---

Intracranial Space-Occupying Lesion (ICSOL)

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Pathophysiology - Monroe-Kellie Doctrine

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Causes (Aetiology)

Cerebral metastases are the most common intracranial tumours, diagnosed in ~25% of all cancer patients.

• Bailey and Love's Short Practice of Surgery, 28th Ed.

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Clinical Features - The Classic Triad

1. Raised ICP

• Headache - classically worse in the morning and on straining/coughing (high-pressure headache)
• Nausea and vomiting (especially morning vomiting)
• Blurred vision and diplopia (from VI nerve palsy - false localizing sign)
• Drowsiness progressing to coma
• Papilloedema on fundoscopy (takes time to develop, may be absent acutely)

2. Seizures

• Focal or generalized
• New-onset adult seizures demand neuroimaging to exclude ICSOL

3. Focal Neurological Deficit

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Special Presentations

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Investigations

Imaging

• CT head - first-line; rapidly identifies mass lesions, bleeds, oedema, hydrocephalus
• MRI - gold standard for characterizing tumours; superior for posterior fossa, brainstem, pituitary lesions
  • Contrast-enhancing ring lesions = glioma or metastasis (also abscess)
  • Diffusion-weighted imaging (DWI) helps distinguish abscess (restricted diffusion) from tumor
  • Meningiomas show uniform dural-based contrast enhancement
  • Metastases show well-demarcated, gadolinium-enhancing lesions with surrounding oedema

• ICP monitoring - gold standard is an external ventricular drain (EVD) or intraparenchymal pressure probe
• Lumbar puncture is CONTRAINDICATED until imaging has excluded an ICSOL (risk of cerebellar tonsillar herniation/"coning")

---

Management

Immediate / Emergency

• Raise head of bed to 30 degrees
• IV mannitol or hypertonic saline - osmotic agents to reduce cerebral oedema acutely
• Anaesthetic/neurosurgical involvement if pupil changes or declining GCS
• Urgent CT imaging

Medical

• Dexamethasone (high-dose glucocorticoid) - reduces vasogenic oedema around tumours and metastases
• Anticonvulsants for seizure control (not routinely prophylactic)
• Treat obstructive hydrocephalus with early external ventricular drainage (EVD), especially for posterior fossa tumours

Surgical

• Craniotomy + resection - for primary tumours (glioma, meningioma) and selected metastases
  • Intraoperative neuronavigation for localization
  • 5-ALA (5-aminolevulinic acid) given pre-op: metabolite protoporphyrin IX accumulates in glioma cells and fluoresces pink under UV, guiding complete resection
• Transsphenoidal approach (endoscopic or microscopic through the nose) for pituitary adenomas
• Stereotactic radiosurgery (e.g. Gamma Knife) for small/deep lesions or vestibular schwannomas
• Ventriculoperitoneal (VP) shunt for hydrocephalus

Adjuvant Treatment (Malignant Glioma)

• High-dose focused radiotherapy + oral temozolomide (alkylating chemotherapy)
• Median survival for glioblastoma (GBM) remains just over 12 months

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Common Tumours Summary

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Key Points for Exams

• Lumbar puncture is contraindicated in raised ICP until ICSOL excluded by imaging
• False localizing sign: unilateral or bilateral VI nerve (abducens) palsy due to raised ICP (not from a lesion at the nerve)
• New-onset seizures in an adult = ICSOL until proven otherwise
• Cushing's triad = very late sign of transtentorial herniation
• Dexamethasone is the drug of choice for perilesional vasogenic oedema
• 5-ALA fluorescence guides glioma resection margins
• Metastases + gliomas = ring-enhancing on contrast CT; meningiomas = uniformly enhancing + dural tail

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DR. RASHIDE'S WEEK 3 - COMPLETE STUDY GUIDE

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TOPIC 1: PANCREATITIS

Acute Pancreatitis

1. Acute onset severe epigastric pain, often radiating to the back
2. Serum amylase or lipase ≥ 3x upper limit of normal
3. Characteristic imaging findings on CT/MRI

