- Intra-luminal: stone, tumour, parasites (Ascaris)
- Luminal: Trauma (Sx), scarring (chronic pancreatitis), strictures (PSC), AIDS-related
cholangiopathy/cholangitis
- Extra-luminal: tumours, cyst, choledochocoele, pancreatic pseudocyst
Symptoms  Obstructive jaundice – jaundice, dark urine, pale stool
 RUQ pain – intermittent
 Nausea, vomiting
 Symptoms of acute pancreatitis
Signs  Jaundice
 RUQ tenderness
Complications  Ascending cholangitis (Gram –ve & anaerobes)
 Gallstone pancreatitis
DDx  Periampullary carcinoma
 HCC/liver mets
 Other ddx as for acute cholecystitis
Ix Blood &  As for acute cholecystitis
urine
Imaging  U/S hepatobiliary – dilated CBD (>8mm), acoustic shadow
 MRCP – confirm stone (may have passed), TRO other pathology e.g. tumour
 ERCP – diagnostic & therapeutic
Mx Supportive  NBM
 IV fluids
 Analgesics
 Antibiotics
 Anti-emetic
 Prepare for ERCP & cholecystectomy
Surgical  ERCP (endoscopic retrograde cholangiopancreatography) & sphincterotomy
- Indications
 Choledocholithiasis & complications (ascending cholangitis,
acute pancreatitis)
 Bile duct strictures
29
  Post-op biliary leaks
 Sphincter of Oddi dysfunction
 Unknown cause of recurrent acute pancreatitis
 Pancreatic duct stones
 Symptomatic pancreatic pseudocyst
- Contraindications
 Patient refusal
 Unstable cardiopulmonary, neurologic, or cardiovascular status
 Existing bowel perforation
 Structural abnormalities of the esophagus, stomach, or small
intestine (esophageal stricture, paraesophageal herniation,
esophageal diverticulum, gastric volvulus, gastric outlet
obstruction, and small bowel obstruction)
 Altered surgical anatomy (partial gastrectomy with Billroth II or
Roux-en-Y jejunostomy)
- Procedure

- Complications
 General
o Contrast allergy
o Oxygen desaturation
o Cardiopulmonary complications
 Specific (Early)
o Bleeding
o Post-ERCP pancreatitis
o Infection - Ascending cholangitis
o Perforation – by passage of endoscope
 Specific (late)
o Stenosis of the ampulla of Vater (sphincterotomy)
o Stone recurrence
 Common bile duct operation (open surgery if ERCP fails)
- To check for residual stones & remove difficult stones
- Longitudinal/transverse incision at CBD
- Stones retrieved by a combination of manipulation, irrigation, grasping
with forceps/Dormia basket, balloon catheter
- Latex T tube inserted to drain bile to the exterior with transverse limb in
the CBD – provide assess to biliary tree for a further cholangiogram (T-
tube cholangiography) 1-week later in order to ensure no stone remains
& oedema @ ampulla settle
 Laparoscopic cholecystectomy during the same admission

Ascending Cholangitis
Definition  Acute bacterial infection superimposed on obstructed biliary tree
 Causes
- CBD gallstone
- Tumour – periampullary (pancreatic head, cholangiocarcinoma, duodenal), porta
hepatis tumour, liver mets
- Stricture, primary sclerosing cholangitis (PSC)
- Choledochocoele
- ERCP
- AIDS cholangiopathy
- Ascaris lumbricoides infections

30
  Common pathogens
- Escherichia coli (27%)
- Klebsiella (16%)
- Enterococcus (15%)
- Streptococcus (8%)
- Enterobacter (7%)
- Pseudomonas aeruginosa (7%)
 Complications
- Liver failure
- Liver abscess
- Sepsis
- Acute renal failure
Symptoms  Charcot’s triad – fever, RUQ pain, jaundice
 Raynold’s pentad – above + hypotension + altered mental status
 Pale stool, dark urine
 Pruritus
 Risk factors – gallstone, recent cholecystectomy, recent ERCP, Hx of cholangitis, AIDS
Signs  Pyrexia
 Tachycardia
 Hypotension
 Altered mental status
 Jaundice
 RUQ tenderness
 Mild hepatomegaly
 Peritonitis (uncommon, look for other causes)
DDx  Acute cholecystitis
 Viral hepatitis
 Liver abscess
 Perforated gastric ulcer
 Pyelonephritis
 Acute pancreatitis
 Acute appendicitis
 Right colon diverticulitis
 Mesenteric ischaemia
 Septic shock
Ix Blood &  FBC –WCC (leucocytosis/leucopenia), Plt (low in sepsis)
urine  LFT – total bilirubin (high), direct/indirect bilirubin (high), ALP (high), AST,
ALT, GGT
 Coagulation profile – coagulopathy, DIVC
 ESR, CRP
 Blood C+S
 Biliary C+S – if drainage done
 Serum amylase – TRO pancreatitis; serum calcium (hypocalcaemia)
 RP – Urea, Cr, electrolyte
 UFEME – urobilinogen
 UPT – women of childbearing age
Imaging  U/S hepatobiliary – stone in CBD (may be obscured), bile duct dilatation,
stones in gallbladder, visualise liver & other structures – pancreas, aorta
 Plain AXR – ileus, radiopaque gallstone, air in biliary tree (emphysematous
cholecystitis, emphysematous cholangitis, cholecystic-enteric fistula),
 MRCP – choledocholithiasis, tumour, stricture
 ERCP – diagnostic & therapeutic – stone removal, stenting, bile sampling

31
  CT (spiral/helical/cholangiogram) – dilated intrahepatic & extrahepatic
ducts, POOR imaging of gallstone, pericholecystic fluid, liver abscess, TRO
tumour, right-sided diverticulitis, pyelonephritis, mesenteric ischaemia,
appendicitis
 Biliary scintigraphy (hepatic 2,6-dimethyliminodiacetic acid [HIDA]) –
functional scan – non-visualization of biliary tree
Mx Supportive  May need ICU admission
 ABC
 Close monitoring of vital signs, watch out for shock
 NBM – bowel rest, prep for cholecystectomy
 IV fluid, correct electrolyte abnormalities
 Analgesia – tramadol, mepiridine
 IV antibiotics – cefuroxime/gentamicin (Gram –ve), metronidazole
(anaerobe)
 Anti-emetic (metochlopromide)/ NG tube for vomiting
Surgical  Urgent ERCP with biliary drainage/percutaneous drainage
 Laparoscopic cholecystectomy after resolution of cholangitis

Pancreatic & Hepatobilliary Tumours

PANCREATIC CARCINOMA
Types of - 90% adenocarcinoma of exocrine ductal cell
pancreatic Ca- 2% exocrine acinar (secretory) cells
- 8% endocrine islet cells – secretes insulin, glucagon, gastrin (remember 90% insulinoma
benign)
Pathology - 80% head, 20% body/tail
- Well-differentiated ductular pattern but highly malignant
- Metastasize early to LN, peritoneum, liver
 Direct  portal vein
 Lymphatics  coeliac axis, porta hepatis, lesser & greater curvatures of stomach,
hilum of spleen
 Blood  liver, lung
- <20% resectable at presentation, poor prognosis
Epidemiology - Mean age – 65
- M=F
- Cigarette smoking, chronic pancreatitis, obesity/T2DM, family Hx
Clinical Common
features - LOW (80%), LOA, dyspepsia
- Abdominal pain (60%) – severe persistent deep gnawing pain, worse at night, sometimes
relieved by sitting forward (locally advanced disease with extrapancretic invasion into
retroperitoneal nerves around coeliac axis)
- Obstructive jaundice (50%) – painless jaundice develops over weeks, pale stool, dark urine
(common bile duct obstruction by head of pancreas Ca  proximal duct dilate  gallbladder
distended  palpable)
“Courvoisier’s Law”: Obstructive jaundice in the presence of palpable GB is not due to stone.
Gall stones cause chronic inflammation  fibrosis or intermittent stone  hypertrophy of GB
wall, preventing its distension. Malignancy  obstruction over short period  non-thickened
wall distends easily
Uncommon
- Ascites

32
 - Abdominal mass
- GOO
- Acute pancreatitis
- DM
- Pancreatic steatorrhoea
- Thrombophlebitis migrans (recurrent superficial venous thromboses)
Ix Blood/ - Urine dipstick – bilirubin
urine - LFT – bilirubin +++, ALP +++, AST +, ALT +
Imaging - US –liver, dilated bile duct, gallstones. Usually can’t see pancreas
- CT scan – tumour extent, liver mets, LN mets, vascular invasion of superior
mesenteric & portal veins, superior mesenteric artery & coeliac axis. High
definition CT – assess mass in detail. Also allows CT-guided biopsy
- EUS-guided needle aspiration cytology (gold standard) – US probe in D2, examine
pancreatic head, vessel, duodenum & ampullary region, assess tumour site, size,
vascular involvement; needle aspiration of lesion via gastric lumen for cytology
- Staging laparoscopy – assess metastasis to liver, nodes, peritoneum
- ERCP – stenting across the obstruction (palliative)
Mx Resectable - Surgical resection - Whipple’s operation (pancretico-duodenectomy)
(15-20%)  1-2% mortality
 15-20% morbidity (pancreatic leaks, delayed gastric emptying, wound
infections)
- Adjuvant chemotherapy – 5-fluorouracil, gemcitabine
Palliation - Good analgesia – includes percutaneous permanent coeliac ganglion blockade
- Biliary stenting – ERCP or percutaneous transhepatic cholangiogram (PTC)
- Surgical (triple) bypass for to relieve obstructive jaundice & duodenal obstruction
 Gastrojejunostomy to bypass duodenal obstruction
 Cholecysto-jejunostomy to bypass obstructed common bile duct
 Jejuno-jenunostomy to divert food away from biliary tract
- Endoscopic stenting/laparoscopic gastroenterostomy for duodenal obstruction

Whipple’s operation

33
OTHER PANCREATIC TUMOURS
Cystic neoplasm of the pancreas - DDx: Serous and mucinous cystadenomas, cystadenocarcinomas
- Incidental finding on CT/US, non-specific abdominal symptoms
- Difficult to differentiate from pancreatic pseudocyst
- Rx: radical resection – all cystic neoplasms have malignant potential
Endocrine tumours Insulinoma - Arise from beta Islet cells of pancreas
of the pancreas - Clinical features – hypoglycaemic attacks
- 90% single, 90% benign & curable by Sx
- Often misdiagnosed as alcoholism, epilepsy, psychiatric disorders
- Rx: enucleation if small, pancreatic resection if large
Glucagonoma - Arise from apha Islet cells of pancreas
- Rare
- Presents as DM & migratory necrolytic erythema
Gastrinoma - Gastrin secreting tumours in pancreatic islets or ectopic cells in
duodenum
- 25% MEN1 – pancreatic islet cell tumour, pituitary adenoma, parathyroid
hyperplasia
- Presents as severe intractable PUD & diarrhoea – Zollinger-Ellison
syndrome
- 60% malignant, grow slowly & mets late
- Rx: excision often curative. Palliative - PPI

TUMOURS OF THE BILIARY SYSTEM

Cholangiocarcinoma - ADC arising from biliary duct epithelium
- Anywhere in the intrahepatic & extrahepatic biliary system but more common near the
confluence of R & L hepatic ducts “Klatskin tumour”
- Intrahepatic cholangiocarcinomas px like HCC but jaundice rare (most biliary sys intact)
- Extrahepatic cholangiocarcinomas usually cause painless obstructive jaundice
- More frequent in PSC
- Dense fibrous stroma, grow along the ducts  smooth elongated stricture
- Ix: ERCP/MRCP/transhepatic cholangiography. Histology – fibrosis
- Slow growing & mets late but LN involvement @ presentation common, extension along
bile ducts & involvement of portal vein & hepatic arterial branches  low operability rate
& lower survival
- Rx: partial hepatectomy with excision of involved biliary tree + ‘en bloc’ portal vein
resection & reconstruction
ADC of ampulla of Vater
- Unusual – polypoid lesion projecting into duodenum, obstruct biliary drainage
- Tumour friable, bleed persistently  FOB positive
- a/w intestinal polyposis
- Dx: ERCP + biopsy
Mx of extrahepatic cholangiocarcinoma & periampullary carcinoma
- Whipple’s pacreatico-duodenectomy
 Distal ½ stomach, entire duodenum, head & body of pancreas, lower end of CBD
removed
 All structures anastomosed to jejunum
Carcinoma of the - Old age
gallbladder - a/w stones – chronic inflammation  carcinogenic
- Early dx – incidental at cholecystectomy, Rx – wide excision of GB + hilar
lymphadenectomy
- Dx often late with jaundice – liver invasion + lymphatic spread – short survival
Primary sclerosing - Rare, autoimmune, a/w longstanding ulcerative colitis (UC)
cholangitis

34
 - Progressive fibrosis & multiple biliary strictures  narrowing of lumen  progressive
obstructive jaundice  secondary cirrhosis
- Ix: ERCP – widespread irregular narrowing of intrahepatic & ectrahepatic bile ducts
- DDx: cholangiocarcinoma
- Mx: endoscopic dilatation of strictures, choleritic drugs to improve bile flow, liver
transplant (1/3 have cholangiocarcinoma in excised liver)

LIVER TUMOURS
Benign Malignant
Liver cyst Secondary metastases
Liver abscess Hepatocellular carcinoma
Haemangiomas Angiosarcoma
Focal nodular hyperplasia (women on OCP,
characteristic central scar, can safely be left.)
Hepatic adenomas (resection recommended since can
lead to HCC)

Liver abscess

 Fever, malaise, upper abdominal pain/tenderness

 Causes
o Amoebiasis (Entamoeba histolytica)
o Hydatid cyst (Echinococcus – dog/sheep)
o Ascending cholangitis
o Appendicular/ diverticular abscess (via portal vein)
o Endocarditis (generalised bacteraemia)
 Rx
o Radiological drainage & long course antimicrobial
o Exception – hydatid cyst – complete surgical excision with antihelminthic cover (mebendazole)
because drainage causes serious risk of peritoneal dissemination & anaphylaxis

Hepatocellular Carcinoma (HCC)/ Hepatoma

Intro - Malignant slow growing tumours that often arise multicentrically & synchronously throughout the
liver
- 6th most common cancer worldwide, very common in Africa & Far East
- 80-90% have pre-existing cirrhosis, 25% >5y cirrhosis develops HCC
- Age: 40-60 in developed countries, 20-40 in developing countries
Aetiology - Chronic hepatitis - Hepatitis C, Hepatitis B
- Alcoholic cirrhosis
- Non-alcoholic fatty liver disease (NAFLD)
- Haemochromatosis
- Aflatoxin from Aspergillus (stored grain & peanuts)
- Parasites – schistosomiasis, echinococcus (tapeworm), clonorchis sinesis (liver fluke)
Clinical - LOA, LOW
features - Abdominal pain, distension
- Stigmata of cirrhosis
- Liver mass
Ix - US
- CT/MRI
- Radiologically guided liver biopsy
Mx - Often widespread by dx

35
 - Small tumours – resection & liver transplant
 <3 tumour
 Each < 3cm
 Single tumour < 5cm
- Palliation
 ‘chemo-embolization’ – local cytotoxic drugs via hepatic intra-arterial cannula
 Radiofrequency ablation
- Early detection – patients with known cirrhosis should be in a 6-monthly US surveillance programme

Secondary Liver Metastases

Intro - Common
Aetiology - Stomach Ca
- Pancreatic Ca
- Colon Ca
- Breast Ca
- Lung Ca
Clinical - Asymptomatic
features - LOA, LOW
- Jaundice at late stage
Mx - Resection generally not beneficial except for colorectal liver mets (10-20% curable)
 Up to 70% liver can be resected due to large reserve capacity & regenerative capability
 Chemotherapy/radiofrequency ablation to downsize tumour pre-op
- Surgically incurable disease
 Chemotherapy to slow growth and reduce pain
 Local cryotherapy
 Radiofrequency ablation
 Laser destruction
 Percutaneous alcohol injection

36
Acute Pancreatitis
Definition 1. Abdominal pain consistent with acute pancreatitis (acute onset of a persistent, severe,
(Atlanta 2012) epigastric pain often radiating to the back)
2. Serum lipase activity (or amylase activity) at least three times greater than the upper
limit of normal
3. Characteristic findings of acute pancreatitis on CECT and less commonly MRI
transabdominal US

1 but serum amylase <3x may be delayed presentation  CECT to diagnose

1 + 2  usually CECT not needed
Types  Interstitial oedematous pancreatitis
- Diffuse enlargement of the pancreas d/t inflammatory oedema
- CECT - relatively homogeneous enhancement, peripancreatic fat usually shows some
inflammatory changes of haziness or mild stranding. May be some peripancreatic fluid
- Clinical symptoms usually resolve within the 1st week
 Necrotising pancreatitis
- 5–10% of patients develop necrosis of the pancreatic parenchyma, the peripancreatic
tissue or both
- The impairment of pancreatic perfusion and signs of peripancreatic necrosis evolve
over several days
- 1st few days - pattern of perfusion of the pancreatic parenchyma may be patchy, with
variable attenuation before the area of impaired enhancement becomes more
demarcated and/or confluent
- After the 1st week - non-enhancing area of pancreatic parenchyma should be
considered to be pancreatic parenchymal necrosis
Clinical Anatomy  12-15cm long, J-shaped, lobulated retroperitoneal organ
 Lies transversely on the posterior abdominal wall behind the stomach across L1-L2
 4 parts – head, neck, body, tail
 2 ducts – pancreatic duct of Wirsung, accessory duct of Santorini
 Relations
- Anterior – stomach (separated by lesser sac), head of pancreas – transverse colon, tail
of pancreas – hilum of spleen
- Posterior – aorta, IVC, SMA, SMV, crura of the diaphragm, coeliac plexus, left kidney
- Hugs the duodenum, opposes IVC, cradles aorta, wraps around superior mesenteric
vessels, hides behind peritoneum of lesser sac, cuddles the left kidney, dallies with the
left renal pedicle, tickles the spleen
 Anomalies – annular pancreas: dorsal & ventral segments surround 2nd part of duodenum

