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Home , Coffee ground vomiting, Oropharyngeal dysphagia

3.3 Gastrointestinal System 3.3.1 Ref: Davidson P. 851, Andre Tan Ch3, WCS51 A. Physiology of Dysphagia Dysphagia: difficulty in

Swallowing: function of clearing food and drink through oral cavity, and oesophagus into stomach at an appropriate rate and speed Phases of swallowing: □ Oral phase: voluntary → Mastication of solids → form food bolus → movement to achieve glossopalatal seal → push food bolus or fluid against hard palate □ Oropharyngeal phase: involuntary → Activation of mechanoreceptors of pharynx → initiation of swallowing reflex → Soft palate elevates (levator veli palatini) → nasal cavity closed off → elevates (suprahyoid muscles) → larynx closed off (by epiglottis) → Pharyngeal muscles contract → food bolus delivered from pharynx into oesophagus □ Oesophageal phase: involuntary → Peristaltic movement of muscularis propria → food bolus delivered into stomach

Dysphagia can be classified as □ → difficulty with initiation of swallowing → Usually functional (i.e. due to neuromuscular diseases) □ Oesophageal dysphagia → failure of peristaltic delivery of food through oesophagus → Can be functional or mechanical (i.e. due to mechanical obstruction)

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B. Approach to Dysphagia

Oropharyngeal Oesophageal Functional Diseases of CNS: Primary motility disorders: Bulbar palsy, pseudobulbar palsy, Parkinson’s Achalasia, diffuse oesophageal spasm, nutcracker disease oesophagus153, hypertensive LES Diseases of motor neurones: Secondary motility disorders: Motor neurone disease, peripheral neuropathy, Diabetic neuropathy, scleroderma, Sjogren’s poliomyelitis, syphilis syndrome, multiple sclerosis Diseases of NMJ/muscles: , myopathies (muscular dystrophy, polymyositis, dermatomyositis) Mechanical [NOT COMMON] Intraluminal causes: Mural causes: Foreign bodies, lower oesophageal rings154, oesophageal webs Pharyngeal pouch, oropharyngeal tumours, strictures Extramural causes: Mural causes: Oesophageal tumours, oesophagitis (peptic, Goitre, lymphadenopathy, cervical , retropharyngeal abscess radiation, chemical, infectious, drug-induced), strictures (long-standing oesophagitis, malignant) Extramural causes: Anterior mediastinal masses (thyroid, thymus, teratoma, terrible lymphoma), CA lung, TB, cardiovascular (rare)155

1. History

153 Nutcracker oesophagus refers to normal oesophageal peristaltic wave but at an increased intensity. 154 Lower oesophageal (Schatzki’s ring) is a lower oesophageal narrowing due to presence of a ring of mucosa. 155 Cardiovascular causes of extraluminal obstruction include thoracic aorta aneurysm (dysphagia aortica), aberrant Rt subclavian a. (dysphagia lusoria) and LA dilatation (dysphagia megalatriensis).

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Is it real dysphagia? □ Globus hystericus: anxious people feel a lump in throat without organic cause □ : during swallowing (can coexist with but ≠ dysphagia) Which phase of swallowing is affected? Oropharyngeal Oesophageal - C/O difficulty in initiating swallowing - C/O food getting stuck in throat or chest - A/w nasal regurgitation, choking and coughing - Region localized is poorly correlated with exact - A/w other neurological signs: site of abnormality Nasal speech (soft palate ) - Note that oesophageal dysphagia my perceive location at cervical region mimicking oropharyngeal dysphagia Drooling of saliva Dysarthria, diplopia - A/w recurrent aspiration

What type of pathology is causing the dysphagia? Mechanical Functional Onset Can be gradual or sudden Usually gradual Progression Often Variable C/O Difficulty swallowing solid >> fluid Difficulty swallowing solid + fluid Response to Usually passes with drinking liquid or Often regurgitation bolus repeated swallowing Variation with None May vary with temperature temperature Intermittent? Webs, rings, oesophagitis, Diffuse oesophageal spasm, nutcracker CVS compression oesophagus Progressive? Strictures Achalasia Others Other relevant Hx (eg. tumour) Hx of , neuromuscular disease

Is it painful? – odynophagia suggestive of □ Oesophagitis: drug-induced, radiation, infectious, reflux Causes of infective oesophagitis: □ Caustic ingestion Healthy: Candida albicans, HSV □ Late CA oesophagus HIV: fungal, viral, mycobacteria, protozoan, ulcers Are there any red-flag features of CA oesophagus? □ RFs: smoker, drinker, chronic GERD, Barett’s oesophagus, achalasia, FHx… □ Dysphagia: recent onset, progressively worsening □ Odynophagia (late feature) □ UGI bleed □ Constitutional symptoms: loss of weight (also in achalasia), loss of appetite, anaemic symptoms □ Local invasion: hoarseness (RLN), T-spine bone pain (vertebral), fever/cough/haemoptysis (trachea), massive haematemesis (aorta) □ Metastasis: neck lump, , bone pain Any suggestive features of individual causes? Oropharyngeal dysphagia Oesophageal dysphagia

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Functional Functional - Hx or features of neurological diseases, - Hx or features of systemic sclerosis, eg. eg. stroke, myopathies Calcinosis, Raynaud’s, (Esophageal 156 Mechanical dysmotility), Sclerodactyly, Telangiectasia - Reflux symptoms, eg. , acid/water Mechanical brash, ↑when lying down → reflux strictures - Reflux symptoms, eg. heartburn, acid/water - Halitosis → pharyngeal diverticulum brash, ↑when lying down → reflux strictures - Hx of caustic ingestion - Drug Hx: tetracyclines, NSAIDs, KCl, alendronate → drug-induced oesophagitis

Any complications? □ □ : fever, cough, SOB (esp at night) □ Tumour spread: hoarseness, bone pain, haemoptysis, neck lump, jaundice…

2. Physical Examination General condition: □ Level of alertness and cognitive status → risk of aspiration? □ Vitals, → hypovolemia from or ↓intake □ Cachexia → nutritional status □ Pallor → UGIB due to tumour, peptic ulcer or oesophagitis □ Jaundice → mets Examination to look for causes: □ Neurological exam for any CN5, 7-12 palsies, PD features, myopathy □ Neck exam for any neck mass □ Bedside swallowing test for direct observation of act of swallowing □ Surgical scars on /chest for previous surgeries or RT □ Abdominal exam for any palpable mass (not likely) □ PR exam for any Examination to look for any complications: □ Aspiration pneumonia: febrile, septic-looking, lung crepitation, ↓AE (usually RUL) □ Metastasis: cervical LN, , Any treatment already given? □ Tube feeding via NG tube, gastrostomy, jejunostomy → look at the colour of aspirate □ TPN

156 Strictly speaking, CREST syndrome is the limited cutaneous form of systemic sclerosis.

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3. Investigations OGD: first-line for oesophageal dysphagia □ Advantage: allows direct visualization, allow tissue Bx (esp in malignancy), allow therapeutic interventions, eg. treat bleeding, stents □ Disadvantage: should NOT be used if suspecting webs or diverticula (risk of perforation)

Barium swallow for OGD negative but still suspect mechanical obstruction □ Advantage: less invasive than OGD □ Disadvantage: dangerous if at risk of aspiration □ Possible findings: → Bird’s beak (rat’s tail) sign in achalasia → Oesophageal diverticulum or pharyngeal pouch → Shouldering in stricture (smooth if benign, right-angled if malignant) → Corkscrew appearance in diffuse oesophageal spasm

High resolution manometry (HRM) for OGD negative but still suspect functional obstruction □ 36 circumferential channels each with 12 sensors down oesophagus □ Gold standard for assessing oesophageal motility □ Reading a manometry contour plot: → Vertical = distance down oesophagus → Horizontal = time □ Chicago classification

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Video fluoroscopic swallowing study (VFSS) and fibreoptic endoscopic evaluation of swallowing (FEES) for oropharyngeal dysphagia □ VFSS: fluoroscopic examination of swallowing of liquid, paste and solid with barium contrast □ FEES: nasal endoscopic examination during swallowing process □ Allow assessment of penetration and aspiration of various consistencies of food during swallowing □ Limited to cervical oesophagus

4. Initial Management Stabilize patient: □ Resuscitate if haemodynacmically unstable □ IV fluid to correct fluid deficits and electrolyte derangement □ Nutrition: fluid-only (if can tolerate), NPO157 + NG tube/TPN (if cannot tolerate fluid) □ Treat aspiration pneumonia: NPO + IV Abx Ix and treatment of underlying cause

157 NPO = nil per os, i.e. nothing taken by mouth.

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3.3.2 Upper GI Bleeding Ref: Davidson P. 853, Andre Tan Ch5, WCS52, 57 A. Causes of Upper GI Bleed Common causes Uncommon causes Peptic ulcer disease* (most common) Oesophageal Gastro-esophageal varices* Oesophageal tumour or duodenitis Stomach 158 Gastric malignancies Portal hypertensive gastropathy, GAVE , Dieulafoy’s lesion*159 Oesophagitis Small bowels Mallory-Weiss syndrome Aortoduodenal fistula160*, angiodysplasia, GI stromal tumour (GIST)161, diverticular bleeding, Crohn’s disease Biliary tree Haemobilia (due to PTBD), haemosuccus pancreaticus162 *Causes that can give rise to severe bleeding

Peptic ulcer disease: accounts for ~25-50% of non-variceal UGIB □ Site: duodenal, gastric, oesophageal, stomal (eg. jejunal side of gastrojejunostomy) → Ulcers high on lesser curve and in postero-inferior wall of D1 bleed more easily (penetrate into Lt gastric and gastroduodenal aa. respectively) □ S/S: variable bleeding ± previous epigastric discomfort □ Suggestive features: → Hx of dyspepsia → Hx of H. pylori infection: urea breath test, OGD, triple therapy → DHx of NSAIDs, antiplatelets, steroids, anticoagulants, TCM → Recent Hx of stress (eg. burns (Curling ulcer163), ↑ICP (Cushing’s ulcer))

Gastro-esophageal varices: accounts for 5% of UGIB but 80% of the mortality □ S/S: usually fresh large volume haematemesis (± haematochezia), rarely coffee ground vomitus □ Usually cannot be distinguished based on Hx alone □ Suggestive features: → Hepatitis carrier status → Hx of cirrhosis and chronic liver disease → Hx of oesophageal varices with banding done

158 GAVE = gastric antral vascular ectasia, otherwise known as watermelon stomach, refers to dilated antral small blood vessels of unknown cause giving rise to erythematous bands (watermelon appearance on endoscopy). It is a/w liver diseases and ct diseases. 159 Dieulafoy’s lesion = a developmental malformation characterized by massive or recurrent bleeding from an area of apparently normal gastric mucosa. It is caused by an AVM, usually in gastric fundus, resulting in a large tortuous submucosal arteriole prone to bleeding. It is often missed by endoscopy as it often retracts into submucosa when it is not bleeding. 160 Note that aorta is situated just behind D4. It can occur primarily with erosion of AAA into oesophagus or secondarily after aortic surgery. 161 GIST are tumours of smooth muscle pacemaker cells (mesenchymal origin). It may ulcerate and bleed when malignant. 162 Haemosuccus pancreaticus = bleeding into pancreatic duct. It commonly occurs secondary to haemorrhagic pancreatitis. 163 Curling ulcer occurs with ↓intravascular volume leading to ischaemia.

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Gastritis and duodenitis: □ S/S: usually small volume bleeding □ Drug-induced due to local (GI) and systemic effect (blood) of aspirin and NSAIDs → Almost all pt on aspirin develop mild haemorrhagic gastritis within 24h → usually minimal and not clinically apparent → adaptation and healing → Bleeding can occur acutely (within first few days) or chronically (after several months) → Usually self-limiting after removal of the drug → Note that enteric coated aspirin still have systemic effect → can cause bleeding □ Alcohol-induced → Can be acute (esp after binge drinking) or chronic → Note that they can occur in patients with existing cirrhosis or portal HTN □ Stress gastritis: → Usually in ICU patients with resp failure, hypotension, sepsis, renal failure, burns… → Only 2-10% has significant bleeding (esp pt with coagulopathy due to eg. DIC, RF)

Mallory-Weiss tears: □ Cause: violent retching leading to longitudinal tears in EGJ mucosa and submucosa (but sparing muscularis cf Boerhaave syndrome with full-thickness tears) □ Suggestive features: → Hx of repeated vomiting → Hx of alcohol intake (note alcoholic liver ds also causes variceal bleeding) → Hx of chemotherapy

Malignancy: uncommon causes of UGIB □ Site: gastric, oesophageal, duodenal □ S/S: bleeding usually mild and self-limiting but can be large volume □ Suggestive features: → Early satiety, chronic epigastric discomfort/ → Loss of weight, loss of appetite

Oesophagitis can arise from □ Reflux: obesity, middle aged, Hx of heartburn, acid regurgitation, acid/water brash □ Irradiation: Hx of H&N and thoracic malignancy □ Infectious: usually in immunocompromised patients (Candida, HSV, CMV) □ Drug-induced: tetracyclines, alendronate, slow K □ Sclerotherapy-induced: Hx of endoscopic intervention □ Caustic substance ingestion

Angiodysplasia (vascular ectasia): □ Site: usually in colon but can occur in stomach and duodenum □ Suggestive features: elderly, aortic valve disease164, chronic renal failure, HHT, prior RT

164 This is due to Heyde’s syndrome where in aortic valve disease, vWF becomes uncoiled (i.e. activated) when passing through the pathologic aortic valve. They are then cleaved by ADAMTS13. Consumption of vWF precipitates bleeding from pre-existing angiodysplasias.

