Surgical Notes PDF

October 8, 2022 | Author: Anonymous | Category: N/A
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Surgery Notes  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 Gastr o-oesophageal Reflux Disease (GORD)  (GORD)  Definitions

  Montreal classification: A condition that develops when the reflux of stomach contents



       

 

 

evidence of oesophageal inflammation

Classification

Clinical Anatomy Risk Factors

  Lower oesophageal sphincter (LES) - zone of high pressure that prevents gastric reflux   Anatomical constriction of oesophagus – oesophagus – cricopharyngeal  cricopharyngeal (15cm), aortic & bronchial (25cm),





         









Pathophysiology



   

 

Symptoms

causes troublesome symptoms and/or complications ≥ 2 heartburn per week, adversely affects individual’s wellbeing  wellbeing  Physiologic reflux - postprandial, short-lived, asymptomatic, rarely during sleep Pathological reflux – reflux – a/w  a/w symptoms or mucosal injury, often including nocturnal episodes Reflux esophagitis = patients with GERD symptoms + endoscopic or histopathologic

diaphragmatic (40cm) Obesity Alcohol Smoking Spicy & fatty food LES dysfunction – dysfunction – initially  initially increased number of transient LES relaxations  decreased LES resting tone  loss of sphincter function Hiatus hernia – hernia – LES  LES not in the abdomen, do not function properly Delayed gastric emptying



Heartburn – Heartburn  – burning  burning sensation in the retrosternal area, worse after meal, on lying flat and   bending forward   Regurgitation Regurgitation –  – perception  perception of flow of refluxed gastric contents (acid/bitter) into i nto mouth or



hypopharynx   Dysphagia Dysphagia –  – d/t  d/t reflux oesophagitis or stricture Odynophagia –  – ulcer  ulcer   Odynophagia   Water brash (hypersalivation)   Globus sensation (constant perception of lump in the throat)   Nausea Extraoesphageal   Chest pain Cough/wheeze –  – aspiration  aspiration   Cough/wheeze   Hoarseness Hoarseness –  – irritation  irritation of vocal cord pain – otitis  otitis media   Ear pain –   Tooth decay

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DDx

           

Infectious oesophagitis Motility disorder e.g. achalasia Oesophageal carcinoma Peptic ulcer disease Coronary artery disease OGDS + biopsy (mandatory) – (mandatory) – Look  Look for oesophagitis, Barrett’s Barrett’s oesophagus, carcinoma, strictures, hiatal hernia (mandatory) – determine  determine LES function, persistent symptoms   Oesophageal manometry (mandatory) – despite medical Rx, investigation of atypical symptoms e.g. chest pain & asthma   Ambulatory 24H oesophageal pH monitoring – monitoring – extent  extent & severity of reflux











Ix







contrast barium swallow – swallow – visualise  visualise mucosal changes, ulcers, delayed gastric   Double emptying



       

ECG, cardiac biomarkers – biomarkers – TRO  TRO MI if chest pain CXR – CXR  – if  if pulmonary symptoms, may have pulmonary fibrosis Grade I – I –  ≥1 ≥1 non-confluent  non-confluent reddish spots +/- exudate Grade II – II – erosive  erosive and exudative lesions in the distal oesophagus that may be confluent, but not circumferential III – circumferential  circumferential erosions in the distal oesophagus, covered by haemorrhagic and   Grade III – pseudomembranous exudate   Grade IV – IV – presence  presence of chronic complications: deep ulcers, stenosis, scarring with Barrett's metaplasia 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 (PPI) – omeprazole  omeprazole 20mg od, pantoprazole   Proton-pump inhibitors (PPI) –   H2 receptor antagonist – antagonist – ranitidine,  ranitidine, cimetidine   Antacids Antacids –  – aluminium  aluminium hydroxide, magnesium hydroxide   Prokinetics Prokinetics –  – metoclopramide,  metoclopramide, domperidone Surgical   Balloon dilatation of stricutures   Laparoscopic Nissen fundoplication -  Indications   Inadequate control by medical therapy 



Savary-Miller Classification of endoscopic appearance on OGDS









Mx





























Poor compliance Patient’s wish (not to take long term medication)  medication)  oesophagus    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,  bleeding, infection, injury to adjacent structures   General common – temporary  temporary dysphagia, gas-bloat   Specific and common – syndrome, increased flatus rare  – slipped  slipped wrap: down onto stomach or up into   Specific but rare – chest – chest  – acute  acute onset chest/upper abdominal pain, dysphagia    





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Complications

       









Reflux oesophagitis Barett’s oesophagus  oesophagus  Oesophageal adeocarcinoma Oesophageal stricture

Oesophageal Carcinoma  Carcinoma  Clinical Anatomy

Epidemiology

th   6  commonest cancer in the world   Mid-late adulthood   Poor prognosis







Types

Squamous cell carcinoma (SCC)   Common   Upper 2/3   RF: Tobacco, alcohol, dietary (hot fluid, nitrosamines), betel nut chewing, predisposing condition (achalasia, oesophageal diverticula & webs, PlummerVinson syndrome, HPV)   Pathophysiology: Exposure of the oesophageal mucosa to noxious or toxic 





Adenocarcinoma   Rising trend   Lower 1/3   RF: Obesity, GERD, Barett’s, smoking  smoking    Pathophysiology: GERD  Barrett’s oesophagus  intestinal metaplasia   dysplasia  CIS  carcinoma 









Spread

   

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Symptoms



 



stimuli  dysplasia  carcinoma in situ   carcinoma Direct – Direct  – aorta,  aorta, tracheobronchial tree Lymphatic – Lymphatic  – early  early local LN invasion (situated in lamina propria), mediastinal LN, coeliac & perihepatic LN (the latter 2 more in ADC) Haematogenous – Haematogenous  – liver,  liver, lung, bone, brain Local effects: -  Dyspepsia -  Progressive dysphagia – dysphagia – solid  solid to liquid -  Odynophagia -  Cough, regurgitation, vomiting -  UGIB Adjacent structures: -  Lungs (fistula) – (fistula) – pneumonia  pneumonia -  RLN RLN –  – hoarseness  hoarseness -  Aorta Aorta –  – massive  massive haemorrhage 4

 

  Distant metastasis: -  Liver Liver –  – jaundice  jaundice -  Lungs Lungs –  – SOB  SOB -  Brain Brain –  – altered  altered behaviour, focal neurological signs -  Bone Bone –  – back  back pain   General -  LOA -  LOW   Normal except spread to LN/ distant mets LN –  supraclavicular (Virchow’s)  (Virchow’s)    LN –   Hepatomegaly   Lung crepitations/ pleural effusion disorders – achalasia  achalasia   Oesophageal motility disorders –   Oesophageal strictures   Bronchogenic carcinoma (compression on oesophagus)   Blood -  FBC FBC –  – Hb  Hb -  LFT LFT –  – liver  liver mets   Imaging -  OGDS + biopsy -  EUS EUS –  – depth  depth of tumour penetration (T) and enlarged local lymph nodes (N) – (N)  – patients  patients





Signs

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DDx

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Ix





-  - 

without distant mets and planned for surgery CT TA – TA – distant  distant mets to lungs, liver PET – PET  – occult  occult LN & bone mets

-  -  -  - 

Laparoscopy – staging Laparoscopy –  staging regional LN Thoracoscopy – Thoracoscopy  – staging  staging regional LN Bronchoscopy – Bronchoscopy  – invasion  invasion of trachea & bronchi Barium swallow (rarely) – (rarely) – studying  studying the distal anatomy in obstructive tumors that are inaccessible by endoscopy   Assess fitness for surgery -  FBC, RP, LFT, coagulation profile -  Cardiovascular risk assessment – assessment – FPG,  FPG, FPL, ECG, ECHO, cardiopulmonary exercise testing -  Fitness for thoracotomy – thoracotomy – spirometry,  spirometry, ABG



TNM staging (AJCC)

Mx

Principles

  Potentially curative vs palliative



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



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



surgery (trimodality therapy)

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  Stage IV – IV – Chemotherapy,  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) 

 



     

 

Surgical



 



Invasion of adjacent structures (RLN, tracheobronchial tree, aorta, pericardium) Severe comorbid (cardiovascular disease, respiratory disease) Impaired cardiac or respiratory function 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



 



   



Chemoradiotherapy



 



Palliative (mainly to relieve dysphagia)

LN, anastomose gastric conduit to proximal oesophagus remnant (Rouxen-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 Mainly neoadjuvant -  Reduce tumour bulk, increase curative resection rate, eliminate/delay elim inate/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 Chemotherapy Radiotherapy

