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
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
DDx
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
Aetiology/ Risk Factors
Pathophysiology
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
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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
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- 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
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-
- -
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
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Symptoms
Painless macroscopic haematuria (20%) +/- Long string blood clots (upper tract) - Loin pain/Ureteric colic (obstruction by blood clot) - Acute urine retention (rapid bleeding with clot causing obstruction) Frequency, urgency, dysuria (25% - think CIS) Obstruction by tumour - Uraemia (bilateral obstruction) - Recurrent UTI - LL oedema (iliac vessels compression) Spread of tumour(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
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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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