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B. Approach to Upper GI Bleed Definition: bleeding from GI tract proximal to ligament of Treitz (duodenojejunal junction) 1. History Taking How does the patient present? – depends on volume and location of bleeding Acute bleeding Chronic bleeding - Small amounts - Haematemesis - Asymptomatic Fe deficiency anaemia - Coffee ground from NG tube - Faecal occult blood +ve on routine checkup - Fresh blood from NG tube Moderate amounts - Melaena - Symptomatic anaemia: lethargy, dizziness, - Haematochezia palpitation, angina, dyspnoea - Abnormal stool colour (eg. melena) - Abnormal Ix (↓Hb, ↓MCV, Fe studies, FOBT+) Coffee ground vomiting: □ Causes: gastric ulcers, gastritis, small amounts of variceal blood (dripping down into stomach) □ Pathology: UGI blood oxidized by gastric acid → vomitus containing methaemoglobin □ Indicates: mild bleeding from stomach or beyond Haematemesis: □ Causes: variceal bleeding, Mallory-Weiss tears, AV malformation □ Pathology: vomiting of fresh, unaltered blood → ↑time spent in stomach → ↑oxidization → red colour turns brown gradually □ Indicates: moderate-to-severe bleeding or from a source proximal to stomach Melaena: passing of black (as black as hair), tarry, loose, sticky, malodorous stools □ Types: distinguished on PR → Fresh melaena: jet black with tarry non-particulate liquid stools → indicates acute ongoing bleeding → Old (stale) melaena: black-grey, dull and mixed with normal stools → indicates bleeding has stopped □ Pathology: → Blood in GI tract digested by enzymes → black haematin in stools → A cathartic165 → usually accompanied with loose stools or diarrhoea □ Indicates: usually upper GI bleeding but can arise down to Rt colon □ Note: must rule-out iron stools due to iron supplements → More likely to be constipated → Usually present with green-black stools → When smeared on gloves after PR, usually will have a green-black hue (cf reddish hue in melena) Haematochezia: usually only if very profuse UGI bleeding

165 Cathartic = diarrhoea-inducing substance.

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Is it true UGI bleed? – rule out □ Haemoptysis: a/w cough, frothy, bright red (aerated), no melaena □ Upper airway bleeding: swallowed blood from epistaxis or oral bleeding

Assess urgency! – should be done before history taking □ Very severe: hypotension, tachycardia, agitation, confusion, drowsiness, coma □ Moderate to severe: postural hypotension (indicates ≥20% reduction in blood volume) → Note that haematocrit does not drop until expansion of ECV → does NOT reflect degree of blood loss □ Proceed to resuscitation first if features above present (see below) Characterize the bleeding: □ Current bleeding: nature, number of times, amount, duration □ Any previous episodes

Is it variceal bleeding? – usually profuse, presents as haematemesis □ Hx and S/S of liver disease: ascites, jaundice, hepatic encephalopathy (these pt can still have ulcers) □ RFs of chronic liver disease: hepatitis carrier status, alcoholism, FHx of HCC/hepatitis □ Hx of previous variceal bleeding: any previous UGIB, OGD, banding Is it peptic ulcer disease? – variable bleeding □ Previous dyspepsia/pain: ↑with eating (gastric) vs ↓with eating (duodenal) □ Hx of peptic ulcer ± bleeding: ulcer recurrence (more common in pre-H. pylori era) □ Hx of H. pylori testing, treatment and F/U: → Peptic ulcer disease is unlikely if Hp is eradicated and is –ve Clues that a pt may be → Still possibility of Hp-negative peptic ulcers (eg. drug-induced) taking NSAIDs - IHD, Hx of chest pain, □ Recent use of NSAIDs and TCM (some TCM may contain NSAIDs) CVA, minor stroke, TIA → Sometimes patient may not be aware of this - Joint pain, seen by → look for certain clues orthopaedic - Given analgesic together □ Recent severe metabolic stress, eg. burns, ↑ICP with antacids Are there worrisome symptoms of malignancy? □ ↓weight, ↓appetite □ Early satiety □ Dysphagia (CA oesophagus) □ FHx of GI malignancies □ Signs of metastasis: jaundice, dyspnoea…

Any other associating symptoms? □ Dysphagia: painful (oesophagitis, ulcers), painless (malignancy) □ Vomiting: eg. repeatedly, a/w alcohol → Mallor-Weiss tears □ Heartburn, acid regurgitation: reflux oesophagitis □ Early satiety: malignancy, peptic ulcer □ Epigastric pain: peptic ulcer, gastritis, malignancy Any potential precipitating factors?

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□ Bleeding tendencies: → Bleeding symptoms: haemoptysis, haematuria, epistaxis, easy bruising → Hx of anticoagulant and antiplatelet use □ Alcohol ingestion: gastritis, Mallory-Weiss tears (if recurrent vomiting), alcoholic cirrhosis □ Ingestion of caustic substances Any complications? □ Symptomatic anaemia: SOB on exertion, dizziness, syncope, chest pain, palpitation, malaise □ S/S of hypovolemic shock: postural hypotension, tachycardia, confusion… □ Acute MI: esp if prev Hx of IHD

2. Physical Examination Confirm the complaint: □ Examine the vomitus □ Examine material from nasogastric tube □ Perform PR exam: fresh vs old melaena Vital signs: erect/supine BP, pulse, haemocue General examination: □ Hydration status: skin turgor, mucosa □ Anaemic signs □ Stigmata of chronic liver disease □ Signs of hereditary vascular anomalies, eg. skin telangiectasia in HHT □ Bleeding source in nose/mouth □ Lymph nodes Abdominal examination: □ Epigastric tenderness □ Abdominal masses □ Hepatomegaly, , ascites □ PR exam Other examination: respiratory to r/o aspiration pneumonia 3. Investigations CBC: □ Hb: usually ↓ after 48h □ MCV: usually normal in acute bleeding but may ↓ if chronic (or thalassaemia) □ Platelet: ↑ (reactive) or ↓ (thrombocytopenia) LFT: underlying liver disease RFT: □ Electrolytes: usually normal □ Urea/creatinine: urea abnormally higher than creatinine → Reason: breakdown of GI blood (indicates UGIB) and hypovolemia (pre-renal failure) Clotting profile: PT/aPTT T/S to prepare for transfusion Erect CXR for aspiration pneumonia and r/o perforation 4. Management General principle to acute management: 80% of ulcer - Page 203 of 360 - bleeding stops spontaneously

□ Resuscitation if in shock (earliest sign is tachycardia) □ Rapid assessment + urgent OGD if ongoing bleeding □ Otherwise Hx, P/E, Ix + late OGD Usually give empirical PPI until diagnosis a. Resuscitation ABC: □ A: intubate if decompensated (confused) or massive haematemesis

□ B: O2 cannula to ↑O2 carrying capacity of blood □ C: large bore IV cannula with colloid/crystalloid infusion ± blood transfusion NPO, NG tube if haematemesis (but NOT if suspect varices) Monitoring by: □ Shock chart hourly □ Vitals: BP/P, RR, body temp166 □ Foley’s catheter: urine output ≥0.5mL/kg/h □ Cardiac monitor, pulse oximetry □ ± CVP line for PAWP167 b. Locate Bleeding Source Choice: □ Upper endoscopy (first-line) □ Colonoscopy for LGI sources □ Capsule endoscopy, double/single balloon enteroscopy for small bowel sources □ RBC scan, angiography for occult bleeding i. OGD Arrange emergency OGD if: □ Shock/haemodynamic instability: OGD after BP stable (requires sedation) □ Features of ongoing bleeding: → Haematemesis → Fresh melaena → Fresh blood from NG tube → Fresh PR bleed → Tachycardia □ Suspected variceal bleeding (covered in later sections)

166 ↓body temperature can cause ↓efficiency of clotting factors. 167 PAWP = pulmonary arterial wedge pressure measures the preload of the heart by the Swan-Ganz catheter. It can guide resuscitation in ICU setting by detecting fluid status to help treat hypovolemic shock without inducing volume overload.

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Role of OGD: □ Diagnostic: → Identify source of bleeding → Biopsy for H. pylori and r/o CA stomach (if gastric ulcers present) □ Prognostic: stratify risk of rebleeding → guide subsequent Tx □ Therapeutic: definitive surgery or temporizing before definitive surgery Forrest’s classification: □ Also called endoscopic stigmata of recent haemorrhage (ESRH) □ Help assess chance of rebleeding □ Guide subsequent Tx Endoscopic Tx modalities: □ Adrenaline injection: volume effect, induce vasoconstriction, attract platelet for thrombosis □ Heat probes: melt wall → stop bleeding Chance of □ Haemoclips Type Tx □ Argon plasma coagulation (usually for rebleeding angiodysplasia) I – active bleeding □ Band ligation (usually for varices) Ia – spurting 80-90% 168 C/I if there is perforation Ib – oozing 30% Risk of endoscopy: Endoscopic II – recent bleeding Tx □ Anaesthetic risk: resp depression, MI, CVA IIa – non-bleeding 20-50% □ Procedure-related: visible vessels → Bleeding and perforation IIb – adherent clot 20-30% → Failure of haemostasis Start → Failure of complete scope (to D2) III – clean base 0-2% feeding, early D/C After endoscopy, □ IV PPI to ↑pH for clot stabilization □ Close monitoring for rebleeding (3-10%) usually in the first 3d Risk factors for recurrent bleeding: → ↑pulse rate - Blood loss: shock on presentation, Hb <8 on presentation, need blood transfusion → Haematemesis - Patient profile: age >60y, comorbidities, → Fresh blood from NG tube coagulopathy, already hospitalized for → Fresh melena other conditions → ↓Hb level - Disease: large ulcers, posterior D1 or high posterior lesser curve Consider surgery if rebleeding (see later section)

168 Pneumoperitoneum can cause abdominal compartment syndrome leading to ↓VR and death and splinting of diaphragm compromising ventilatory movement.

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ii. Other Diagnostic Modalities Considered if OGD -ve Usual approach: □ Colonoscopy for LGI sources □ Capsule endoscopy, double/single balloon enteroscopy for small bowel sources □ RBC scan, angiography for occult bleeding Capsule endoscopy: □ Principle: swallow capsule with cameras → transmit images to receiver → entire small bowel examined □ Indications: detect SB pathologies, eg. coeliac disease, Crohn’s disease, tumours, NSAID-induced GI damage, polyposis syndromes → Obscure GI bleeding or Fe deficiency anaemia with OGD/colonoscopy –ve → Suspected or known small bowel pathologies □ Usually only as guidance for enteroscopy □ C/I: → Known/suspected GI obstruction/strictures (may be stuck) → Pacemakers or implanted electromedical devices (cannot function) → Swallowing disorders or severe motility problems (cannot pass into SB) □ Limitations: expensive, diagnostic only, long viewing time, insensitive, inability to determine exact site Enteroscopy: □ Principle: → SB extremely long with elastic wall → cannot use extremely long scopes or else may perforate while pushing → Use of flexible overtube with a balloon system allows shortening of intestines → visualize entire small bowel □ Types → Double balloon enteroscopy: two balloons to grip bowel and shorten it - Can visualize deeper parts of SB but slower intubation → Single balloon enteroscopy: one balloon combined with up and down angulation of scope to grip bowel and shorten it □ Approach: anterograde (from mouth) or retrograde (from anus) □ Advantage: → Allow Bx and therapeutic interventions → Avoid surgical Tx for conditions in which it is previously required, eg. bleeding, mucosal tumours, benign Crohn’s strictures in distal small intestines RBC scan: □ Principle: RBC labelled in vitro by 99m-Tc pertechnetate → visualize GI bleeding on scintigraphy □ Advantages: → Readily available, low cost, no complications → Can detect intermittent and slow bleeding (more sensitive than angiography) → Allow sequential scans □ Disadvantages: cannot perform intervention Angiography: □ Advantage: → Can be performed intra-operatively → inject dye to guide surgery → Can diagnose non-bleeding lesions, eg. angiodysplasia, SB tumours □ Disadvantage: not sensitive for slow and intermittent bleed c. Treatment Modalities Acute management:

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□ Endoscopic therapy: see above, often 1st line for UGI bleed □ Sengstaken-Blakemore tube: balloon tamponade for acute severe variceal bleeding □ Medical therapy: → Octreotide, terlipressin for variceal bleeding → PPI: empirical until diagnosis, post-endoscopy IV infusion if diagnosed ulcer Management of rebleeding: □ Repeat OGD □ Surgery (see below) □ Mesenteric angiogram for embolization Treatment of underlying condition: triple therapy etc. i. Surgery for Bleeding Ulcers Rarely required Indications: □ Therapeutic endoscopist not available □ Massive bleeding □ Failed endoscopy □ Rebleeding after endoscopic therapy Usual procedures for ulcer bleeding □ Plication: closure of ulcer and ligation of bleeding vessels □ Additional procedures: → DU: truncal vagotomy169 and pyloroplasty170 → GU: Billroth I or II gastrectomy - Billroth I: resection of pylorus with gastroduodenostomy - Billroth II: resection of antrum with gastrojejunostomy171

169 Note that PN stimulation is important for stimulating gastric acid secretion and gastrin release. Denervation of PN supply to stomach results in ↓acidity of stomach and facilitates DU healing. 170 PN stimulation is important for gastric emptying. Therefore, pyloroplasty (vertical incision at pylorus and suturing the incision transversely) is required to widen the pylorus and facilitate gastric emptying. 171 Jejunum is joined to the greater curvature to ↓tension at anastomosis and therefore ↓risk of leakage.

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3.3.3 and Vomiting Ref: Davidson P. 853, Talley Ch13, WCS76 Terminology: □ Nausea: sensation of wanting to vomit □ Vomiting: forcible involuntary expulsion of stomach content through mouth → Preceded by nausea and autonomic symptoms (eg. salivation) □ Regurgitation: sudden, effortless return of small amount of gastric content into pharynx/mouth → No preceding autonomic symptoms □ Rumination: repetitive effortless regurgitation of recently ingested food into mouth → ± re- and re-swallowing or expulsion A. Causes Vomiting centre is activated by □ Visceral afferents (mAChR, H1, D2, 5HT3) detecting visceral stimuli □ Chemoreceptor trigger zone (D2, 5HT3) detecting chemical stimuli □ Cerebellum (H1, mAChR) detecting vestibular stimuli □ Higher centres detecting pain, emotional, repulsive sights/smell stimuli

Groups Acute causes Chronic causes Stomach - Food poisoning – - Mechanical (GOO) – PUD, CA S. aureus, Bacillus cereus stomach, lymphoma, CA pancreas - Gastroenteritis - Functional (motility) – gastroparesis, - GOO functional dyspepsia Other visceral - SB obstruction - Small bowel dysmotility - – acute appendicitis, (pseudo-obstruction) – drugs, , pancreatitis scleroderma, DM, amyloidosis, jejunal - Hepatitis diverticulosis, SB myopathy/neuropathy Neurological - CNS disorders – meningitis, - CNS disorders - ↑ICP migraine, ↑ICP - Psychogenic – psychogenic (after - Vestibular disorders – vestibular stress), bulimia nervosa neuronitis - Cyclical vomiting syndrome - Psychogenic – after stress Metabolic and - Pregnancy - Pregnancy others - Alcoholism - Alcoholism - Endocrine – DKA, Addison’s disease - Endocrine – hyperthyroidism, Addison’s - Uraemia disease - Drugs – narcotics, digitalis, chemo - Drugs – narcotics, digitalis, chemo

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B. Approach 1. History Is it true vomiting? – What happens during a typical episode? □ Vomiting: nausea/autonomic S/S → abdominal contraction → forceful expulsion of gastric content □ Regurgitation: no nausea/autonomic S/S → no contraction → effortless return of gastric content How is the vomiting? □ Duration, number of times – acute vs chronic □ Timing – esp relationship with meals → Delayed >1h after meal → GOO or gastroparesis → Early morning, before eating → pregnancy, (alcoholism, ↑ICP) □ Vomitus → Undigested food → Old food (eaten a few hours) → GOO → Bilious → open connection between duodenum and stomach (eg. SB obstruction) → Blood → PUD (or other causes of UGIB) → Feculent → distal IO Is the cause gastric or abdominal? □ → likely organic aetiology, consider acute abdomen □ → intestinal obstruction □ Diarrhoea ± fever → food poisoning, GE □ TOCC → food poisoning, GE Is the cause neurological? □ Abnormal mental status → CNS causes □ Vertigo, gait instability → vestibular neuronitis Any other causes? □ Drug Hx □ Constitutional symptoms → malignancy (red flag!) Any complications? □ Symptoms of dehydration □ Symptoms of electrolyte disturbance: hypokalemia, metabolic alkalosis □ Emetogenic injury, eg. Mallory-Weiss tears