• Serum amylase: peaks within hours, elevated 3-5 days (half-life 10 h)
• Serum lipase: more specific; elevated 8-14 days (half-life 6.9-13.7 h) - preferred marker, especially if patient presents >48 h
• Amylase can be falsely elevated in: peptic ulcer, parotitis, cholecystitis, mesenteric ischemia, renal failure
• Elevated ALT in the setting of pancreatitis = 95% PPV for biliary (gallstone) pancreatitis

• Gallstones (most common in adults, ~40%)
• Ethanol/alcohol
• Trauma
• Steroids
• Mumps / infections (viruses - coxsackievirus, EBV)
• Autoimmune / hyperCalcaemia
• Scorpion sting / hypertriglyceridemia
• Hyperlipidaemia
• ERCP (post-procedural)
• Drugs (valproate, L-asparaginase, 6-MP, prednisone)

• Epigastric tenderness with peritonism
• Cullen's sign - periumbilical bruising (retroperitoneal bleed)
• Grey Turner's sign - flank bruising (retroperitoneal bleed)
• Both are RARE but indicate haemorrhagic pancreatitis
• Tetany (from hypocalcaemia)

• USS - first-line to identify gallstones (sensitivity 95%)
• CT (portal venous phase, 65-70s post-contrast) - gold standard for severity, necrosis, complications
• MRCP - for unexplained/recurrent cases, pancreatic duct anatomy; NOT in acute setting
• Plain AXR: non-specific - may show "sentinel loop" (isolated ileum), "cut-off colon sign"

Severity Assessment - Ranson's Criteria

• Score ≥3 = severe acute pancreatitis
• APACHE II score ≥8 also defines severe pancreatitis

Management of Acute Pancreatitis

• IV fluid resuscitation (crystalloids) - aggressive early hydration
• Analgesia: NSAIDs (IV metamizole) or opioids (buprenorphine IV); avoid morphine (causes Sphincter of Oddi spasm)
• NBM initially; early oral feeding as tolerated

• ICU care, monitoring
• Early enteral nutrition (NG or nasojejunal) preferred over TPN
• High-dose dexamethasone or antibiotics if infected necrosis
• External ventricular drain/pancreatic drain for collections
• Early ERCP only if: coexisting cholangitis or proven biliary obstruction (hyperbilirubinaemia)
• Early laparoscopic cholecystectomy (within 3 days) for mild biliary pancreatitis = standard of care

• Peripancreatic fluid collections (early, usually resolve)
• Pancreatic pseudocyst - fluid collection encapsulated after ≥4 weeks
• Walled-off necrosis (WON) - solid debris encapsulated; needs drainage
• All drained endoscopically if in apposition to stomach/duodenum

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TOPIC 2: LIVER SEGMENTS (COUINAUD)

RIGHT LOBE                    LEFT LOBE
Segments V, VI, VII, VIII     Segments I, II, III, IV
                              (Caudate lobe = Segment I)

• Boundaries between segments differ from the visible anatomical right/left lobe boundary
• Left lobe = medial (segment IV) + lateral (segments II & III) parts
• Each segment has its own portal triad: branch of portal vein + hepatic artery + bile duct (= Glisson triad)
• Blood drains inward along sinusoids between hepatocytes, into the central vein → hepatic veins → IVC
• Kupffer cells (hepatic macrophages) line the sinusoidal endothelium
• Ito cells (hepatic stellate cells) in the perisinusoidal space (Disse space) - store fat; become activated in fibrosis

• Zone 1 (periportal) - first to receive oxygen; most metabolically active; first affected by toxic injury
• Zone 3 (centrilobular) - last to receive oxygen; first affected by ischaemia and in alcoholic hepatitis

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TOPIC 3: INFLAMMATORY BOWEL DISEASE (IBD)

Crohn's Disease vs. Ulcerative Colitis

Clinical Features of Crohn's Disease

• Insidious onset; chronic exacerbations and remissions
• Recurrent RIF pain (from terminal ileal involvement or ileocaecal mass)
• Diarrhoea (malabsorption of fats + bile salts)
• Weight loss; growth retardation in children
• Perianal disease: fistulae, skin tags, abscesses

• Arthritis/spondylitis (20%)
• Skin: pyoderma gangrenosum, erythema nodosum (5%)
• Iritis/uveitis (3%)
• Cholangitis/liver involvement