      Argon plasma tissue coagulation   Laser therapy Stenting –  – food  food has to be liquefied, take fizzy drinks after food to cleanse   Stenting











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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

Prevention

       









(lower)tocan cause severe sepsis & death -  Injury RLN RLN –  – hoarseness  hoarseness Late -  Anastomotic stricture -  Dysphagia, early satiety, reflux (antacid) Smoking cessation Reduce alcohol intake High fibre & vitamin diet Treatment of GERD/Barrett’s oesophagus  oesophagus  -  GERD GERD –  – fundoplication  fundoplication -  Barrett’s – endoscopic – endoscopic ablation using radiofrequency ablation, photodynamic therapy or cryotherapy

Peptic Ulcer Disease (PUD)  (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

                   

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Aetiology/ Risk Factors















Pathophysiology



 



 



   

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Very common in developed countries – countries  – 10%  10% Incidence of duodenal ulcer decreased, gastric ulcer constant H. pylori infection NSAIDs Smoking Alcohol Stress/anxiety Spicy/fatty food Gastrinoma: Zollinger-Ellison syndrome (rare) 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 – (Gram –ve 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) -  -  -  -  - 

Clinical features

First part of duodenum Gastric antrum along the lesser curve Lower end of oesophagus Meckel’s diverticulum with ectopic ectopic gastric mucosa Jejunal site of gastrojejunal anastomosis Duodenal ulcer (more common) Epigastric pain – pain –     Pain before meal & middle of gnawing, burning night, relieved by food & milk   Pain radiating to the back suggests posterior penetrating ulcer causing pancreatitis Other GI   Dyspepsia symptoms   Heartburn, chest discomfort less common 

Gastric ulcer   Pain aggravated by eating 



  Dyspepsia   Heartburn, chest discomfort









  Malaena>haemaemesis



common

  Haematemesis >malaena



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  Bloating, nausea, vomiting



       

LOW Complications



  

Well-built Anterior ulcer – ulcer – perforation  perforation Posterior ulcer – ulcer – bleeding  bleeding Usually not a/w malignancy

         











several hours after meal suggest GOO Ill-built Gastric outlet obstruction Perforation Bleeding Gastric carcinoma

Classification

DDx

               

Functional dyspepsia Crohn’s disease  disease  Zollinger-Ellison syndrome GERD Cholecystitis/ascending cholangitis Oesophagitis/oesophageal rupture ACS Laboratory -  H. pylori test biopsy – rapid  rapid urease test (CLOtest), histopathology & culture   Endoscopic biopsy –   Stool antigen test   Serology (IgG)   Urea breath test -  FBC FBC –  – anaemia  anaemia -  Iron studies -  LFT amylase – TRO  – TRO hepatobiliary & pancreatic causes -  Serum gastrin – gastrin – if  if suspect Zollinger-Ellison syndrome   Imaging -  OGDS + biopsy – biopsy – direct  direct visualisation, detect H. pylori, malignancy (benign) – well-defined,  well-defined, punched out, smooth base with whitish   Gastric ulcer (benign) –















Ix





fibrinoid exudate, surrounding mucosa shows radiating folds Duodenal ulcer - well-demarcated break in the mucosa that may extend into the muscularis propria -  Erect CXR – CXR – air  air under diaphragm when perforation suspected -  Barium meal – meal – GOO,  GOO, perforation (largely replaced by OGDS) -  Angiography Angiography –  – massive  massive UGIB in which OGDS cannot be performed Conservative   Avoid aggravating food   Reduce alcohol intake Medical (2/52) – standard  standard   Triple therapy (2/52) – -  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  

Mx









-  -  - 

PPI, standard dose, or ranitidine 150 mg, PO bid Bismuth 525 mg PO qid Metronidazole 500 mg PO qid 9

 

 



     





Surgical



-  Tetracycline 500 mg PO qid Maintenance therapy with PPI/H2-receptor antagonists in patients with wi th recurrent, refractory, or complicated ulcers Discontinue NSAIDs, change to selective COX-2 inhibitor or cover with PPI Other: cytoprotective – cytoprotective – misoprotol,  misoprotol, sucralfate See perforated ulcer

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Upper GI Bleed  Bleed  Definition Clinical Anatomy

  Bleeding in the GIT proximal to ligament of Treitz Variceal   Splenic vein + SMA  portal vein  L & R





Non-variceal   Blood supply of oesophagus -  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) a nd 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 D 1. CHA continues as hepatic artery proper

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-  - 



Right gastric artery (RGA) is a branch o f 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 offthe theRGEA LGEA which runs along the greater curvature and joins

  Blood supply of the duodenum





Epidemiology

  6.4% UGIB in Malaysia   Cirrhosis -  Present in 60% decompensated & 30% compensated cirrhosis at

 

-  - 

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   Bleeding PUD commonest cause   80% stop spontaneously, 20% may have persistent/recurrent bleed   10% mortality

time of diagnosis 30% will bleed Major cause of death – death  – 30-50%  30-50% within 6/52 (1 st bleed)

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Aetiology

  Risk factors for oesophageal varices bleed -  Severity of liver dysfunction -  Size (large) of varices -  Presence of endoscopic wale signs -  HPVG >12mmHg -  Previous bleed (70% recurrent haemorrhage)



  Cirrhosis from -  Alcoholic liver disease -  Chronic hepatitis B, C

Risk factors



Pathophysiology



  Normal hepatic venous pressure gradient (HPVG) 10mmHg

 risk of developing varices Portal HPT  portosystemic collaterals inc gastro-oesophageal varices     Majority bleeding are from oesophageal varices, 20-30% from gastric varices, but mortality is higher with the latter

Classification

Japanese classification of oesophageal varices 1 – small  small straight varices not disappearing with insufflations   Grade 1 – 2 – medium  medium varices occupying 1/3 lumen   Grade 2 – 3 – large  large varices occupying >1/3 lumen   Grage 3 –

  Commonest: PUD (64% of all UGIB) , acute erosive gastritis  - NSAIDs,



steroids, alcohol (16.5%), oesophagitis, oesophageal ca, gastric ca (malignancy 3.6%) Oesophagus –  – GERD,  GERD, oesophagitis, oesophageal ulcer, oesophageal   Oesophagus ca, Mallory-Weiss tear Stomach –  – gastric  gastric ulcer, erosive gastritis, haemorrhagic gastritis,   Stomach gastric polyp, gastric ca, gastric lymphoma, leiomyoma, hereditary haemorrhagic telangiectasia, angiodysplasia, Dieulafoy lesion (large tortuous arteriole in submucosa) Duodenum –  – duodenal  duodenal ulcer, duodenal erosion, duodenal polyps,   Duodenum ampullary Ca, Ca pancreas, haemobilia, AVM, aorto-duodenal fistula bowel – stomal  stomal ulcer, diverticulum (inc Meckel’s), M eckel’s), tumour,   Small bowel – AVM   H. pylori   NSAIDs   Aspirin PUD –  – amount  amount of bleeding depends on size of vessel. Posterior    PUD duodenal ulcer can erode the gastroduodenal artery causing massive bleeding oesophagitis – erosion  erosion of BV   Gastritis, oesophagitis – syndrome – acute  acute GOJ tear - severe vomiting/retching   Mallory-Weiss syndrome – Boerrhaave’s ’s syndrome – full – full thickness tear   Boerrhaave carcinoma  – ulcerative  ulcerative stage   Oesophageal/ gastric carcinoma – Forest Classification for Bleeding Peptic Ulcer

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I – continuation  continuation of oesophageal varices, extend 2-5cm along lesser   GOV I –



curvature

II – extend  extend towards fundus of stomach   GOV II – I – fundus  fundus of stomach   IGV I – II – ectopic,  ectopic, anywhere   IGV II –

Major – Major  – Ia,  Ia, b, IIa, b





Rockall Score for Prognosis



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8 = bad prognosis (41% re-bleeding risk, 41% mortality) Clinical features

             



Haematemesis – Haematemesis  – fresh  fresh coffee ground (gastric breaks down Hb into ha ematin) Malaena Malaena –  – black,  black, tarry,blood sticky,orloose, malodorous stool acid (degradation of blood in intestine) Rarely haematochezia – haematochezia – life-threatening  life-threatening massive bleeding  Iron deficiency anaemia (chronic) – (chronic)  – SOB,  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) -  Coagulation profile   Blood -  ABG -  FBC FBC –  – Hb  Hb (anaemia), HCT, WCC, Plt -  GXM -  RP – RP – Urea  Urea (blood meal, dehydration), Cr, electrolyte inbalance -  LFT LFT –  – albumin  albumin (liver function), bilirubin, AST, ALT (liver disease),   Imaging -  OGDS (urgent) GGT (alcohol), ALP PUD Bleed Oesophageal Varices 