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2. Investigations Largely based on symptomatology For abdominal pain, work up for □ Amylase for pancreatitis □ Erect/supine AXR for pneumoperitoneum (perforation), obstruction □ USG for cholecystitis and cholangitis □ CT/MRI as indicated For fever/, workup for food poisoning □ Stool for microscopy (RBC, WBC) and rapid GI panel (for eg. coronavirus, E. coli) Complications of vomiting □ CBC for anaemia, leukocytosis □ RFT for hydration status, electrolyte disturbance □ ABG for metabolic alkalosis For chronic diarrhea, may consider tests for gastric emptying □ Gastric emptying scan: 99mTc-DTPA meal/drink to visualize gastric emptying via scintigraphy → Gold standard for gastric emptying □ Barium studies (alternative, cannot evaluate emptying of solid food) □ CT/MRI for change in gastric volume □ Real-time ultrasound □ Gastric impedance (only for research)

3. Anti-emetics : dimenhydrinate, promethazine, meclizine, cyclizine □ Useful for vestibular causes eg. motion sickness : scopolamine □ Useful for vestibular causes eg. motion sickness Dopamine antagonists: □ Phenothiazines: prochlorperazine, chlorpromazine □ Haloperidol □ D2 blocker: metoclopramide, domperidone Serotoninergic agents: □ 5HT3 blocker: ondansetron □ 5HT4 agonist: cisapride, molsapride, itopride (prokinetic) Erythromycin (prokinetic)

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3.3.4 Approach to Dyspepsia and Functional Dyspepsia Ref: Davidson P. 852, 876, UpToDate, JC (A) TC on dyspepsia A. Approach to Dyspepsia Dyspepsia: chronic or recurrent pain or discomfort centred in upper abdomen □ Extremely common complaint (~25% in the West) but ~25% may have organic cause

Causes: Gastrointestinal Non-gastrointestinal Peptic ulcer disease Drug-induced dyspepsia: NSAIDs, steroids, oral Gastro-esophageal reflux disease antibiotics, iron, digoxin, metronidazole, alendronate, slow K… Biliary pain172 Abdominal wall pain Gastroesophageal CA Functional dyspepsia Pancreatic pathologies, eg. chronic pancreatitis Electrolyte disturbances, eg. hyperCa, hyperK Infiltrative gastric diseases, eg. Crohn’s disease Thyroid and parathyroid diseases Coeliac disease Chronic renal failure Intestinal parasitic infestation Coronary artery disease (basal myocardial ischaemia) Bowel ischaemia due to coeliac artery compression Other abdominal cancers, eg. HCC, HBP malignancies

Clinical approach: main aim is to r/o organic causes of dyspepsia Hx: Alarm features in dyspepsia: □ Alarm features for malignancy (see RHS) (1) Age >40y □ PUD: predominant upper abd pain but may also be a/w (2) Unintentional weight loss dysmotility-like discomfort (due to visceral hypersensivity) (3) Dysphagia or odynophagia □ GERD: dominant Hx of heartburn or regurgitation173 (4) Unexplained Fe def anaemia □ Biliary pain: episodic constant NON-colicky intense dull pain (5) Persistent vomiting → In RUQ or epigastrium ± radiation to back or scapula (6) UGIB → Often a/w diaphoresis, nausea or vomiting (7) Palpable mass or LNs → NOT ↑by movement, not ↓by squatting, bowel mov’t or passage of flatus (8) FHx for UGI cancers → Can be a/w post-prandial discomfort □ Drug-induced: +ve drug Hx

P/E: usually normal, epigastric discomfort NOT diagnostically valuable □ Carnett sign: ↑local tenderness during muscle tensing → indicates abdominal wall origin □ Other findings: anaemia, jaundice, wasting, abd mass, LN, ascites

172 Biliary can be a/w post-prandial pain, as eating a fatty meal is a common trigger for GB contraction. 173 GERD is overdiagnosed in dyspepsia! → do NOT conclude as GERD unless w/ typical symptoms.

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Evaluation: □ Depends on setting and presence of alarm symptoms □ Monitoring of progress: refer if symptoms persist or progressive

Workup Involves Indicated for Upper endoscopy for any organic disease Age >40y H. pylori testing should be done on Bx sample Unexplained weight loss or Upper Subsequent management: anaemia endoscopy □ Manage/workup on underlying cause if +ve UGIB, vomiting □ Treat HP infection if HP +ve Dysphagia or odynophagia □ Treat as functional dyspepsia if -ve FHx +ve for UGI cancers Urea breath test or stool antigen test Age <40y and NO alarm Subsequent management: HP testing features □ HP eradication therapy if HP +ve HP not tested in previous OGD □ Treat as functional dyspepsia if –ve Empirical antisecretory therapy: PPI proven Empirical to ↓dyspepsia symptoms Age <40y and NO alarm drug Tx features Prokinetics and TCA if fail PPI treatment i.e. treat as Persistent symptoms despite FD Should be reinvestigated by OGD should documented HP eradication symptoms persist despite multiple Tx

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3.3.5 Abdominal Pain Ref: Browse Ch 15, Andre Tan Ch2, WCS53, 55, 60, 64 A. General Principles of Abdominal Pain Abdominal pain originates from irritation of peritoneum Can be broadly divided into: Visceral Parietal Referred pain Origin and Visceral peritoneum Parietal peritoneum Innervation shared by both innervation innervated bilaterally by innervated unilaterally by somatic nerves and visceral autonomic nerves somatic nerves organs Cause Stretching, inflammation, Irritation (inflammatory or (Visceral causes) ischaemia mechanical) Site Midline in upper (foregut), Well-localized over irritated Well-localized in a distant central (midgut) or lower area area abdomen (hindgut) Character Dull, poorly localized Sharp, severe Sharp

In general, causes of acute abdominal pain can be divided into: Examples Pathology Typical S/S Inflamed Signs of local inflammation (early) viscus - Appendicitis or generalized peritonitis (late): Initially local inflammation of - Ileitis - Pain, tenderness, guarding, rebound visceral peritoneum tenderness - Colitis → later generalized - Diverticulitis - ↓bowel sounds - Tachycardia, fever

Perforated - Peptic ulcer GI content enters peritoneal viscus cavity → chemical or bacterial Signs of generalized peritonitis - Ischaemic bowel peritonitis Obstructed Colicky pain, vomiting, viscus - IO Luminal obstruction distension, absolute - (Ureteric colic) → intestinal distension depending on level of obstruction - (Biliary colic) (cardinal signs) Strangulation Local/generalized peritonitis Infarcted - Mesenteric ischemia Ischaemic damage of nerve Local/generalized peritonitis viscus - Ischemic colitis endings → severe pain Signs of hypovolemic shock (late) Intra-abd or Irritation of peritoneum Signs of generalized peritonitis - Ruptured AAA retroperitoneal Cullen’s sign, Grey Turner’s sign, - Ruptured spleen Bleeding into peritoneal cavity haemorrhage , shoulder pain - Ectopic pregnancy Bleeding → hypovolemia Signs of hypovolemic shock (early) Extra-GI - Pleurisy causes - MI Various / - DKA…

D/dx of abdominal pain: RUQ Epigastric LUQ Liver: hepatitis, hepatomegaly, Oesophagus: oesophagitis, Spleen: rupture, infarct,

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liver abscess GERD, Boerhaave’s syndrome splenomegaly Biliary: cholangitis, cholecystitis, Stomach: gastritis, peptic ulcer, Pancreas: pancreatitis cholelithiasis, choledocholithiasis gastric volvulus, gastric outlet Thoracic: pneumonia, pleural Thoracic: pneumonia, pleural obstruction, CA stomach effusion, MI effusion Pancreas: pancreatitis, CA Others: subphrenic abscess pancreas Thoracic: MI, pericarditis (Hepatobiliary) Others: rAAA, R flank Para-umbilical R flank Kidney: pyelonephritis, renal Small bowels: small bowel Kidney: pyelonephritis, renal infarct, obstructive uropathy obstruction, gastroenteritis, early infarct, obstructive uropathy (hydronephrosis), renal stone, appendicitis, mesenteric (hydronephrosis), renal stone, RCC ischaemia, IBD RCC (Biliary) Retroperitoneal: ruptured AAA, (Splenic) pancreatitis RLQ Hypogastric LLQ Ileum: ileitis (Crohn’s disease, Large bowels: large bowel Sigmoid colon/Lt colon: colitis Yersinia), Meckel’s diverticulitis obstruction, colorectal CA (infective, IBD, radiation), Caecum/Rt colon: acute Urological: AROU, bladder diverticulitis, CA Lt appendicitis, diverticulitis, caecal stones, cystitis/UTI colon/sigmoid ischaemia, colitis (infective, IBD, O/G: PID, degenerating fibroid, O/G: torsion/rupture of ovarian radiation), CA Rt colon/caecum adenomyosis/endometriosis, cyst, ectopic pregnancy, PID O/G: torsion/ruptured of ovarian ectopic pregnancy Urological: ureteric colic, cysts, ectopic pregnancy testicular torsion Urological: ureteric colic, Others: strangulated testicular torsion inguinal/femoral Others: strangulated inguinal/femoral hernia, mesenteric adenitis Diffuse/non-specific abdominal pain Bowels: gastroenteritis, constipation, uncomplicated bowel obstruction Peritoneum: generalized peritonitis, intra-abdominal haemorrhage, ruptured viscus Medical causes: DKA, hypercalcemia, herpes zoster, anaphylaxis, porphyria

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1. Causes of Upper Abdominal Pain Acute causes Pathology Hx Signs Heartburn - Severe retrosternal burning Refluxing of acid - Ppt by bending, stooping, heavy lifting from stomach up - Occur when lying flat through LES onto Oesophagitis, Acid regurgitation squamous Usually unremarkable GERD epithelium of - Bitter taste develop ± cough oesophagus Dysphagia → pain - Chronic reflux → stricture - Should r/o achalasia, CA oesophagus/cardia Epigastric discomfort/pain - Usually described as indigestion - Can be burning (ulcer-like) or distension, N/V, early satiety, belching (dysmotility-like) - Gastric ulcer: Usually pain immediately after Acute Irritation of meal → often afraid of eating174 Epigastric tenderness gastritis, gastric/duodenal ↓ by vomiting mucosa due to ± guarding if severe duodenitis, - Duodenal ulcer: ↓mucosal defense ± anaemia if chronic bleeding peptic ulcer ↓pain after eating → usually good appetite Pain ~2h after meal UGI bleed (haematemesis/ melena) Drug Hx: ask about ANY drug ingested - Esp aspirin, NSAIDs, alendronate Cigarette smoking, stress may be risk factors Sudden severe and constant epigastric pain Distressed, lying completely - Usually begins in epigastrium still, tachycardia, shallow Acid erosion of - Quickly reaches max intensity and respiration remains severe for hours gastric/duodenal Localized tenderness and - Gradually extends to whole of abdomen Perforated wall to visceral guarding (early) peritoneum peptic ulcer - ↑ by movement → usually lie still on bed → chemical and Any history of previous dyspepsia Generalized peritoneal signs then bacterial (late) with intense guarding Hx of steroids and NSAIDs peritonitis (board-like rigidity) Note: pain and guarding may ↓after 4-6h as the acid gets diluted but the peritonitis is still ± ↓liver dullness progressing. (pneumoperitoneum) Fat, female, fertile, forty Severe colicky pain in upper abdomen Spasms of - Severe, constant with excruciating Distressed Gallstone or gallbladder or exacerbations Jaundice (1/5) 175 biliary colic cystic duct to - Usually lasts < a few hours unless Tenderness, guarding in upper push stones complicated by acute cholecystitis abdomen Nausea, vomiting Hx of dyspepsia or upper abdominal pain

174 After eating, food enters the stomach, stimulating gastric acid and duodenal alkaline secretion and closure of pylorus. Therefore, acid stays within the stomach to irritate gastric ulcers whereas duodenal ulcers are spared. 175 Gallstone colic is caused by spasm of gallbladder as it tries to force a gallstone down the cystic duct.

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Fat, female, fertile, forty Distressed, lying still Sudden RUQ pain radiating to shoulder Pyrexia, tachycardia Obstruction in - Often radiates to the back to tip of right cystic duct scapula ± jaundice leading to - Continuous, last >6h RUQ tenderness/guarding Acute distension, - ↑ by moving and breathing cholecystitis chemical Palpable gallbladder (early on inflammation and - ↓ only by analgesics before guarding develops) secondary Nausea, vomiting Murphy’s sign176 infection ± obstructive jaundice (dark urine, pale stools, itchy skin) Bowel sounds usually present Hx of indigestion or abdominal pain unless infarcted/ruptured Agonizing pain but Sudden, progressive epigastric pain insignificant signs - Begins suddenly and then steadily Distressed, lying still increases in severity until very severe - Usually radiates to back Pale, sweating, tachycardia (due to hypovolemic shock177) - ↑ by movement, ↓ by sitting up and Activated leaning forward ± jaundice (gallstone) pancreatic Acute Persistent nausea with frequent vomiting, enzymes High fever not common retching pancreatitis autodigest the (suggests complication) pancreatic gland Hx of unusually large meal or alcohol Tenderness and guarding in intake upper abdomen Hx of indigestion or abdominal pain due to gallstone disease Grey Turner’s sign, Cullen’s Hx of alcohol intake sign (LATE signs, see below) Hx of exposure to mumps Bowel sounds usually present unless paralytic ileus Chronic causes M > F, more common in 20-60y Indigestion/dyspepsia associated with meals Loss of weight due to fear of food in gastric No anaemia, cervical ulcers 178 lymphadenopathy (suggests Chronic Long-standing Night pain in duodenal ulcers cancer) - Wakes pt, unrelated with food peptic ulcer, erosion/irritation Mild epigastric tenderness gastritis, of gastric or - Epigastric pain radiating to back or RUQ Epigastric distension + visible duodenitis duodenal mucosa - Continuous gnawing/boring ache peristalsis + succession splash - Periodicity: usually occurs for 2-3w at a time before resolving spontaneously if pyloric stenosis Water and acid brash 179 in duodenal ulcers UGI bleed (haematemesis, melena) M > F, more common in 50-70y Wasting, pallor Variable indigestion or epigastric pain Signs of metastasis CA stomach - May be mild/related to food but often / constant and not solely due a/w food - Jaundice or lymphoma - May present as a change in nature of pain - Supraclavicular LN in chronic PU pt - Pleural effusion Loss of appetite and weight - Ascites

176 Murphy’s sign: put your hand at Rt costal margin and ask the patient to take a deep breath. Pt with cholecystitis will experience a sharp pain that prevents further inspiration when the liver and the attached gallbladder descend and strike the palpating hand. 177 Hypovolemic shock develops in pancreatitis due to interstitial oedema. 178 This is thought to be caused by ↓pH in stomach at night when they are no longer buffered by presence of food. 179 Acid brash refer to effortless regurgitation of acid into mouth. Water brash refers to excessive salivation. Both occur as a reflexive response to irritation in GI tract (eg. duodenal ulcer).