37
Epidemiology  5-80 per 100,000 population worldwide
 2-6% mortality
 15% severe
 F>M but male more likely to have recurrent attacks
 Peak incidence 50-60
Aetiology/ Risk  I – idiopathic
Factors  G – gallstone
 E – ethanol (alcohol)
 T – trauma
 S – steroids
 M – mumps
 A – autoimmune
 S – scorpion/snake
 H – hyperlipidaemia/hypercalcaemia
 E – ERCP

38
  D – drugs (SAND – Steroids & Sulphonamides, Azathioprine & 6-mercaptopurine,
Antibiotics (metronidazole, tetracycline), NSAIDs, Diuretics – frusemide, thiazides,
didanosine)
Obstruction  Gallstones (30-70%)
 Congenital abnormalities – pancreas divisum with accessory duct
obstruction, choledochocoele, duodenal diverticula
 Ampullary/pancreatic tumours
 Abnormally high pressure in sphincter of Oddi
 Ascariasis
Drugs &  Alcohol excess (30-70%)
toxins  Drugs – as above)
 Scorpion venom
 Snake bites
Iatrogenic &  ERCP (2-6%)/endoscopic sphincterotomy
traumatic  CABG
 Blunt trauma
 Repeated marathon running
Metabolic  Hypertriglyceridaemia (>11mmol/L)
 Hypercalcaemia
 Hypothermia
 Pregnancy
Infection  AIDS – secondary infection with CMV etc
 Other: mumps, chickenpox, Cocksackie, Hep ABC
Idiopathic  No identifiable cause (10-12%)
Pathophysiology  Normal function of pancreas
- Exocrine – amylase, trypsin, lipase
- Endocrine – insulin, glucagon
 Diverse factors initiate cellular injury & membrane stability
 Lysosomal and zymogen (pre-enxyme) granule compartments fuse
 Activation of trypsinogen to trypsin
 Intracellular trypsin triggers the entire zymogen activation cascade
 Inflammation causing interstitial oedema
 Most remain mild and self-limiting – minimal peritoneal exudation, no pancreatic changes.
Areas of fat saponification (white patches) on great omentum & mesentery
 Severe
- Calcium sequestration  hypocalcaemia
- Systemic inflammatory response syndrome
- Multi-organ failure: shock, ARDS, renal failure, DIVC
- Acute peri-pancreatic fluid collection
- Infection from Gram –ve bacteria translocated from the bowel (increase mortality)
- Pancreatic abscess formation (better prognosis)
- Pancreatic necrosis with grossly inflamed & semi-digested peritoneal surface,
peritoneal cavity filled with dark, blood-stained inflammatory exudate containing fine
lipid droplets (acute haemorrhagic pancreatitis)
Hx  Abdominal pain
- Epigastric, diffuse
- Dull, boring, steady
- Sudden onset
- Increasing to a plateau
- Radiates to the back
- Relieved by leaning forward
- May lie still if chemical peritonitis
 A, N, V, D

39
PE  General
- Vital signs – fever, tachycardia, hypotension (shock), dyspnoea (diaphragm irritation,
pleural effusion, ARDS)
- Jaundice (periampullary oedema), pallor, diaphoresis, listlessness
- Stigmata of chronic alcohol use – spider naevi, caput medusa
 Abdomen
- Distension
- Cullen sign (periumbilical bluish discolouration)
- Grey-Turner sign (reddish-brown discolouration around the flanks)
- Tenderness
- Guarding/rigidity – peritonitis
- Hepatomegaly
- Murphy sign (gallstone)
- Pulsatile abdominal mass (AAA)
- Diminished/absent bowel sound (ileus)
- Shifting dullness (ascites) /hyperresonance (pneumoperitoneum)
 Lungs
- Left sided
- Basal crepitations
- Atelectasis
- Pleural effusion
 Other (rare)
- Erythematous skin nodules (focal subcutaneous fat necrosis on extensor surfaces)
- Polyarthritis
- Purtscher retinopathy
Complications  Local
- Acute peri-pancreatic fluid collection
- Acute pseudocyst
- Infected pancreatic necrosis (previously known as pancreatic abscess)
 Extraluminal gas in the pancreatic and/or peripancreatic tissues on CECT or
 Percutaneous, image-guided, fine-needle aspiration (FNA) is positive for
bacteria and/or fungi on Gram stain and culture
- Intra-abdominal infection
- Pancreatic necrosis
- Haemorrhage into GIT, retroperitoneal or peritoneal cavity (erosion of large vessels)
- Ileus
- Pleural effusion
 Systemic
- Cardio - Arrhythmias
- Respi - ARDS
- Renal - Renal failure
- Haemato - DIVC
- Metabolic - Hypocalcaemia, hyperglycaemia, hyperlipidaemia
- Neuro - Confusion, irritability, encephalopathy, visual disturbances
- MSK - Subcutaneous fat necrosis, arthralgia
- Vascular – portal vein thrombosis, transverse colon ischaemia (pressure effect,
inflammation, hypotension), pseudoaneurysm e.g. splenic artery
- Internal pancreatic fistula pancreatic ascites, mediastial pseudocyst, enzymatic
mediastinitis, pancreatic pleural effusions
 Late
- DM
- Intestinal malabsorption
DDx  Perforated PUD
 AAA

40
  Ascending cholangitis
 Lower lobe pneumonia
 Inferior MI
Ix Blood  FBC – WCC, HCT (haemoconcentration)
 LFT – AST, ALT (>150 U/L = gallstone pancreatitis), ALP, GGT (alcohol),
bilirubin (jaundice), albumin
 RP – Urea, Cr (dehydration), electrolyte imbalance
 CRP – ≥10mg/dL = severe pancreatitis
 ABG – if tachypnoeic
 Serum amylase > 1000
- Normal – late presentation (short T ½ ) or severe pancreatic damage
- other causes of high amylase: salivary gland inflammation, RF, cirrhosis,
peritonitis, cholecystitis, perforated PUD, strangulated bowel, ruptured
ectopic, salpingitis
 Serum lipase – longer T ½
 Serum calcium – hypoCa (saponification), hyperCa (cause)
 Serum LDH – Ranson criteria
 RPG – hyperglycaemia (insulin from damaged beta cells)
 FPL – hypertriglyceridaemia
 IgG4 – autoimmune
Imaging  Ultrasound hepatobiliary – gallstone
 Plain AXR – ground-glass appearance, absent bowel gas except ‘sentinel
loop’ of dilated adynamic small bowel, radio-opaque gallstone
 CXR – perforation, atelectasis, pleural effusion
 CT (helical/multislice with pancreas protocol)
- Changes take days to appear
- Help in equivocal diagnosis
- Severe pancreatitis – necrosis
 Grade A - Normal pancreas
 Grade B - Focal or diffuse gland enlargement
 Grade C - Intrinsic gland abnormality recognized by haziness on
the scan
 Grade D - Single ill-defined collection or phlegmon
 Grade E - Two or more ill-defined collections or the presence of
gas in or nearby the pancreas
Other  ERCP + sphincterotomy /MRCP
- Gallstone pancreatitis
- TRO other causes after recovery – small pancreatic/periampullary
tumours, pancreatic duct stricture, congenital pancreas divisum, high
pressure sphincter of Oddi

41
Severity

Mx Supportive  NPO2 – risk of ARDS, pleural effusion, hypoxaemia due to pain

 IV fluids (3rd space sequestration), monitor CVP/urine output
 NBM, NG tube, nutritional support (enteral or TPN), begin orally as pain
subsided
 Analgesics – PCM, tramadol, meperidine
 Antibiotics
- Not routine, fever is due to inflammation
- Imipenem if infected pancreatic necrosis
Underlying  Gallstone
cause - Ductal  ERCP within 72 hours
- Laparoscopic cholecystectomy – same admission if possible because
deferring increases chance of another attack
 Alcohol – discourage abuse

42
 Surgical  Surgical debridement (necrosectomy) +/- continuous peritoneal irrigation
 Indications:
- Necrotic pancreas
 Does not opacify on CECT (lost blood supply)
- Infected peri-pancreatic fluid collection
 Gas bubbles in peripancreatic fluid collections
 Confirm by percutaneous aspiration (microscopy, C+S)
Mx of Local  Acute peripancreatic fluid collection
complications - Most resolve spontaneously, CT-guided percutaneous drainage if not
 Pancreatic pseudocyst (1-8%)
- Collection of pancreatic enzymes, inflammatory fluid & necrotic debris
encapsulated within lesser sac, >6/52
- Palpable upper abdominal mass
- CT scan to confirm
- <6cm & asymptomatic – observe for up to 6/12
- >10cm / unresolved – laparoscopic/open marsupialization of the
pseudocyst into posterior wall of stomach
 Pancreatic abscess (1-4%)
- Recurrent high swinging fever
- Necrotic pancreas form a discrete grey mass lying free in pancreatic bed
& bathed in pus
- Sx resection of necrotic tissue & abscess drainage
Prognosis  15% admitted patients have severe disease
 10% initially mild  severe
 10-30% mortality in severe (2-5% mortality in all cases)
 50% die within 1st week from ARDS & pulmonary failure, MODS
 Infective complications of pancreatic necrosis adds to death after 1st week

43
Intestinal Obstruction
Definition  Any condition that interferes with normal propulsion and passage of intestinal contents
Clinical
Anatomy

 Ascending – ileocolic & right colic arteries (SMA)

 Transverse (proximal 2/3) – middle colic artery (SMA)
 Descending – left colic & superior sigmoid arteries (IMA)
 Sigmoid – sigmoidal artery (IMA)
Classification  Mechanical vs. functional
 Partial vs. complete (absolute constipation)
 Simple vs. strangulated (vascular impairment)
 Acute vs. chronic
Aetiology/ Risk Mechanical (Dynamic) Functional (Adynamic)
Factors Physical blockage of intestinal lumen due to Atony of the intestine with loss of normal
extramural, intramural, intraluminal causes. peristalsis, in the absence of any mechanical
Peristalsis is working against the obstruction. cause.

Extramural  Paralytic ileus (post-op most common)

 Adhesions  Mesenteric vascular occlusion
 Congenital bands (rare)  Pseudo-obstruction
 Hernia  Spinal injury
 Volvulus

44
  Intussusception
 Tumours
Intramural
 Congenital atresia
 Stricture – Crohn’s, diverticular disease,
drug-induced (NSAIDs)
 Tumours, lymphomas

Intraluminal
 Stool impaction
 Gallstone
 Foreign body
 Bezoars – phytobezoar (vegetable matter),
tricobezoar (hair)
Symptoms  Abdominal pain – colicky
 Abdominal distension
 Vomiting
- Time of onset – earlier with proximal obstruction
- Nature – bile-stained fluid  upper GI; thick & faeculent  lower GI
 Absolute constipation
- No faeces or flatus passed (complete obstruction)
- Exceptions: Richter’s hernia, gallstone obstruction, mesenteric vascular occlusion,
partial obstruction by faeces/tumour (diarrhoea may occur)
Signs  Dehydration – vomiting, lack of fluid  Dehydration – vomiting, lack of fluid
intake, fluid sequestration in obstructed intake, fluid sequestration in obstructed
bowel bowel
 Surgical scar  Abdominal distension – larger with more
 Abdominal distension – larger with more distal obstruction
distal obstruction  No visible peristalsis
 Visible peristalsis  Central resonance to percussion with flank
 Abdominal tenderness (MUST be dx as dullness – gas-filled bowel loops rise
strangulation or perforation)  Absent bowel sound
 Guarding – perforation with peritonitis
 Abdominal mass
 Central resonance to percussion with flank
dullness – gas-filled bowel loops rise
 Loud, frequent, high-pitch, tinkling bowel
sounds
 Succussion splash (GOO)
 Hernias
DDx  Ascites
 Medications – TCA, narcotics
 Mesenteric ischaemia
 Perforated viscus, peritonitis
Ix Laboratory  FBC – Hb (bleeding tumour), WCC (infection/inflammation), HCT
 RP – Urea, creatinine (dehydration), electrolyte balance
 ABG – acidosis/alkalosis
Imaging  Plain supine AXR – dilated bowels
 Erect CXR – TRO perforation
 Barium studies – small bowel vs colon; partial vs complete; mechanical vs
functional
 CT increasingly used
- Level of obstruction
45
 - Degree of obstruction
- Degree of ischaemia
- Cause of obstruction – volvulus, hernia, luminal & mural causes
- Free fluid & gas – perforation
Mx  Resuscitation
- NBM
- IV fluids (NS or Hartmann’s)
- IV antibiotic prophylaxis
- NG tube & aspiration – controls N & V, remove swallowed air, reduce gaseous
distension, minimise risk of inhalation (induction of anaesthesia)
 Conservative Mx if uncomplicated – spontaneous resolution
- Indications
 Incomplete obstruction
 Previous abdominal surgery
 Advanced malignancy
 Diagnostic doubt – possible ileus
 Faecal impaction  enemas, manual removal of faeces
 Surgery to relieve obstruction
- Indications
 Peritonitis
 Perforation
 Irreducible hernia
 Palpable mass lesion
 Virgin abdomen
 No resolution after 48H conservation Rx
- Steps
 Identify caecum  dilated = large bowel obstruction
 Operative decompression
 Assess viability of intestine, resect gangrenous bowel
 Large bowel obstruction
o Palpate liver for metastases, inspect colon for synchronous tumours
o Right hemicolectomy, extended right hemicolectomy, Hartmann’s,
stoma may be done

46
Small Bowel Obstruction

- Dilated bowel loops located centrally

- Presence of valvulae conniventes – extend across whole width of lumen; step-ladder pattern – regularly
spaced
- Multiple air-fluid levels in erect AXR

Large Bowel Obstruction

- Dilated bowel loops located peripherally

- Presence of haustrations – do not extend across whole width of
lumen, irregularly spaced

47
48
Colorectal Carcinoma
Clinical Blood supply of the colon
Anatomy

 Arterial
- Ascending – ileocolic & right colic arteries (SMA)
- Transverse (proximal 2/3) – middle colic artery (SMA)
- Descending – left colic & superior sigmoid arteries (IMA)
- Sigmoid – sigmoidal artery (IMA)
- Watershed area – terminal branches of SMA & IMA meet – prone to ischaemia
 Venous
- Superior mesenteric vein follows the SMA
- Inferior mesenteric vein drains into splenic vein
- SMV + splenic vein  portal vein
 Lymphatics
- Epiploic (surface of colon), paracolic, mesocolic (around vessels) lymph nodes
- Follow the vessels into superior mesenteric nodes and inferior mesenteric nodes (part
of pre-aortic nodes)  cisterna chyli  thoracic duct

Blood supply of the rectum

49
  Arterial
- 1 superior rectal artery from inferior mesenteric artery
- 2 middle rectal arteries from the internal iliac arteries
- 2 inferior rectal arteries from the internal pudendal artery which is a branch of internal
iliac artery
 Venous
- Follow arteries
 Lymphatics
- Upper inferior mesenteric nodes
- Middle & Lower  internal iliac nodes
 Nerve supply – inferior hypogastric plexuses. Rectum only sensitive to stretch

Blood supply, lymphatics & innervation of the anal region

 Arterial
- Upper ½ - superior rectal artery (IMA)
- Lower ½ - inferior rectal artery (internal pudendal artery)
 Venous
- Upper ½ - superior rectal vein  IMV  portal vein
- Lower ½ - inferior rectal vein  internal pudendal vein  systemic circulation
 Lymphatics
- Upper ½  para-rectal nodes  inferior mesenteric LN
- Lower ½  superficial inguinal LN
 Nerve supply
- Upper ½  visceral motor (sympathetic & parasympathetic) & sensory nerves
- Lower ½  somatic motor & sensory nerves
Epidemiology  2nd most common cancer in women & 3rd most common cancer in men
 Increase with age – rare <50, common >60
 M=F
Aetiology/ Risk  Age >50
Factors  Chinese
 Western low-fibre, high fat diet
 Alcohol
 Smoking
 Obesity
 Family Hx
 Personal Hx of colon, ovarian, uterine cancers
 IBD - Ulcerative colitis, Crohn’s disease
 Inherited conditions
- Familial Adenomatous Polyposis (FAP) – 1% colorectal ca
50
  Autosomal dominant
 APC gene mutation on 5q21 (also occurs in sporadic cases)
 Numerous adenomatous polyps throughout GIT- min 100, can be >2000
 100% develop colon ca by 40
 Variants
o Gardner’s syndrome – multiple adenomas, epidermoid cyst (skin),
fibromatosis (soft-tissue), osteomas (bone), abnormal dentition.
Increased risk of duodenal ca and thyroid ca
o Turcot’s syndrome – colorectal adenomatous polyps & brain tumours
(gliomas)
- Hereditary Non-polyposis Colorectal Cancer (HNPCC) – 6%
 Autosomal dominant
 Mismatch repair gene mutation - hMLH1, hMSH2, hMSH6, hPMS1, hPMS2
 Microsatellite instability
 Lower no of polyps than FAP
 40% lifetime risk of colon ca
 Also at increased risk of urothelial, ovarian & endometrial ca
Pathophysiology  Multi-hit hypothesis (cumulative gene alteration)
- Microsatellite instability (HNPCC)
- Inactivation/mutation of other allele of APC
 Activation of K-ras (12p)
 Loss of DCC gene (18q)
 Loss of p53 (17p)
 Activation of telomerase
- Adenoma-carcinoma sequence