Ix

Mx

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

15

 

  C: 2 large bore IV brannula/ central veno us access, bloods, GXM,



cautious transfusion of packed RBC to keep Hb around 8g/dL/ HCT 24% (Overtransfusion can increase portal pressure & exacerbate bleeding), correct coagulopathy   Monitor vital signs closely, monitor for continuous bleeding

2. Pharmacological Rx   Start IV vasoactive drug as early as possible to reduce blood flow & pressure within varices -  Terlipressin (synthetic vasopressin analogue): 2mg bolus and 1mg every 6 hours x 2-5/7 -  Somatostatin: 250mcg bolus, then 250mcg/hour infusion x 5/7 -  Octreotide (somatostatin analogue): 50mcg bolus, then 50mcg/hour x 5/7 prophylaxis – reduce  reduce rate of infection, SBP, re-bleeding.   Antibiotic prophylaxis – -  IV 3rd gen cephalosporin (ceftriaxone 1g daily) o r x 1/52 -  PO fluoroquinolones (norfloxacin 400mg bd, ciprofloxacin 500mg bd) x 1/52 3. Surgical Rx   OGDS a.s.a.p. If unavailable  consider balloon tamponade & send to tertiary centre bleeding – endoscopic  endoscopic variceal ligation (EVL) recommended,   Control of bleeding – use endoscopic sclerotherapy if EVL difficult -  EVL EVL –  – more  more effective, fewer complications, more difficult to perform -  Sclerotherapy Sclerotherapy –  – easier  easier to perform, more complications (ulceration, stricture) bleeding – repeat  repeat OGDS, TIPS, Sx, consider ba lloon   Persistent bleeding – tamponade -  TIPS TIPS –  – effective  effective but high morbidity & mortality -  Sx Sx –  – oesophageal  oesophageal transection +/- devascularisation, portosystemic shunts, liver transplantation. High mortality -  Balloon tamponade – tamponade – effective  effective but high re-bleeding rate, complications e.g. ulceration, perforation, aspiration pneumonia. Only as temporary bridge for max 24 H

  C: 2 large bore IV brannula/ ce ntral venous access, bloods, GXM, IV



crystalloids (Hartmann’s or normal saline)  saline)   -  Indications of blood transfusion:   SBP 110 bpm   Postural hypotension Hb 4 mm), pericholecystic fluid, subserosal edema, intramural gas, and sloughed mucosa), complications e.g. gangrene, gas formation, perforation, TRO other pathology Supportive NBM –  – bowel  bowel rest, prep for cholecystectomy c holecystectomy   NBM

                

















Ix





















Mx



  IV fluid, correct electrolyte abnormalities Analgesia –  – tramadol,  tramadol, mepiridine   Analgesia





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  IV antibiotics – antibiotics – cefuroxime/gentamicin  cefuroxime/gentamicin (Gram – (Gram –ve), ve), metronidazole



   





Surgical

   





(anaerobe) Anti-emetic (metochlopromide)/ NG tube for vomiting Plan for immediate/delayed laparoscopic cholecystectomy (4-6 weeks for inflammation to subside) Laparoscopic cholecystectomy is the standard Timing -  Emergency Emergency –  – complicated  complicated cases e.g. gangrene, perforation -  Immediate Immediate –  – within  within 72H admission -  Delayed Delayed –  – 4-6  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 – perforation – abscess,  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 Infection –  – including  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) – infected)  – drain  drain should be left in situ for 5 days -  Bowel injury





Postcholecystectomy syndrome – syndrome – persistent/recurring  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)  



-

Symptoms

Luminal: Trauma (Sx), scarring (chronic pancreatitis), strictures (PSC), AIDS-related A IDS-related cholangiopathy/cholangitis -  Extra-luminal: tumours, cyst, choledochocoele, pancreatic pseudocyst   Obstructive jaundice – jaundice – jaundice,  jaundice, dark urine, pale stool   RUQ pain – pain – intermittent  intermittent   Nausea, vomiting   Symptoms of acute pancreatitis   Jaundice   RUQ tenderness   Ascending cholangitis (Gram – (Gram –ve ve & anaerobes)   Gallstone pancreatitis   Periampullary carcinoma   HCC/liver mets   Other ddx as for acute cholecystitis Blood &   As for acute cholecystitis urine Imaging hepatobiliary – dilated  dilated CBD (>8mm), acoustic shadow   U/S hepatobiliary –   MRCP MRCP –  – confirm  confirm stone (may have passed), TRO other pathology e.g. tumour ERCP –  – diagnostic  diagnostic & therapeutic   ERCP Supportive   NBM   IV fluids   Analgesics   Antibiotics   Anti-emetic   Prepare for ERCP & cholecystectomy Surgical   ERCP (endoscopic retrograde cholangiopancreatography) & sphincterotomy -  Indications 







Signs





Complications





DDx







Ix









Mx















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

  Contrast allergy o  Oxygen desaturation o  Cardiopulmonary complications

o

 

Specific (Early) Bleeding o  pancreatitis    Post-ERCP Infection - Ascending cholangitis o  Perforation – Perforation  – by  by passage of endoscope

o

o

 

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 c atheter -  Latex T tube inserted to drain bile to the exterior with transverse limb in the CBD – CBD – provide  provide assess to biliary tree for a further cholangiogram (Ttube 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 Tumour –  – periampullary  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%)  (27%) -  Klebsiella (16%) -  Enterococcus (15%) -  Streptococcus (8%) -  Enterobacter  (7%)  (7%) -  Pseudomonas aeruginosa (7%)   Complications -  Liver failure -  Liver abscess





Symptoms

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









Signs

















DDx





















Ix

























MRCP – choledocholithiasis,  choledocholithiasis, tumour, stricture   MRCP –   ERCP – diagnostic  – diagnostic & therapeutic – therapeutic – stone  stone removal, stenting, bile sampling

 

31

 

  CT (spiral/helical/cholangiogram) – (spiral/helical/cholangiogram) – dilated  dilated intrahepatic & extrahepatic



 



Mx

Supportive

       





 

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]) – [HIDA]) –   functional scan – scan – non-visualization  non-visualization of biliary tree May need ICU admission ABC Close monitoring of vital signs, watch out for shock NBM – NBM  – bowel  bowel rest, prep for cholecystectomy c holecystectomy

  IV fluid, correct electrolyte abnormalities Analgesia –  – tramadol,  tramadol, mepiridine   Analgesia   IV antibiotics antibiotics –  – cefuroxime/gentamicin  cefuroxime/gentamicin (Gram – (Gram –ve), ve), metronidazole



 

(anaerobe)   Anti-emetic (metochlopromide)/ NG tube for vomiting   Urgent ERCP with biliary drainage/percutaneous drainage   Laparoscopic cholecystectomy after resolution of cholangitis



Surgical

 

Pancreatic & Hepatobilliary Tumours PANCREATIC CARCINOMA Types of pancreatic Ca

Pathology

-  90% adenocarcinoma of exocrine ductal cell -  2% exocrine acinar (secretory) cells -  8% endocrine islet cells – cells – secretes  secretes insulin, glucagon, gastrin (remember 90% insulinoma benign) -  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 -  5y cirrhosis develops HCC -  Age: 40-60 in developed countries, 20-40 in developing countries -  Chronic hepatitis - Hepatitis C, Hepatitis B -  Alcoholic cirrhosis -  Non-alcoholic fatty liver disease (NAFLD) -  Haemochromatosis -  Aflatoxin from Aspergillus (stored grain & peanuts) -  Parasites Parasites –  – schistosomiasis,  schistosomiasis, echinococcus (tapeworm), clonorchis sinesis (liver (l iver fluke) -  LOA, LOW -  Abdominal pain, distension -  Stigmata of cirrhosis -  Liver mass -  US

Mx

- CT/MRI -  Radiologically guided liver biopsy -  Often widespread by dx

Intro

Aetiology

Clinical features

 

35

 

-  Small tumours – tumours – resection  resection & liver transplant   11mmol/L) Hypercalcaemia Hypothermia Pregnancy AIDS – AIDS  – secondary  secondary infection with CMV etc Other: mumps, chickenpox, Cocksackie, Hep ABC