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Dysphagia and regurgitation for cardia Epigastric tenderness tumours causing EGJ obstruction Hard, irregular, dull Vomiting of undigested food, epigastric distension, discomfort for pyloric tumours epigastric mass that moves Other S/S of metastasis with respiration Hx of peptic ulcer180, pernicious anaemia, Epigastric distension + visible atrophic gastritis, gastrectomy peristalsis + succession splash

Hx of triple therapy, B12 supplementation if pyloric stenosis Middle aged male Progressive Severe, recurrent epigastric pain radiating destruction of Often few physical sign pancreas to the back Chronic occurring de novo - Gnawing, persistent, dull ache Weight loss pancreatitis in chronic alcohol - Often a/w episodes of excessive alcohol Jaundice abuse or multiple drinking Palpable pseudocyst attacks of acute Weight loss, nausea pancreatitis Hx of alcohol abuse Persistent epigastric pain radiating to back - Continuous, dull, boring pain No physical signs (early or - ↑ at night, ↓ by sitting forward tail/body tumours) - Can radiate to RUQ (head) or LUQ (tail) Obstructive jaundice CA pancreas 85% in head of Progressive obstructive jaundice (90%) pancreas Weight loss Palpable gallbladder Steatorrhoea, epigastric bloating, Hepatomegaly , diarrhoea, vomiting, Signs of distant metastasis constipation (20-30%) Paraneoplastic obstruction Fat, female, fertile, forty Upper abdominal postprandial discomfort - Usually begins gradually 15-30min after meal and lasts for 30-90min Gallstones - May extend to RUQ and radiates through ± jaundice Chronic causing chronic or recurrent to the back RUQ tenderness cholecystitis gallbladder - ↓only by analgesics, ↑after fatty meal ± palpable gallbladder infection Postprandial belching Nausea/vomiting during acute exacerbations Obstructive jaundice if CBD stone Floating stools (fatty stools) Constant dull RUQ aching pain Distension of General malaise, weight loss if tumour Hepatomegaly liver capsule Hepatomegaly Jaundice if liver derangement Hyperfunctioning, Splenomegaly infiltration, or Dull, persistent LUQ pain congestion

180 Hx of peptic ulcer/Abx usage indicates previous H. pylori infection.

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2. Causes of Central Abdominal Pain

Acute causes Pathology Hx Signs True colic Abdominal distension - Severe central gripping pain interspersed with periods of little or no pain High-pitched, hyperactive Peristalsis to - Usually occur every 2-20 min bowel sounds Small bowel propel bowel Bile-stained or non-bile stained vomitus Abdominal scars for adhesion obstruction contents across Distension in centre of abdomen Hernial orifices for obstruction - May be a/w visible peristalsis strangulated hernia Absolute constipation with no passage of ± RLQ palpable mass in faeces or flatus (occurs late in small bowel intussusception IO) Usually due to ischaemia (from Small bowel Sudden onset central abdominal pain volvulus) or a progressing to generalized peritonitis Generalized peritoneal signs perforation closed loop obstruction Agonizing pain but Severe acute central abdominal pain insignificant signs when early Thromboemboli, - Usually poorly localized Lie still, pale, sweating, volvulus, - Later quickly develop signs of peritonitis Mesenteric dissecting tachycardia Nausea and vomiting ischaemia aneurysm, Tenderness/guarding can be Irreducible and painful hernia venous mild in initial stages thrombosis Hx of atherosclerosis, vasculitis Hx of abdominal surgery, hernia BS can be normal in early stages but becomes reduced Pain Usually due to - Usually mild but can be severe, colicky Gastroenteritis Campylobacter Usually few signs or viruses Vomiting and diarrhoea - Usually predominant picture Renal angle tenderness Infection of renal Pain in loin region or renal angle Kidney enlargement, bladder Pyelonephritis pelvicalyceal - May spread to centre of abdomen enlargement for system - May fluctuate in intensity hydronephrosis Urine examination Abdominal distension Large central tender expansile pulsating epigastric or Hx of smoker, atherosclerotic diseases paraumbilical mass Sudden onset of central abdominal pain Infrarenal (below costal margin) vs Rupturing of radiating to back or to groin along course of suprarenal (cannot get above) abdominal aortic Ruptured AAA genitofemoral nerve aneurysm Cullen’s and Grey Turner’s S/S of shock (pale, sweating, breathless, sign181 (late, 3-4d) palpitation, collapse) Generalized peritoneal signs Signs of hypovolemia (tachycardia, pale, sweating, postural hypotension) Chronic causes

181 Cullen’s sign = bruising around umbilicus. Grey’s Turner’s sign = bruising in the flanks. They are signs of intraperitoneal and retroperitoneal haemorrhage and are not specific to rAAA

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Intermittent abdominal pain Ill-defined ill-localized Irritable bowel Functional GI Change in frequency and abdominal sensitivity on syndrome disorder consistency of stools palpation Abdominal distension No other physical sign Typically presents at age of 20s ± palpate thickened small Long Hx of acute flares of colicky bowels Inflammatory Crohn’s disease central/lower abdominal pain with (most commonly Extraabdominal bowel disease ileocecal region) remission manifestations (Finger clubbing, A/w diarrhoea, mucus/blood in erythema nodosum, arthritis, aphthous stools ulcers, uveitis/episcleritis…)

Recurrent Previous Recurrent IO symptoms Abdominal scar adhesive abdominal obstruction surgery Hx of abdominal surgery Abdominal distension ‘Intestinal angina’ – begins insidiously after Mesenteric Less acute meals with umbilical/epigastric cramps, ± abdominal bruit ischaemia occlusions vomiting, diarrhoea Anorexia, weight loss 3. Causes of Lower Abdominal Pain Acute causes Pathology Hx Signs Unwell, low-grade pyrexia183 Often young adults and teenagers Tachycardia Classically a migratory pain (50%): Fetor oris (halitosis) Begins as vague ‘colicky’ paraumbilical Limited lower abd resp movt pain182 RLQ tenderness and Shifts to Rt iliac fossa and becomes more guarding (max over severe, constant and localized after a few 184 Unknown, likely hours-days McBurnley’s point ) 185 obstruction by S/S depends on exact site of appendix Rovsing’s sign faecolith, Acute Retrocaecal (64%) → RLQ, flank pain 186 lymphoid Cough sign appendicitis hyperplasia, Pelvic (32%) → bladder (dysuria, Obturator sign187 stricture, frequency), large bowel (diarrhoea) S/S 188 carcinoid tumour Post/preileal (1.5%) → terminal ileum IO Nausea, vomiting after onset of pain Tenderness of other sites Anorexia (~75%) before onset of pain depending on location Fever often after 6h Flank (retrocaecal), RUQ when peritoneum becomes affected (subhepatic) Generalized peritonitis if progressed: ± RLQ tender mass generalized abd pain, N/V, sweating, rigors (Indistinct, dull on percussion) BS present (unless perforated) Meckel’s Inflammation of S/S indistinguishable from acute Meckel’s appendicitis but pain felt more towards Similar to acute appendicitis diverticulitis diverticulum centre of abdomen than in Rt iliac fossa

182 The central pain is a referred pain as the visceral innervation of appendix is at the T10 level. As dermatomes in different persons vary, this may present as a retrosternal pain in some patients. It is therefore important to note that the initial pain is at midline instead of its precise level. 183 High-grade pyrexia should suggest other pathologies or generalized peritonitis a/w ruptured appendix. 184 McBurnley’s point = 1/3 distance from Rt ASIS to umbilicus. 185 Rovsing’s sign = pressure on Lt iliac fossa cause pain in Rt iliac fossa as it causes movement of inflamed appendix. 186 Cough sign = Rt iliac fossa pain on coughing due to localized peritonitis. 187 = RIF pain on internal rotation of flexed Rt hip due to spasm of obturator internus. 188 Psoas sign = RIF pain on Rt hip flexion due to inflamed retrocaecal appendix is lying on psoas muscles.

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(2% pop’n, 2ft Central abd pain if ectopic gastric or from ileocecal pancreatic mucosa becomes ulcerated or junction, 2 inch inflamted long, presents at Colicky abd pain if acting as head of 2y/o) intussusception or congenital band causes SB obstruction or volvulus Similar to acute appendicitis Inflammation of Usually in children Often only mild tenderness mesenteric LNs Mesenteric Preceding URTI and cervical LN ± rebound tenderness (common mimic adenitis of acute Usually central abd pain but can cause Pain may move at lateral appendicitis) RLQ pain decubitus position when glands move over with mesentery Usually 50-70y, Westerners Lie still, pyrexia, tachycardia Inflammation of Gradual onset of mild intermittent lower IF tenderness and guarding colonic abd pain tender sausage-shaped diverticula due Shift to L/R iliac fossa and becomes more ±IF mass to obstruction severe and constant dull on percussion Acute but can be 190 Nausea, ↓appetite but rarely vomiting Reversed Rovsing’s sign complicated by diverticulitis Peritoneal signs if generalized localized Constipation but a few develop diarrhea peritonitis abscess, purulent Dysuria, ↑frequency if diverticulum lies peritonitis or against bladder PR may show pain when finger fecal peritonitis Hx of diverticular disease, flatulence, is pushed high into Lt side of pelvis distension, L/RIF pain189 PR/sigmoidoscopy to r/o CA colon Agonizing pain but insignificant signs Acute Elderly with Hx of AF or IHD obstruction of Constant, severe non-specific abdominal Lie still, pale, sweating, colonic blood pain, progressively worsening tachycardia Ischaemic colitis vessels leading Rectal bleeding, bloody diarrhoea Tenderness/guarding can be to bowel ± preceded by classical colic (strangulated mild in initial stages ischaemia obstruction) BS can be normal in early stages but becomes reduced o Sexually active F, <40y High fever (38-39.5 C) Preceded by a few months of menstrual Lower abd tenderness, irregularities and dysmenorrhoea guarding Preceded by purulent yellow-white Often bilateral but may be asymm. Salpingitis and vaginal discharge by a few days Usually lower and nearer to midline associated Gradual onset of constant lower abd pain cf acute appendicitis infection of ± radiation into back PID supporting PV shows Sweating, rigors but no N/V or changes in tissues around Yellow-white introital discharge bowel habits adnexa Adnexal tenderness on bimanual Often a/w dysuria and urinary frequency palpation Often a/w dyspareunia191 Chandelier sign192 Hx of previous gyne procedures, IUD, or Pus discharge from cervical canal in STDs speculum examination

Sudden severe unilateral lower abd pain ± lower abd tenderness and Torsion/ruptured Complicated during agitating movement (eg. exercise) guarding of ovarian cyst ovarian cyst ± S/S of intra-abdominal bleeding S/S of intraabdominal bleed ± S/S of hypovolemic shock S/S of haemodynamic

189 Note that diverticular disease is almost exclusively in sigmoid colon (95%) in Caucasians but more commonly to be in Rt colon in Asians. 190 Reversed Rovsing’s sign = pressure on Rt side of abdomen may induce pain on left. 191 Dyspareunia = painful intercourse. 192 Chandelier’s sign = painful cervical excitation.

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collapse Female in child-bearing age S/S of pregnancy (morning sickness, amenorrhoea, breast swelling, +ve test) Preceded by a few days of mild abd pain Signs of hypovolemia (tachycardia, pale, sweating, Ectopic Tubal pregnancy Sudden onset severe lower abdominal ± rupture into pain on side of ectopic pregnancy postural hypotension) pregnancy abdominal cavity Becomes generalized and a/w S/S of shock Generalized signs of (fainting, collapse) if ruptured peritonitis Shoulder tip pain if blood collects beneath the diaphragm Hx of PID, fertility problems Severe, gripping true colic radiating down from renal angle, parallel to inguinal ligament into groin (base of penis, scrotum or labia majora) May have renal angle tenderness Obstruction in Point of beginning is a reliable indicator of Ureteric colic ureter due to level of obstruction Urinalysis shows gross or ureteric stones Severe, colicky with pain-free remission microscopic haematuria ↓ by rolling around bed or walking around Otherwise unremarkable Autonomic symptoms (sweating, N/V) Gross or microscopic haematuria Chronic causes

Chronic Diverticula in Middle-aged or elderly RIF tenderness ± mass diverticular colon Episodes of dull or colicky central R/O CA colon by DRE and disease ± inflammation or lower Rt sided pain sigmoidoscopy Pallor, cachexic Symptoms of anaemia RIF tenderness ± some Fatigue and SOB guarding RIF/R lumbar firm irregular CA Rt colon or Constitutional symptoms / mass (fixed or freely mobile, dull on caecum Dull RIF pain percussion) Colicky pain if SB obstruction ± hepatomegaly Self-palpated RIF mass DRE sigmoidoscopy normal ± FOBT +ve >50y or young adults with ulcerative Pallor, cachexic colitis or familial polyposis LIF/L lumbar mass ± Change in bowel habits tenderness (if a/w inflammation) 193 CA Lt colon, Alternating constipation and diarrhoea Dull on percussion 194 195 sigmoid or / Mucoid or pencil-thin stools ± hepatomegaly rectum Tenesmus 196 ± ↑BS, generalized peritonitis Haematochezia if complicated by IO and 197 Sigmoid/Lt colon: not common, dark and perforation plum colored with clots if occur PR palpable mass/nodules

193 Constipation is caused by obstruction. Diarrhoea is caused by liquefaction of faeces above the obstruction, inflammation of colonic mucosa and excessive secretion of mucus. 194 Mucoid stools are caused by excessive mucus secretion by the tumour 195 Pencil-thin stools are caused by colonic obstruction. 196 Tenesmus is a constant intense desire to defecate and may be a/w pain. When defecating, nothing or small amount of mucus and loose feces due to SOL in lumen or wall of rectum may be passed out. It occurs because rectosigmoid tumours are space-occupying lesions that simulate stools stored in the rectum. 197 Perforation is usually perforation of caecum secondary to LB obstruction instead of the tumour itself.