 Tumours in the proximal colon tend to grow as polypoid lesions “cauliflower”, may ulcerate
 occult bleeding  iron deficiency anaemia in an adult (especially a male) = colon cancer
until proven otherwise
 In the distal colon tend to be annular, encirculing lesions “Napkin ring”  constriction with
symptoms and signs of obstruction (rectal bleeding and changing bowel habits)

Malignancies in the GIT

 Adenocarcinoma
- May produce mucin
- Well, moderately or poorly differentiated
- Invades through bowel wall
- Metastasize to LN, liver & lungs
 Carcinoid (neuroendocrine) tumours
- Present throughout GIT
- Commonest: appendix, small bowel, rectum, stomach, colon
- Secretes
 Serotonin  carcinoid syndrome (only in massive liver mets) – skin flushing,
diarrhoea, cramps, bronchospasm, systemic fibrosis, hepatomegaly
 Gastrin  Zollinger-Ellison syndrome  PUD
 ACTH  Cushing’s syndrome
 Insulin  hypoglycaemia
- Low grade malignant tumour
 Gastrointestinal stromal tumours (GISTs)
- Mesenchymal neoplasm of the GIT arising from pacemaker interstitial cell of Cajal
- 2/3 in stomach, ¼ in small intestine, <10% colorectal
- Benign & malignant
- Mutations in c-kit proto-oncogene or PDGFRA  Tyrosine activity
- Tyrosine activity can be blocked by imatinib (Gleevec)

51
  Lymphoma
- Commonest primary extra-nodal location
- Risk factors

 H. pylori infection (B- cell gastric lymphoma= MALTOMA)

 Coeliac disease (T-cell lymphoma - proximal bowel)
 Immunodeficiency ( B-cell lymphoma) – Congenital, HIV, Immunosuppressive
therapy
 Mediterranean lymphoma (B-cell lymphoma)
 Secondaries
- Melanoma
- Ovarian
- Endometrial
- Prostatic
Symptoms Right-sided Left-sided Rectal
 Often asymptomatic until  Obstructive symptoms  PR bleed – end of
advanced (solid faecal matter, defaecation
 Anaemia (chronic low- smaller diameter, annular  Tenesmus
grade bleeding) type tumour) – colicky  Abdominal pain
 Malaena abdominal pain,  Diarrhoea
 Less likely to cause constipation, vomiting  Perforation with pericolic
obstruction (liquid faecal  PR bleeding – melaena/ abscess formation
matter, large diameter, fresh blood (rectosigmoid) – LIF pain,
ulcerative type tumour)  Altered bowel habit – swinging fever
 Can present with palpable diarrhoea & constipation
mass on the right side  Colicky dull aching pain
 Perforation with pericolic
abscess formation
(rectosigmoid) – LIF pain,
swinging fever
 LOA, LOW
 Metastases – jaundice, bone pain, SOB
 Perforation with peritonitis
 Malignant fistula into stomach, bladder (pneumaturia, faecaluria), uterus, vagina (faeculent
vaginal discharge), skin
Signs  Cachexia
 Anaemia
 Palpable mass in the abdomen
 DRE – blood in stool, may feel the mass in rectal ca
 Hepatomegaly, ascites
 Bone tenderness
 Pleural effusion
DDx  Inflammatory bowel disease
 Diverticular disease
Ix Blood  FBC – Hb (anaemia), MCV, MCH, WCC (infection causing diarrhoea)
 RP – Urea (dehydration), Cr, electrolytes (imbalance in intestinal
obstruction)
 LFT – liver mets
 Tumour marker: serum carcinoembryonic antigen (CEA) level – baseline.
After removal CEA should drop within 4 weeks. If not = inadequate
resection/ distant mets

52
 Imaging  Initial – U/S abdomen, plain AXR (dilated bowel in case of obstruction),
CXR
 CT TAP – assess extent of tumour, mets to adjacent structures, liver, lungs
 Pelvic MRI or endorectal U/S – local extent of rectal tumours
 PET-CT – to detect metastatic deposits not seen on other modalities
Other  Colonoscopy + biopsy (gold standard)
Staging T  Tis – carcinoma in situ
 T1 – invades submucosa
 T2 – invades muscularis propria
 T3 – invades through muscularis propria into pericolorectal tissues
 T4a – penetrates surface of visceral peritoneum
 T4b – directly invades/adherent to other organs & structures
N  N0 – no RLN mets
 N1 – mets in 1-3 RLN
 N2 – mets in 4 or more RLN
 M0 – no distant mets
 M1 – distant mets
M1a – confined to 1 organ/site (liver, lung, ovary, non-RLN)
M1b - >1 site or peritoneum
AJCC stage
grouping

Duke’s

Mx of colon ca Principles  MDT – surgeons, oncologist, radiologist, geneticist, palliative care

physicians, colorectal specialist nurses
 Surgical resection is the main treatment
- Curative for localized disease (stage I-III) and limited metastatic
disease in liver/lung (stage IV)
- Palliative resection to relieve obstruction (stenting is another
option)/prevent continuing blood loss

53
 - Neoadjuvant chemotherapy may be given to shrink tumour pre-op
 Adjuvant chemotherapy for stage III to increase chance of cure. Marginal
benefits for stage II
 Chemotherapy as the standard management for metastatic disease
Surgical  Affected segment removed with a margin of 5cm proximally & distally
 Lines of resection determined by distribution of mesenteric BV
- Ascending colon – right hemicolectomy
 Ileocolic, right colic, and right branch of the middle colic
vessels are divided and removed
 Care must be taken to identify the right ureter, the ovarian or
testicular vessels, and the duodenum
 If omentum is attached to the tumour, remove en bloc
- Hepatic flexure/ proximal/ middle transverse colon – extended right
hemicolectomy
 Ileocolic, right colic, and middle colic vessels are divided and
the specimen is removed with its mesentery
- Splenic flexure/descending colon – left hemicolectomy
 left branch of the middle colic vessels, the inferior mesenteric
vein, and the left colic vessels along with their mesenteries
are included with the specimen
- Sigmoid colon – sigmoid colectomy
 Inferior mesenteric artery is divided at its origin, and
dissection proceeds toward the pelvis until adequate margins
are obtained
 Care must be taken during dissection to identify the left ureter
and the left ovarian or testicular vessels
- Total abdominal colectomy with ileorectal anastomosis for FAP,
HNPCC, metachronous cancers in separate segments
Adjuvant  Chemotherapy
therapy - 5-FU is the main agent, given together with folinic acid (biomodulator)
- Combinations: 5-FU + oxaliplatin, 5-FU + leucovorin and oxaliplatin
 Biologic agents – monoclonal antibodies against VEGF &EGFR, tyrosine
kinase inhibitor & decoy receptor for VEGF
- Bevacizumab, cetuximab, panitumumab, regorafenib, ziv-aflibercept
Surveillance  85% recurrence occur within 3 years of resection, 95% within 5 years
 Follow up for 5 years with regular review of Hx, PE, CEA every 3-6 months
 Surveillance colonoscopy 1 year after resection
 Annual CT abdomen chest for 3 years
 Maintain healthy body weight, be physically active, healthy diet
Mx of rectal ca Principles  Sphincter-saving procedures for rectal cancer are now considered the
standard of care provided the lower edge of tumour is 1-2cm above the
anal sphincter
 Rectal ADC are radiosensitive – may be delivered pre-op, intra-op or post-
op +/- chemotherapy
 5-FU based chemotherapy for stage II & III
Radical  Anterior resection/low anterior resection
surgery - Sphincter saving
- Excise the tumour with appropriate length of bowel + an intact
envelope of fat around it (mesorectum containing local LN)
- Proximal bowel anastomosed to distal stump/ create pelvic reservoir
using a J-pouch technique – reduce frequency & urgency of
defaecation
- A temporary defunctioning ileostomy/colostomy is sometimes used to
aid healing of a low anastomosis
54
  Abdomino-perineal resection of rectum
- Sphincter involved
- Entire rectum & anus removed
- Proximal end of bowel brought out as end colostomy
 Hartmann’s operation
- Unable to perform the definitive Sx at the point of time or for frail &
debilitated patient
- Lesion resected, proximal end of bowel made into end colostomy, cut
end of distal remnant closed with sutures/staples
- Several months later decision to reconnect the bowel made
depending on fitness & preference of the patient
Local surgery/  Transanal excision – early stage small tumours (<3cm) with no nodal
radiotherapy involvement. A/w higher rate of recurrence.
for early stage  Endocavitary radiotherapy – similar selection criteria to transanal excision,
delivered via a special proctoscope and is performed in an operating room
with sedation. 6x over 6 weeks.
 Transanal endoscopic microsurgery (TEM) - local excision that uses a
special operating proctoscope that distends the rectum with insufflated
carbon dioxide and allows the passage of dissecting instruments. Can be
used on lesions located higher in the rectum and even in the distal sigmoid
colon
Radiotherapy  Neoadjuvant
- Advantages:
 Down-staging to increase in resectability, possibly permitting
the use of a sphincter-sparing procedure
 Decrease in tumour viability to decrease the risk of local
recurrence
- Disadvantages:
 Delay in definitive resection
 Possible loss of accurate pathologic staging
 Possible over-treatment of early-stage (I and II) rectal cancer
 Increased postoperative complications and morbidity and
mortality rates secondary to radiation injury
 Intra-op
- Advantage: improve local disease control for large, bulky, fixed,
unresectable cancers
 Post-op
- Advantages:
 Immediate definitive resection
 Accurate pathologic staging information before ionizing
radiation
- Disadvantages:
 Possible delay in adjuvant radiation therapy if postoperative
complications ensue
 No effect on tumor cell spread at the time of surgery
 Decreased effect of radiation in tissues with surgically-induced
hypoxia
Chemotherapy  Stage II and above
 +/- radiotherapy
 Regimens
- Infusional fluorouracil, folinic acid, and oxaliplatin (FOLFOX)
- Capecitabine and oxaliplatin (CapeOx)
Surveillance  As colon cancer above

55
  Pelvic CT scanning should be performed in patients with rectal cancer
annually for 3-5 years
 In patients who have not received pelvic radiation, a rectosigmoidoscopy
should be performed every 6 months for 2-5 years
Pre-op  Low-residue diet & enemas. Oral purgatives no longer given – dehydration
preparations  Prophylactic antibiotics – cefuroxime 750mg (ciprofloxacin 200mg if penicillin allergy) +
metronidazole 500mg
Complications  Early
of surgery - Local
 Inadvertent damage to other organs – ureter, bladder, duodenum, spleen
 Haemorrhage – slipped ligature
 Wound infection – cellulitis, abscess, wound-edge necrosis
 Intra-abdominal abscess – site of Sx, pelvic, subphrenic

- Regional
 Anastomotic leak – local/general peritonitis
 Stoma problems – retraction etc
 Compartment syndrome in legs (prolonged elevation during perineal Sx) – rare
- Systemic
 A fib, A flutter – anastomotic breakdown
 Systemic sepsis  MODS
 Late
- Diarrhoea – short bowel
- Sexual/bladder dysfunction – division of pelvic parasympathetic nerves
- Small bowel obstruction – adhesions, tangling of small bowel with
colostomy/ileostomy, complication of radiotherapy
Screening  Faecal occult blood & colonoscopy
- Asymptomatic: FOB from 50 years old, colonoscopy if FOB+
- High risk (FH of FAP/HNPCC/strong FH of colorectal ca): start 8-10 years before the
youngest age of diagnosis – FOB yearly, colonoscopy 5 yearly

56
57
Inguinal Hernia
Definition  Hernia = condition in which the content of a cavity protrudes through the wall of the cavity
containing it
Clinical Inguinal canal
Anatomy

 4cm
 Content – ilioinguinal nerve, spermatic cord in male, round ligament in female
 Anterior wall – external oblique aponeurosis, internal oblique lateral 1/3
 Posterior wall – conjoint tendon of internal oblique and transverse abdominis medially,
transversalis fascia laterally
 Roof – fibres of internal oblique and transversus abdominis
 Floor – inguinal ligament

 Deep ring (origin of indirect inguinal hernia) – opens at transversalis fascia 2.5cm above
midpoint between ASIS and pubic tubercle. Bounded by inferior epigastric artery medially,
inguinal ligament below and conjoint muscle above and laterally
 Superficial ring – opens at external oblique aponeurosis above and medial to the pubic
tubercle
 Hesselbach’s triangle (origin of direct inguinal hernia) – rectus abdominis medially, inferior
epigastric artery laterally, inguinal ligament below
Spermatic cord
 3 layers – external spermatic fascia, cremasteric fascia, internal cremasteric fascia
 3 arteries – testicular artery, cremasteric artery, artery to vas deferens
 3 nerves – cremasteric nerve, sympathetic nerve, genital branch of the genito-femoral
nerve, ilioinguinal nerve (not in cord)
 3 others – vas deferens, pampiniform plexus, lymphatics

58
Types Indirect Direct
 Passage of abdominal content, leaving  Abdominal content leaves the abdomen
deep inguinal ring, through inguinal canal, through a weakness/split in the
exiting through superficial ring towards transversalis fascia (Hesselbach’s triangle),
scrotum/labium does not enter scrotum
 Aetiology: patent processus vaginalis  Aetiology: weakness in abdominal wall
 Origin: lateral to inferior epigastric artery  Origin: medial to inferior epigastric artery
 Neck of sac narrow (limited by borders of  Neck of sac broad - risk of incarceration of
deep ring) - potential for incarceration & large but low risk of strangulation
strangulation
Hx Hx
 Younger <50  Older >50
PE PE
 After reduction, can be prevented from  Cannot be controlled by digital pressure
reappearing during cough by digital over the deep ring
pressure over the deep ring
Epidemiology  Commonest hernia in males and females
 Male>female due to abdominal wall deficiency secondary to testicular descent
 Any age but most common <5 or after middle age
Pathophysiology  Raised intra-abdominal pressure
- Obesity
- Constipation
- Straining at micturition
- Chronic coughing
- Continued heavy lifting
- Repeated pregnancy
- Infant: a period of severe crying/coughing  acute indirect hernia
 Previous surgery esp. appendicectomy – division of ilioinguinal/subcostal nerve causing
weakness of abdominal wall muscles
 Indirect & direct as above
 Reducible  irreducible (adhesion)  incarcerated (not reducible but not strangulated) 
strangulated (impaired blood supply)
 Strangulation – hernia content becomes constricted by the neck of sac or twisting 
- Obstruction of venous return  swelling  arterial obstruction  infarction
- Intestinal obstruction
 bowel perforation  peritonitis

Other types
 Pantaloon hernia = direct & indirect occurring on the same side
 May consist of merely peritoneum & extraperitoneal fat but if large, usually contain
omentum or small bowel, less commonly large bowel or appendix
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  Sliding hernia = retroperitoneal viscus ‘slides’ down the posterior abdominal wall &
herniates directly/indirectly into the inguinal canal, dragging overlying peritoneum with it –
hence visceral content lie behind & outside the peritoneal sac. E.g. descending colon,
sigmoid colon, bladder
 Spigelian hernia = herniation through a fascial defect in linea semilunaris at the lateral
border of rectus abdominis. Hernia sac lies btwn layers of int & ext oblique or transverse
abdominis. Lies higher than inguinal hernia & difficult to palpate
Symptoms  Mass in the groin – disappears on lying, reappears on standing, coughing, straining
 Pain – dragging sensation/aching. Groin/testicular pain during work/exercise in indirect.
Very painful & tender: strangulated
 Intestinal obstruction – nausea, vomiting, colicky abdominal pain, abdominal distension,
absolute constipation, no flatus
Signs  Above and medial to the pubic tubercle (femoral hernia is below and lateral)
 Positive cough impulse
 Skin red and tender if strangulated
 Elastic/doughy/granular if non-strangulated, tense, hot and tender if strangulated
 Visible peristalsis, resonant percussion, bowel sound if contains bowel
Diagnosis  Side, type, complication, content
Ix Blood  Pre-op assessment: FBC, RP, LFT
Imaging  Plain AXR – intestinal obstruction
 Erect CXR – bowel perforation
 U/S – TRO scrotal masses & other masses below inguinal ligament
 CT abdomen pelvis – difficult cases – spigelian or obturator hernia
Mx Conservative  Small reducible direct hernias in older men can safely be left
 Truss to keep hernia reduced at the deep ring – when surgery inappropriate
or unacceptable to patient
Surgical  Timing
- Asymptomatic – elective
- Intermittently irreducible, pain, tenderness, intermittent intestinal
obstruction symptoms – early operation
- Strangulated – emergency (within 4H to save ischaemic bowel)
 Hernioplasty
- LA/GA
- Open or laparoscopic herniotomy + repair of posterior wall by filling the
gap btwn conjoined muscle & inguinal ligament
- Lichtenstein ‘tension-free mesh repair’ technique is the current
standard
 Using a patch of non-absorbable open-weave mesh
(polyprophylene) to repair and reinforce defect rather than
pulling muscle & fascia layers together under tension
 Advantages:
 Easily learned, trainee surgeons can produce reliable
good results
 Less post-op pain, increased mobility & earlier return to
normal activity
 Low recurrence rate
- Laparoscopic
 Transperitoneal/retroperitoneal route
 Less post-op pain, faster return to normal activity
 Slightly higher risk of major complications
 Recommended for recurrent hernia & bilateral repair
- Post-op
 Keep the area clean & wash carefully especially after
clips/suture removed
60
  Able to bathe immediately
 Early mobilization is important but
 1st week – avoid activities likely to strain the repair – heavy
lifting, driving
 Next 2-3 weeks – gradually return to normal inc sexual activity
 Modification of posture – squat and lift rather than bending, use
trolleys to move heavy objects
 Management of COPD to reduce coughing
 Take laxative if constipated post-op
 Herniorraphy (Bassini & Shouldice)
- Largely replaced by Lichtenstein mesh repair
- Bassini repair - apposition of the transversus abdominis, transversalis
fascia, and lateral rectus sheath to the inguinal ligament under tension
- Shouldice technique - uses two layers of continuous suture in a similar
fashion
 Herniotomy
- Children & young adults with good musculature
- Separate sac from cord structures
- Reduce sac content
- Ligation of sac
- Excise redundant sac
Consent  Surgery offered
 Indication/benefits – prevent/treat strangulation & intestinal obstruction
 Procedure
- GA/LA, usually as day case
- Laparoscopic/open
- Mesh implant to prevent protrusion of abdominal content
 Complications
- Intra-op
 Bleeding – injury to femoral & inferior epigastric vessels
 Injury to adjacent structure – bladder, bowel, nerves (ilioinguinal,
iliohypogastric), spermatic cord
- Early
 Urinary retention (specific)
 Scrotal haematoma/bruising – 30%
 Seroma
 Wound infection – 1%
 Pain – discharge with analgesics, 5% persists as chronic groin pain
 Ischaemic orchitis – 0.5% (thrombosis of the pampiniform plexus due to
dissection more medial than pubic tubercle/ previous Hx of vasectomy)
- Late
 Chronic groin pain – inadvertent trapping of ilioinguinal/another nerve in repair
 Testicular atrophy – inadvertent damage to testicular artery
 Recurrent hernia
o Inappropriate technique (Bassini)
o Operator inexperience (Shouldice & laparoscopy have long learning
curve)
o Technical failure – to recognize & remove indirect sac, insufficient
coverage of defect, suture/mesh failure
o Missed dx of concomitant femoral hernia
o Inherently poor musculature, chronic cough, urinary obstruction,
constipation, resumption of heavy work too soon after repair
o Impaired healing d/t DM, smoking
 Mesh infection, migration, erosion