• Colonoscopy + biopsy - granulomas are diagnostic
• Small bowel MRI or contrast study - "cobblestone" pattern, rose-thorn ulcers, strictures

• Sulphasalazine (5-ASA) - maintenance
• Corticosteroids - acute flares
• Azathioprine / 6-MP - immunomodulator
• Anti-TNF (infliximab, adalimumab) - severe/refractory
• Surgery: resection of complicated segments (not curative; recurs)

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TOPIC 4: COLORECTAL CARCINOMA (CRC)

Epidemiology

• Greatest cause of cancer mortality in non-smokers in the West
• Incidence increases with age
• Risk factors: high red meat / low fibre diet; IBD; hereditary syndromes
• ~10% hereditary - Familial Adenomatous Polyposis (FAP), HNPCC (Lynch syndrome)

Pathogenesis - Adenoma-Carcinoma Sequence

• FAP: hundreds/thousands of polyps; near 100% malignant transformation → prophylactic colectomy

Staging - Dukes' Classification

Modern staging also uses TNM (T1-T4, N0-N2, M0-M1)

Clinical Features

• Change in bowel habit (most common)
• Rectal bleeding (distal lesions)
• Iron deficiency anaemia (occult bleeding from proximal/caecal tumours)
• Weight loss
• Palpable abdominal mass
• 50% are in sigmoid colon or rectum
• Complications: obstruction, perforation, fistula, bleeding

Treatment

• Surgical resection is primary - right hemicolectomy, left hemicolectomy, anterior resection, abdominoperineal resection (APR) for low rectal
• Adjuvant chemotherapy (FOLFOX - oxaliplatin + 5-FU) for stage III/IV
• Radiotherapy for rectal cancer (neoadjuvant to downsize)
• Surveillance colonoscopy post-op

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TOPIC 5: LIVER PATHOLOGIES

A. Hepatocellular Carcinoma (HCC)

• Cirrhosis from ANY cause (alcohol, NAFLD, viral hepatitis)
• Hepatitis B - can cause HCC WITHOUT cirrhosis
• Hepatitis C - HCC develops after long-standing cirrhosis
• Aflatoxin exposure
• Fibrolamellar HCC variant - younger patients, no underlying cirrhosis

• CT/MRI: arterial hyperenhancement + portal venous washout = diagnostic in chronic liver disease
• LI-RADS 5 = diagnostic of HCC (no biopsy needed in most cases)
• Tumour marker: AFP (alpha-fetoprotein) - elevated in HCC
• Staging: BCLC (Barcelona Clinic Liver Cancer) staging system used clinically

• Liver transplantation - treatment of choice in cirrhosis + limited HCC (Milan criteria)
• Surgical resection - for Child-Pugh A patients without portal hypertension; perioperative mortality <5%
• Thermal ablation - for small HCC (<2-3 cm); equivalent outcomes to resection in small tumours
• TACE (transarterial chemoembolisation) - for intermediate HCC
• Sorafenib / Atezolizumab + bevacizumab - systemic therapy for advanced HCC

B. Liver Abscess

• Incidence: ~1/5000 hospital admissions
• Organisms: Klebsiella, E. coli, Streptococcus milleri group (usually polymicrobial)
• Routes of infection:
  • Biliary tract pathology - most common (35%)
  • Portal spread (from appendicitis, diverticulitis) - 20%
  • Contiguous spread, bacteraemia, cryptogenic (10%)
• Increased risk: elderly, diabetics, immunosuppressed

• Fever, anorexia, malaise, right upper quadrant pain/discomfort
• Raised WCC, elevated LFTs, CRP

• USS / CT - multiloculated cystic mass with rim enhancement and possible air-fluid level
• Aspiration for culture and sensitivity

• Aspiration + antibiotics (metronidazole + cephalosporin or aminoglycoside + metronidazole for anaerobic/Gram-negative cover)
• Percutaneous drainage for large/complex abscesses
• Surgery rarely required

C. Viral Hepatitis

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TOPIC 6: COMPLICATIONS OF PANCREATITIS