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Rectum: usually bleeding > abdominal pain if in apex of loop of sigmoid colon or and obstruction secondary deposits in pelvis Mild lower abdominal colic/ache PR blood becoming a persistent pain in LIF S/S of large bowel obstruction: colicky pain, distension LOW/LOA Uncommon in early stages LOW usually precedes anorexia Self-palpated mass

B. Approach to the Acute Abdomen Acute abdomen: presence of abdominal pathology which if left untreated (<72h) will result in patient morbidity and mortality Characterized by sudden onset of severe abdominal pain 1. History Taking Onset/duration: □ Within seconds: → Infarction, eg. MI, mesenteric occlusion → Haemorrhage, eg. ruptured AAA → Perforation, eg. PPU □ Within minutes: → Inflammatory, eg. acute appendicitis, pancreatitis, diverticulitis → Colic, eg. biliary colic, ureteric colic, IO → Ischaemia, eg. mesenteric ischaemia, strangulated IO, volvulus □ Over hours: → Inflammatory, eg. appendicitis, cholecystitis → Obstruction, eg, non-strangulated IO, urinary retention → Mechanical, eg. ectopic pregnancy, perforating tumours Quality: □ Constant pain due to inflammation, infiltration, ischaemia or infarction → Severe, persistent, made worse by local or general movement □ Colicky pain due to hyperperistalsis against obstruction → Waxing and waning gripping pain → Intestinal obstruction/ureteric colic: with periods of complete cessation (true colic) → Biliary colic: severe, constant with painful exacerbations but no complete pain-free periods □ Stretching pain due to prolonged obstruction to outflow of hollow viscus → Constant stretching pain but not colicky

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Site □ Localized vs diffuse vs vague □ Any shifting, eg. acute pancreatitis shift from periumbilical to RLQ Radiation: □ Back: pancreatitis, AAA, aortic dissection, posterior stomach/duodenal ulcer □ Shoulder tip: haemoperitoneum (eg. ruptured ectopic, splenic ruptured) □ Scapular spine: gallbladder □ Loin to groin: renal colic □ Testicles to flank: testicular pain □ Flanks: pyelonephritis, retroperitoneal haematoma, AAA Severity Time course: □ Constant, eg. ulcers □ Colicky ± pain-free remissions, eg. intestinal, renal, biliary colic □ Steady increase then constantly severe, eg. biliary colic, pancreatitis □ Progressive, eg. appendicitis, diverticulitis □ Catastrophic onset, eg. rAAA Exacerbating and relieving factors: □ Peritonitis: ↑ by movement, ↓ by staying still □ Colic: often ↓ by movement □ I/O: ↓ by vomiting

Associating symptoms: screen UGI, LGI, Uro and O/G systems □ Nausea/vomiting:

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→ After onset of pain: appendicitis → Before onset of pain: GE, food poisoning → Bilious vomit: process distal to duodenum □ Dysphagia → oesophagitis □ Heartburn, acid/water brash, ↑upon lying supine → reflux disease □ UGIB → oesophagitis, peptic ulcers, gastritis □ Abdominal distension (relieved by vomiting) → IO □ Obstructive jaundice → cholangitis, CBD stones □ Mucoid stools, diarrhoea → inflammatory process □ Absolute constipation → IO □ Haematochezia → LGI pathologies □ Tenesmus → CA colon □ Dysuria/haematuria → UTI, ureteric colic □ Vaginal discharge → PID □ Fever/chills → inflammatory or infectious process □ Constitutional symptoms or change in bowel habits → malignancy □ Chest pain, dyspnoea → basal pneumonia, MI Past medical Hx: □ RF for AAA/mesenteric ischaemia: peripheral vascular disease, coronary artery disease… □ RF for bowel obstruction/perforation: cancer, PUD, previous abdominal surgery □ Medical conditions: DKA, porphyria, sickle cell crisis… □ LMP to exclude ectopic pregnancy Drug Hx: □ RFs for PUD: NSAIDs □ Other medications: → may mask signs of inflammation → Abx may mask pain by peritonitis and may cause pseudomembranous colitis → Opioid analgesia usually not a/w ↓diagnostic accuracy Relevant social Hx and family Hx Menstrual and sexual Hx may be relevant to r/o O/G causes Systemic review

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2. Physical Examination General appearance: □ Lying motionless → local or generalized peritonitis □ Restless, writhing in pain → ureteric colic, intestinal colic □ Bending forward → pancreatitis Vitals + hydration status: □ Haemodynamic instability → RESUSCITATE FIRST before performing any P/E □ High-grade fever → consider abscess, cholangitis, PID or pneumonia □ Hydration status → look for skin turgor, postural hypotension, mucosal membrane □ Other peripheral signs, eg. jaundice, pallor, cold extremities Abdominal examination: □ Inspection → Distension, visible peristalsis → IO → Surgical scars → previous OT → Bulging masses → Pulsations → AAA → Skin changes □ Palpation → Peritoneal signs: tenderness, guarding, rebound tenderness → Palpable masses → Hernial orifices (incisional, umbilical, inguinal, femoral) → incarcerated198 hernia → Pain out of proportion of PE findings → acute pancreatitis, mesenteric ischaemia □ Percussion: → Dullness over bladder → AROU → Resonance over distended bowel → I/O □ Auscultation: → Absent BS → possibly paralytic ileus from generalized peritonitis → High-pitched tinkling BS → IO □ Per- □ Examination of external genitalia Per-vaginal examination Others: □ Chest examination: pleurisy, AMI, basal pneumonia □ Peripheral vascular examination: embolization □ Signs of coagulopathy

198 Incarcerated = irreducible. Strangulation = loss of blood supply. An incarcerated hernia may not be strangulated.

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3. Investigations Bedside tests: □ Urinalysis: dipstick, microscopy → urological causes □ Urine pregnancy test → ectopic pregnancy Blood test: □ CBC: → RBC indices for signs of chronic bleeding (takes 48h for haemodilution to set in after bleeding) → WBC for infection (inflammatory source may cause left shift on differential) □ Clotting profile, T/S for surgery □ LFT: hepatic vs obstructive jaundice □ RFT: → Hydration status → HypoK/hypoCl → prolonged vomiting → HypoK/hypoCa → can cause ileus but can arise from 3rd spacing → Cr → suitability of contrast scans □ Amylase: peaks at 6-24h, >1000 diagnostic of acute pancreatitis □ ± Cardiac enzymes, ECG to r/o basal MI □ ± Glucose to r/o DKA □ ± ABG: → Metabolic acidosis, ↑lactate → intestinal ischaemia → Metabolic alkalosis → prolonged vomiting Radiography: □ Erect CXR for free gas under diaphragm → perforation □ Supine AXR/KUB for → Proximal dilatation (>3cm in SB, >5cm in LB) + distal collapse → IO → Coffee bean sign → sigmoid volvulus → Radio-opaque stones → 90% urinary stones, 15% gallstones (only pigmented stones are radio-opaque, majority cholesterol stones) → Sentinel loop sign → localized ileus (dilated bowel) → indicating local inflammation (eg. pancreatitis) → Pancreatic calcification → chronic pancreatitis □ Erect AXR for air-fluid levels (>5 diagnostic of IO) USG: □ Gallstones: highly sensitive, 95% positive □ Acute cholecystitis: thickened GB wall (>3mm), pericholecystic fluid, stone at neck of HB, sonographic Murphy’s sign199 Contrast CT abdomen: increasingly used in many pathologies □ Acute mesenteric ischaemia by CTA □ Retroperitoneal structures, eg. leaking AAA, renal stones Endoscopy as indicated

199 Sonographic Murphy’s sign = tenderness is maximal when US probe press on visualized gallbladder

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4. Initial Management Schema for all surgical Mx Diet: Diet – NPO, IV fluid □ NPO Activity – (bed rest) □ IV fluid: Vitals – resuscitate early → Secure IV access (large bore if resuscitation required) Ix – as indicated 200 → IV fluid: routinely 2D1S Q8h Drugs – as indicated - Clinically dehydrated → give 500mL bolus crystalloid then reassess by UO - Subsequent fluid replacement guided by electrolytes and urine output □ NG tube decompression if IO Vitals: □ Haemodynamic status: BP/P □ Fever: body temperature □ Fluid balance: Foley’s catheter (keep UO > 0.5mL/kg/h) ± CVP Ix as indicated □ Serial abd examination to assess changes in abdominal pathology Drugs as indicated □ IV broad-spectrum Abx if infective aetiology □ Analgesics as indicated

200 Daily fluid requirement is usually ~1.5L. D and S refer to dextrose 5% and normal saline 0.9% and 2D1S refer to the ratio. Q8h = one packet (500mL) every 8h.

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3.3.6 Lower GI Bleeding Ref: Browse Ch 16, Andre Tan Ch6, WCS62 A. Causes Haematochezia: bleeding from gut distal to ligament of Treitz □ Epidemiology: 20-27/100k annual incidence, usually elderly with ↑incidence over age Massive upper GI (<10%) Large bowels (vast majority) Peptic ulcer, variceal bleed Diverticular disease* (17-40%) Small bowels (~5%) Angiodysplasia* (2-30%) Colitis (9-11%): Diverticulum: Meckel’s*, jejunoileal diverticula Infective: C. dificile, CMV, amoebic, TB Vascular lesions: angiodysplasia, haemangioma Inflammatory: ulcerative colitis, Crohn’s disease Small bowel tumours Ischaemic* Small bowel ulcers: NSAID-induced Radiation Enteritis: Crohn’s disease, TB Neoplasm (7-33%): carcinoma, large polyps, Aortoenteric fistula post-polypectomy Anorectal (~10%) Haemorrhoids Fissure-in-ano Anal or rectal ulcers Rectal varices* *can present with heavy bleeding.

Diverticular disease: acquired outpouching of colonic wall □ Bleeding occurs in ~17% of pt with diverticulosis → Usually from a ruptured vasa rectum from a single diverticulum → Can be in Rt and Lt colon in Asians (cf mostly in Lt colon in West) → Varying severity, stops spontaneously in 80-85% □ Diagnosis: endoscopy, angiography □ Tx: endoscopic therapy, surgical resection → Rebleeding in ~20-30% → Semi-elective surgery after 2nd bleeding episode

Angiodysplasia: acquired degenerative condition □ Usually in elderly (2/3 pt >70y/o) □ Pathology: ectasia of submucosal vessels → Can occur through whole colon but more commonly in Rt colon → A/w vascular malformations in other parts of GI (Osler-Weber-Rendu disease201) → A/w aortic stenosis (Heyde’s syndrome) □ Bleeding: less severe than diverticular haemorrhage, tends to be intermittent → Stops spontaneously in ~85-90%, rebleed in 25-85% □ Tx: endoscopic, surgery Inflammatory bowel disease (IBD):

201 Osler-Weber-Rendu disease (hereditary haemorrhagic telangiectasia, HHT) is a rare autosomal dominant genetic disorder caused by TGFβ1 receptor mutation. It is a/w telangiectasiae in skin, mucosa and arteriovenous malformations.

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□ S/S: usually as bloody diarrhoea, not life-threatening → More common to have bleeding in ulcerative colitis than Crohn’s disease □ Tx: high chance of rebleeding → recommend → Total colectomy or segmental small bowel resection (for Crohn’s enteritis)

Radiation proctocolitis: □ Pathology: damage of rectal mucosa → vascular telangiectasiae → Can occur more than 10y after RT of pelvic malignancies □ Tx: → Medical Tx: steroids → Endoscopy: IR coagulation, argon beam coagulation, laser, 4% formalin injection → Surgery for unstoppable bleeding - Diversion, eg. to external stoma - Proctectomy (high mortality and morbidity)

Anorectal causes: haemorrhoids, fissure-in-ano, anal or rectal ulcer □ Dx: rectal and proctoscopic examination □ Rectal varices: a/w portal hypertension, present with severe bleeding → Tx: injection sclerotherapy (local), TIPS (if uncontrolled bleeding)

B. Approach to Lower GI Bleeding 1. History Taking How does the bleeding occur? □ What is the presentation? → Acute (recent ± haemodynamic compromise) vs chronic (over days) → Occult (FOBT +ve or anaemic S/S) vs overt (blood found in stools) □ How is the blood found? → Blood mixed with faeces: from above sigmoid → Blood on surface of stools: from anus/rectum → Blood on toilet paper: usually mild bleeding from sources close to anal margin → Blood after : from anus, eg. haemorrhoids → Blood by itself: torrential bleeding, eg. diverticular disease, angiodysplasia □ How ‘heavy’ is the bleeding? → Mild (usually mixed with stools): anorectal pathologies, carcinoma, colitis → Heavy (usually pass by itself): diverticular disease, angiodysplasia, Meckel’s diverticulum, ischaemic colitis, rectal varices □ What is the colour of blood? – more distal pathologies give ‘fresher’ blood □ Any previous history of bleeding episodes? – duration, recent changes, previous investigations

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How is the bowel output? – frequency, consistency, colour, anorectal symptoms □ Passing mucus, diarrhoea → colitis or □ Anorectal symptoms (eg. pain, pruritus) → anorectal pathologies □ Worrying signs of colorectal CA: alternating diarrhoea and constipation, passage of mucus, tenesmus, pencil-thin stools Are there any other GI symptoms? □ Any signs of upper GI bleed? – haematemesis, coffee ground vomitus, melaena □ Any abdominal pain? – painful GI pathologies Are there worrying symptoms suggestive of malignancy? □ Risk factors: >50y, male, smoker, FHx, Hx of IBD, polyps and colorectal CA □ Bowel habits: alternating constipation and diarrhoea, pencil thin stools, tenesmus □ Constitutional symptoms: loss of appetite, loss of weight, malaise □ S/S of spread: intractable pain (sacral n. invasion), irritative urinary symptoms (bladder), ascites (peritoneal), jaundice/RUQ discomfort (liver), bone pain (bone), SOB (lungs)

Any features that would suggest a specific pathology?

Aetiology Features UGI bleed - Melena, haematemesis, coffee ground vomitus Diverticular ds - Painless, usually profuse haematochezia (not chronic) Angiodysplasia - Usually in elderly, may be a/w vascular malformations (eg. HHT) and aortic stenosis - Painless, less severe than diverticular but tends to be intermittent Colorectal carcinoma - >50y, male, smoker, FHx, Hx of IBD, polyps and colorectal CA - Alternating diarrhoea and constipation, pencil-thin stools, tenesmus - Loss of appetite, loss of weight, malaise - Intractable pain, jaundice/LUQ pain, dyspnoea, bone pain Colitis Inflammatory - Usually bloody diarrhoea - Extra-intestinal manifestations: arthritis, episcleritis/uveitis, erythema nodosum… Ischaemic - CVS risk factors, acute MI, stroke Infective - Fever, chills, rigors, night sweats, nausea/vomiting, diarrhoea, pain - TOCC, immunosuppression (CMV colitis) - Previous TB exposure/infection, BCG vaccination status Radiation - Hx of abdominal irradiation Haemorrhoids - Blood coating stools or bleeding following defecation - May note perianal prolapsing mass, pruritus (mucus secretion) ± pain (if thrombosed) Anal fissure - Hx of constipation - Severe sharp pain upon defecation

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Are there any complications? □ Shock: extreme thirst, confusion, pallor, oliguria □ Symptomatic anaemia: SOB on exertion, postural dizziness, syncope, chest pain, palpitation, lethargy or fatigue

Any other important things to note in history taking? □ Important comorbidities: → Cardiopulmonary disease (more susceptible to hypoxaemia) → HF or RF (predispose to fluid overload) → Bleeding disorders, eg. liver disease □ Drug Hx: → NSAIDs: can give rise to small bowel ulcers202 → Antiplatelets, anticoagulants

2. Physical Examination Vitals: □ Haemodynamic stability: BP/P, RR, postural BP □ Fever General examination: □ Anaemia: pallor, tachycardia □ Dehydration: capillary refill time, dry tongue □ Any extra-abd manifestation of IBD Abdominal examination: usually normal □ Mass □ Tenderness Digital rectal examination + proctoscopy: □ Confirm haematochezia □ Look for any anorectal pathologies, eg. haemorrhoids, fissure-in-ano, masses

3. Investigations and Management Principles of approach: □ Save the patient: resuscitation and stabilization of haemodynamics □ Find the bleeding: localization of bleeding site 75% of bleeding □ Stop the bleeding: endoscopy, angiography, surgery stops spontaneously a. Resuscitation ABC: □ A: intubate if decompensated (confused) or massive haematemesis

□ B: O2 cannula to ↑O2 carrying capacity of blood □ C: large bore IV cannula with colloid/crystalloid infusion ± blood transfusion

202 NSAID-induced enteropathy is a separate phenomenon from peptic ulcers and it can cause mucosal disruption by a different mechanism.