61
Femoral Hernia & DDx
FEMORAL HERNIA

Definition  Protrusion of peritoneum into the potential space of the femoral canal
Clinical
Anatomy

Femoral Canal
 Medial compartment of femoral sheath
 Its upper opening into abdominal cavity is the femoral ring
 Conical shape, apex directed downwards
 Relations
- Anterior – inguinal ligament
- Posterior – pectineal line & ligmanet
- Medial – Gibernat’s/lacunar ligament
- Lateral – femoral vein
 Contents
- Fat
- Lymph node of cloquet
Aetiology/ Risk  Female
Factors  Increased intra-abdominal pressure
 Pregnancy
Pathophysiology  Course – femoral ring  femoral canal  sephaneous opening (4cm below & lateral to
pubic tubercle)  travel upwards in subcutaneous tissue  may reach inguinal ligament
 Covering – skin, superficial fascia, cribiform fascia, anterior layer of femoral sheath, fatty
content of femoral canal, femoral septum, peritoneum
 Sac may contain abdominal viscera e.g. small bowel or omentum
 40% present with strangulation (narrow opening)
Symptoms  Swelling at the inguinal region – R>L
- Appears on standing & straining
- Disappears on lying down
 Pain – if adhered to greater omentum
 Strangulation
- No obvious localizing sign
- Distal small bowel obstruction – abdominal pain, vomiting, absolute constipation

62
 - Ritcher’s hernia (30%) – only a portion of bowel circumference trapped. Lumen remains
patent – continues to pass flatus but obstruction sufficient to cause vomiting
Signs  Femoral hernia: BELOW & LATERAL to pubic tubercle; Inguinal hernia: ABOVE & MEDIAL to
pubic tubercle
 Globular (small) or retort (large) shape
 Cough impulse rarely detected d/t narrow femoral canal
 Usually irreducible
 Firm & doughy consistency (omentum/fat)
DDx  Inguinal hernia
 Lipoma
 Enlarged inguinal lymph node
 Saphena varix
 Femoral artery aneurysm
Mx  Surgical repair for all femoral hernia (even if asymptomatic) without delay – prone to
strangulation
- Isolate, empty & excise peritoneal sac
- Close femoral canal with non-absorbable sutures/plug placed btwn pectuneus fascia &
inguinal ligament
- Approach
 Femoral/low approach
 Lotheissen/high approach – via post wall of inguinal canal
 McEvedy/pararectus extraperitoneal approach (laparotomy) – rarely
- Indications of laparotomy
 Hernia containing small bowel cannot be safely reduced via low approach
 Bowel of doubtful viability escapes back into peritoneal cavity

DDx of Femoral Hernia

Enlarged  Multiple small firm shotty nodes, normal if <1cm

inguinal LN  3 groups which drain the lower abdominal wall, lower back, perineum, anal canal, penis,
scrotal skin, LL
 Causes of enlargement – infection, lymphoma, metastases
- Foot infection
- Skin diseases
- STI
- Tumours – malignant melanoma, anal ca, penile ca
- Lymphoma
- AIDS
- Glandular fever
- TB
Saphena varix  Dilatation of the long saphenous vein in the groin just proximal to its junction with the
femoral vein
 Soft & diffuse swelling
 Blue tinge
 Disappears on lying down
 Empties with minimal pressure, refills on release
 Cough impulse present
 Fluid thrill present on tapping varicose vein distally
Femoral artery  Dilatation of common femoral artery just below inguinal ligament
aneurysm  Aneurysm elsewhere (aorta, iliac, popliteal) or isolated
 Lump lies just below midpoint of inguinal ligament
 Expansile pulsation

63
Psoas abscess  Tuberculous abscess of lumbar vertebra tracking down inside sheath of psoas muscle/
pyogenic abscess originating in the abdomen/abscess from renal stone (rare)
 TB - Swelling/ ‘cold abscess’ below inguinal ligament
 Pyogenic abscess – ‘hot’
Lipoma

64
Varicose Veins
Definition  Dilated, tortuous, elongated and prominent superficial veins in the lower limb
Clinical  Superficial (to the deep fascia) veins of the LL:
Anatomy - Long/great saphenous vein – arise from medial
side of the dorsal venous arch  in front of
medial malleolus  up medial side of the
lower limb  penetrates deep cribiform fascia
4cm below & lateral to pubic tubercle  enter
the femoral vein at the saphenofemoral
junction (SFJ)
- Short/small saphenous vein – arise from lateral
side of the dorsal venous arch  up lateral
side of the leg  goes medially to join the
popliteal vein at the spahenopopliteal junction
7.5cm above popliteal fossa. Relation: Sural
nerve

 Deep veins:
- Femoral veins
- Popliteal veins
- Anterior & posterior tibial veins
- Medial & lateral plantar veins
- Plantar venous arch
- Metatarsal veins
- Digital veins

 Perforator veins – connect superficial & deep

- SFJ
- SPJ
- Mid-thigh - Mid Hunterian perforator/Dodd’s
(GSV & femoral vein)
- Below knee perforator/Boyd (GSV & PTV)
- 1 lateral ankle perforator (SSV & peroneal vein)
- 3 medial ankle perforators (GSV & PTV 5, 10,
15 cm above medial malleolus)
Return of the venous blood to the heart aided by:
- Negative pressure in thorax during inspiration
- Soleal muscle pump on walking
- Competent valves
- Vis-a-tergo – pressure from arterial tree to venous system
- Venae comitantes – pulsation of nearby accompanying artery

Tributaries at the SFJ

- Superficial external pudendal vein
- Superficial epigastric veins
- Superficial circumflex iliac veins
- Deep external pudendal vein
Epidemiology  20% at 20, 80% at 60
 Female > male
 90% GSV, 25% SSV

65
Aetiology/ risk  Valve incompetence (SFJ, SPJ, perforators)  uninterrupted column of blood from the
factors heart  progressive dilation of superficial veins down the limb

 Hereditary
- Family Hx
- Congenital absence of valve in iliac veins
- Abnormal vein wall elasticity (Marfan’s)
- Multiple congenital AVM (Klippel-Trenaunay syndrome)
 Pregnancy
- Progesterone causes changes in collagen structure & smooth muscle relaxation
- Pressure of gravid uterus on pelvic veins restricting venous return
 Pelvic mass, retroperitoneal LN, fibrosis
 Iliac vein thrombosis, DVT
 Increasing age - elastic lamina of the vein becomes atrophic and smooth muscle layer
begins to degenerate
 Lifestyle: obesity, sedentary, OCP
 Occupation: surgeons, lecturer
Hx  Dilated tortuous vein on the leg
 Dull aching improved by ambulation & elevation
 Bursting (venous claudication) pain
 Pruritus
 Bleeding of varicose veins when traumatized
 Ankle swelling
 Ulcer
 Venous eczema
 Recurrent superficial thrombophlebitis
PE  See OSCE
DDx  Cellulitis
 PAD
 Lymphoedema
Diagnosis  Aetiological - Primary vs secondary (post-thrombotic)
 GSV or SSV or both
 +/- SFJ or SPJ or perforator incompetence
 +/- complications
 Deep vein patency
CEAP  C0 - No visible or palpable signs of venous disease
Classification  C1 - Telangiectasias, reticular veins, malleolar flares
 C2 - Varicose veins
 C3 - Edema without skin changes
 C4 - Skin changes ascribed to venous disease (eg, pigmentation, venous eczema,
lipodermatosclerosis)
 C5 - Skin changes as defined above with healed ulceration
 C6 - Skin changes as defined above with active ulceration
Ix  Hand-held ultrasound Doppler
- Assess reflex at SFJ, SPJ, within LSV, SSV
- Probe placed over junction, calf pressed, listen for significant reflex on release
 Colour-flow Doppler ultrasonography
- Gold-standard
- Identify & quantify points of reflux within the superficial venous system
- Patient in upright position
- Assess the deep vein – DVT, deep system insufficiency
 MRV – more sensitive
 Other specialised tests – venous refilling time, MVO, MPEF
66
Mx Conservative  Maintain proper weight
 Leg elevation above the heart level several times a day
 Foot & ankle exercises – move blood back to the heart
 Compression/elastic stocking/compression bandage - minimise venous
distension
 Clean ulcer with NS, povidone iodine & hydrogen
 Proper debridement (slough)
Medical  Aspirin – speed ulcer healing
 Antibiotics when there is infection
 Stasis dermatitis – moisturizers, steroid cream/ointment
Surgical  Endovenous ablation – LA
1. Foam Sclerotherapy
- Sclerosing substance (sodium tetradecylsulfate, polidocanol,
hypertonic saline) is injected into the abnormal vessels to produce
endothelial destruction that is followed by formation of a fibrotic
cord and eventually by reabsorption of all vascular tissue layers
- Detergent sclerosing agent is first mixed with air or CO2 to create a
foam prior to injection
- Indications: (1) small-medium sized varicose in the absence of reflux
in saphenous trunks (2) recurrent varicosities after operation (3)
below knee varicosities due to incompetent perforators
- CI: (1) DVT (2) SF incompetence
2. Laser ablation
- Perform preprocedural DUS for mapping of the venous segments to
be treated
- Mark the course of the vein(s) to be treated and important
anatomical landmarks associated with the ablation on the skin,
including the proposed venous access site(s) and deep vein
junctions
- Placing the patient in a reverse Trendelenburg or partly sitting
position prior to the venous puncture keeps the vein more
distended and may facilitate venous access
- Anesthetize the access site. Nick the skin just large enough to
facilitate entry of the sheath through the skin
- Insert the access needle into the great saphenous vein (GSV) under
sonographic guidance, place the guidewire, place the introducer
sheath over the guidewire, position the sheath and remove the
guidewire, introduce the laser fiber into the sheath
- Activate the laser and withdraw the fiber and sheath at the speed
that is dependent on the amount of energy
3. Radiofrequency ablation
-
 Surgery

67
Complications  Thrombophlebitis
 Haemorrhage (ruptured varicose vein)
 Vein calcification
 Brown/black skin pigmentation (RBC breakdown)
 Venous eczema (RBC breakdown)
 Venous ulcer
 Periostitis (venous ulcer over tibia)
 Equinus deformity (patient walking on toe to reduce pain caused by shortening on tendon
Achilles)

Abdominal Aortic Aneurysm (AAA)

Definition  Aneurysm = localised area of pathologically excessive dilatation
 Abdominal aorta – AP diameter ≥3 = aneurysm
Clinical
Anatomy

Epidemiology  85% mortality after rupture (shock, post-op MI, post-op RF), 5% mortality if elective surgery
Aetiology/ Risk  Male
Factors  Age >65
 Hypertension
 Smoking
 Marfan’s syndrome, Ehler-Danlos syndrome
 Mycotic aneurysm
 Uncommon: cystic medial necrosis, arteritis, trauma
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Pathophysiology  Degeneration of the elastin & collagen of the arterial wall  fusiform, slowly expanding 
thinning of vessel wall  expansion accelerates  risk of rupture
 Patterns:
- Abdominal aorta only
- Abdominal aorta & common iliacs
- Abdominal aorta & internal iliacs
(External iliacs are never aneurysmal)
Symptoms  Asymptomatic
 Incidental finding on plain AXR (calcification), CT, U/S
 Pressure symptoms caused by aneurysm
- Vein – LL oedema, DVT, embolism (livedo reticularis/blue toe syndrome)
- Bone – vertebrae erosion  back pain
- Adjacent organs – stomach pushed anteriorly  early satiety, nausea, vomiting
 Symptoms of leaking/dissection/rupture
- Tearing abdominal pain radiating to the back
- May have flank, back, groin pain
- Fainting/syncope (cardiovascular collapse)
- Aorto-venous (vena-cava) fistula - tachycardia, congestive heart failure (CHF), leg
swelling, abdominal thrill, machinery-type abdominal bruit, renal failure, and peripheral
ischemia
- Aorto-duodenal fistula – massive haematemesis
 Sudden death (fatal cardiovascular collapse, often misdx as MI)
Signs  Signs of shock – cyanosis, mottling, altered mental status, tachycardia, hypotension
 Pulsatile & expansile abdominal mass
 Thrill & bruits
 Grey-turner sign – flank ecchymosis
 Weak distal pulses
Complications  Death
 Ischaemia
- Colon ischaemia (mesenteric artery)
- Renal failure (renal artery)
 Embolism
- Acute limb ischemia
- Blue toe syndrome
 Fistula
- Aorto-venous
- Aorto-duodenal/aorto-enteric
 Inflammation/infection of the aneurysm
DDx  Other causes of acute abdomen
 Renal colic
 Lumbar spine disease
Ix Blood  FBC – Hb, WCC
 RP, LFT – pre-op assessment
 Blood GXM including clotting factors & platelets
Imaging Non-ruptured AAA
 U/S Abdomen
- Assess size
- Periodic monitoring

69
  CT abdomen
- Define aortic size
- Rostral-caudal extent
- Involvement of visceral arteries e.g. renal arteries
- Extension into the suprarenal aorta (5% extend above requiring thoraco-
abdominal approach)
- Detect aneurysms in iliac arteries
- Detect inflammatory aneurysm (thickened anterior surface may make Sx
difficult)
- Chest CT TRO thoracic aneurysm
 Angiogram
- If evidence of LL ischemia
Leaking/Ruptured AAA
 If haemodynamically stable, CT Abdomen
- Plan Rx, whether EVAR is practicable
- Relationship to renal arteries and visceral arteries
- Secondary iliac aneurysms
- Other abdominal pathology e.g. liver mets (influences decision to
operate)
Pre-op  Cardiac status – ECG, ECHO
 Pulmonary function
Mx Conservative  Diet control – reduce salt, fat intake
 Smoking cessation
Medical  Antihypertensives
 Statins
 Treat syphilis if present
Surgical  Indications
- Leaking/rupturing aneurysms (Emergency – 50% reach hospital alive &
50% survive after Sx)
- Symptomatic aneurysm - pain, ureteric obstruction, embolism
- Expanding aneurysm - >0.5cm per year
- Size >5.5cm or saccular aneurysm
 Open AAA Surgery
- Advantages:
 Less expensive
 Distance between normal aorta & renal arteries can be <15mm
 Discharge at 3 months, rescan after 5-7 years
 Reintervention unlikely
- Disadvantages
 Invasive
 Higher mortality (5%)
 Longer hospital stay
 More likely needing ICU/HDU care
 More difficult with previous abdominal Sx/peritonitis

- Pre-op anticoagulation with IV heparin to prevent distal thrombosis

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 - Long midline/transverse abdominal incision
- Aorta reached via peritoneal cavity/extraperitoneal approach
- Clamps applied to iliac arteries, then to aorta and inferior mesenteric
artery
- Aneurysm opened & thrombus removed
- Bleeding lumbar arteries opening into the posterior aortic wall underrun
with sutures
- IMA retained for re-implanation later if necessary
- Dacron prosthetic graft sutured inside aorta to healthy tissue, proximal
anastomosis 1st
- Test by clamping the graft & releasing aortic clamp
- Distal anastomosis performed ensuring there are no proximal/distal
clots before final closure
- If iliacs are aneurysmal (aorto-iliac aneurysm) , bifurcation (‘trouser’)
graft used with distal graft ends sutured to an area of normal iliac artery
- The aneurysm sac is left in-situ and later closed around the graft (inlay
grafting – seperates graft from intestine, reduce risk of aorto-intestinal
fistula arising from anastomoses)

 Endovascular Aneurysm Repair (EVAR)

- Advantages:
 Minimally invasive
 Lower mortality (1.7%)
 Shorter hospital stay
 Less need for ICU/HDU care
 Unaffected by previous abdominal Sx
- Disadvantages
 More expensive
 Needs 15mm of normal aorta below renal arteries
 Potential endovascular leaks
 High reintervention rates
 Need lifelong follow up
- GA/LA
- Performed using mobile X-ray image intensifier
- Stent graft consists of self-expanding metal framework with non-porous
cloth covering
- Short transverse incisions to assess femoral arteries in the groin
- Main device passed into 1 femoral artery & guided proximally using
radiological guidance to its position below renal arteries
- Check with angiogram
- Remove constraining mechanism – stent opens & expands against
vessel wall
- Contralateral femoral artery exposed & guide-wire passed proximally to
enter main graft body through the short leg
- The second limb of the stent-graft is completed by passing another
covered stent over guide-wire, secure to main graft body & iliac artery
- Completed device looks like a pair of trousers & extends from iliac
arteries to common iliacs
Complications  General
of surgery - CVS – MI, HF, arrhythmas, stroke, renal failure, intestinal ischemia (pre-existing risk
factors, prolonged anaesthesia, aortic clamping, heavy blood loss)