A. Hypovolaemic Shock

• Plasma leaks into the retroperitoneal and peritoneal spaces
• Vomiting adds to volume loss
• Haemoconcentration occurs → raised Hct and BUN (Ranson criteria items)
• Reduced circulating volume → decreased preload → reduced cardiac output → shock

B. Septic SIRS (Systemic Inflammatory Response Syndrome)

• Temperature >38°C or <36°C
• Tachycardia >90/min OR tachypnoea >20/min
• WBC >12 × 10⁹/L or <4 × 10⁹/L

C. DIC (Disseminated Intravascular Coagulation)

1. Bleeding - from factor/platelet consumption and FDPs
2. Thrombosis - fibrin deposition in microvessels → ischaemia of kidneys, brain, skin

• Treat underlying cause (the most important step)
• If active bleeding: FFP (fresh frozen plasma) + cryoprecipitate (fibrinogen) + platelet transfusion
• If thrombosis predominates: heparin (selected cases - purpura fulminans)
• Goal: stop depletion of clotting factors; monitor fibrinogen, platelet count, and FDPs

D. GI Bleeding in Pancreatitis

• Stress ulceration of the gastric/duodenal mucosa (from splanchnic ischaemia)
• Splenic artery pseudoaneurysm - pancreatic enzymes erode the splenic artery → life-threatening haemorrhage
• Haemosuccus pancreaticus - bleeding into the pancreatic duct → haematemesis or melaena
• Portal hypertension from splenic vein thrombosis → gastric varices (left-sided/sinistral portal hypertension)

• Resuscitate with blood products
• OGD for stress ulcer bleeding; proton pump inhibitors
• Angiography + embolisation for pseudoaneurysm
• Surgery if embolisation fails

E. Perforation in Pancreatitis

• Usually involves the colon (transverse colon most common - "colonic necrosis")
• Mechanism: peripancreatic inflammation and necrosis extends to involve the mesocolon and bowel wall
• Can also cause duodenal perforation or small bowel necrosis
• Presents with: peritonitis, free air on AXR/CT, sudden deterioration
• Management: Emergency laparotomy; resection of perforated segment; defunctioning stoma; drain necrosum

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QUICK SUMMARY TABLE

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ACUTE PANCREATITIS - COMPLETE GUIDE

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OVERVIEW

• 80-90% = mild, self-limiting
• 10-20% = severe, with systemic complications and MODS
• Mortality: mild <1% | severe 10-50%
• Death is bimodal: early (first 2 weeks) from MODS; late (after 2 weeks) from septic complications

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PATHOPHYSIOLOGY

Step-by-Step Mechanism

Precipitating cause (gallstone / alcohol / etc.)
            ↓
Zymogen granules + lysosomes COLOCALIZE inside acinar cells
            ↓
Lysosomal cathepsin B activates trypsinogen → TRYPSIN
            ↓
Trypsin activates other proenzymes:
  - Elastase → blood vessel digestion → haemorrhage
  - Phospholipase A2 → cell membrane destruction
  - Lipase → fat necrosis
  - Complement + kinin systems activated
            ↓
Acinar cell injury/death (apoptosis + necrosis)
            ↓
Release of proinflammatory cytokines: TNF-α, IL-1, IL-2, IL-6
            ↓
Neutrophil & macrophage recruitment into pancreas
            ↓
Local: pancreatic oedema → necrosis → abscess / pseudocyst
            ↓
Systemic: cytokine storm → SIRS → MODS → MSOF

• SPINK1 (Serine Protease Inhibitor Kazal Type 1) - binds and inactivates ~20% of trypsin
• Mesotrypsin and enzyme Y degrade active trypsin
• Low intra-acinar calcium prevents autoactivation
• Separation of zymogens from lysosomes in the Golgi apparatus

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AETIOLOGY

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CLINICAL FEATURES

Symptoms

• Epigastric pain radiating to the back - cardinal symptom; constant, severe, non-colicky
• Pain typically does NOT radiate to the shoulder (that is diaphragmatic irritation)
• Nausea and vomiting in ~90% - does NOT relieve the pain (unlike peptic ulcer)
• If pain disappears suddenly → consider another diagnosis (perforation?), or fat necrosis becoming walled off