Idiopathic   No identifiable cause (10-12%)   Normal function of pancreas -  Exocrine Exocrine –  – amylase,  amylase, trypsin, lipase -  Endocrine Endocrine –  – insulin,  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 – self-limiting  – minimal  minimal peritoneal exudation, no pancreatic changes. c hanges. Areas of fat saponification (white patches) on great omentum & mesentery   Severe -  Calcium sequestration  hypocalcaemia 

Pathophysiology





 

 





 

--  -  -  -  - 

Hx

Systemic inflammatory response Multi-organ failure: shock, ARDS, syndrome renal failure, DIVC Acute peri-pancreatic fluid collection Infection from Gram – Gram –ve ve bacteria translocated from the bowel (increase mortality) Pancreatic abscess formation (better prognosis) Pancreatic necrosis with grossly inflamed inf lamed & semi-digested peritoneal surface, peritoneal cavity filled with dark, blood-stained inflammatory exudate containing fine lipid droplets (acute haemorrhagic pancreatitis)   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 – signs – fever,  fever, tachycardia, hypotension (shock), dyspnoea (diaphragm irritation, i rritation,



pleural effusion, ARDS) -  Jaundice (periampullary oedema), pallor, diaphoresis, listlessness -  Stigmata of chronic alcohol use – use  – spider  spider naevi, caput medusa   Abdomen -  Distension -  Cullen sign (periumbilical bluish discolouration) -  Grey-Turner sign (reddish-brown discolouration around the flanks) -  Tenderness



-  Guarding/rigidity Guarding/rigidity –  – peritonitis  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 o n extensor surfaces) -  Polyarthritis





Complications

-  Purtscher retinopathy   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



 



 



DDx

   





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 Vascular –  – portal  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 Perforated PUD AAA 40

 

  Ascending cholangitis   Lower lobe pneumonia   Inferior MI Blood FBC –  – WCC,  WCC, HCT (haemoconcentration)   FBC   LFT LFT –  – AST,  AST, ALT (>150 U/L = gallstone pancreatitis), ALP, GGT (alcohol), 





Ix





       

   

               

     

Imaging





bilirubin (jaundice), albumin RP – RP – Urea,  Urea, Cr (dehydration), electrolyte imbalance CRP – CRP  –  ≥10mg/dL = severe pancreatitis ABG – ABG  – if  if tachypnoeic Serum amylase > 1000 -  Normal Normal –  – late  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 – lipase – longer  longer T ½ Serum calcium – calcium – hypoCa  hypoCa (saponification), hyperCa (cause) Serum LDH – LDH – Ranson  Ranson criteria RPG – RPG  – hyperglycaemia  hyperglycaemia (insulin from damaged beta cells) FPL – FPL  – hypertriglyceridaemia  hypertriglyceridaemia IgG4 – IgG4  – autoimmune  autoimmune Ultrasound hepatobiliary – hepatobiliary – gallstone  gallstone Plain AXR – AXR – ground ground-glass glass appearance, absent bowel gas except ‘sentinel loop’ of dilated adynamic small bowel, radio-opaque radio-opaque gallstone



CXR – perforation, CXR –  perforation, atelectasis, pleural effusion    CT (helical/multislice with pancreas protocol) -  Changes take days to appear -  Help in equivocal diagnosis -  Severe pancreatitis – pancreatitis – necrosis  necrosis   Grade A - Normal pancreas   Grade B - Focal or diffuse gland enlargement   Grade C - Intrinsic gland abnormality recognized by haziness on



Other

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   ERCP + sphincterotomy /MRCP -  Gallstone pancreatitis





TRO other causes after recovery – recovery – small  small pancreatic/periampullary tumours, pancreatic duct stricture, congenital pancreas divisum, high pressure sphincter of Oddi

41

 

Severity

Mx

Supportive

NPO2 – risk  risk of ARDS, pleural effusion, hypoxaemia due to pain   NPO2 –   IV fluids (3rd space sequestration), monitor CVP/urine output   NBM, NG tube, nutritional support (enteral or TPN), begin orally as pain

 



subsided Analgesics –  – PCM,  PCM, tramadol, meperidine   Analgesics   Antibiotics -  Not routine, fever is due to inflammation -  Imipenem if infected pancreatic necrosis   Gallstone -  Ductal  ERCP within 72 hours

 

Underlying cause



 

-

Laparoscopic cholecystectomy cholecystectomy –  – same  same attack admission if possible because deferring increases chance of another   Alcohol Alcohol –  – discourage  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)   Acute peripancreatic fluid collection -  Most resolve spontaneously, CT-guided percutaneous drainage if not   Pancreatic pseudocyst (1-8%)

 

Mx of complications

Local







Collection of pancreatic enzymes, inflammatory fluid & necrotic debris encapsulated within lesser sac, >6/52 -  Palpable upper abdominal mass -  CT scan to confirm -  10cm / unresolved – unresolved – laparoscopic/open  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 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 1 st week 

Prognosis

         



 

 

43

 

Intestinal Obstruction  Obstruction  Definition Clinical Anatomy

  Any condition that interferes with normal propulsion and passage of intestinal contents



`

  Ascending – Ascending – ileocolic  ileocolic & right colic arteries (SMA)   Transverse (proximal 2/3) – 2/3) – middle  middle colic artery (SMA)

 

Descending – left Descending –  left colic & superior sigmoid arteries (IMA) Sigmoid – Sigmoid  – sigmoidal  sigmoidal artery (IMA) Mechanical vs. functional Partial vs. complete (absolute constipation) Simple vs. strangulated (vascular impairment) Acute vs. chronic Mechanical (Dynamic) Functional (Adynamic) 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.

           





Classification









Aetiology/ Risk Factors

Extramural   Adhesions 



bands (rare)    Congenital Hernia   Volvulus



  Paralytic ileus (post-op most common)   Mesenteric vascular occlusion





   Pseudo-obstruction Spinal injury







44

 

  Intussusception   Tumours





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





Intraluminal    Stool impaction 

  Gallstone   Foreign body   Bezoars Bezoars –  – phytobezoar  phytobezoar (vegetable matter),







Symptoms

     

 



 



Signs

 



   





   





     

 



 



tricobezoar (hair) Abdominal pain – pain – colicky  colicky Abdominal distension Vomiting -  Time of onset – onset – earlier  earlier with proximal obstruction -  Nature Nature –  – bile-stained  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, oc clusion, partial obstruction by faeces/tumour (diarrhoea may occur) Dehydration Dehydration –  – vomiting,  vomiting, lack of fluid intake, fluid sequestration in obstructed bowel Surgical scar Abdominal distension – distension – larger  larger with more distal obstruction Visible peristalsis Abdominal tenderness (MUST be dx as strangulation or perforation) Guarding – Guarding  – perforation  perforation with peritonitis Abdominal mass Central resonance to percussion with flank dullness – dullness  – gas-filled  gas-filled bowel loops rise Loud, frequent, high-pitch, tinkling bowel

 



 



   





 



Dehydration – Dehydration  – vomiting,  vomiting, lack of fluid intake, fluid sequestration in obstructed bowel Abdominal distension – distension – larger  larger with more distal obstruction No visible peristalsis Central resonance to percussion with flank dullness – dullness  – gas-filled  gas-filled bowel loops rise Absent bowel sound

sounds   Succussion splash (GOO)   Hernias   Ascites   Medications Medications –  – TCA,  TCA, narcotics   Mesenteric ischaemia   Perforated viscus, peritonitis Laboratory   FBC FBC –  – Hb  Hb (bleeding tumour), WCC (infection/inflammation), HCT RP – Urea,  Urea, creatinine (dehydration), electrolyte balance   RP –   ABG ABG –  – acidosis/alkalosis  acidosis/alkalosis Imaging   Plain supine AXR – AXR – dilated  dilated bowels   Erect CXR – CXR – TRO  TRO perforation studies – small  small bowel vs colon; partial vs complete; mechanical vs   Barium studies – 



DDx









Ix













functional

  CT increasingly used -  Level of obstruction



45

 

-  -  -  -  Mx

Degree of obstruction Degree of ischaemia Cause of obstruction – obstruction – volvulus,  volvulus, hernia, luminal & mural m ural causes Free fluid & gas – gas – perforation  perforation