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 Local
- Haemorrhage
 Intra-op
o Venous tears more difficult to repair, inaccessible, difficult to identify &
control
o Massive blood loss can result in consumption coagulopathy – give plt,
cryoprecipitate, FFP
o Organic-based glue to seal bleeding areas, protamine to reverse
heparin effect if necessary
o Cell-saving devices – collect patient’s spilled blood, wash, concentrate
and reinfuse
 Post-op – anastomotic leak (usually pinhole)
o Further operation if does not stop spontaneously with blood and
clotting factor transfusions
- Embolism
 Dislodged thrombus from within the aneurysmal sac
 Preventable by clamping outflow vessels before manipulation of aneurysm
 Can cause infarction of digits/whole foot (trash foot) – needs amputation
- Thrombosis
 Sluggish blood flow due to faulty anastomotic technique (luminal obstruction),
dissection of distal vessel wall creating ‘flap valve’, twisting/kinking of graft, in-
situ thrombosis during clamping
 Prevention – pre-op anticoagulation, ensure satisfactory flow in the
reconstruction & good peripheral perfusion at the end of Sx, secure
haemostasis
 Rx: re-operation
- Graft infection
 Uncommon but devastating
 Patient’s skin/intestinal flora
 Prevention: avoid opening the bowel, meticulous asepsis & haemostasis,
perioperative antibiotics (gentamicin + flucoxacillin), soak protein-coated
Dacron grafts in anti-staph (rifampicin) before use, antibacterial silver
impregnated graft
 Death from sepsis or anastomotic breakdown with massive bleeding
 Rx: extra-anatomic (axillo-femoral) graft & remove infected graft
- False aneurysm formation
 Slow anastomotic leak  slowly expanding blood-filled cavity 
rupture/thrombosis
 Low grade infection
 May leak into duodenum producing aorto-duodenal fistula  major
haematemesis

72
Breast Carcinoma
Clinical  15-20 lobes consisting of lobules which are made up of acini
Anatomy  Supported by Astley Cooper’s ligament
 Lies over pectoralis major and minor
 Axillary tail of Spence

Epidemiology  1 in 10 women develop breast ca

 1 in 18 die from it
 Mortality fallen due to earlier diagnosis and improved treatment
 Most common cancer in Malaysia (30%)
 Peak age 50-59 in Malaysia
 Chinese>Indian>Malay

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Aetiology/ Risk High risk:
Factors  Personal history of invasive breast ca
 LCIS and DCIS
 Benign breast disease with atypical hyperplasia
 First degree family members with breast ca
 BRCA1 (Chr 17) and BRCA2 (Chr 13) mutation
 Ionizing radiation
Moderate risk:
 Age
 Early menarche <12
 Late menopause >55
 Nulliparity
 Benign breast disease without atypia
 Dense breast
Low risk
 1st full term pregnancy >30
 OCP
 HRT
 Alcohol
 Obesity
Pathophysiology

Symptoms  Breast lump

 Change in breast size/shape
 Nipple retraction
 Nipple discharge (esp bloody)
 Skin dimpling
 Skin ulceration
 Arm swelling
 SOB
 Jaundice, abdominal distension
 Bone pain/#
 Localizing neurological signs, altered cognitive function
 Symptoms of hypercalcaemia
Signs (Ms Leow) Inspection
 Breast – symmetry (any fullness in 1 side), scar, skin changes (dimpling, peau d’orange,
hyperpigmentation), dilated veins
 Nipple-areolar complex – everted/inverted/retracted, spontaneous discharge
 Axilla – scar (axillary clearance), accessory breast
 Supraclavicular fossa – fullness (LN)
 Back – scar (chest drain for pleural effusion)
 UL – lymphoedema

74
 Palpation
 Breast
- Any pain?
- Temperature tenderness
- Site size shape surface
- Mobility (skin tethering, muscle tethering)
- Edge – well/ill-defined
- Consistency – hard
 Nipple – discharge, mass behind
 Axilla – apical central anterior lateral posterior groups
 Neck – supraclavicular and cervical LN
Completion
 Bone – tenderness
 Lung – signs pleural effusion
 Abdomen – hepatomegaly, ascites
DDx  Fibroadenoma
 Breast cyst
 Phylloides tumour (massive)
Classification  In situ
- Ductal carcinoma in situ (DCIS) – best prognosis
- Lobular carcinoma in situ (LCIS) – best prognosis
- Paget’s disease of the nipple
 Invasive
- Invasive ductal carcinoma (IDC) - 85%
- Invasive lobular carcinoma (ILS) - 10%
- Tubular
- Medullary
- Colloid
- Signet ring cell (worst)
 Other
- Lymphoma (non-hodgkin’s)
- Sarcoma
- Secondary – melanoma/ carcinoma from other sites
Ix: Triple Clinical  Hx & PE
Assessment Radiological  Mammogram
- First modality for women >35
- Medial-lateral-oblique (MLO) and cranial-caudal (CC) views
- Speculated mass lesion (dense centre with radiating lines)
- Malignant type fine linear/granular microcalcification (needs to be
calculated), pleomorphic clustered calcification
- Architectural distortion
- Asymmetry
- Skin thickening
- Lymph nodes
 Ultrasound
- First modality for women <35 – dense breast tissue
- Can be supplementary to mammogram
- Distinguish solid vs cystic lesion
- Hyper/hypoechoic
- Posterior enhancement
- Vascularity
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 - Disrupted halo
- Taller than wide
 MRI
- For pre-op assessment – reduces risk of incomplete excision
- Consider in
 Invasive lobular cancer
 Suspicion of multicentricity
 Genetic high risk (BRCA1 & 2)
 T0 N+ disease
 Breast implants/foreign bodies
 Diagnosis of recurrence
 Follow-up after neo-adjuvant treatment
 Dense breast

Breast Imaging Recording and Database System (BI-RADS)

Histological  Fine needle aspiration cytology (FNAC)

- Cannot distinguish in-situ vs invasive cancers
- Features: Nucleus, nuclear-cytoplasmic ratio, mitotic activity
 Trucut core biopsy
- Enable visualization of architecture
- Invasive vs in-situ (basement membrane)
- Ductal vs lobular
- ER, PR, HER2 status (if immunohistochemistry of HER2 is 2+ or 3+,
perform FISH to confirm)
Staging Ix  CXR
 Liver US
 CT TAP
 Bone scintigraphy/CT/MR
 PET if suspicious of metastasis
TNM T T0 – no evidence of primary tumour
(see below) Tis – DCIS, LCIS or Paget’s
T1 – <2cm
T2 – 2-5 cm
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 T3 – >5cm
T4 – any size with direct extension to the chest wall/skin (ulceration/skin
nodules)
N N0 – no regional LN metastasis
N1 – mobile ipsilateral level I, II axillary LN
N2 – clinically fixed/matted ipsilateral level I, II axillary LN or clinically
detected ipsilateral internal mammary LN
N3 – ipsilateral infraclavicular (level III) or internal mammary + axillary or
supraclavicular LN
M M0 – no distant metastases
M1 – distant metastases
Reporting Minimum  Location (side, quadrant), max diameter, multifocality
parameters  Tumour type (histology)
 Histological grade (Scarff-Bloom-Richardson) – see below
 LN involvement
 Resection margins (post-op)
 Lymphovascular invasion
 Non-neoplastic breast changes
 ER/PR status
 HER2 status
Mx Early Def: Stage I, IIa, IIb – has not spread beyond breast or axillary LN
 Disclose Dx to the patient
 Offer surgery
- To the breast
 Breast-conserving surgery (BCS) + radiotherapy
o Selection criteria:
1. Single lesion clinically & mammographically
2. ≤3cm (4cm in larger breast)
3. >2cm away from nipple/areola
4. Low histological grade
5. No extensive in situ component
6. No extensive nodal involvement
o CI:
1. Ratio of tumour size to breast size or location of
tumour will result in unacceptable cosmesis
2. Multifocal/multicentric disease
3. Local radiotherapy contraindicated (previous
radiotherapy at the site, CTD, pregnancy)
o Remove the tumour and 1cm margin of macroscopically
normal tissue, followed by radiotherapy to minimise
local recurrence
o Impalpable tumour – directed by US-guided skin
marking or mammogram-guided hook wire insertion
o 10% possibility that margin is not clear and need 2nd
WLE or mastectomy
 Mastectomy
o Remove the whole breast with preservation of
pectoralis major and minor in most cases
o May need radiotherapy (see indication below)
- To the axilla
 Sentinel LN biopsy +/- axillary clearance
o Selection criteria:
1. Early breast ca with no clinically palpable LN or
2. Impalpable LN but radiologically detected, FNAC –ve

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 o Dual technique: Radioactive isotope (Tc99m) injected
next to tumour 12H before Sx, then blue dye
(methylene blue/ isosulphan blue) injected at the start
of Sx into periareolar area  detect sentinel LN by
gamma probe & direct visualisation of blue colour 
excise & examine by frozen section  +ve  axillary
clearance in the same seating (2nd seating if frozen
section facility not available)

 Primary axillary clearance

o To treat proven axillary disease & fully stage the axilla
o Level II clearance is accepted by most surgeons
o Level III clearance causes higher morbidity & only
performed when higher nodes palpable
o 10-15 LN retrieved, at least 1 section from each
assessed by haematoxylin & eosin (H&E)
 Breast reconstruction surgery
- Immediate or delayed
- Immediate – skin sparing surgery – remove breast via periareolar
incision, the place implant (silicone gel/silicone with saline) or expander
(will be changed to permanent impalent) deep to pectoralis muscle
- Myocutaneous flap using skin, fat, muscle
 Abdominal wall – ‘TRAM’: transverse abdominis myocutaneous
flap or ‘DIEP’: deep inferior epigastric perforator flap
 Back – ‘LD’: Latissimus dorsi flap
 Buttock
 Inner thigh
 Plan for adjuvant therapy
- Systemic
 Chemotherapy
o 5-FU based
 FEC (5-fluorouracil, epirubicin,
cyclophosphamide)
 FAC (5-fluorouracil, Adriamycin/doxorubicin,
cyclophosphamide)
 CMF (cyclophosphamide, methotrexate, 5-
fluorouracil)
o Taxanes – doclitaxel, paclitaxel
o S/E: N, V, alopecia, mucositis, neutropenia, premature
ovarian failure, induction of early menopause Hormonal
(ER +ve)
1. Tamoxifen
o Selective oestrogen receptor modulator (SERM)
o Blocks peripheral action of oestrogen in the breast by
binding to the ER
o For pre-menopausal or post-menopausal women with
ER+ breast ca
o S/E: Menopausal symptoms (vaginal dryness, hot
flushes), osteoporosis, visual disturbances, DVT
o Increased risk of endometrial cancer due to stimulating
effect on ER in uterus (previously ≤5 years, now ≤10
years recommended)
2. Aromatase inhibitor e.g. letrozole, anastrozole
o Only in post-menopausal women

78
 o Prevent oestrogen synthesis in peripheral adipose tissue
by blocking the conversion of androgen to oestrogen by
enzyme aromatase
o S/E: osteoporosis & fractures
3. Ovarian ablation using LHRH analogues (buserelin,
goserelin) /oophorectomy (not routine)
 Biological: Trastuzumab/Herceptin (HER2 +ve)
o Humanised monoclonal antibody to HER/neu (cerbB2)
transmembrane receptor which is overexpressed in 30%
breast ca & carries a poor prognosis
o Given after Sx & chemo at 3-weekly interval for 1 year
- Local
 Radiotherapy
o External beam radiation 40-50Gy over 3-5 weeks
o Indications (see below)
o Advantage: reduce local recurrence up to 50%
o Disadvantage: lymphoedema, lymphangiosarcoma,
radiation necrosis, radiation pneumonitis,
cardiomyopathy
 Surveillance
- Annual mammogram especially for BCS
- Follow up 3-monthly for the 1st year, 6-monthly for 5 years, annual
review thereafter
 Psychosocial support
Locally Def: Stage IIIa, IIIb, IIIc – primary tumour >3cm, skin/chest wall involvement, +/-
advanced regional LN involvement
 Mastectomy + primary axillary clearance + adjuvant therapy, or
 Neoadjuvant therapy to downsize tumour to enable BCS in operable
tumours or to downsize inoperable tumours to operable + primary axillary
clearance + adjuvant therapy
Metastatic Def: Systemic involvement
 Palliative
 Resection of primary tumour may be considered to improve local control
 Resection of limited metastasis may be considered
 Adjuvant therapy
- Radiotherapy for bone metastases to reduce pain or control locally
advanced skin, breast, chest wall, LN disease, bleeding
- Systemic chemotherapy to slow progression of disease
 Symptomatic
- Aspiration/pleurodesis for pleural effusion
- Peritoneal tap for ascites
Consent  Offer treatment - as above
 Indications/benefits – cure vs palliative
 Complications
- Surgery to the breast/axilla
 Early
o Bleeding
o Injury to the nerve – long thoracic nerve of Bell (winging of scapula),
intercostal brachial nerve (loss of sensation to inner arm)
o Wound infection
o Seroma
 Late
o Lymphoedema
Screening  Mammogram 2-yearly in women 50-74 years old
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(Malaysian CPG)  Breast self-examination to raise awareness instead of as screening tool
 Screen women from high risk group from age 30 with both mammogram and MRI
 MRI not recommended for high risk group with LCIS and atypical hyperplasia
 Early referral to surgical department for
- Women >40 presenting with a breast lump
- Lump >3cm at any age
- Clinical signs of malignancy
Familial breast  Genetic counselling for women with FH associated with BRCA1, BRCA2 and tp53 genes
cancer - ≥2 1st/2nd degree relative on same side of family with breast/ovarian ca at any age
- ≥2 1st/2nd degree relative on same side of family with breast ca, 1 dx ≤50 years old
- ≥2 1st/2nd degree relative on same side of family with ovarian ca at any age
- 1st degree relative with breast ca dx ≤40
- 1st degree relative with breast + ovarian ca at any age
- 1st degree relative with bilateral breast ca at any age
- 1st degree relative with male breast ca
- FH of breast ca + BRCA-related ca e.g. pancreas, prostate, oesophageal ca on same side
of family
- FH of early onset breast ca + other TP53-related ca e.g. sarcoma, multiple childhood ca
on same side of family
 Screen women from high risk group from age 30 with both mammogram and MRI
 Risk reducing salpingo-oophrectomy once childbearing is complete
 Bilateral prophylactic mastectomy
 Contralateral prophylactic mastectomy for breast ca with BRCA1/2

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Benign Breast Diseases
ANDI (Aberrations in the Normal Development and Involution of the breast) Classification
Normal Aberration Disease
Early Ductal development Single duct obstruction Mammary duct fistula
reproductive Nipple eversion Nipple inversion Subareolar abscess
years (<25)
Lobular development Fibroadenoma Giant/multiple fibroadenoma

Stromal development Adolescent hyperplasia Gigantomastia (severe)

Mature Cyclical changes

reproductive - Hormonal Mastalgia (Severe form of each)
years (25-40) Nodularity

- Epithelial Ductal papilloma (fibrocystic

disease)

Epithelial hyperplasia of Bloody nipple discharge

pregnancy

Lactation Galactocoele & inappropriate

lactation
Involution (35-55) Lobular involution – Macrocyst, adenosis,
microcysts sclerosing lesions (fibrocystic
disease)

Ductal involution
- Dilation Mammary duct ectasia Periductal mastitis/abscess
- Fibrosis/sclerosis Nipple inversion/retraction

Epithelial turnover Hyperplasia Lobular hyperplasia with

atypia
Ductal hyperplasia with
atypia
Intracystic papilloma

84
Benign Thyroid Diseases
Developmental
Condition Pathophysiology Clinical Features
Thyroglossal - Cyst formation anywhere along - Uncommon
cyst embryological descent pathway of thyroid - Children/young adults
from the foramen of caecum (junction - Smooth, well-defined, rounded swelling in
btwn ant 2/3 and post 1/3 of the tongue) the midline of neck
via the hyoid bone to the neck - Anywhere from submental area to thyroid
isthmus
- Moves up with swallowing and tongue
protrusion
- Becomes symptomatic when infected by
oral bacteria
- Rx: Sistrunk operation – excision of cyst &
whole thyroglossal duct
Thyroglossal - Incomplete removal of a thyroglossal cyst - Rare
fistula causing a fistula - Fistula opening near midline of the neck
- Intermittent discharge – serous/pus
Ectopic thyroid - Part/all of thyroid lying anywhere along - Uncommon
the thyroglossal tract - Usually asymptomatic
- Swelling near foramen caecum

Inflammatory/Autoimmune
Condition Pathophysiology Clinical Features
Hashimoto’s - Diffuse lymphocytic infiltration of thyroid - Common
thyroiditis gland, Hurthle cells - Adult, F>M
- Progressive destruction of thyroid follicles - Mild, diffuse, sometimes tender thyroid
– atrophy & fibrosis enlargement (often not enlarged)
- Cause: Anti-thyroid antibodies (anti-TPO) - Euthyroid/hyperthyroid hypothyroid
in high titres, may be a/w other AI - Rx: Levothyroxine. Thyroidectomy if
disorders e.g. pernicious anaemia suspect lymphoma/papillary carcinoma
Graves’ disease - Diffuse thyroid hyperplasia - Fairly common
- Cause: Circulating Ig ‘long-acting thyroid - Diffuse thyroid enlargement +/- bruit
stimulator’ (LATS) – mimic TSH effect  ↑ - Hyperthyroidism – heat intolerance,
T3/4 increased appetite, LOW, tremor,
diarrhoea, tachycardia, atrial fibrillation,
thyroid eye disease
De Quervain’s - Diffuse inflammation of the thyroid gland - Uncommon
thyroiditis - Neutrophilic  lymphocytic/histiocytic - Middle-aged females
infiltration - Diffuse moderate thyroid enlargement
- Cause: viral - Pain + tenderness
- +/- systemic symptoms
- Episode lasts weeks-months, often
recurrent
- Usually euthyroid, may be hyperthyroid
initially
- Rx: NSAIDs, corticosteroid, Sx if
unresponsive