Signs

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DIAGNOSIS

Revised Atlanta Classification (RAC) - Needs 2 of 3:

1. Acute onset severe persistent epigastric pain ± radiation to back
2. Serum amylase or lipase ≥ 3x upper limit of normal
3. Characteristic imaging findings

Biochemistry

Imaging

• Abdominal USS - First-line; high sensitivity (95%) for gallstones; limited view of pancreas by bowel gas
• CT abdomen with IV contrast (portal venous phase) - Gold standard for severity, necrosis assessment; best at 72-96 hours after onset
  • Shows: pancreatic swelling, peripancreatic fat stranding, fluid collections, non-enhancing areas (= necrosis), extraluminal gas (= infected necrosis)
• MRCP - Best for pancreatic/biliary duct anatomy; used in unexplained/recurrent pancreatitis (NOT in acute setting)
• Plain AXR - Non-specific: "sentinel loop" (isolated ileus), "cut-off colon sign" at splenic flexure, pancreatic calcifications (chronic disease)

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SEVERITY ASSESSMENT

Revised Atlanta Severity Classification (2012)

• Shock: systolic BP <90 mmHg
• Pulmonary insufficiency: PaO₂ <60 mmHg
• Renal failure: creatinine >2 mg/dL after resuscitation
• GI bleed >500 mL/24 h

Ranson's Criteria (gallstone pancreatitis)

CT Severity Index (Balthazar)

• CTSI 0-3: mortality 3%, morbidity 8%
• CTSI 4-6: mortality 6%, morbidity 35%
• CTSI 7-10: mortality 17%, morbidity 92%

BISAP Score (Bedside Index of Severity in AP - calculated at admission):

• BUN >25 mg/dL
• Impaired mental status
• SIRS present
• Age >60
• Pleural effusion
• Score 0-1: mortality <1% | Score 4-5: mortality >20%

Other markers:

• APACHE II score ≥8 = severe pancreatitis
• CRP >150 mg/L at 48-72 h = severe pancreatitis
• Serum procalcitonin, IL-6 also correlate with severity (not widely available)

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LOCAL COMPLICATIONS - REVISED ATLANTA CLASSIFICATION

• Pseudocyst = no solid debris, entirely fluid; can be drained simply
• WON = contains solid necrotic debris; needs step-up drainage approach

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MANAGEMENT

Cornerstones (for ALL severities):

1. Aggressive IV fluid resuscitation - Lactated Ringer's (LR) preferred over normal saline (LR associated with decreased SIRS odds at 24 h, OR 0.38)
2. Pain control
3. Early nutrition

Fluid Resuscitation

• Hypovolaemia = unfavourable prognostic factor
• Rate must be individualised based on: age, comorbidities, vital signs
• Monitor: urine output (target ≥0.5 mL/kg/hr), BUN, Hct, vital signs

Pain Management

• NSAIDs (e.g. IV metamizole 2 g/8 h) for mild pain
• Opioids for moderate-severe pain: buprenorphine 0.3 mg/4 h IV, pentazocine, meperidine
• AVOID morphine - causes Sphincter of Oddi spasm (worsens biliary obstruction)

Nutrition

• Early enteral nutrition (NG or nasojejunal) = strongly preferred over TPN
• Lower infection rates, lower cost with enteral feeding
• NG feeding as effective as NJ in most cases; NJ preferred if gastric retention from duodenal oedema
• TPN only if enteral route not tolerated

Antibiotics

• NOT indicated for mild-moderate sterile pancreatitis
• Indicated for:
  • Documented infected necrosis
  • Concurrent cholangitis
  • Secondary infections
• Carbapenems = first choice (best pancreatic penetration)
• Alternatives: quinolones + metronidazole, 3rd-gen cephalosporins, piperacillin

Specific Interventions

• ERCP only if: concurrent cholangitis or proven biliary obstruction (hyperbilirubinaemia + dilated CBD)
• Early ERCP for ALL mild biliary pancreatitis = NOT recommended
• Early cholecystectomy (within 3 days) for mild biliary pancreatitis = standard of care

• Most resolve spontaneously
• Drain if: symptomatic, infected, expanding, causing obstruction
• Endoscopic internal drainage (EUS-guided transgastric stenting) preferred