  Resuscitation -  NBM -  IV fluids (NS or Hartmann’s)  Hartmann’s)   -  IV antibiotic prophylaxis -  NG tube & aspiration – aspiration – controls  controls N & V, remove swallowed air, reduce gaseous



distension, minimise risk of inhalation (induction of anaesthesia) uncomplicated – spontaneous  spontaneous resolution   Conservative Mx if uncomplicated – -  Indications   Incomplete obstruction   Previous abdominal surgery   Advanced malignancy doubt – possible  possible ileus   Diagnostic doubt –   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 Palpate liver for metastases, inspect colon for synchronous tumours o  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 – conniventes – extend  extend across whole width of lumen; step-ladder pattern pattern –  – regularly  regularly spaced Multiple air-fluid levels in erect AXR Large Bowel Obstruction -  Dilated bowel loops located peripherally -  Presence of haustrations – haustrations – do  do not extend across whole width of lumen, irregularly spaced

47

 

48

 

Colorectal Colorect al Carcinoma  Carcinoma  Clinical Anatomy

Blood supply of the colon

  Arterial -  Ascending Ascending –  – ileocolic  ileocolic & right colic arteries (SMA) -  Transverse (proximal 2/3) – 2/3) – middle  middle colic artery (SMA) -  Descending Descending –  – left  left colic & superior sigmoid arteries (IMA) -  Sigmoid Sigmoid –  – sigmoidal  sigmoidal artery (IMA) -  Watershed area – area – terminal  terminal branches of SMA & IMA meet – meet – prone  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 inf erior 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





supply – inferior  inferior hypogastric plexuses. Rectum only sensitive to stretch   Nerve supply –



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   2nd most common cancer in women & 3 rd most common cancer in men   Increase with age – age  – rare  rare 60   M=F   Age >50   Chinese   Western low-fibre, high fat diet   Alcohol   Smoking   Obesity   Family Hx   Personal Hx of colon, ovarian, uterine cancers









Epidemiology







Aetiology/ Risk Factors

















  IBD - Ulcerative colitis, Crohn’s disease   Inherited conditions -  Familial Adenomatous Polyposis (FAP) – (FAP) – 1%  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 Gardner’s syndrome – multiple – multiple adenomas, epidermoid cyst (skin), o  fibromatosis (soft-tissue), osteomas (bone), abnormal dentition. Increased risk of duodenal ca and thyroid ca o  Turcot’s syndrome – colorectal – colorectal adenomatous polyps & brain tumours (gliomas)



Pathophysiology

Hereditary Non-polyposis Colorectal Cancer (HNPCC) – (HNPCC) – 6%  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   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 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 mets) – skin  skin flushing,   Serotonin  carcinoid syndrome (only in massive liver mets) – diarrhoea, cramps, bronchospasm, systemic fibrosis, hepatomegaly   Gastrin  Zollinger-Ellison syndrome  PUD syndrome    ACTH  Cushing’s syndrome    Insulin  hypoglycaemia -  Low grade malignant tumour   Gastrointestinal stromal tumours (GISTs) -  Mesenchymal neoplasm of the GIT arising from fr om pacemaker interstitial cell of Cajal -  2/3 in stomach, ¼ in small intestine, 1 site or o r peritoneum

AJCC stage grouping

Duke’s   Duke’s

Mx of colon ca

Principles

  MDT MDT –  – surgeons,  surgeons, oncologist, radiologist, geneticist, palliative care c are



physicians, colorectal specialist nurses   Surgical resection is the main treatment -  Curative for localized disease (stage I-III) and limited metastatic





disease liver/lungto(stage IV)obstruction (stenting is another Palliativeinresection relieve option)/prevent continuing blood loss 53

 

 



     



Surgical





-  Neoadjuvant chemotherapy may be given to shrink tumour pre-op 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 Affected segment removed with a margin of 5cm proximally & distally Lines of resection determined by distribution of mesenteric BV -  Ascending colon – colon – right  right hemicolectomy o f the middle colic   Ileocolic, right colic, and right branch of vessels are divided and removed   Care must be taken to identify the right ureter, the ovarian or testicular vessels, and the duodenum



Adjuvant therapy

 



 



Surveillance

     







  If omentum is attached to the tumour, remove en bloc

Hepatic flexure/ proximal/ middle transverse colon – colon – extended  extended right hemicolectomy   Ileocolic, right colic, and middle colic vessels are divided and the specimen is removed with its mesentery -  Splenic flexure/descending colon – colon – left  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 – colon – sigmoid  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 Chemotherapy -  5-FU is the main agent, given together with folinic acid (biomodulator) -  Combinations: 5-FU + oxaliplatin, 5-FU + leucovorin and oxaliplatin Biologic agents – agents – monoclonal  monoclonal antibodies against VEGF &EGFR, tyrosine kinase inhibitor & decoy receptor for VEGF -  Bevacizumab, cetuximab, panitumumab, regorafenib, ziv-aflibercept 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   Sphincter-saving procedures for rectal cancer are now considered the



Mx of rectal ca

Principles



standard of care provided the lower edge of tumour is 1-2cm above the anal sphincter radiosensitive  – may  may be delivered pre-op, intra-op or post  Rectal ADC are radiosensitive – op +/- chemotherapy   5-FU based chemotherapy for stage II & III   Anterior resection/low anterior resection -  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 – technique – reduce  reduce frequency & urgency of





Radical surgery





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   Hartm Hartmann’s ann’s operation  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 clo sed with sutures/staples Several months later decision to reconnect the bowel made depending on fitness & preference of the patient

Local surgery/ radiotherapy for early stage

  Transanal excision – excision – early  early stage small tumours (female due to abdominal wall deficiency secondary to testicular descent Any age but most common L  R>L -  Appears on standing & straining -  Disappears on lying down   Pain Pain –  – if  if adhered to greater omentum   Strangulation 









Aetiology/ Risk Factors







Pathophysiology









Symptoms







-  - 

No obvious localizing sign Distal small bowel obstruction – obstruction – abdominal  abdominal pain, vomiting, absolute constipation

62

 



Signs

 



                   









DDx











Mx



Ritcher’s hernia (30%) – only –  only a portion of bowel circumference trapped. Lumen remains patent – patent  – continues  continues to pass flatus but obstruction sufficient to cause vomiting Femoral hernia: BELOW & LATERAL to pubic pubic tubercle; Inguinal h hernia: ernia: 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) Inguinal hernia Lipoma Enlarged inguinal lymph node Saphena varix Femoral artery aneurysm Surgical repair for all femoral hernia (even if asymptomatic) without delay – delay – prone  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 approach – via  via post wall of inguinal canal   Lotheissen/high approach – (laparotomy)  – rarely  rarely   McEvedy/pararectus extraperitoneal approach (laparotomy) – -  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 inguinal LN

Saphena varix

 



 



 

     

Femoral artery aneurysm

  Multiple small firm shotty nodes, normal if male   90% GSV, 25% SSV





65

 

Aetiology/ risk factors

  Valve incompetence (SFJ, SPJ, perforators)  uninterrupted column of blood from the



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)  (Marfan’s)  -  Multiple congenital AVM (Klippel-Trenaunay syndrome)   Pregnancy -  Progesterone causes changes in collagen structure & smooth muscle relaxation





     







               





Hx









 



                                





PE DDx

 





Diagnosis

 







CEAP Classification



-  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 Dilated tortuous vein on the leg Dull aching improved by ambulation & elevation Bursting (venous claudication) pain Pruritus Bleeding of varicose veins when traumatized t raumatized Ankle swelling Ulcer Venous eczema Recurrent superficial thrombophlebitis See OSCE Cellulitis PAD Lymphoedema Aetiological - Primary vs secondary (post-thrombotic) GSV or SSV or both +/- SFJ or SPJ or perforator incompetence +/- complications Deep vein patency C0 - No visible or palpable signs of venous disease



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   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 – vein – DVT,  DVT, deep system insufficiency   MRV MRV –  – more  more sensitive tests – venous  venous refilling time, MVO, MPEF   Other specialised tests –



Ix









66

 

Mx

Conservative

       



 



           





Medical

 



Surgical



Maintain proper weight Leg elevation above the heart level several times a day Foot & ankle exercises – exercises – move  move blood back to the heart Compression/elastic stocking/compression stocking/compression bandage - minimise venous venous distension Clean ulcer with NS, povidone iodine & hydrogen Proper debridement (slough) Aspirin – Aspirin  – speed  speed ulcer healing Antibiotics when there is infection Stasis dermatitis – dermatitis – moisturizers,  moisturizers, steroid cream/ointment Endovenous ablation – ablation – LA  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 c reate 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 v enous 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 gr eat 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 o f 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)  (AAA)  Definition

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





Clinical Anatomy

Epidemiology Aetiology/ Risk Factors

               