85
 Riedel’s - Dense fibrosis of the thyroid gland - Very rare
thyroiditis - Cause: autoimmune - Middle-aged females
- Extremely hard ‘woody’ goitre, often
asymmetrical (mimic malignancy)
- +/- compressive symptoms
- Rx: corticosteroid

Hyperplastic/Metabolic
Condition Pathophysiology
Simple non- - Benign, diffuse or multinodular
toxic colloid hyperplasia of thyroid follicles
goitre - Cause: Unknown, ?minor abnormality of
thyroid hormone synthesis
Endemic goitre - Diffuse hyperplasia of thyroid follicles
- Cause: Dietary iodine deficiency (inland
mountain areas), goitrogenic food
Drug-induced - Diffuse thyroid hyperplasia
goitre - Cause: interference with thyroid hormone
synthesis – carbimazole, lithium,
aminoglutethimide
Dyshormono- - Diffuse thyroid hyperplasia
genesis - Cause: a variety of uncommon genetic
(recessive) defects affecting thyroid
hormone synthesis
Physiological - Diffuse thyroid hyperplasia
- Cause: pregnancy, puberty
Clinical Features
- Very common
- F>M
- Diffuse/ multinodular thyroid
enlargement/ single ‘adenomatous’
nodule/ cyst
- Clinically euthyroid, TFT normal
- Inland mountain areas
- Diffuse, often massive thyroid
enlargement, may later become nodular
- Low/normal T4, high TSH
- Uncommon
- Diffuse thyroid enlargement
- Usually euthyroid
- Can be prevented using ‘block & replace’
regimen
- Very uncommon
- Presents at birth/childhood
- Thyroid enlargement & severe cretinism
- Diagnosed by neonatal screening test
- Common
- Mild diffuse thyroid enlargement
- Euthyroid

86
Approach to a Thyroid Swelling
Clinical  2 lobes joined by an isthmus – butterfly-shaped
Anatomy  Pyramidal lobe may be present, extends superiorly from the isthmus and can reach hyoid
 Site: anterior neck below the thyroid cartilage, extends from C5-T1
 Anatomical relationships
- Anterior: strap muscles – sternothyroid, thyrohyoid, sternohyoid; superior belly of
omohyoid, sternocleidomastoid
- Posterior: parathyroid glands, trachea, oesophagus, recurrent laryngeal nerve, carotid
sheath

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  Lymphatic drainage: periglandular  pretracheal (Delphian)  paratracheal  superior
mediastinal nodes. Also superior and inferior deep cervical nodes
 Nerve supply: sympathetic & parasympathetic
Hx  Swelling – site, onset, duration, progress
 Pain – painful  thyroiditis, haemorrhage, malignant infiltration of nerves, anaplastic ca
 Pressure effect
- SOB, stridor (tracheal compression, tracheomalacia)
- Dysphagia (oesophagus)
- Hoarseness (RLN)
- Horner’s syndrome (ptosis, myosis, anhidrosis, enopthalmos)
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  Symptoms of hyperthyroidism
- Heat intolerance
- Excessive sweating
- Increased appetite
- Weight loss
- Diarrhoea
- Amenorrhoea/oligomenorrhoea
- Anxiety
- Palpitations
- Eye signs – double vision, pain, change in appearance
 Symptoms of hypothyroidism
- Cold intolerance
- Reduced appetitie
- Weight gain
- Constipation
- Menorrhagia/amenorrhoea
- Lethargy
- Hoarseness
 Constitutional symptoms of malignancy
- LOA, LOW
- Bone pain
- SOB
- Jaundice
 PMH/PSH – Hx of irradiation (papillary ca), longstanding endemic goitre (follicular ca),
hashimoto’s (lymphoma, papillary ca), thyroglossal cyst (papillary ca)
 Medication – thyroxine/anti-thyroid drugs
 FH – goitre, thyroid ca (medullary – MENIIa, IIb)
 SH – diet (iodine deficiency), cabbage/soy (goitrogen), living area
PE  General
- Respiratory distress
- Nutritional status – underweight/overweight/cachexic/anaemic
 Neck
- Inspection

- Palpation

- Percussion – over the manubrium for retrosternal extension
- Auscultation – vascular bruits in Graves’
- Special test
 Pemberton’s sign – raise arm over head  facial flushing, respiratory distress
(SVCO due to restrosternal extension)
 Berry’s sign – inability to feel the carotid pulse due to malignant infiltration of
the carotid sheath
 Hand
 Eye
 Leg
 Other system
- CVS – evidence of HF – cardiomegaly, pedal oedema
- Respi – lung mets, pleural effusion
- Abdomen – hepatomegaly
- Bone – mets
Ix Blood  TFT – T4/TSH
 Thyroid antibodies
- TSH receptor antibody – Graves’
89
 - anti-thyroglobulin – autoimmune thyroiditis
- anti-thyroid peroxidase antibody (anti-TPO) – Hashimoto’s
 TSH suppression test – not suppressed in carcinoma
 Serum thyroglobulin – tumour marker for papillary & follicular ca
(surveillance)
 Serum calcium & calcitonin – raised in medullary ca
Imaging  Thyroid U/S
- Size, number of nodules, cystic vs solid , margin, echogenicity,
calcification, invasion of local structures, lymph nodes, vascularity
(Colour Doppler U/S)
- Benign nodule: large cystic component, hyperechoic solid, comet tail
artefact
- Malignant nodule: hypoechoic solid, microcalcifications, large (>10mm),
taller than wide, local invasion of surrounding structures, suspicious LN,
intranodular blood flow
- Allows aspiration of cyst, send fluid for cytology
- Guides FNAC
 Radioactive iodine study (Tc99m)
- Less commonly used
- Differentiate hot vs cold nodules
- Hot nodules: increased uptake, rarely malignant – Grave’s, toxic MNG,
toxic adenoma
- Cold nodules: malignancy (10%), haemorrhage
 CT neck/thoracic outlet
- Retrosternal extension, compression of trachea, oesophagus, SVC
 Indirect laryngoscopy
- Vocal cord function, as pre-op baseline
Histology  Fine needle aspiration cytology (FNAC)
- With or without local lidocaine anesthesia
- Repetitively moving a 23 to 27-gauge needle through the nodule
- The needle is attached to a 10 mL syringe
- Aspirated material is smeared directly on slides, fixed, and stained, or
collected in a liquid preservative
- Thin-layer preparations are made
- Advantages: simple, quick, low risk of infection, allows aspiration if
cystic, easily repeatable for multiple nodule
- Disadvantages: might miss target if small nodule, may no be
representative if small sample taken, cannot differentiate follicular
adenoma vs carcinoma, operator dependent
Bethesda FNAC Result Explanation Action
Class

I Non diagnostic Insufficient sample and Repeat FNAC

diagnosis is not possible under
ultrasound
guidance
II Benign Non cancerous. Continue
observation
Follow up with
ultrasound

90
 III Atypia of Lesions that are not Repeat FNA in 2
undetermined convincingly benign but to 3 months
significance or do not have definitive
follicular lesion features of a follicular
of neoplasm and are not
undetermined highly suspicious of
significance malignancy

IV Follicular Benign adenomas or Lobectomy

neoplasm or well-differentiated
suspicious for a follicular or follicular
follicular variant of papillary
neoplasm cancers of the thyroid.
V Suspicious for Lesions with some Lobectomy/
malignancy features suggestive of Total
but not definitive for thyroidectomy
thyroid cancer.
VI Malignant Papillary cancer, Total
medullary cancer, thyroidectomy
thyroid lymphoma,
anaplastic cancer, and
cancer metastatic to
the thyroid
 Trucut core biopsy
- Shows architecture hence differentiate follicular adenoma vs carcinoma
Other  ECG – A fib
 FBC, RP, LFT, coagulation profile based on case
Mx Medical Anti-thyroid drugs
 Curative for small, non-toxic goitre
 For patients who refuse surgery
 Pre-RAI ablation & pre-Sx
 Carbimazole
- Inhibits iodination & coupling
- Start dose: 20-40mg od, gradual reduction to 5mg od if hyperthyroidism
controlled, discontinue once euthyroid on 5mg od
- Block & replace regimen – full dose carbimazole + levothyroxine 50-
100µg od
- S/E: agranulocytosis, SJS, hepatitis, jaundice, aplastic anaemia,
peripheral neuritis, polyarteritis, vasculitis, teratogenicity – Aplasia cutis
congenital (congenital focal absence of epidermis with or without
evidence of other layers of the skin)
 Propylthiouracil
- Inhibits peripheral conversion of T4 to T3
- Can be used in pregnancy
- Starting dose 100-200mg TDS
- Gradual dose titration is similar to that of carbimazole
- S/E: rash, urticaria, arthralgia, GI upset, agranulocytosis
 Propanolol (Beta-blocker)
- Reduce sympathetic stimulation, reduce peripheral conversion of T4 to
T3
- Symptomatic control, stabilize patient before surgery
- Starting dose 40-80mg TDS or QID

91
 - Avoid in asthma, use with caution in heart failure
- Stop when clinically and biochemically euthyroid
Thyroid hormone replacement
 Levothyroxine
- To treat all causes of hypothyroidism
- To suppress TSH after thyroidectomy & RAI
Radio-iodine  Administered orally as sodium iodide-131 (131-I) in solution or a capsule
 Indications:
- Graves’ disease
- Toxic adenoma
- Multinodular goitre
- Relapse after medical/surgical Rx
- Contraindicated for medical/surgical Rx
 Contraindications:
- Pregnancy – cross placenta & ablate foetal thyroid – cretinism
- Breastfeeding mother
- Severe opthalmopathy – worsening of eye disease
 A/E: hypothyroidism, increased risk of malignancy
Surgical  Indications
- Malignancy
- Compression symptoms – trachea, oesophagus
- Failure of medical therapy
- Cosmetic reason
 Types
- Total thyroidectomy
- Subtotal thyroidectomy
- Hemithyroidectomy
Consent  Surgery offered, indications, benefits
 Procedure
 Complications
- Anaesthesia
 Trauma to teeth, trachea, vocal cord, sore throat, hypoxia, vomiting
- Early
 Bleeding
 RLN injury
 Hypoparathyroidism
 Thyroid storm
- Late
 Hypothyroidism

92
Thyroid Malignancies
Types Features Metastasis Mx
Papillary

Follicular

Medullary

Anaplastic

Lymphoma

Management of Thyroid Malignancies

93
Urolithiasis
Clinical
Anatomy

Ureter
 Retroperitoneal, 25-30cm long
 3 constriction points
 Start - Pelvi-ureteric junction (PUJ)
(Descends over psoas)
 Middle - Cross iliac bifurcation overlying SIJ
 End – vesico-ureteric junction (VUJ) – medial to ischial spine
 Blood supply
 Upper 1/3 – renal artery
 Middle 1/3 – gonadal artery
 Lower 1/3 – internal iliac artery
 Innervation
 Automomic – sympathetic & parasympathetic
 Visceral afferent fibres return to T10-L2 dermatome “loin to groin pain”
Types of urinary Type % Aetiology Clinical features
stones Calcium oxalate/ 70  Idiopathic  Small, smooth ‘hemp-seed’
phosphate  Urinary stasis stones
 Infection  Small irregular ‘mulberry’
 Foreign bodies stones
 Hyperparathyroidism  Small spiculated ‘jack’ stones
 Hypercalcaemia  Radio-opaque
 Idiopathic hypercalciuria
 Hyperoxaluria
Magnesium 15  Infection – Proteus (urease  Large ‘staghorn’ calculi of
ammonium splits urea forming ammonia pelvi-calyceal system
phosphate in alkaline urine)  Bladder stones
(struvite/staghorn)
Uric acid 8  Gout  Yellow/brown
 Chemotherapy (leukaemia,  Radiolucent
mueloproliferative disorders)
Cysteine/xanthine 2  Autosomal recessive  Cysteine – hexagonal,
disorders translucent, white crystals in
 Excess urinary excretion of acidic urine/ pink/yellow but
cysteine/xanthine change to green when
exposed to air. Radio-opaque
94
  Xanthine – smooth round
brick red with lamellation
Epidemiology  2-5% lifetime risk (Asia)
 Peak age 35-45
 M>F
Aetiology/ Risk  Urinary stasis – congenital abnormalities (horseshoe), hydronephrosis, BPH, neurogenic
Factors bladder
 Chronic UTI – Proteus
 Excess urinary excretion of stone-forming substances – idiopathic hypercalciuria, hyperPTH,
hyperoxaluria, gout, cysteinuria, xanthinuria
 Foreign bodies – fragments of catheter tubing, parasites (schistosome ova), diseased tissue
(renal papillary necrosis)
 Diet – high calcium/dairy, low water intake
 Other – prolonged immobility, children in developing world (uric acid stone), multiple
fractures & paralysis (skeletal decalcification)
Pathophysiology  Obstruction at PUJ  hydronephrosis  progressive parenchymal damage  renal
impairment/failure
 Pass into ureter  impacted  ureteric colic & hydroureter/hydronephrosis +/- renal
impairment
 Pass into ureter  bladder  nidus for larger bladder stone  bladder outlet obstruction
 urinary retention
 Pass into ureter  bladder  sandy urine, dysuria, haematuria
 Stasis  bacteria multiply  UTI  acute pyelonephritis  perinephric abscess
 Stasis  bacteria multiply  UTI  cystitis
 Local irritation in PUJ/ureter  stricture
 Prolonged irritation in bladder  squamous metaplasia  squamous carcinoma

Site Kidney Ureter Bladder

Hx  Asymptomatic  Ureteric colic (loin to groin  Asymptomatic
 Loin pain pain)  Suprapubic pain
 Haematuria  Haematuria  Dysuria
 Frequency
 Nocturia
 Urgency
 Intermittency
 Urinary retention
 Haematuria
 Fever (UTI)
PE  Anaemia  Unwell, distress  Suprapubic tenderness
 Renal punch/percussion  Tenderness/rigidity  Palpable bladder
 Ballotable kidney  Ballotable kidney  Ballotable kidney
(pyelonephrosis/ (pyelonephrosis) (pyelonephrosis)
pyelonephritis) - rare  Retracted testis
(cremasteric spasm)
Ix Blood &  Urine FEME – haematuria, leukocytes & nitrites (UTI), pH (acidic in uric acid
Urine stone, alkaline in infection), crystals
 Urine C+S – culture
 FBC – Hb (anaemia), WCC (infection)
 RP – Urea, Cr (impaired renal function), electrolytes
 Serum calcium, phosphate, oxalate, uric acid, ALP
 24H urinary excretion of calcium, uric acid, cysteine

95
 Imaging  X-ray KUB – 90% stone radio-opaque
 U/S KUB – stone in renal pelvis, hydronephrosis (less well in demonstrating
ureter), urinary retention, stones in bladder with acoustic shadow
 Non-contrast CT abdomen pelvis – better to visualize ureter
 Intravenous urogram (less used) – able to detect radiolecent stone as well.
Filling defect, hydroureter, hydronephrosis
Other  Cystoscopy – bladder stones
 Percutaneous (antegrade) pyelography or ascending (retrograde) ureterography
 Biochemical analysis of recovered stones
Acute Mx  IV fluids
 Analgesics – NSAIDs e.g. ibuprofen, diclofenac; narcotics if needed
 Antiemetic e.g. metolopromide
 Antibiotics for UTI
 Rule out obstruction & infection – if both present  emergency surgical decompression by
urethral/double J stent (endoscopic) or percutaneous nephrostomy (fast & safe for unstable
patients)  treat infection  definitive treatment
 <5mm likely to pass spontaneously

Active Medical Expulsive Therapy (MET) – example of regime

 Pain relief
 Ketorolac 10 mg PO tds x 5/7
 Paracetamol 1g PO tds x 7/7
 Oral opioid pain medication (oxycodone-acetaminophen) as needed for breakthrough
pain
 Anti-spasmodic
 Nifedipine XL 30 mg/d PO x 7/7
 Tamsulosin
 Antibiotic
 Trimethoprim/sulfamethoxazole DS od x 7/7
 Steroid
 Prednisolone 20 mg PO bd x 5/7

Uric acid stone

 Alkalinazation of urine using potassium citrate

Indications for stone removal

 Obstruction of urinary flow
 Infection
 Persistent (>48H), recurrent or severe pain
 Stone likely to cause obstruction/infection
 Small ‘metabolic’ stones likely to grow rapidly in size
 Professions where colic could be disastrous e.g. pilot
 Solitary kidney
Surgical Mx  Extracorporeal shock wave  Extracorporeal shock wave 
lithotripsy (ESWL) lithotripsy (ESWL)
 Percutaneous  Rigid/flexible ureteroscopy
nephrolithotomy (PCNL) (URS)
 Nephrolithotomy/ - Rx of choice for middle
pyelolithotomy (open) & lower ureter stone
- Failed ESWL

96
 Complications  

Extracorporeal Shockwave Lithotripsy (ESWL)

 Principles
- High energy shock waves produced by an electrical discharge
- Shock waves transmitted through water & directly focused onto a renal/ureteral stone with the aid of
biplanar fluoroscopy
- The change in tissue density between the soft renal tissue and the hard stone causes a release of energy
at the stone surface  fragments the stone