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Transfuse if □ Profuse bleeding □ Persistent haemodynamic instability despite crystalloid resuscitation □ Symptomatic anaemia □ Acute MI/unstable angina with low Hb

Monitor haemodynamic status by: □ Shock chart hourly □ Vitals: BP/P, RR, body temp203 □ Foley’s catheter: urine output ≥0.5mL/kg/h □ Cardiac monitor, pulse oximetry □ ± CVP line for PAWP

Take blood for: □ CBC: Hb, haematocrit □ RFT: hydration status, pre-renal failure, electrolyte imbalance □ LFT, clotting profile: coagulopathy □ T/S for transfusion b. Localization of Bleeding Site and Management Modalities: failure in localization in 8-12% □ Proctoscopy, sigmoidoscopy to exclude bleeding from anorectal pathology □ NG tube: bile-stained aspiration → bleeding from upper GI tract excluded □ Endoscopy: → Colonoscopy for lower GI bleeding → Enteroscopy for small bowel bleeding → Upper endoscopy to exclude upper GI bleeding → Intraoperative endoscopy during laparotomy to assess both intra- and extraluminal pathologies □ Angiography □ Radionuclude scans: RBC scan, sulphur colloid scan □ Other imaging: CT scan, small bowel contrast

Colonoscopy: □ Diagnostic yield = 75-90%, low complication rate □ Should be performed early (to obtain a diagnosis before bleeding stops) □ Bowel preparation: → ↑diagnostic yield but does not ↑morbidity → NOT feasible in unstable patients □ Therapeutic modalities: esp effective in angiodysplasia and diverticulitis → Sclerosant/vasoconstrictor injections, heat probe, electrocoagulation, laser, haemoclips, argon beam coagulation

203 ↓body temperature can cause ↓efficiency of clotting factors.

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Angiography: □ Procedure: selective catheterization of SMA, IMA and coeliac artery by Seldinger technique □ Can detect 1-1.5mL/min bleeding, diagnostic yield 27-67% □ Positive test defined by extravasation of contrast204 □ Therapeutic measures: usually not done because of high risk → Embolization: risk of bowel ischaemia and infarction → Vasopressin injection: CVS side effects □ Complications: contrast allergy, renal failure, bleeding from puncture site

Radionuclide scan: □ Principle: Tc-99m labelled sulphur colloid or tagged RBC □ Advantage: high sensitivity (detects bleeding as slow as 0.1mL/min) □ Disadvantage: no therapeutic value, less specific (only detect the rough site of bleeding) □ Usually only as a screening tool to confirm bleeding prior to angiography for non-life-threatening bleeding

Surgery: required in ~15-20% of patients with acute lower GI bleed □ Indications: → Haemodynamic instability → Require ≥6 units of blood → Persistent bleeding → Rebleeding within one week □ Procedures: → With localization: segment resection → Without localization - Subtotal colectomy if bleeding from colon - Intraoperative colonoscopy or enteroscopy for localization □ Outcome: → Segmental resection with localization: rebleeding 0-15%, mortality 0-13% → Blind segmental resection: rebleeding up to 75% → Subtotal colectomy: mortality 0-40%

204 Sometimes angiography may detect abnormal vessels but they may not actually be the source of bleeding as angiodysplasia is very common in elderly.

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i. Obscure GI Bleeding Obscure GI bleeding: bleeding of unknown origin persisting or recurring after a –ve initial colonoscopy ± upper endoscopy Modalities: □ Repeat upper endoscopy or colonoscopy (can identify 35% of bleeding lesions) □ Look for small bowel sources by → Enteroscopy → Angiography: may be difficult to interpret → may require intra-op angiography → RBC scan: non-specific → CT scan → Small bowel enema: low yield (10%), cannot detect vascular lesions

Enteroscopy: small bowel endoscopy □ Push enteroscopy: upper endoscopy extending beyond DJ flexure → Tool: paediatric colonoscope or long endoscope with overtube → Usually well-tolerated with few complications and provide channel for therapeutic measures → Problem: does not visualize whole small bowel □ Capsule enteroscopy: diagnostic capsule endoscopy (see upper GI bleed) □ Double and single balloon enteroscopy □ Spiral endoscopy □ Intraoperative endoscopy: used in situations without prior localization → Route: peroral, transanal, through enterotomy, laparoscopically assisted → Bowel prep by on-table anterograde irrigation from Foley’s catheter inserted through appendicotomy or enterotomy to anus → Allows complete examination of the small bowels

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3.3.7 Acute Diarrhoea and Gastroenteritis Ref: Talley Ch13, Davidson P. 306, 857, JC68, JC123, GI26 Diarrhoea is defined as ↑daily stool volume, frequency and fluidity □ Stool weight: >250g/24h □ Frequency: ≥3 times/day □ Fluidity: increased

May be divided into: □ Acute diarrhoea (>4 weeks): → Mostly infective but consider metabolic, drugs and toxin causes □ Chronic diarrhoea (>4 weeks) → Due to a variety of pathologies → Irritable bowel syndrome as the commonest cause

Mechanisms of diarrhoea and presentation: □ Watery diarrhoea: watery diarrhoea w/o any pus, blood or excess fat → Secretory diarrhoea → persists despite fasting → Osmotic diarrhoea → resolves w/ fasting → Motility issues → resolves w/ fasting □ Inflammatory diarrhoea: mucoid diarrhoea ± blood w/ PMN in stools □ Fatty diarrhoea (malabsorptive): undigested food w/ steatorrhoea + weight loss + nutrient deficiency

A. Acute Diarrhoea Causes: predominantly infective (due to infective GE) □ Infective: → Gastroenteritis (vast majority) → C. difficile infection → Other GI infections, eg. diverticulitis → Malaria □ GI non-infective: → IBD → CA colon □ Metabolic: → DKA → Hypocalcaemia → Uraemia → Thyrotoxicosis → Neuroendocrine diseases □ Drugs: antibiotics, NSAIDs, cytotoxic agents □ Toxins: ciguatera fish poisoning, heavy metal poisoning

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Classification of acute GE: Food poisoning Non-inflammatory Inflammatory Invasive (small-bowel type) (large-bowel type) Bacteriology B. cereus V. c h o le ra e EHEC* Salmonella typhi S. aureus Enterotoxigenic E. coli Shigella* Salmonella paratyphi Clostridium perfringens Norovirus Campylobacter (Yersinia) Rotavirus (children) Non-typhoidal Giardia lamblia Salmonella Cryptosporidium parvum Clostridium difficile Entamoeba histolytica* Pathogenesis Ingestion of heat-stable Ingestion of bacteria Mucosal invasion w/ Systemic infection, pre-formed toxins producing exotoxins, cytotoxin production, mainly at terminal ileum → secretory diarrhoea mainly at prox SB mainly at colon → → enteric fever → secretory diarrhoea inflammatory diarrhoea Incubation Short (<6h) 12-72h 12-72h 12-72h period Presentation Nausea, vomiting Watery diarrhoea Mucoid diarrhoea Enteric fever Watery diarrhoea ± blood (dysentery*) Fecal finding / / ↑WBC ↑WBC (mononuclear)

Viral causes: majority of acute GE, usually mild Small bowel Large bowel □ Norovirus: accounts for >1/3 of outbreaks Toxin-mediated – <16h incubation → Esp common in winter months B. cereus, S. aureus, Clostridium perfringens and spp □ Other viruses: usually causes ds in children Bacterial – 12h-5d incubation → Eg. rotavirus, adenovirus, astrovirus Enterohemorrhagic E. coli Bacterial causes: ↑↑prevalence for severe diarrhoea Enterotoxigenic E. coli Non-typhoidal Salmonella □ Toxin-mediated: a/w food poisoning Vibrio chloerae Campylobacter spp Aeromonas spp and Shigella spp → S/S: prominent N/V w/ short incubation Plseiomonas shigelloides Yersinia spp → Eg. B. cereus typically a/w rice Listeria monocytogenes Non-chlorae Vibrio → Eg. S. aureus typically a/w prepared food Clostridium difficile □ SB pathogens: a/w non-inflammatory diarrhea Viral – 12-72h incubation Norovirus → S/S: watery, large volume diarrhoea a/w Cytomegalovirus Rotavirus abdominal cramping, bloating and gas Adenovirus Astrovirus → Rarely a/w fever and usually no blood or Parasitic – >5d incubation WBC detected in stools Cryptosporidium parvum □ LB pathogens: a/w inflammatory diarrhoea Giardia lamblia Entameoba histolytica → S/S: frequent, regular, small volume and Microsporidium spp often painful bowel movements *bolded = common causes → Often a/w fever and bloody/mucoid stools w/ WBC and RBC +ve Parasitic causes, eg. Giardia lamblia, Cryptosporidium parvum □ Usually a/w a longer incubation period

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Clinical evaluation: □ Diarrhoea: syndrome, duration, amount, frequency, presence of blood, mucus or fat □ Associating symptoms: abdominal pain, fever, N/V, poor Food-related pathogens: appetite Fried rice: Bacillus cereus □ Food history: see RHS, also note incubation period Raw seafood: → <6h → preformed toxin (S. aureus, B. cereus) Norovirus, Vibrio spp, hepatitis A → 8-16h → C. perfringens infection Raw eggs: Salmonella spp → >16h → viral or other bacterial infections Undercooked meat or poultry: Salmonella spp, Campylobacter spp, □ Travel, occupation, contact, cluster EHEC, C. perfringens □ Dehydration: frequent profuse watery diarrhoea, vomiting, Unpasteurized milk or juice: poor fluid intake, concurrent fever, dry lips, oliguria Salmonella spp, Campylobacter spp, EHEC, Yersinia enterocolitica □ Other Hx: recent Abx use, immunodeficiency Unpasteurized soft cheeses: □ P/E: Salmonella spp, Campylobacter spp, → Hydration status: dry mucous membrane, diminished skin EHEC, Yersinia enterocolitica, Listeria turgor, postural or frank hypotension, altered sensorium monocytogenes → Abdominal exam: r/o other significant abd pathologies Homemade canned food: C. botulinum Raw hot dogs, Pâté: L. monocytogenes Laboratory evaluation: □ Indications: NOT for ALL patients, most would recover w/ expectant management Some useful questions in → Severe illness, eg. necessitating hospitalization evaluating food Hx: - Usual intake → Inflammatory diarrhoea, eg. bloody, mucoid, high fever ≥38.5oC - Recent changes in content or → High-risk hosts, eg. age ≥70y, comorbidities, I/C, prior IBD or preparation (person, method, pregnant utensils) → Persistent diarrhoea for >1w - Intake of unhygienic food, eg. undercooked food, raw □ Basic metabolic panel: CBC, L/RFT, electrolytes ± blood culture food, eating out □ Stool examination: - FHx → Stool culture for bacterial pathogen → Stool microscopy for RBC, WBC, ova and cyst (if inflammatory or persistent) → Multipathogen panel for bacterial, viral and parasitEic pathogens (if inflammatory) → Specific toxin tests: E. coli O157:H7 test, Shiga toxin test, C. difficile toxin testing □ Malaria workup: thick/thin blood smear if returning traveler □ Endoscopy if persistent to r/o IBD

Mx: based on clinical setting □ Dietary changes: avoid dairy products205 □ ORS: replace established deficits in 4h + ongoing loss + normal daily requirement → IV fluid if shock, unconscious, paralytic ileus or fail oral rehydration □ Abx: NOT indicated unless inflammatory, severe watery diarrhoea or high-risk patients → Empirical Tx: azithromycin (if inflammatory) or fluoroquinolones → Specific Tx: metronidazole (C. dificile), amoxicillin/cotrimoxazole (Listeria) □ Anti-diarrhoeal, eg. loperamide (Imodium) → To be used with caution in afebrile inflammatory diarrhoea → Antimotility agents may prolong/exacerbate illness in inflammatory diarrhoea → bismuth salicylate as alternative

205 Dairy products may be difficult to digest in presence of diarrhoea due to secondary lactose malabsorption.

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3.3.8 Chronic Diarrhoea and Protein-losing Enteropathy Ref: Talley Ch13, Davidson P. 306, 857, WCS68 Inflammatory Watery Fatty Causes Inflammatory bowel ds Secretory Malabsorptive Crohn’s disease Endocrine tumours: VIPoma, Enteropathy: celiac disease, short Ulcerative colitis carcinoid syndrome, gut syndrome, Crohn’s disease Zollinger-Ellison syndrome Chronic infections Pancreatic insufficiency: chronic Bile salt malabsorption206 pancreatitis, CA pancreas, CF C. dificile Laxative abuse M. tuberculosis Osmotic Other colonic diseases Lactase deficiency CA colon Osmotic laxative Chronic ischaemia (Malabsorption) Motility IBS Metabolic: hyperthyroidism Clinical Mucoid, bloody stools Watery diarrhoea Watery diarrhoea features PMN in stools Changes w/ fasting + steatorrhoea ↓ in osmotic, motility + weight loss Persists in secretory + nutritional deficiency (usually large volume) Ix CBC, L/RFT, APR CBC, L/RFT, APR CBC, L/RFT, APR Stool microbiology Spot stool for Na/K Spot ± timed stool Appropriate imaging Appropriate imaging Appropriate imaging Ileocolonoscopy ± Bx Endoscopy as indicated Endoscopy as indicated

Drug-induced diarrhoea:

□ Acid-suppressing agents: antacids (esp Mg-containing), H2RA, PPI □ Alcohol □ Antibiotics □ Caffeine: coffee, tea, cola □ Sorbitol/mannitol: dietectic food, gums, mints (osmotic diarrhoea) □ Others: β-blocker, NSAID/5-ASA, colchicine, misoprostol, theophylline, vitamin and mineral supplements, herbal products P/E: □ Hydration status: extent of fluid and electrolyte depletion □ Causes for diarrhoea: → Hyperthyroidism: goitre, thyrotoxic signs → IBD: episcleritis/uveitis, oral ulcers, arthritis, skin rashes, flushing □ Abdominal examination → Peritoneal signs suggestive of acute inflammation → Anorectal exam, esp note anal involvement in Crohn’s disease

206 Bile acid malabsorption occurs when terminal ileum fails to reabsorb bile acids. It may cause osmotic diarrhoea and induce secretory diarrhoea (at higher level). This can occur in ileal resection or ileal diseases.