 



85% mortality after rupture (shock, post-op MI, post-op RF), 5% mortality if elective surgery Male Age >65 Hypertension Smoking Marfan’s syndrome, Ehler-Danlos Ehler-Danlos syndrome Mycotic aneurysm Uncommon: cystic medial necrosis, arteritis, trauma 68

 

Pathophysiology

  Degeneration of the elastin & collagen of the arterial wall  fusiform, slowly expanding  



 



Symptoms

     



 

 



               



Signs



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) Asymptomatic Incidental finding on plain AXR (calcification), CT, U/S Pressure symptoms caused by aneurysm -  Vein Vein –  – LL  LL oedema, DVT, embolism (livedo reticularis/blue toe syndrome) -  Bone Bone –  – vertebrae  vertebrae erosion  back pain -  Adjacent organs – organs – stomach  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 – fistula – massive  massive haematemesis Sudden death (fatal cardiovascular collapse, often misdx as MI) Signs of shock – shock – cyanosis,  cyanosis, mottling, altered mental status, tachycardia, hypotension



Pulsatile & expansile abdominal mass Thrill & bruits Grey-turner sign – sign – flank  flank ecchymosis Weak distal pulses Death Ischaemia -  Colon ischaemia (mesenteric artery) -  Renal failure (renal artery)   Embolism -  Acute limb ischemia -  Blue toe syndrome   Fistula -  Aorto-venous -  Aorto-duodenal/aorto-enteric



 

Complications









Inflammation/infection of the aneurysm Other causes of acute abdomen Renal colic Lumbar spine disease Blood FBC –  – Hb,  Hb, WCC   FBC   RP, LFT – LFT – pre-op  pre-op assessment   Blood GXM including clotting factors & platelets Imaging Non-ruptured AAA   U/S Abdomen -  Assess size -  Periodic monitoring

       



DDx







Ix









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 



-  -  -  Pre-op

               





Mx

Conservative

 

Medical







Surgical



 



Relationship to renal arteries and visceral arteries Secondary iliac aneurysms Other abdominal pathology e.g. liver mets (influences decision to operate) Cardiac status – status – ECG,  ECG, ECHO  Pulmonary function  Diet control – control – reduce  reduce salt, fat intake Smoking cessation Antihypertensives Statins Treat syphilis if present Indications -  Leaking/rupturing aneurysms (Emergency – (Emergency – 50%  50% reach hospital alive & 50% survive after Sx) -  Symptomatic aneurysm - pain, ureteric obstruction, o bstruction, 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 Indian>Malay













73

 

Aetiology/ Risk Factors

High risk:   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 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 Inspection   Breast Breast –  – symmetry  symmetry (any fullness in 1 side), side), scar, skin changes (dimpling, peau d’orange, hyperpigmentation), dilated veins   Nipple-areolar complex – complex – everted/inverted/retracted,  everted/inverted/retracted, spontaneous discharge Axilla –  – scar  scar (axillary clearance), accessory breast   Axilla 























Signs (Ms Leow)







fossa – fullness  fullness (LN)   Supraclavicular fossa – Back –  – scar  scar (chest drain for pleural effusion)   Back UL –  – lymphoedema  lymphoedema   UL

  

74

 

Palpation   Breast -  Any pain? -  Temperature tenderness -  Site size shape surface -  Mobility (skin tethering, muscle tethering) -  Edge Edge –  – well/ill-defined  well/ill-defined 

-  Consistency Consistency –  – hard  hard Nipple –  – discharge,  discharge, mass behind   Nipple   Axilla Axilla –  – apical  apical central anterior lateral posterior groups Neck –  – supraclavicular  supraclavicular and cervical LN   Neck Completion   Bone Bone –  – tenderness  tenderness   Lung Lung –  – signs  signs pleural effusion Abdomen –  – hepatomegaly,  hepatomegaly, ascites   Abdomen   Fibroadenoma   Breast cyst   Phylloides tumour (massive)   In situ -  Ductal carcinoma in situ (DCIS) – (DCIS)  – best  best prognosis 











DDx







Classification



Ix: Triple

-  Lobular carcinoma in situ (LCIS) – (LCIS)  – best  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) (non-hodgkin’s)   -  Sarcoma -  Secondary Secondary –  – melanoma/  melanoma/ carcinoma from other sites 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 radiati ng 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 3cm, skin/chest wall involvement, +/+/ regional LN involvement   Mastectomy + primary axillary clearance + adjuvant therapy, or   Neoadjuvant therapy to downsize tumour to enable BCS in operabl operable e tumours or to downsize inoperable tumours to operable + primary axillary clearance + adjuvant therapy 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 

Locally advanced





Metastatic









-  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  cure vs palliative   Indications/benefits   Complications -  Surgery to the breast/axilla   Early Bleeding o  Injury to the nerve – nerve  – long  long thoracic nerve of Bell (winging of scapula), o 



 

intercostal brachial nerve (loss of sensation to inner arm) o  Wound infection o  Seroma  

Late

  Lymphoedema

o

Screening

o ld   Mammogram 2-yearly in women 50-74 years old



79

 

(Malaysian CPG)

       

  



Familial breast cancer

 



       

  



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 Genetic counselling for women with FH associated with BRCA1, BRCA2 and tp53 genes -  ≥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  old   st nd -  ≥2 1 /2  degree relative on same side of family with ovarian ca at any age -  1st degree relative with breast ca dx ≤40  ≤40  st -  1  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

80

 

81

 

82

 

83

 

Benign Breast Diseases  Diseases  ANDI (Aberrations in the Normal Development and Involution of the breast) Classification Classification Early reproductive years (M -  Mild, diffuse, sometimes tender thyroid enlargement (often not enlarged) -  Euthyroid/hyperthyroid hypothyroid -  Rx: Levothyroxine. Thyroidectomy if suspect lymphoma/papillary carcinoma -  Fairly common -  Diffuse thyroid enlargement +/- bruit -  Hyperthyroidism Hyperthyroidism –  – heat  heat intolerance, increased appetite, LOW, tremor, diarrhoea, tachycardia, atrial fibrillation, thyroid eye disease -  Uncommon -  Middle-aged females -  Diffuse moderate thyroid enlargement -  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 thyroiditis

-  Dense fibrosis of the thyroid gland -  Cause: autoimmune

-  Very rare -  Middle-aged females -  Extremely hard ‘woody’ goitre, often asymmetrical (mimic malignancy) -  +/- compressive symptoms -  Rx: corticosteroid

Hyperplastic/Metabolic Condition Simple nontoxic colloid goitre

Pathophysiology -  Benign, diffuse or multinodular hyperplasia of thyroid follicles -  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 goitre

-  Diffuse thyroid hyperplasia -  Cause: interference with thyroid hormone synthesis – synthesis  – carbimazole,  carbimazole, lithium, aminoglutethimide

Dyshormonogenesis

Physiological

-  Diffuse thyroid hyperplasia -  Cause: a variety of uncommon genetic (recessive) defects affecting thyroid hormone synthesis -  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  Swelling  Clinical Anatomy

       









2 lobes joined by an isthmus isthmus –  – butterfly-shaped  butterfly-shaped 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 – muscles – sternothyroid,  sternothyroid, thyrohyoid, sternohyoid; superior belly of - 

omohyoid, sternocleidomastoid Posterior: parathyroid glands, trachea, oesophagus, recurrent laryngeal nerve, carotid sheath

87

 

  Lymphatic drainage: periglandular  pretracheal (Delphian)  paratracheal  superior



       



Hx

 



mediastinal nodes. Also superior and inferior deep cervical nodes Nerve supply: sympathetic & parasympathetic Swelling – Swelling  – site,  site, onset, duration, progress Pain – Pain  – painful  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)  enopthalmos) 

88

 

  Symptoms of hyperthyroidism -  Heat intolerance -  Excessive sweating -  Increased appetite -  Weight loss -  Diarrhoea -  Amenorrhoea/oligomenorrhoea -  Anxiety -  Palpitations -  Eye signs – signs – double  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  









       

  

PE



 



PMH/PSH – PMH/PSH  – Hx  Hx of irradiation (papillary ca), longstanding endemic goitre hashimoto’s (lymphoma, papil papillary lary ca), thyroglossal cyst (papillary ca) (follicular ca), Medication – Medication  – thyroxine/anti-thyroid  thyroxine/anti-thyroid drugs FH FH –  – goitre,  goitre, thyroid ca (medullary – (medullary – MENIIa,  MENIIa, IIb) SH SH –  – diet  diet (iodine deficiency), cabbage/soy (goitrogen), living area General -  Respiratory distress -  Nutritional status – status – underweight/overweight/cachexic/anaemic  underweight/overweight/cachexic/anaemic Neck -  Inspection  