Percutaneous Nephrolithotomy (PCNL)

 Indications
- Large (>2 cm in diameter)
- Complex calculi (filling the majority of the intrarenal collecting system e.g. staghorn calculi)
- Cysteine stones (relatively resistant to ESWL)
- Anatomic abnormalities (horseshoe kidneys, PUJ obstruction)
- Stones within calyceal diverticula
 Procedure
- Supine position
- A retrograde ureteral catheter is placed using a 15F flexible cystoscope
- Turn the patient to prone position
- Assess renal collecting system via an 18G needle under fluoroscopic guidance
- Dilation of the tract with a nephrostomy balloon dilator
- A working sheath is placed into the renal collecting system
- All calculi are extracted with grasping forceps (rigid and/or flexible nephroscope)/ fragmented using
ultrasonic/ pneumatic/ combined lithotripsy probe using a rigid nephroscope
- Following successful stone removal, leave a 10F Cope catheter in the renal pelvis as a nephrostomy
tube with a 5F catheter placed down the ureter
 Complications
- Bleeding
- Sepsis

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Renal Cell Carcinoma
Definition  Primary malignant tumour of the renal parenchyma
 A.k.a hypernephroma/Grawitz tumour
Clinical
Anatomy

 Retroperitoneal organ
 Receives 20% cardiac output
 Relations
- Anterior relations
 Right – right adrenal, liver, D2, hepatic flexure, small intestine
 Left – left adrenal, stomach, spleen, pancreas, splenic flexure, descending
colon, jejunum
- Posterior relations – rib 11,12, psoas major, quadratus lumborum, transversus
abdominis muscles
 Renal fat & fascia – renal capsule, perirenal fat, Gerota’s fascia, pararenal fat
 Structures – cortex, medulla (pyramids & renal papilla), pelvis (major & minor calyces)
 Blood supply
- Arterial – L & R renal arteries from aorta at L1, R longer than L, pass behind IVC. Each
divides into 5 segmental arteries.
- Venous – segmental veins  L & R renal veins  IVC
Epidemiology  3% adult malignencies
 M>F x2
 Peak age 50-70
Aetiology/ Risk  96% Sporadic
Factors  4% Familial – Von-Hippel-Lindau, hereditary papillary renal carcinoma, Birt-Hogg-Dube
syndrome, and hereditary renal carcinoma
Von-Hippel-Lindau
- Autosomal dominant
- 50% develop RCC, often bilateral & multifocal
- Present in 3rd, 4th, 5th decade
- A/w phaeochromocytoma, renal & pancreatic cysts, cerebellar haemangioblastomas,
retinal angiomas, epididymal cystadenomas
- Loss of both copies of VHL (tumour suppressor genes)  upregulation of VEGF
 Acquired cystic renal disease (1/3 after 3 years of dialysis. Risk of RCC 3-6x higher)
 Smoking
 Other: western diet, obesity, low SE class, asbestos, HPT
Pathophysiology  Adenocarcinomas arising from proximal tubules
- Large tumour cells with clear cytoplasm (glycogen & lipid) hence “clear cell carcinoma”
- Multifocal in 7-20%
- Spread

98
  Direct – adrenal
 Vascular – renal vein (5% at presentation), IVC, RA – thrombosis
 Lymphatics (only when tumour breaches Gerota’s fascia) – hilar & para-aortic
LN
 Blood – lung (75%), bone (20%), liver (18%), brain (8%)
 Other neoplasms in the kidney
- Benign – adenoma, angioma, angiomyolipoma (a/w tuberous sclerosis, contain fat, can
bleed), oncocytoma
- Malignant – wilm’s tumour, TCC, SCC

Clinical features  Asymptomatic, >50% incidental finding on imaging

 Classic triad: Pain, flank mass, haematuria in <10% & indicates advanced disease
 Haematuria (40%)
 Flank pain (40%)
 Flank mass (25%)
 Constitutional symptoms – LOW, fever, night sweats, malaise
 Metastatic (25%) – haemoptysis, bone pain
 Non-reducing left varicocoele (2% male, spread to left renal vein)
 LL oedema
 Paraneoplastic syndrome (10-40%)
- Polycythaemia (excess erythropoietin)
- Hypercalcaemia 10-20% (due to production of parathormone-like hormone)
- Cushing’s (ectopic secretion of ACTH)
- Hypertension (excess renin production, renal artery compression)
- Iron deficiency anaemia
- Pyrexia of unknown origin
- Elevated ESR
- Stauffer’s syndrome (Non-metastatic hepatic dysfunction, fever, anorexia)
DDx  Acute pyelonephritis
 Chronic pyelonephritis
 Bladder carcinoma
 Non-Hodgkin’s lymphoma
 Wilm’s tumour
Ix Blood &  FBC – Hb (anaemia, polycythaemia), WCC (infection)
urine  RP – assess remaining renal function
 LFT – liver mets, Stauffer’s, ALP increase in bone mets
 Serum calcium – hypercalcaemia
 ESR – raised in paraneoplastic syndrome
 Blood C+S – TRO infection in pyrexic patients
 Serum erythropoietin, renin
 Urine FEME – haematuria, UTI
 Urine C+S – TRO pyelonephritis
Imaging  Renal U/S
 CECT (triphasic)
- Cystic vs. solid masses
- Lymph node, renal vein, IVC involvement
 MRA – renal vein involvement

99
  CXR – lung mets
 Bone scan – bone mets
 CT brain – brain mets
 PET scan
Other  Percutaneous cyst puncture and fluid analysis - evaluation of potentially
malignant cystic renal lesions detected by US/CT
 Transoesphageal ECHO – right atrium involvement
Staging T  T1 – ≤7 cm, limited to the kidney
- T1a - ≤4 cm
- T1b - >4 cm but ≤7 cm
 T2 – >7 cm, limited to the kidney
 T3 – Extends into major veins/ directly invades adrenal gland/ perinephric
tissues but not beyond Gerota fascia
- T3a – directly invades adrenal gland or perinephric tissues but not
beyond Gerota fascia
- T3b – grossly extends into renal vein(s) or vena cava or its wall below
diaphragm
- T3c – grossly extends into vena cava or its wall above diaphragm
 T4 – directly invades beyond Gerota fascia
N  N0 – No regional lymph node metastasis
 N1 – 1 regional lymph node
 N2 – >1 regional lymph node
M  M0 – No distant metastasis
 M1 – Distant metastasis
AJCC Stage
grouping

Mx Principles

100
Consent

Complications

Prognosis  Confined to kidney – 79% 5-year survival

 Nodes/IVC – 40%
 Metastasis – 8%

Bladder Carcinoma
Clinical
Anatomy

 Blood supply
- Arterial – branches of the internal iliac artery
 Superior vesical arteries
 Inferior vesical arteries (vaginal arteries in females)
 Obturator artery
 Inferior gluteal artery
 Uterine branches (female only)
- Veins – follow arteries into internal iliac vein
 Lymphatics – external/internal iliac nodes
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Normal  Continence - synergic relaxation of detrusor muscles & contraction of the bladder neck and
physiology pelvic floor muscles (during bladder filling & urine storage)
 Normal adult bladder accommodates 300-600 mL of urine
 A CNS response is usually triggered when volume reaches 400 mL  perceived as sensation
of bladder fullness & need to void.
 However, urination can be prevented by cortical suppression of the PNS/ voluntary
contraction of the external urethral sphincter
Epidemiology  Common urological cancer
 >90% are transitional cell carcinoma
 Rare <50
 M>F
 Malay>Chinese>indian
Aetiology/ Risk  Age
Factors  Smoking
 Industrial carcinogens – aniline dyes, aromatic amines, rubber, cable, printing
 Pharmaceutical compounds – saccharin, phenacetin, insecticides
 Cyclophosphamide
 Schistosomiasis (SCC)
Pathophysiology  TCC can be found anywhere from renal pelvis, to urethra but commonest site is bladder
 Well-differentiated tumours form papillary frond-like lesions
 Poorly differentiated tumours form plaque-like lesions which invade underlying muscle &
tissues
 “Field abnormality” - tumours are commonly associated with areas of dysplasia of various
grades elsewhere in the urinary tract. Often present initially as low grade superficial
tumours with patient presenting subsequently with additional lesions which are
progressively of higher grade and a more advanced stage
 Carcinoma in situ presents with frequency & dysuria & often misdiagnosed as prostatitis.
Can be picked up by cytology. Infiltrate rapidly if untreated
Histopathology Histological subtypes
 Transitional cell carcinoma (>90%)
- Carcinoma in situ – 10%
- Non-muscle invasive – 70%
- Muscle-invasive – 20%
 Squamous cell carcinoma (schistosomiasis) – 1-7%
 Adenocarcinoma (fistula) – 2%
 Others e.g. sarcomas – 1%

Morphology of TCC
 70% papillary
- Usually G1 or G2
- Usually superficial – confined to the mucosa (Ta)/ submucosa (lamina propria (T1))
- T1G3 more aggressive, 40% subsequently upstaged to muscle invasive
 10% mixed papillary and solid
 10% solid
- Usually G3, and half are muscle invasive at presentation
 10% CIS
- Does not invade through the basement membrane into the lamina propria
- 40-83% of CIS will progress to muscle-invasive TCC if untreated
- CIS is therefore most aggressive form of superficial TCC
Spread
 Adjacent structures – peri-vesical fat, prostate, rectum, vagina, pelvic side wall
 Lymphatics – pelvic nodes, para-aortic nodes
 Vascular – lung, liver, bone, brain

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Symptoms  Painless macroscopic haematuria (20%) +/-
- Long string blood clots (upper tract)
- Loin pain/Ureteric colic (obstruction by blood clot)
- Acute urine retention (rapid bleeding with clot causing obstruction)
 Frequency, urgency, dysuria (25% - think CIS)
 Obstruction by tumour
- Uraemia (bilateral obstruction)
- Recurrent UTI
- LL oedema (iliac vessels compression)
 Spread of tumour
- Incontinence (tumour invading bladder neck)
- Constant pain in the pelvis (extravesical spread)
- Referred suprapubic, groin, perineum, anal, thigh pain (late)
Signs  Palpable suprapubic mass
 DRE/bimanual examination – large tumours, fixation of pelvic structures
DDx  Cystitis, UTI
 Nephrolithiasis
 RCC
 Trauma
Ix Blood &  Urine FEME – haematuria, raised WCC, nitrites (UTI)
urine  Urine C+S – UTI
 Urine cytology – high pick-up rate for CIS, invasive ca
 FBC – Hb (anaemia), WCC (Infection), Plt (bleeding disorder)
 RP – Urea, Cr (obstructive uropathy), baseline before CT (contrast), also
baseline before intravesical Rx
 LFT – liver mets, baseline as BCG Rx can cause acute hepatitis
 Coagulation profile – bleeding disorder, warfarin
 Tumour markers – not widely used as non-specific
Imaging  U/S KUB – renal/bladder mass, hydronephrosis in ureteric involvement,
blood clots, stones
 CECT/MRI TAP – extent of tumour, staging
 IVU/CT urogram – filling defect, irregular bladder wall, hydronephrosis
Other  Bimanual examination under anaesthesia
 Cystoscopy + biopsy – examine lining of bladder & urethra & take biopsy
Grading & Grade
Staging

103
T

 Ta - Non-invasive papillary carcinoma

 Tis - Carcinoma in situ: "flat tumour"
 T1 - Invades subepithelial connective tissue/lamina propria
 T2 - Invades muscle
- T2a - superficial muscle (inner half)
- T2b - deep muscle (outer half)
 T3 - Invades perivesical tissue
- T3a - Microscopically
- T3b - Macroscopically (extravesical mass)
 T4 - Invades any of the following: prostate, uterus, vagina, pelvic wall,
abdominal wall
- T4a - Tumour invades prostate, uterus or vagina
- T4b - Tumour invades pelvic wall or abdominal wall
N  N0 – no regional LN mets
 N1 – 1 RLN ≤2 cm
 N2 – 1 RLN >2 cm but ≤5 cm, or multiple RLN, none >5cm
 N3 – 1 RLN >5 cm
M  M0 – no distant mets
 M1 – distant mets

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 Stage
grouping

Mx Non-muscle  Tis & T1 – Intravesical instillation of BCG (Bacillus Calmette-Guérin)

invasive (Ta, - Induce immune reaction that facilitates the destruction of cancer cells
Tis, T1) - A/E
 Minor reactions common
 Fever occurs in 3% requiring anti-TB drugs
 Granulomatous prostatitis occurs in 0.9%
 BCG SEPSIS: intravascular absorption of a lethal dose, 20%
mortality, treat with steroids & anti-TB medications
 Tis refractory to BCG instillation/diffuse CIS (most become muscle-invasive)
– radical cystectomy/cysto-prostatectomy
 Ta – Transurethral resection of bladder tumour (TURBT) + intravesical
instillation of either BCG vaccine or chemotherapy 2-4 weeks after
- TURBT – diagnostic, staging & therapeutic
 Electrocautery or laser fulguration of the bladder tumour is
sufficient for low-grade, small-volume, papillary tumours
 Bulky, high-grade, or multifocal tumours should undergo a
second procedure to ensure complete resection and accurate
staging 4-6 weeks after the initial TURBT
Muscle  Radical cystoprostatectomy for men
invasive - Removal of the bladder, peritoneal covering, perivesical fat, distal
(T2-4) ureters, prostate, seminal vesicles, vas deferentia, +/- membranous or
entire urethra
- + Bilateral pelvic lymphadenectomy (PLND)
- + urinary diversion
 Anterior pelvic exenteration for women
- Cystectomy, urethrectomy, hysterectomy, salpingo-oophorectomy, and
partial anterior vaginectomy
- + Bilateral pelvic lymphadenectomy (PLND)
- + urinary diversion
 Urinary diversion
- Incontinent – ileal conduit (small segment of ileum taken out with
mesentery to preserve its blood supply, ureters anastomosed to 1 end
and the other end brought out as stoma to abdominal wall)
- Continent – Indiana pouch, orthoptic neobladder
 Neoadjuvant chemotherapy
- Cis-platin based
- Treat micrometastatic disease, pathologic downstaging
- Less evidence to support the use of adjuvant chemotherapy
 Radiation therapy – EBRT
Metastatic  Palliative care
disease  Radiotherapy – primary tumour & bone mets
 Chemotherapy - Methotrexate, vinblastine, doxorubicin (Adriamycin), and
cisplatin (MVAC) is a standard combination regimen

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Treatment  Radical cystectomy
complications - 2-3% peri-operative mortality
- 7-8% 6-month mortality
- Commonest: small bowel obstruction, uretero-enteric stricture
- Impotence (S2-4 parasympathetic nerves removed)

 Urinary diversion (ileal conduit)

- Hyperchloremic metabolic acidosis - If the ileum or colon is used
- Urinary tract infections (UTIs)
- Urinary calculi
- Ureterointestinal stenosis leading to hydronephrosis
- Stomal - peristomal inflammation, hernia, or stenosis
- Vitamin B-12 deficiency - For diversions affecting the terminal ileum
Prognosis  High grade P3 tumours - <30% 5-year survival.
 Grade 1 non-invasive carcinomas (Pa) - >90% 5-year survival. (Not all patients develop
subsequent tumours of a higher grade and stage)

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Benign Prostatic Hyperplasia (BPH)
Clinical  See prostate carcinoma
Anatomy  Transitional zone affected
Epidemiology  Common, affects ½ men >50, 95% men >85
Pathophysiology  Nodular hyperplasia of the cellular elements of the prostate, involving the stromal and
epithelial elements in the periurethral and transitional zones
 Depends on potent androgen dihydrotestosterone (DHT)
 Type II 5-alpha-reductase metabolizes circulating testosterone into DHT, which works
locally
 As the prostate enlarges, the surrounding capsule prevents it from radially expanding,
potentially resulting in urethral compression
 Obstruction also induces bladder dysfunction that contributes to LUTS
 Bladder wall becomes thickened, trabeculated, and irritable when it is forced to
hypertrophy and increase its own contractile force (detrusor overactivity)
 Gradually weaken and lose the ability to empty completely, leading to increased residual
urine volume and, possibly, acute or chronic urinary retention
 Large numbers of alpha-1-adrenergic receptors are located in the smooth muscle of the
stroma and capsule of the prostate, as well as bladder neck. Blockade of these can
reversibly relax these muscles, with subsequent relief of LUTS
Complications  Urinary retention (acute/chronic)
 Recurrent UTI
 Overflow incontinence (in chronic retention)
 Bladder diverticula & calculi
 Hydronephrosis & renal impairment
Symptoms  Hesitancy – difficulty initiating, straining
 Poor flow
 Terminal dribbling
 Sense of incomplete bladder emptying
 Double micturition
 Frequency
 Nocturia
 Urgency
 Dysuria (UTI)
 Urinary retention (inability to pass urine)
 Overflow incontinence

International Prostate Symptom Score (I-PSS)

1. Straining to begin micturition
2. Poor stream
3. Intermittent flow
4. Incomplete bladder emptying
5. Frequency
6. Nocturia
7. Urgency
- Each symptom graded 1-5
- 0-7 = mild; 8-19 = moderate; 20-35 = severe
Signs  DRE – smooth enlarged prostate with preservation of median sulcus, freely mobile rectal
mucosa
 Palpable bladder (AUR)