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1. Workup Principle: □ No firm rule, directed by Hx and P/E □ Minimum Ix includes Causes of eosinophilia: → Blood tests and stool examination - Neoplasm → Imaging - Allergy → Endoscopy ± Bx - Collagen vascular diseases Blood tests: - Parasite infestation □ CBC: anaemia, leukocytosis, eosinophilia, thrombocytosis - Eosinophilic gastroenteritis □ APR: ESR, CRP □ LFT: albumin (malabsorption, protein-losing enteropathy) □ RFT: electrolyte disturbance, hydration □ Serology: → AutoAb for IBD: p-ANCA (UC), ASCA (CD) → Serum Ig level: hypogammaglobulinaemia → recurrent GE → ± HIV Ab if noted lymphopenia □ TFT for hyperthyroidism Spot stool analysis: □ Stool for occult blood: routinely unless gross blood Stool osmolal gap □ Stool for Na, K: = stool osmolarity – 2[Na] – 2[K] → Stool osmolal gap: ↑ in osmotic, ↓ in secretory □ Stool for pH: Stool calprotectin → <5.6 → carbohydrate malabsorption - 24kDa dimer of Ca-binding proteins □ Stool for leukocytes for inflammatory cause - ↑ in (1) infectious diarrhoea; (2) CD or UC; □ Stool for microbiology for infective vs inflammatory (3) Cancer → C. dificile toxin - Stable in room temperature → Culture for Aeromonas, Plesiomonas → Microscopy for ova and cyst for protozoan and parasites □ Fecal calprotectin: ↑ in inflammatory conditions → Usually for triage → -ve unlikely to have serious pathology 24h stool fat excretion: NOT commonly performed □ Use: only when suspecting malabsorption or maldigestion □ Findings: → Normal = <9% of intake → Malabsorption/maldigestion = >18g/d while on standard 100g fat/d diet - Malabsorptive → <8g/100g stool - Maldigestive → >8g/100g stool (pancreatic insufficiency or biliary steatorrhoea) Imaging □ AXR: calcifications in chronic pancreatitis □ Ba studies for mucosal abnormalities → Esp Ba follow through/SB enema for SB mucosal abnormalities □ USG for pancreatic disease □ CT/MR enterography for IBD and its complications □ Lymaphangiogram for lymphagiectasia

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Endoscopy: □ Modalities: OGD, enteroscopy, colonoscopy, sigmoidoscopy(esp for UC F/U) → If suspecting IBD, should r/o strictures w/ CT/MR enteroclysis first before performing capsule endoscopy □ Use: obtain mucosal Bx for → IBD → Opportunitistic infections, eg. CMV colitis → Microscopic colitis

2. Management Specific Tx vs cause of disease Supportive Tx: □ ?Abx □ Antidiarrhoeal drugs, eg. Lomotil, Imodium □ Octreotide: ↓motility, useful in neuroendocrine tumour □ Intraluminal absorbants, eg. charcoal □ Bile acid-binding resin (cholestyramine) for bile acid malabsorption □ Bismuth compounds Mx of malabsorption:

□ Dietary supplements: Ca, Mg, Fe, folate, vitamin A, B12, D, K □ Pancreatic enzyme supplement, eg. pancreatin □ Enteral and parenteral supplementation

B. Protein-losing Enteropathy Causes: □ Inflammatory exudation (erosions/ulcers present): IBD, GI malignancies, CD pseudomembranous colitis, erosive gastritis and multiple gastric ulcers, radiation/chemo-induced gastroenteritis □ ↑mucosal permeability (erosions/ulcers absent): coeliac disease, tropical sprue, Whipple’s disease, Menetrier’s disease, eosinophilic gastroenteritis, congenital hypogammaglobulinaemia □ Lymphatic obstruction: primary intestinal lymphagiectasia, constrictive pericarditis or right heart failure, portal hypertension, retroperitoneal lymphadenopathy Clinical features: peripheral oedema and hypoalbuminaemia w/ normal LFT and no proteinuria Workup: □ R/o proteinuria □ Labelled serum albumin scan for localization of source

□ α1-antitrypsin: → Resistant to enzymatic degradation → can be used to document excessive GI protein loss

→ Fecal α1-antitrypsin concentration

→ Serum α1-antitrypsin clearance □ Lymphangiogram for lymphangiectasia Mx: □ Dietary therapy to improve nutrition □ Treatment of underlying condition

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3.3.9 Jaundice Ref: Davidson P. 936, Andre Tan Ch10, WCS56, Block A TC (jaundice), GI block L17 A. Physiology of Bilirubin Excretion Bilirubin: non-toxic breakdown product of heme □ Formed in reticuloendothelial system (RES) □ Two forms: → Unconjugated (indirect) bilirubin: - Not water soluble → bound to plasma protein - Cannot be excreted directly in urine → Conjugated (direct) bilirubin: - Water soluble - Can be excreted directly in urine

Hepatic handling: □ Unconjugated bilirubin taken up by hepatocytes □ Bilirubin conjugated by UDP-glucuronyl transferase □ Secreted into bile canaliculi into duodenum

Enterohepatic circulation: □ Conjugated bilirubin reduced into urobilinogen by intestinal flora → 10% reabsorbed into portal circulation → secreted in kidney as urobilin → confers straw colour of urine □ Unabsorbed urobilinogen oxidized into stercobilinogen and then stercobilin → confers brown colour of faeces

Features of cholestatic jaundice: □ Tea-coloured urine: excretion of conjugated bilirubin in urine (bilirubinuria) □ Pale stools: reduced stercobilin content in stools □ Pruritus: retention of bile acid in blood

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B. Causes of Jaundice Pre-hepatic Hepatic Post-hepatic Suggestive - Lemon yellow jaundice - Yellow jaundice - Greenish jaundice features - Dark stools (↑stercobilin) - Normal stools - Pale stools - Normal urine - Tea-coloured urine - Tea-coloured urine - Pruritus ± scratch marks LFT - ↑unconj. bilirubin - ↑conj. bilirubin - ↑conj. Bilirubin - AST/ALT normal - ↑↑↑AST/ALT - ↑AST/ALT - ALP/GGT normal (AST>ALT = toxins) - ↑↑↑ALP/GGT (ALT>AST = viral) - Albumin normal - Albumin normal - ↑ALP/GGT - ↓albumin (if subacute) Causes Haemolytic anaemia Acute liver injury Cholangitis/RPC - Congenital: - Viral hepatitis: A, B, E Choledocholithiasis Membrane - Alcoholic hepatitis Malignant biliary (spherocytosis) - Drug-induced hepatitis obstruction (MBO) Metabolic (G6PD) - Autoimmune hepatitis - Cholangiocarcinoma: hilar Hb (thalassaemia) Chronic liver disease (Klatskin tumour), CBD - Acquired: - Viral hepatitis: B, C - LNs: HCC, gallbladder, lymphoma Immune (auto-, allo-, - Alcoholic liver disease drug-induced) - Non-alcoholic fatty liver - CA head of pancreas - CA ampulla or duodenum Fragmentation disease (microangiopathic) - Metabolic: Wilson’s disease, Benign strictures haemochromatosis, Infection (parasitic, - Post-ERCP α -antitrypsin deficiency bacterial) 1 - Stones, chronic pancreatitis - Autoimmune: autoimmune Drugs and toxins hepatitis Other obstruction Congenital causes - HCC - Mirizzi syndrome - Gilbert syndrome Congenital causes - Choledochal cyst - Crigler-Najjar syndrome - Dubin-Johnson syndrome - Biliary atresia (very rare) - Rotor syndrome Medical causes - PBC - PSC - Cholestatic phase of viral hepatitis Ix CBC with reticulocyte Clotting profile U/S of HBP Peripheral blood smear AFP ERCP/MRCP if dilated LDH, haptoglobin Hepatitis serology: biliary system Direct Coomb’s test Acute: anti-HBc + anti-HAV IgM Autoimmune panel ± liver Chronic: HBsAg, anti-HCV biopsy if no dilated biliary Autoimmune panel: system ANA, anti-smooth muscle, AMA for PBC anti-LKM1 (for AI hepatitis) p-ANCA for PSC (if segmental Metabolic screen: dilatation on ERCP) Cu: ceruloplasmin, 24h urine Cu Fe: iron profile Abdominal USG: Cirrhosis, splenomegaly, ascites *Cannot distinguish between hepatic vs post-hepatic by direct:indirect ratio (both ~2:1).

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C. Approach to Jaundice 1. History Is it truly jaundice? – r/o other causes of yellow skin □ Inspect the mucous membrane of sclera, mouth, palms and soles under natural light → Protected from the sun → minimizes photodegradation of bilirubin □ Other causes of yellow skin: → Diet: consumption of large quantity of food with lycopene or carotene207 → Drugs: rifampicin, quinacrine, TCMs Is it conjugated or unconjugated hyperbilirubinaemia? □ Conjugated (direct): → Tea-coloured urine → Pale stools → Pruritus ± scratch marks □ Unconjugated (indirect): none

Is it hepatic jaundice? Hepatic causes of jaundice: □ Chronic liver disease: Hx of chronic liver disease and its All medical doctors aren’t very happy complications Alcohol, Metabolic, Drugs, □ Alcoholic: Hx of alcohol abuse Autoimmune, Virus, HCC □ (Metabolic) □ Drugs: recent drug Hx, TCM intake □ (Autoimmune: Hx of autoimmune diseases) □ Virus: → Feco-oral (A/E): travel Hx, ingestion of seafood → Blood-borne (B/C): hep B/C status, FHx of hepatitis and HCC, blood transfusion, risk factors for blood-borne transmission (transfusion, IVDU, needle stick injury, MSM) □ (HCC) Is it post-hepatic jaundice? □ Cholangitis: → Charcot’s triad: jaundice, fever, RUQ pain → Reynold’s pentad: jaundice, fever, RUQ tenderness, hypotension, confusion → Past episode (recurrent pyogenic cholangitis) □ Choledocholithiasis (CBD stone): → Episodic, painful jaundice in young individuals → Biliary colic symptoms: episodes of severe RUQ pain → Hx of gallstone diseases, past surgery, ERCP □ Malignant biliary obstruction: → New onset, painless, progressive jaundice in old individuals → CA pancreas: constant, dull, boring epigastric pain radiating to back (usually late feature) → Constitutional symptoms: LOA, LOW, malaise → Metastatic symptoms: bone pain, dyspnoea, neck lump □ Post-ERCP jaundice Are there any complications? □ Liver decompensation: encephalopathy, hepatic fetor, worsening ascites

207 Lycopene = 茄紅素. Carotene = 胡蘿蔔素.

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□ Acute pancreatitis: abdominal pain radiating to the back with nausea and vomiting → Due to stone disease □ Fat malabsorption: → Steatorrhoea: fatty, loose stools (floaters) → Vitamin deficiency (A, D, E, K): coagulopathy 2. Physical Examination General examination □ Vitals: fever, haemodynamic stability □ General inspection: jaundice, distension, ankle oedema Abdominal examination □ Scars: previous HBP surgeries □ Stigmata of chronic liver disease: ascites, caput medusae, gynaecomastia □ Generalized distension: ascites can be due to malnutrition, peritoneal malignancy, malignant portal vein obstruction □ Palpable masses: Courvoisier’s law: → Hepatomegaly: primary liver tumour, metastatic Presence of palpable gallbladder in a disease, biliary obstruction (usually mild) patient with painless obstructive → Enlarged palpable gallbladder: indicates malignant jaundice indicates malignancy rather biliary obstruction if painless jaundice than stone disease. → Splenomegaly: portal hypertension Reason: a gallbladder that gives rise to CBD Digital rectal examination for pale stools stone is likely to have been chronically inflamed leading to fibrosis and therefore Metastatic screen: would not be palpable. □ LNs: cervical, supraclavicular Exceptions: □ Bony tenderness (1) Double stone (CBD + cystic duct) □ Respiratory examination (2) Recurrent pyogenic cholangitis Epigastric mass + jaundice can be: (3) In situ CBD stones (4) Mirizzi syndrome (rare) □ Hepatomegaly (mild) due to biliary obstruction (5) Pancreatic stone (rare) □ Hepatomegaly due to metastasis or HCC □ LN metastasis to coeliac axis and porta hepatis □ CA stomach with metastatic LN in porta hepatis □ Tumour obstructing both duodenum and bile duct → distended stomach + jaundice

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3.3.10 Cholestatic Jaundice - Hepatitis - Drugs Intrahepatic - Cirrhosis - Primary biliary cholangitis Intraluminal - Cholangocarcinoma - Gallstones Extramural - Cholangitis or RPC - Mirizzi syndrome Extrahepatic Mural - Pancreatitis - Benign strictures: post-instrumentation, - Carcinoma of head of pancreas gallstones, chronic pancreatitis - Malignant LN at porta hepatis - Primary sclerosing cholangitis

1. Investigations Blood: □ LFT showing classical obstructive pattern → ↑bilirubin → ↑ALP (± GGT) > AST/ALT (classical picture more often in CA than gallstones) → Mildly ↑AST/ALT □ CBC for anaemia, leukocytosis and thrombocytopenia □ RFT for hydration status, hepatorenal syndrome, suitability of contrast CT □ Amylase for any concomitant acute pancreatitis □ Clotting profile for coagulopathy due to vit K malabsorption, DIC or liver disease □ Tumour markers: Goals of imaging → CA19-9 for CA pancreas and cholangiocarcinoma (1) Extrahepatic vs intrahepatic → CEA for adenocarcinoma cholestasis → AFP for HCC (>400 diagnostic of HCC) (2) Level of obstruction □ Blood C/ST for biliary sepsis (3) Identify exact cause □ T/S for operation (4) Staging of cancer Imaging: □ Trans-abdominal ultrasound of hepatobiliary system (US HBS) → As first-line to confirm extrahepatic cholestasis (cf intrahepatic cholestasis) □ Direct cholangiography: gold standard, by → Endoscopic retrograde cholangiopancreatography (ERCP) → Percutaneous transhepatic cholangiography (PTC) if ERCP C/I □ MR cholangiopancreatography (MRCP) if intervention is not required □ If malignancy present, then → Triphasic CT scan for diagnosis ± staging (can skip US if highly suspicious of malignancy) → Endoscopic US (EUS) for diagnosis, staging and Bx → ± PET-CT for staging □ Triphasic CT scan → Done if malignancy suspected to aid staging

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Ultrasound of hepatobiliary system: first-line imaging □ Main aim: look for any dilated biliary system → indicates extrahepatic cholestasis □ Other possible findings: → Choledocholithiasis: dilated CBD (>6mm), CBD stone → Gallstone disease: GB stone/sludge, thickened GB wall, pericholecystic oedema, stranding (if cholecystitis) → Cholangitis: thickened CBD wall → Liver parenchyma: HCC, cirrhosis, fatty liver □ Disadvantages: → Unable to detect malignancy well → Unable to visualize distal CBD, ampulla, pancreas (behind D2) CT abdomen: can replace US as 1st line if likely MBO □ Suspected perforated gallbladder (air around gallbladder in lung window) □ Suspected malignant pathology → allow staging and planning of management → Double duct sign indicates CA ampulla or CA head of pancreas Endoscopic retrograde cholangiopancreatography (ERCP): □ Setting: usually as outpatient with IV sedation and analgesia + LA spray in throat □ Role: as diagnostic as well as therapeutic procedure □ Precautions: → Correct coagulopathy + stop anticoagulants x5d if sphincterotomy anticipated → Abx prophylaxis if suspected biliary obstruction, known pancreatic pseudocyst or ductal leak □ Complications: → Pancreatitis (3-4%): usually transient, due to contrast irritation of pancreatic duct or oedema when removing stone → Infections (1-2%): cholecystitis, cholangitis → Haemorrhage (1-2%): due to sphincterotomy → Perforation (0.5%): duodenal or biliary → CVS/analgesia-related (1-2%)

Disease Available ERCP modality Biliary - Choledocholithiasis (mainly therapeutic) Diagnostic: filling defect Therapeutic: sphincterotomy and stone extraction (balloon or wire basket) ± stenting - Biliary strictures (benign or malignant) Diagnostic: brush biopsy, FNAC Therapeutic: balloon dilatation ± stenting - Cholangitis Therapeutic: biliary decompression Pancreatic - CA pancreas Diagnostic: brush biopsy (in pancreatic duct), FNAC Ampullary - Sphincter of Oddi dysfunction Therapeutic: sphincterotomy - Ampullary carcinoma Diagnostic: endoscopic biopsy Therapeutic: snare ampullary resection (not curative)

Percutaneous transhepatic cholangiography or biliary drainage (PTC, PTBD):

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□ Procedure: percutaneous needle insertion to intrahepatic bile duct for contrast injection □ Indication: confirmed extrahepatic cholestasis but not candidate for ERCP □ Types: → External: drain externally into bag only → External-internal: drain both externally and internally into duodenum (more secure but more prone to ascending infections) □ Role: → Diagnostic: - Assess intrahepatic ductal disease - Brushing, biopsies for malignancy → Therapeutic: - Drainage of infected bile in cholangitis - Extraction of biliary stones - Dilatation of benign biliary strictures - Stenting across malignant strictures □ Complications: cholangitis (~2%), haemobilia

Endoscopic ultrasound (EUS): □ Identification of periampullary tumours208 □ Assessment of vascular and LN involvement □ FNAC for suspected lesions

Staging investigation: □ CT abdomen + pelvis for T, N and liver/intra-abd mets □ CT thorax for pulmonary metastasis □ EUS for T and N staging □ Bone scan if indicated □ PET-CT if indicated

Periampullary tumours = tumours arising within 2cm of ampulla of Vater - CA head of pancreas - Distal cholangiocarcinoma (CBD) - Periampullary duodenal CA - CA ampulla

208 EUS is essential for identifying masses in pancreas, bile duct and gallbladder as they are often obscured by bowel loops in trans-abdominal ultrasound.