Palpation



Percussion – Percussion  – over  over the manubrium for retrosternal extension

 

-  - 

Auscultation –  vascular bruits in Graves’  Auscultation – Graves’  Special test – raise arm over head  facial flushing, respiratory distress   Pemberton’s sign – raise (SVCO due to restrosternal extension) – inability to feel the carotid pulse due to malignant infiltration of   Berry’s sign – inability the carotid sheath   Hand   Eye   Leg   Other system -  CVS CVS –  – evidence  evidence of HF – HF – cardiomegaly,  cardiomegaly, pedal oedema -  Respi Respi –  – lung  lung mets, pleural effusion -  Abdomen Abdomen –  – hepatomegaly  hepatomegaly -  Bone Bone –  – mets  mets Blood TFT –  – T4/TSH  T4/TSH   TFT   Thyroid antibodies -  TSH receptor antibody – antibody –  Graves’ Graves’   







Ix





89

 

   





   



Imaging



 



 

-  anti-thyroglobulin anti-thyroglobulin –  – autoimmune  autoimmune thyroiditis -  anti-thyroid peroxidase antibody (anti-TPO) – (anti-TPO) –  Hashimoto’s Hashimoto’s   TSH suppression test – test – not  not suppressed in carcinoma Serum thyroglobulin – thyroglobulin – tumour  tumour marker for papillary & follicular ca (surveillance) Serum calcium & calcitonin – calcitonin – raised  raised in medullary ca 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 – 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   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



Histology



representative if small sample taken, cannot differentiate follicular adenoma vs carcinoma, operator dependent

Bethesda Class 

FNAC Result 

Explanation 

Action 

I

Non diagnostic

Insufficient sample and diagnosis is not possible

Repeat FNAC under ultrasound guidance

II

Benign

Non cancerous.

Continue observation Follow up with ultrasound

90

 

III

Atypia of undetermined significance or follicular lesion of undetermined significance

Lesions that are not convincingly benign but do not have definitive features of a follicular neoplasm and are not highly suspicious of malignancy

Repeat FNA in 2 to 3 months

IV

Follicular

Benign adenomas or

Lobectomy

neoplasm or suspicious for a follicular neoplasm

well-differentiated follicular or follicular variant of papillary cancers of the thyroid.

V

Suspicious for malignancy

Lesions with some features suggestive of but not definitive for thyroid cancer.

Lobectomy/ Total thyroidectomy

VI

Malignant

Papillary cancer, medullary cancer, thyroid lymphoma, anaplastic cancer, and cancer metastatic to

Total thyroidectomy

the thyroid

  Trucut core biopsy -  Shows architecture hence differentiate follicular adenoma vs carcinoma   ECG ECG –  – A  A fib   FBC, RP, LFT, coagulation profile based on case



Other

 

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 – regimen – full  full dose carbimazole + levothyroxine 50100µg od -  S/E: agranulocytosis, SJS, hepatitis, jaundice, aplastic anaemia, peripheral neuritis, polyarteritis, vasculitis, teratogenicity – teratogenicity – Aplasia  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   Administered orally as sodium iodide-131 (131-I) in solution or a capsule   Indications: -  Graves’ disease  disease  

Radio-iodine





 

--  Toxic adenoma Multinodular goitre -  Relapse after medical/surgical Rx -  Contraindicated for medical/surgical Rx   Contraindications: -  Pregnancy Pregnancy –  – cross  cross placenta & ablate foetal thyroid – thyroid – cretinism  cretinism -  Breastfeeding mother -  Severe opthalmopathy – opthalmopathy – worsening  worsening of eye disease   A/E: hypothyroidism, increased risk of malignancy   Indications -  Malignancy -  Compression symptoms – symptoms – trachea,  trachea, oesophagus -  Failure of medical therapy -  Cosmetic reason





Surgical



  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 Thyr oid Malignancies  Malignancies  Types Papillary

Features

Follicular

Medullary

Anaplastic

Lymphoma

Management of Thyroid Malignancies

Metastasis

Mx

93

 

Urolithiasis   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  vesico-ureteric junction (VUJ) – (VUJ) – medial  medial to ischial spine   End   Blood supply   Upper 1/3 – 1/3 – renal  renal artery 1/3 – gonadal  gonadal artery   Middle 1/3 –   Lower 1/3 – 1/3 – internal  internal iliac artery   Innervation   Automomic Automomic –  – sympathetic  sympathetic & parasympathetic   Visceral afferent fibres return to T10-L2 T10- L2 dermatome “loin to groin pain”  pain”  Type % Aetiology Clinical features 70 Calcium oxalate/ ‘hemp-seed’   Small, smooth ‘hemp  Idiopathic phosphate stones   Urinary stasis   Small irregular ‘mulberry’   Infection stones   Foreign bodies   Small spiculated ‘jack’ stones  stones     Hyperparathyroidism   Radio-opaque   Hypercalcaemia 























Types of urinary stones





















  Idiopathic hypercalciuria   Hyperoxaluria Infection –  – Proteus  Proteus (urease   Infection





Magnesium ammonium phosphate (struvite/staghorn) Uric acid

Cysteine/xanthine

15



splits urea forming ammonia in alkaline urine) 8

2

  Gout   Chemotherapy (leukaemia,













mueloproliferative disorders)   Autosomal recessive



disorders

  Excess urinary excretion of



cysteine/xanthine



  Large ‘staghorn’ calculi of pelvi-calyceal system   Bladder stones

  Yellow/brown   Radiolucent Cysteine –  – hexagonal,  hexagonal,   Cysteine translucent, white crystals in acidic urine/ pink/yellow but change to green when exposed to air. Radio-opaque

94

 



  Xanthine Xanthine –  – smooth  smooth round brick red with lamellation

       

Epidemiology

2-5% lifetime risk (Asia) Peak age 35-45 M>F Urinary stasis – stasis – congenital  congenital abnormalities (horseshoe), hydronephrosis, BPH, neurogenic bladder   Chronic UTI – UTI – Proteus  Proteus   Excess urinary excretion of stone-forming substances – substances  – idiopathic  idiopathic hypercalciuria, hyperPTH,







Aetiology/ Risk Factors



 

hyperoxaluria, gout, cysteinuria, xanthinuria

  Foreign bodies – bodies – fragments  fragments of catheter tubing, parasites (schistosome ova), diseased tissue



   

 

 

Pathophysiology



 



 



   





     







Site Hx

(renal papillary necrosis) Diet – Diet  – high  high calcium/dairy, low water intake Other – Other  – prolonged  prolonged immobility, children in developing world (uric acid stone), multiple fractures & paralysis (skeletal decalcification) 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

Kidney   Asymptomatic   Loin pain   Haematuria







Ureter   Ureteric colic (loin to groin pain)   Haematuria





                         





















PE

  Anaemia   Renal punch/percussion   Ballotable kidney

















Blood & Urine

 



     

  

   





Urinary retention Haematuria Fever (UTI) Suprapubic tenderness Palpable bladder Ballotable kidney (pyelonephrosis)

(pyelonephrosis)   Retracted testis (cremasteric spasm) Urine FEME – FEME – haematuria,  haematuria, leukocytes & nitrites (UTI), pH (acidic in uric acid stone, alkaline in infection), crystals Urine C+S – C+S – culture  culture FBC – FBC  – Hb  Hb (anaemia), WCC (infection) RP – RP – Urea,  Urea, Cr (impaired renal function), f unction), electrolytes Serum calcium, phosphate, oxalate, uric acid, ALP 24H urinary excretion of calcium, uric acid, cysteine

(pyelonephrosis/ pyelonephritis) - rare Ix

  Unwell, distress   Tenderness/rigidity   Ballotable kidney



Bladder Asymptomatic Suprapubic pain Dysuria Frequency Nocturia Urgency Intermittency



95

 

Imaging

  X-ray KUB – KUB – 90%  90% stone radio-opaque   U/S KUB – KUB – stone  stone in renal pelvis, hydronephrosis (less well in demonstrating

 

   

 

Other

     

 



Acute Mx

ureter), urinary retention, stones in bladder with acoustic shadow Non-contrast CT abdomen pelvis – pelvis – better  better to visualize ureter Intravenous urogram (less used) – used) – able  able to detect radiolecent stone as well. Filling defect, hydroureter, hydronephrosis Cystoscopy – Cystoscopy  – bladder  bladder stones Percutaneous (antegrade) pyelography or ascending (retrograde) ureterography Biochemical analysis of recovered stones