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DDx  Prostatic carcinoma
 Bladder neck obstruction – tumour, calculi
 Urethral stricture (double stream)
Ix Blood &  RP – impaired renal function d/t obstructive uropathy
urine  UFEME – haematuria, WCC, nitrites
 Urine C+S
- UTI may result from obstruction
- May ppte AUR
- Needs to be Rx re-op to reduce infection & secondary haemorrhage
 Serum PSA – >35 indicates prostate ca
Imaging  Ultrasound KUB
- Hydronephrosis
- Bladder size
- Measure urinary flow rate & volume of residual urine (if insignificant
think of overactive bladder)
 TRUS + biopsy
- Assess prostate size
- TRO prostate ca
Other  Urodynamic studies
 Cystoscopy – TRO malignancy at bladder neck, foreign body, urethral
stricture
Mx Conservative  Watchful waiting for mild/moderate symptoms on IPSS & uncomplicated
 Catheterization
- Indications
 Chronic urinary retention
 Large volume of residual urine (>750ml)
 Abnormal renal function
 Upper tract dilatation on renal U/S
- Aim
 Allow detrusor tone to recover (few days)
 Allow self-correction of reversible renal failure (3 weeks)
- Anticipate massive diuresis & Rx appropriately – fluids & electrolytes
 Long term catheterization (suprapubic/urethral) or stenting (prone to
displacement, haemorrhage, local irritation, blockage) via cystoscopy if
unsuitable for surgery
Medical  5-α-reductase inhibitor e.g. finasteride, dutasteride
- Prevent conversion of testosterone to dihydrotestosterone
- S/E: decreased libido, erectile dysfunction, ejaculation disorder
 α-blocker e.g. tamsulosin, afluzosin, prazosin
- Relaxation of smooth muscles
- S/E: orthostatic hypotension, dizziness, fatigue, ejaculatory disorder,
nasal congestion, Intra-operative floppy iris syndrome (IFIS) – ask
patient for any planned cataract surgery before starting
Surgical  Transurethral resection of the prostate (TURP)
- Indications
 AUR
 Failed voiding trials
 Recurrent gross haematuria
 Urinary tract infection
 Renal insufficiency secondary to obstruction
 Failure of medical therapy
 Desire to terminate medical therapy
 Financial constraints associated with medical therapy
- Significant risk of morbidity (18%) and mortality risk (0.23%)
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 - Regional/general anaesthesia
- Remove bulk of prostate but leave the least compressed normal
peripheral tissue – protect subcapsular venous plexus that may bleed
profusely
- Chips/strips of tissue excised with resectoscope using a cutting
diathermy wire loop
- Care taken to preserve the sphincter mechanism immediately distal to
veru montanum
- Prostatic chips examined histologically TRO carcinoma
- Sterile glycine solution used to irrigate the blood & debris to allow
visibility
- TUR syndrome – large volume of glycine solution absorbed & result in
dilutional HypoNa & hyperammonaemia with drastic plasma electrolyte
changes
- If obstruction caused by bladder neck hypertrophy – bladder neck
incision done using a diathermy point via the resectoscope
 Other modalities (less bleeding but TURP remain the most successful)
- Holmium laser enucleation of prostate (HOLeP)
- Laser ablation
 Open (retropubic) prostatectomy
- Very large prostates (>75 g)
- Concomitant bladder stones or bladder diverticula
- Patients who cannot be positioned for transurethral surgery
Complications  Early
of TURP & open - Haematuria – minor bleed expected. Secondary haemorrhage d/t
prostatectomy infection/unsuspected cancer may be profuse  clot retention
- Temporary incontinence
 Late
- Retrograde ejaculation
- Erectile dysfunction
- Urethral strictures

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Prostate Carcinoma
Clinical
Anatomy

 The prostate lies below the bladder and encompasses the urethra
 Surrounded by a capsule, external to this is rich venous plexus – direct connection with the
vertebral extradural plexus (bone mets more common)
 Separated posteriorly from the rectum by fascia of Denonvillers (spread to rectum less
common)
 3cm long, 3 cm diameter, 10-15g
 Blood supply – inferior vesical artery from internal iliac artery
 3 Zones – central, peripheral (carcinoma), transitional (BPH)
 5 Lobes – anterior, median (BPH), posterior, 2 lateral
 Median groove – dividing the 2 lateral lobes, exaggerated in BPH, obliterated in advanced
prostatic Ca

Epidemiology  Common >65, 90% men >90 have microscopic prostate ca

 Many patients >70 die with prostate ca rather than from it
Risk Factors  Age
 FH
 High meat & fat consumption
Pathophysiology  Arises in the peripheral prostatic gland, causes obstruction late
 Almost all are ADC except ca of prostatic duct (urothelial origin)
 Most are well-differentiated & contained within capsule, slowly invading, sometimes
involves bladder neck/sphincter
 Spread
- Direct – seminal vesicle, rectum, bladder
- Lymphatics – pelvic LN: obturator, iliac, presacral, para-aortic
- Blood – bone (commonest), lungs, liver
 Most secrete glycoprotein – prostate specific antigen (PSA) >10-15 suggestive of ca, >35
advanced ca
Symptoms  Asymptomatic
 Incidental – detected by doctor, PSA, TURP for BPH
 LUTS – hesitancy, poor stream, terminal dribbling, sense of incomplete bladder emptying,
double micturition, frequency, nocturia
 Spread to adjacent structures
- Rectum – tenesmus, changing bowel habit
- Ureter (obstruction) – renal failure
- Urethral sphincter – incontinence
- Recent incompetence
 Nodal disease
- Local compression – LL swelling
- Impaired lymphatic drainage – penile & genital oedema
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  Metastasis
- Bone – back pain, malaise, anaemia, pathological fracture, spinal cord compression
- Lungs (pulmonary carcinomatous lymphangitis) – SOB, haemoptysis (uncommon)
- Liver – jaundice (uncommon)
 DVT
Signs  DRE
- T1 – normal/ smoothly enlarged by BPH
- T2 – nodular, asymmetrical surface
- T3 – large, hard, irregular gland extending beyond capsule/ into seminal vesicle
- T4 – fixed to bone/bladder/rectum
- Obliteration of median sulcus, rectal mucosa may not be mobile over prostate
 Advanced – pelvic wall, encircle rectum – pelvis ‘frozen’ solid with tumour
 Pedal, penile, genital oedema
 Bone tenderness
 Pleural effusion, reduced air entry
 Jaundice, hepatomegaly
 Palpable bladder, ballotable kidneys
DDx  BPH
 Other ca – bladder, rectal, urethral with local spread
Ix Blood  FBC – anaemia
 RP – renal impairment secondary to obstruction
 LFT – liver mets, ALP for bone mets
 PSA - >10-15 suggestive, >35 advanced
(can also be raised in prostatitis, BPH, recent sex, instrumentation)
 UFEME – haematuria
 Urine C+S – if stasis causes UTI
Imaging  Transrectal ultrasound + biopsy
 X-ray abdomen – osteosclerotic bone mets
 Radionuclide bone scan – clinical suspicion of bone mets/ PSA>20
 CT TAP – mets to lungs, liver, adjacent structures
Other  HPE from resected prostate
TNM Staging T  T1 - Clinically inapparent tumor not palpable or visible by imaging
 T2 - Confined within prostate
 T3 - Extending through the prostatic capsule
3a - Extracapsular extension (unilateral or bilateral)
3b - Tumour invading seminal vesicle(s)
 T4 - Fixed to or invading adjacent structures other than seminal vesicles (eg,
bladder neck, external sphincter, rectum, levator muscles, pelvic wall)
N  N0 - No regional lymph node metastasis
 N1 - Metastasis in regional lymph node(s)
M  M0 - No distant metastasis
 M1 - Distant metastasis
1a - Nonregional lymph node(s)
1b - Bone(s)
1c - Other site(s)
G  G1 – well differentiated (Gleason 2-4)
 G2 – moderately differentiated (Gleason 5-6)
 G3-4 – poorly differentiated (Gleason 7-10)

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 AJCC Stage
Grouping

Gleason Grading  Assesses degree of differentiation, prognostic factor

System  Primary grade – dominant pattern (>50%)
 Secondary grade – next most common pattern (at least 5%)
 Primary + secondary = Gleason score

Mx Early (T1/T2, Options

N0, M0)  Low grade, impalpable, organ-confined  Active monitoring until evidence
of increased disease activity (rising PSA, palpable nodule)
 Radical prostatectomy – potentially curative
- Removal of entire prostate and seminal vesicles with anastomosis of
urethra to bladder
- Approaches – retro-pubic, perineal, laparoscopic
- Indications
 <70
 >10 life expectancy
 Fit for Sx
 Organ-confined disease (T1, T2)
- Advantages
 Cure local disease (88-92%)
 Good long term survival
 Once-off
- Disadvantages
 Major surgery
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  Mortality <1%
 Significant morbidities – bleeding, ED, incontinence
 Radical radiotherapy – potentially curative
- External beam radiotherapy (EBRT) or brachytherapy
- Indications
 Organ-confined disease (T1, T2)
 Patient preference
 Poor candidate for surgery
 Life expectancy <7-10 years
- Advantages
 Cure rate similar to radical prostatectomy
 No surgery
 Painless
 Can be done as outpatient
- Disadvantages
 Many treatments
 Time & cost
 Prostate still left in-situ
 Complications
o Urinary symptoms
o Erectile dysfunction
o Cystitis
o Proctitis
o Urethral stricture
Locally  Adjuvant radiotherapy +/- hormonal therapy
advanced  TURP may relieve urinary symptoms but risk permanent incontinence if
(T3/T4, N0, tumour has invaded sphincter mechanism
M0)
Metastatic  Hormonal therapy
(N1, M1) - LHRH antagonist e.g. goserelin
 4-12 weekly injection
 Initial stimulation of LH for 2/52 followed by competitive
inhibition of LHR  anorchic state
 S/E – hot flushes, sexual dysfunction
 Usually ‘flare’ of symptoms in 1st 2/52  cover with anti-
androgen
- Anti-androgen e.g. cyproterone acetate, flutamide
 Block the binding of DHT to receptor at cellular level – block
both testicular & adrenal testosterone
 Flutamide may preserve potential for sexual arousal for longer
- Bilateral subcapsular orchidectomy
 Remove testes, capsules filled with blood clot to preserve shape
 Removes 95% testosterone
 Prostate ca eventually escapes androgen dependency & become
refractory to hormonal Rx at about 2y. Rx: diethylstilbestrol (DES) –
synthetic androgen, blocks LHRH secretion, high rate of serious
thromboembolic S/E
 Palliative radiotherapy/IV radioactive strontium for painful bone metastases

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114
Testicular Tumours
Clinical
Anatomy

 Blood supply – testicular artery from abdominal aorta, collaterals from artery to vas
deferens and cremasteric artery
 Venous drainage – pampiniform plexus  testicular vein  IVC on the right, left renal vein
on the left
 Lymphatics
- R testis along IVC  inter-aortocaval region  pre-aortic & PARA-AORTIC lymph
nodes (L1-2), with possible cross-over with retroperitoneum
- L testis  pre-aortic & PARA-AORTIC lymph nodes around left renal hilum  inter-
aortocaval region without cross-over
- Retroperitoneal LN – anterior to T11 to L4 vertebral bodies concentrated at L1-L3
Epidemiology  1-2% of male malignancies
 But most common solid tumour in young males (20-45)
 Highest incidence in Whites, American Indian but low in Black and Asians
 90% are germ cell tumours, 48% are seminomas (SGCT), 42% are non-seminomas (NSGCT)
 Highly curable even when metastatic (seminomas have the best prognosis)
Aetiology/ Risk  Age
Factors - 20-45: GCT
- 20-35: teratoma
- 35-45: seminoma
- >60: 50% lymphoma
 Family history (2%)
 Genetic change in sporadic form – Chr12[i(12p)]
 Undescended testis (5-15x compared with normal)
 Infertility
Pathophysiology  Spread
- Direct – adnexae, scrotum
- LN (seminomas) – common iliac  para-aortic  mediastinal  supraclavicular
- Blood (embryonal) – lungs (teratomas), liver, bones
Symptoms  Painless unilateral testicular swelling/nodule
 Sense of heaviness in the scrotum/lower abdomen
 Scrotal/lower abdominal pain
 Trauma usually brings attention to pre-existing nodule
 Metastatic symptoms (10%)
- Local – anorexia, nausea, GI symptoms
- LN – palpable LN in the abdomen (rare), supraclavicular LN

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 - Lungs – cough, chest pain, haemoptysis, SOB (mediastinal LN or lung parenchyma)
- Bones – neurological symptoms, bone pain rare, back pain from LN infiltration
 Gynaecomastia – HCG from choriocarcinoma
 Hyperthyroidism – HCG ++
Signs  SOLID TESTICULAR LUMP MUST BE ASSUMED TO BE A TUMOUR UPO
 Testicular mass/nodule – hard, irregular, nodular (teratoma)/ smooth (seminoma), non-
tender, non-transilluminable, can get above
 Secondary hydrocele (10%) – involvement of testicular capsule
 Thickening of spermatic cord (infiltration)
 Epididymis may be difficult to palpate (inseparable)
 Para-aortic/supraclavicular lymphadenopathy
 Inguinal lymphadenopathy not present UNLESS scrotal skin involved
 Hepatomegaly
 Reduced A/E, dull percussion, increased vocal resonance (tumour) or pleural effusion
 Bone tenderness
 Ankle oedema (IVC obstruction)
DDx  Epididymo-orchitis
 Syphilitic gumma, TB
 Haematoma
 Hydrocele, spermatocoele
WHO  Germ cell tumours (GCT) – 90%
Classification - Seminoma (SGCT) – 48%
Characteristic: Pale, creamy white, homogenous cut surface (potato tumour), resemble
mature germ cells
- Non-seminoma (NSGCT) – 42%
 Teratoma
Characteristics: Resemble foetal tissue - consists of ectoderm (sq epithelium),
mesoderm (cartilage & smooth muscle), endoderm (respiratory endothelium)
tissues. Variegated with cystic areas, patches of necrosis, haemorrhage.
 Embryonal
Characteristic: Undifferentiated epithelial-like.
 Yolk sac
Characteristic: Resemble yolk sac elements. More common in children.
 Choriocarcinoma
Characteristic: Cytotrophoblasts and syncytiotrophoblasts. Resemble placental
tissues. Very aggressive.
- Mixed
 Sex cord/gonadal-stromal tumours – 3%
- Leydig cell
- Sertoli cell
- Granulosa cell
- Fibroma/thecoma
- Mixed
 Miscellaneous – 7%
- Carcinoid
- Ovarian epithelial type
- Tumours of collecting ducts & rete – adenoma, carcinoma
- Tumours of paratesticular structures – ADC, mesothelioma
- Lymphoma, leukaemia
- Metastatic
Ix Blood  FBC
 Serum LDH – non-specific, 10-20% seminomas, assess tumour bulk
 Serum alpha-fetoprotein (AFP)
- Non-seminomas – yolk sac tumour, teratomas
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 - Also positive in liver, pancreas, lung tumours
 Serum beta-HCG (B-HCG)
- Syncytiotrophoblastic component
- All choriocarcinoma, 40-60% embryonal, 5-10% seminomas
Imaging  Trans-scrotal U/S
- Cystic vs solid
- Hypoechoic, homogenous (SGCT) vs hyperechoic, heterogenous (NSGCT)
 CXR – staging
 CT (T)AP – staging
Histology  Biopsy NOT recommended
 Surgical exploration via inguinal approach (not cutting through scrotal skin –
seeding)
- Spermatic cord clamped to prevent venous spread
- Testis brought out for inspection & palpation
- If doubt, testicular biopsy sent for frozen section
- Obviously malignant – radical inguinal orchidectomy +/- retroperitoneal
LN dissection (RPLND)
- RPLND is the only reliable method to identify nodal micrometastases
and provide accurate pathologic staging of the retroperitoneal disease
TNM Staging T  pT0 – No evidence of primary tumor (eg. histologic scar in testis)
 pTis – Intratubular germ cell neoplasia (carcinoma in situ)
 pT1 – Limited to the testis & epididymis without vascular/lymphatic
invasion, or tumour invasion into the tunica albuginea but not the tunical
vaginalis
 pT2 – Limited to the testis & epididymis + vascular/lymphatic invasion, or
tumour extending through the tunica albuginea + involvement of the tunica
vaginalis
 pT3 – Invades the spermatic cord +/- vascular/lymphatic invasion
 pT4 – Invades the scrotum +/- vascular/lymphatic invasion
N  N0 – No regional lymph node metastasis
 N1 – 1 RLN ≤2cm in greatest dimension; or multiple RLN, none >2 cm
 N2 – 1 RLN >2cm but ≤5cm; or multiple RLN lymph nodes, any one >2cm but
≤5cm
 N3 – 1 RLN >5cm
M  M0 – No distant metastasis
 M1 – Distant metastasis
 M1a – Non-regional LN or pulmonary
 M1b – Other metastasis
S

117
AJCC Stage
grouping

 Stage I – confined to testis

 Stage II – retroperitoneal LN involvement
 Stage III – above diaphragm confined to LN
 Stage IV – extralymphatic mets
Mx Principle  After obtaining tumour marker levels suspicious of malignant tumours 
radical inguinal orchidectomy with high ligation of spermatic cord
(diagnostic & therapeutic)  complete staging  further mx
 Discuss sperm baking with patient before any procedure that may cause
infertility – Sx, RT, chemo
 Long term surveillance with tumour markers & CT, recurrent disease often
successfully Rx with chemo, radio or Sx
Seminoma  Stage I – no further Rx after Sx
 Stage IIa, IIb – radical radiotherapy to ipsilateral para-aortic & iliac LN
 Stage IIb – chemotherapy is alternative to radiotherapy using EP (etoposide,
cis-platin) or PEB (cisplatin, etoposide, bleomycin)
NSGCT  25% with stage I will relapse without further Rx, radiotherapy has NO role
 Stage I
- Immediate chemotherapy
- Retroperitoneal lymph node dissection (RPLND)
 Include precaval, retrocaval, paracaval, interaortocaval,
retroaortic, preaortic, para-aortic, common iliac LN
 Disadvantage – damage sympathetic nerve fibres causing
ejaculatory failure
- Surveillance & Rx if metastasis occur
 Metastatic – chemotherapy with BEP has 85% cure rate

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