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2. Management of Malignant Biliary Obstruction Approach: □ Assess operability: general and tumour status □ Laparotomy if clinically and radiologically operable → Bypass if spread → Radial resection if confined □ Palliative biliary drainage if inoperable → PTBD → Endoprosthesis: biliary stenting by ERCP

Assessment of general status: □ Age □ Known comorbidities □ Screen for unknown comorbidities: → Spirometry for lung function → ECG for cardiovascular function → Blood sugar for DM → Renal function

Assessment of tumour status: □ Clinical examination for any signs of inoperability → Lt supraclavicular LNs (Bx can be performed if uncertain) → Hepatomegaly with irregular surface (indicates liver mets) → Sister Joseph’s nodule (indicates peritoneal mets) → Ascites (indicates peritoneal mets) → Rectovesical pouch deposits (indicate peritoneal mets) □ Radiological examination (USG, CT, MRI) for any signs of inoperability → Liver secondaries → LN metastasis → SMA encasement → SMV, portal vein encasement (relative C/I as they can be resected and re-anastomosed easily)

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Laparotomy if □ Indications: → General condition is fit → Tumour is confined □ Radical dissection if tumour is confined → Tumour and part of organ of origin → Regional LNs → Tumour-free resection margin □ Bypass surgery if tumour has spread → Single bypass: choledochojejunostomy or hepaticojejunostomy - Relieve biliary obstruction → Double bypass: CJ/HJ + gastrojejunostomy - Relieve biliary + duodenal obstruction → Triple bypass: CJ/HJ + GJ + pancreaticojejunostomy - Relieve biliary + duodenal + pancreatic obstruction - Seldom done209 □ Note: no promise of resection until laparotomy finding shows no spread □ Outcome: very risky (26-28% mortality) due to → Cancer cachexia → malnutrition → Liver function impairment → Often superimposed biliary infections

Perioperative management of MBO: □ Clinical manifestation of pathophysiological disturbances of MBO: → ↓clotting factor synthesis → bleeding tendency, bleeding gastric erosion, poor wound healing, poor anastomosis healing → ↓reticuloendothelial and cell-mediated immunity → infections → Renal failure (reason unknown, ?related to bilirubin deposition in renal tubules) □ Measures to ↓complications of MBO surgery: → Nutritional support → Vitamin K → FFP during surgery → Abx cover → Mannitol, dopamine to prevent renal failure

→ H2 antagonist to ↓stress ulcers □ Biliary obstruction should be relieved before surgery! → Modality: ERCP with endoprosthesis, PTBD → Target bilirubin: <50 or <20μmol/L (if concomitant partial hepatectomy)

209 The reason of this is because the only symptom of pancreatic duct obstruction is pain and it is usually well-controlled by analgesics. Moreover, triple bypass is more risky as anastomotic leakage will lead to digestion of surrounding tissues and therefore chemical and secondary bacterial peritonitis.

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3.3.11 Deranged Liver Function Ref: Davidson P. 928, 935, GI teaching clinic (jaundice), UpToDate Components of liver function test: □ Liver enzymes: → Parenchymal enzymes: alanine aminotransferase (ALT), aspartate aminotransferase (AST) → Ductal enzymes: alkaline phosphatase (ALP), γ-gutamyl transferase (GGT) □ Proteins: albumin and globulin □ Bilirubin: total, conjugated, unconjugated □ Others: LDH, PT, INR (sometimes included) Significance: □ Liver injury is reflected by ↑serum liver enzymes level (released by injured liver into serum) □ Liver function is reflected by → ↓albumin due to ↓production by liver - Half-life = 25d → insensitive, only ↓ in subacute liver diseases - Reversed A:G ratio (i.e. G>A) in cirrhosis210, multiple myeloma, nephrotic syndrome, SLE → ↑bilirubin due to ↓excretion by liver → ↑PT (or INR) due to ↓production of coagulation factors by liver

- Most sensitive marker for liver synthetic function (t1/2 of F VII only 12h) Three main patterns of LFT abnormalities211: □ Hepatocellular pattern: ALT/AST elevation >> ALP → ± ↑bilirubin, ↓synthetic function □ Cholestatic pattern: ALP/GGT elevation >> ALT/AST → ± ↑bilirubin, ↓synthetic function □ Isolated hyperbilirubinaemia, i.e. jaundice

A. Hepatocellular Pattern Significance: usually indicates liver parenchymal damage Alanine transaminase (ALT) Aspartate transaminase (AST) Ref range 29-33 IU/L (M); 19-25 IU/L (F) 10-40 IU/L (M); 9-32 IU/L (F) Distribution Liver (more specific) Liver, skeletal muscle, kidney, brain… Location Exclusively cytosol Cytosol + mitochondria Transfer of amino group from L-alanine to Transfer amino group from aspartate to Function α-ketoglutarate, forming pyruvate and L-glutamate α-ketoglutarate, forming oxaloacetate and glutamate Also called Serum glutamate-pyruvate transaminase (SGPT) Serum glutamic oxaloacetic transaminase (SGOT)

210 Postulated mechanisms include (1) opening of portosystemic shunt leading to ↓removal of antigens; (2) cirrhotic liver produces Ag and stimulate immune response. 211 Abnormalities of markers of liver function are seldom seen in isolation and when they do, it is usually due to extra-hepatic diseases such as coagulopathies and nephrotic syndrome.

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Degree of elevation has aetiological implications (see next page) De Ritis ratio (AST/ALT): □ For most liver diseases, ALT > AST □ Reversed de Ritis ratio (i.e. AST > ALT) in → Alcoholic liver disease (macromitochondria) → HCC or metastasis (↑mitochondrial content) → NASH, viral hepatitis: occ reversed but AST:ALT often low (<2:1) → Wilson’s disease: often >2

Marked/moderate elevation (>5× ULN) Mild elevation (<5× ULN) Acute viral hepatitis Chronic viral hepatitis Acute hepatitis A-E Chronic hepatitis B, C, D Acute exacerbation of hepatitis B Non-alcoholic fatty liver disease Drug-induced liver injury Non-alcoholic steatosis Paracetamol, idiosyncratic Non-alcoholic steatohepatitis (NASH) Toxic liver injury Alcoholic liver disease TCM, Amanita phalloides poisoning Alcoholic steatosis Common Alcoholic steatohepatitis causes Ischaemic liver injury Others Autoimmune hepatitis Acute autoimmune hepatitis Chronic insidious form Acute alcoholic steatohepatitis Others Acute hepatitis of Wilson’s disease Chronic hepatitis of Wilson’s disease Budd-Chiari and veno-occlusive disease Haemochromatosis Pregnancy-related liver disease, eg. HELLP syndrome, Extrahepatic causes: thyroid disorders, muscle Acute fatty liver of pregnancy disorders, coeliac disease, adrenal insufficiency Hx of alcohol and drug use (esp TCM) Hx of alcohol and drug use Acetaminophen level and toxicology screen HBsAg, anti-HBs and anti-HBc IgM anti-HAV and IgM anti-HEV Anti-HCV HBsAg, anti-HBs and IgM anti-HBc USG for fatty liver Workup Anti-HCV and HCV RNA Ig pattern, ANA, anti-smooth muscle Ab Ig pattern, ANA, anti-smooth muscle Ab Doppler USG for vascular pathologies Serum ceruloplasmin and K-F rings Serum ceruloplasmin and urine copper Serum iron, TIBC and Tf saturation Pregnancy test in woman with childbearing potential Thyroid function tests Liver Bx if all –ve Liver Bx if all -ve

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B. Ductal Pattern Alkaline phosphatase (ALP) Gamma-glutamyl Transpeptidase (GGT) Ref range 45-115 IU/L (M); 30-100 IU/L (F) 8-61 IU/L (M); 5-36 IU/L (F) Source Liver and bone (and intestines) Liver only Alcoholism due to enzyme induction Drugs eg. phenytoin, rifampicin, cimetidine, Isolated ↑bone turnover when there is ↑osteoblast activation212 elevation Physiological: puberty, pregnancy NAFLD in Pathological: osteomalacia, bone metastasis Others, eg. pancreatic disease, MI, renal failure, COPD, DM,… When elevated, can distinguish between bone Sensitive but not specific for liver disease and liver origin by: NOT usually measured as part of routine Use Heat stability index (HSI): bone burns, liver lasts LFT to avoid unnecessary workup GGT level: ↑GGT = liver disease Only used when ALP is elevated

Causes: ≥4× ULN more specific for Marked elevation (≥4× ULN) Mild to moderate elevation (<4× ULN) Extrahepatic cholestasis Hepatic causes Choledocholithiasis ± cholangitis ANY hepatic disease Malignant biliary obstruction Eg. cholestatic phase of hepatitis Biliary strictures Primary sclerosing cholangitis with extrahepatic stricture Non-hepatic causes Recurrent pyogenic cholangitis Physiological in puberty and pregnancy Iatrogenic, eg. post-ERCP, post-LT High bone turnover Parasitic infections, eg. liver flukes, Ascaris lumbricoides Growth Intrahepatic cholestasis Healing fractures Drug-related, eg. androgenic steroids, phenytoin, ACEIs Osteomalacia Primary biliary cholangitis Hyperthyroidism and hyperparathyroidism Bone metastasis SOL of liver Liver abscess Other extrahepatic diseases HCC and metastatic tumour Eg. DM, peritonitis, myeloid metaplasia, subacute thyroiditis, gastric ulcers, extrahepatic tumours Amyloidosis Primary sclerosing cholangitis TPN-related cholestasis Intrahepatic cholestasis of pregnancy Benign post-operative cholestasis

212 Note that ALP is not elevated in multiple myeloma as it involves osteoclasts only.

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Evaluation of ↑ALP: □ Confirm hepatic origin: GGT level and heat-stability index (HSI) □ Hyperbilirubinaemia vs normobilirubinaemia: → ↑bilirubin indicates complete obstruction → Normal bilirubin indicates SOL of liver pressing onto hepatic sinusoids213 □ USG liver for dilated intrahepatic ducts → indicates extrahepatic cholestasis → May also indicate underlying pathology, eg. gallstones, SOL of liver □ For extrahepatic cholestasis (i.e. with dilated bile duct), should workup for → ERCP, PTC or MRCP for direct visualization of obstruction ± Bx ± intervention → ANA, ANCA for primary sclerosing cholangitis □ For intrahepatic cholestasis (i.e. no dilated bile duct), should workup for → Clinical Hx for drugs, TPN use and infiltrative diseases → Anti-mitochondrial antibody (AMA) and Ig pattern for PBC → IgM anti-HAV, HBsAg/anti-HBc, anti-HCV, IgM anti-HEV for cholestatic phase of hepatitis → Liver biopsy if persistently >2× ULN for >6mo w/o identifiable cause

3.3.12 RUQ Pain Ref: Andre Tan Ch8-10, WCS64, UpToDate Cause Features Biliary (commonest) Fat, female, fertile, forty as risk factors for cholesterol gallstone Intense, dull discomfort in RUQ or epigastrium Biliary colic - Severe, constant with excruciating exacerbations (false colic) (and Sphincter of Oddi dysfunction) - Usually last ≥30min and plateau within 1h and resolves ≤6h if uncomplicated - P/E: upper abdominal tenderness and guarding or may be normal Often a/w nausea, vomiting, diaphoresis ± jaundice (if CBD stone) Sudden, prolonged RUQ or epigastric pain - May radiate to back or tip of right scapula Acute cholecystitis - Prolonged (>4-6h), exacerbated by moving and breathing - P/E: upper abdominal tenderness and guarding with Murphy’s sign A/w fever Charcot’s triad and Reynold’s pentad: RUQ pain Acute cholangitis Fever: intermittent fever with chills Obstructive jaundice: scleral icterus, pale stools, dark urine ± mental obtundation and hypotension Liver (due to liver capsule distension) Dull mild RUQ ache due to liver capsule distension - Characteristically mild and occurs in the pre-icteric phase (1-2w before onset of jaundice) Acute hepatitis A/w viral syndrome (low-grade fever, anorexia, fatigue, myalgia) A/w GI upset (vomiting, nausea, diarrhoea) if hep A or E Followed by marked jaundice with cholestatic features (dark urine, pale stools)

213 Bilirubin can be re-secreted into bile in other areas of liver, but ALP/GGT cannot. As long as bile duct obstruction is not extensive, bilirubin elevation may not occur.

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RUQ pain a/w guarding or rebound tenderness Fever is a prominent feature (occurs in 90%) Liver abscess ± hepatomegaly, jaundice (if compress onto bile ducts) ± diarrhoea (due to intestinal Amoebiasis) Travel history to endemic region (ameobic) or I/C state (pyogenic) HCC or metastasis: underlying cirrhosis or HBV carrier, other primary tumours Budd-Chiari syndrome: RUQ pain with massive ascites, LL oedema, jaundice, features of portal Others hypertension, often a/w acute liver failure, thrombotic RFs Portal vein thrombosis: background cirrhosis, acute RUQ pain, fever, dyspepsia Fitz-Hugh-Curtis syndrome: pleuritic RUQ pain ± radiation to right shoulder Pancreatic Sudden onset progressive upper abdominal pain that radiates to the back - Usually occurs in epigastrium but may be felt in RUQ or LUQ Acute pancreatitis - Typically ↓by sitting up and leaning forward Prominent nausea and frequent vomiting Hx of gallstone disease, unusually large meal or alcohol intake Gastrointestinal Upper abdominal burning pain that is characteristically related to eating - May occasionally be experienced in RUQ Peptic ulcer disease May be a/w UGIB symptoms and with Hx of NSAID intake and H. pylori infection Colorectal diseases May be due to diseases of the hepatic flexure. Others Urological Pyelonephritis, renal infarct, obstructive uropathy, renal stone, RCC conditions Thoracic conditions Basal pneumonia, pleural effusion, basal MI Other conditions Herpes zoster, abdominal wall pain

Approach: □ Basic: CBC/D, L/RFT, amylase/lipase □ USG HBS: 1st line, can visualize most hepatobiliary pathologies → Problem: sonographic Murphy’s sign may be equivocal, distal bile duct obscured by bowel gas □ MRCP: 2nd line (if a/v), more sensitive than CT □ CT abdomen □ ERCP: diagnostic ± therapeutic for gallstone disease and cholangitis □ Operation for definitive Mx

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