IV fluids Analgesics – Analgesics  – NSAIDs  NSAIDs e.g. ibuprofen, diclofenac; narcotics if needed Antiemetic e.g. metolopromide Antibiotics for UTI Rule out obstruction & infection – infection – if  if both present  emergency surgical decompression by urethral/double J stent (endoscopic) or percutaneous nephrostomy (fast & safe for unstable patients)  treat infection  definitive treatment   48H), recurrent or severe pain Stone likely to cause obstruction/infection Small ‘metabolic’ stones likely to grow rapidly in size  size   Professions where colic could be disastrous e.g. pilot Solitary kidney Extracorporeal shock wave   Extracorporeal shock wave lithotripsy (ESWL) lithotripsy (ESWL)   Percutaneous   Rigid/flexible ureteroscopy nephrolithotomy (PCNL) (URS) -  Rx of choice for middle   Nephrolithotomy/ & lower ureter stone pyelolithotomy (open) -  Failed ESWL



              









 

Surgical Mx











 



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 c ystoscope -  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

97

 

Renal Cell Carcinoma  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  right adrenal, liver, D2, hepatic flexure, small intestine   Right Left –  – left  left adrenal, stomach, spleen, pancreas, splenic flexure, descending   Left







     

 



Epidemiology

     







Aetiology/ Risk Factors

  96% Sporadic Familial – Von-Hippel-Lindau,  Von-Hippel-Lindau, hereditary papillary renal carcinoma, Birt-Hogg-Dube   4% Familial –





       







Pathophysiology

colon, jejunum -  Posterior relations – relations – rib  rib 11,12, psoas major, m ajor, quadratus lumborum, transversus abdominis muscles Renal fat & fascia – fascia –  renal capsule, perirenal fat, Gerota’s fascia, pararenal fat  fat  Structures – Structures  – cortex,  cortex, medulla (pyramids & renal papilla), pelvis (major & minor calyces) Blood supply -  Arterial Arterial –  – L  L & R renal arteries from aorta at L1, R longer than L, pass behind IVC. Each divides into 5 segmental arteries. -  Venous Venous –  – segmental  segmental veins  L & R renal veins  IVC 3% adult malignencies M>F x2 Peak age 50-70



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, c lass, asbestos, HPT Adenocarcinomas arising from proximal tubules -  Large tumour cells with clear cytoplasm (glycogen & lipid) hence “clear cell carcinoma”  carcinoma”  -  Multifocal in 7-20% -  Spread

98

 

 

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



Clinical features

             



 





 

Asymptomatic, >50% incidental finding on imaging Classic triad: Pain, flank mass, haematuria in 4 cm but ≤7 cm   T2 T2 –  – >7  >7 cm, limited to the kidney   T3 T3 –  – Extends  Extends into major veins/ directly invades adrenal gland/ perinephric

 

         



N

 



M



 



AJCC Stage grouping

Mx

Principles

tissues but not beyond Gerota fascia -  T3a T3a –  – directly  directly invades adrenal gland or perinephric tissues but not beyond Gerota fascia -  T3b T3b –  – grossly  grossly extends into renal vein(s) or vena cava or its wall below diaphragm -  T3c T3c –  – grossly  grossly extends into vena cava or its wall above diaphragm T4 T4 –  – directly  directly invades beyond Gerota fascia N0 – N0  – No  No regional lymph node metastasis N1 – N1  – 1  1 regional lymph node N2 – N2  – >1  >1 regional lymph node M0 – M0  – No  No distant metastasis M1 – M1  – Distant  Distant metastasis

100

 

Consent

Complications

Prognosis

kidney – 79%  79% 5-year survival   Confined to kidney –   Nodes/IVC – Nodes/IVC  – 40%  40% Metastasis –  – 8%  8%   Metastasis

  

Bladder Carcinoma Clinical Anatomy

  Blood supply -  Arterial Arterial –  – branches  branches of the internal iliac artery   Superior vesical arteries   Inferior vesical arteries (vaginal arteries in females)   Obturator artery   artery Uterine gluteal branches (female only)   Inferior -  Veins Veins –  – follow  follow arteries into internal iliac vein   Lymphatics Lymphatics –  – external/internal  external/internal iliac nodes





101

 

Normal physiology

  Continence - synergic relaxation of detrusor muscles & contraction of the bladder neck and



   

 

 



Epidemiology

   





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 Common urological cancer >90% are transitional cell carcinoma



Rare F Malay>Chinese>indian Age Smoking Industrial carcinogens – carcinogens – aniline  aniline dyes, aromatic amines, rubber, cable, printing Pharmaceutical compounds – compounds – saccharin,  saccharin, phenacetin, insecticides Cyclophosphamide Schistosomiasis (SCC) 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 l esions which invade underlying muscle & tissues   “Field abnormality” - tumours are commonly associated with areas of o f 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 f requency & dysuria & often misdiagnosed as prostatitis. Can be picked up by cytology. Infiltrate rapidly if untreated Histological subtypes   Transitional cell carcinoma (>90%) -  Carcinoma in situ – situ – 10%  10% -  Non-muscle invasive – invasive – 70%  70% -  Muscle-invasive Muscle-invasive –  – 20%  20%   Squamous cell carcinoma (schistosomiasis) – (schistosomiasis) – 1-7%  1-7%   Adenocarcinoma (fistula) – (fistula) – 2%  2% sarcomas – 1%  1%   Others e.g. sarcomas –

                      





Aetiology/ Risk Factors













Pathophysiology











Histopathology









Morphology of TCC   70% papillary -  Usually G1 or G2 -  Usually superficial – superficial – confined  confined to the mucosa (Ta)/ submucosa (lamina propria (T1)) -  T1G3 more aggressive, 40% subsequently upstaged to muscle invasive i nvasive   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 







structures – peri-vesical  peri-vesical fat, prostate, rectum, vagina, pelvic side wall   Adjacent structures – Lymphatics –  – pelvic  pelvic nodes, para-aortic nodes   Lymphatics   Vascular Vascular –  – lung,  lung, liver, bone, brain

  

102

 

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(tumour invading bladder neck) -  Incontinence -  Constant pain in the pelvis (extravesical spread) -  Referred suprapubic, groin, perineum, anal, thigh pain (late)   Palpable suprapubic mass   DRE/bimanual examination – examination – large  large tumours, fixation of pelvic structures   Cystitis, UTI   Nephrolithiasis   RCC   Trauma Blood &   Urine FEME – FEME – haematuria,  haematuria, raised WCC, nitrites (UTI) ( UTI) urine C+S – UTI  UTI   Urine C+S –   Urine cytology – cytology – high  high pick-up rate for CIS, invasive ca FBC –  – Hb  Hb (anaemia), WCC (Infection), Plt (bleeding disorder)   FBC 







Signs





DDx









Ix









RP – Urea,  Urea, Cr (obstructive uropathy), baseline before CT (contrast), also   RP –



       

  

Imaging



       

 

Other





Grading & Staging

Grade

baseline before intravesical Rx LFT – LFT  – liver  liver mets, baseline as BCG Rx can cause acute hepatitis Coagulation profile – profile – bleeding  bleeding disorder, warfarin Tumour markers – markers – not  not widely used as non-specific U/S KUB – KUB – renal/bladder  renal/bladder mass, hydronephrosis in ureteric involvement, blood clots, stones CECT/MRI TAP – TAP – extent  extent of tumour, staging IVU/CT urogram – urogram – filling  filling defect, irregular bladder wall, hydronephrosis Bimanual examination under anaesthesia Cystoscopy + biopsy – biopsy – examine  examine lining of bladder & urethra & take biopsy

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) - Invades perivesical tissue   T3 -  T3a - Microscopically -  T3b - Macroscopically (extravesical mass)   T4 - Invades any of the following: prostate, uterus, vagina, pelvic wall,





N

           



  

M

 

abdominal wall -  T4a - Tumour invades prostate, uterus or vagina -  T4b - Tumour invades pelvic wall or abdominal wall N0 – N0  – no  no regional LN mets N1 – N1  –  1 RLN ≤2 ≤2 cm N2 – N2  – 1  1 RLN >2 cm but ≤5 cm, cm, or multiple RLN, none >5cm N3 – N3  – 1  1 RLN >5 cm M0 – M0  – no  no distant mets M1 – M1  – distant  distant mets

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