• Delay intervention as long as possible to allow WON to develop (>4 weeks ideal)
• Step-up approach:
  1. IV antibiotics (carbapenems)
  2. Percutaneous drainage (CT/USS-guided)
  3. Endoscopic internal drainage (EUS-guided, through stomach wall) - preferred if collection adjacent to stomach
  4. Minimally invasive necrosectomy (video-assisted retroperitoneal debridement - VARD)
  5. Open surgical necrosectomy - last resort (high morbidity/mortality)

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SYSTEMIC COMPLICATIONS

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KEY EXAM POINTS

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ACUTE CHOLANGITIS - COMPLETE GUIDE

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DEFINITION

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PATHOPHYSIOLOGY

Normal Biliary Defence Mechanisms (that protect against infection):

1. Sphincter of Oddi - mechanical barrier preventing reflux of duodenal bacteria
2. Laminar bile flow - continual flushing flushes ascending bacteria out of the biliary tree
3. Bile salts - bacteriostatic properties that inhibit bacterial colonization

How Choledocholithiasis Causes Cholangitis:

Gallstone enters CBD (choledocholithiasis)
            ↓
Partial or complete biliary obstruction
            ↓
Bile flow disrupted → stasis of bile
            ↓
Bacteria enter biliary tree via:
  1. Reflux from duodenum through incompetent/bypassed Sphincter of Oddi
  2. Haematogenous spread via portal vein
            ↓
Bacteria proliferate in stagnant bile (bactibilia in 90% of CBD obstruction)
            ↓
Intraluminal pressure ↑ → cholangiovenous reflux → bacteria enter bloodstream
            ↓
Bacteraemia → sepsis → septic shock (Reynolds pentad)
            ↓
Pyogenic liver abscess (if not treated)

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CAUSES OF ACUTE CHOLANGITIS

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CLINICAL FEATURES

Charcot's Triad (classic but low sensitivity <50%):

1. Fever (and/or rigors/shaking chills)
2. Jaundice (obstructive - dark urine, pale stools, pruritus)
3. Right upper quadrant (RUQ) pain

Jaundice is actually the least common of the three findings

Reynolds Pentad (= Charcot's triad + 2 additional ominous signs):

1. Hypotension (septic shock)
2. Altered mental status (confusion, drowsiness)

Reynolds pentad = suppurative (severe) cholangitis - mortality approaches 100% without prompt treatment

Additional Features:

• Tender hepatomegaly
• Signs of sepsis: tachycardia, tachypnoea, high fever
• Dark urine, pale/clay-coloured stools, pruritus (obstructive jaundice features)

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INVESTIGATIONS

Laboratory Workup

Microbiology - Common Pathogens

ESBL-producing organisms (Extended-Spectrum Beta-Lactamase) are increasingly common - always consider local resistance patterns

Imaging

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DIAGNOSTIC CRITERIA - TOKYO GUIDELINES 2018

Suspected Diagnosis: 1 item from A + 1 item from B or C

Definite Diagnosis: 1 item from A + 1 item from B + 1 item from C

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SEVERITY GRADING - TOKYO GUIDELINES 2018

Severity should be reassessed at: time of diagnosis, within 24 hours, and at 24-48 hours

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MANAGEMENT

Principles:

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Step 1: Immediate Resuscitation

• IV access, IV fluids (aggressive crystalloid resuscitation)
• NBM
• Urinary catheter (monitor urine output ≥0.5 ml/kg/hr)
• ICU admission for severe/Grade III cholangitis
• Vasopressors if septic shock (norepinephrine first-line)

Step 2: Antibiotic Therapy

• Take blood cultures FIRST, then start antibiotics immediately
• Cover gram-negative rods (E. coli, Klebsiella) + gram-positive (Enterococcus) + anaerobes

• 4-7 days after source control obtained
• 14 days if bacteraemia is present (risk of endocarditis)

Step 3: Biliary Drainage

Biliary drainage within 24 h of diagnosis = associated with increased survival rate Delay >48 h = associated with higher costs and longer hospital stay

• PTC (Percutaneous Transhepatic Cholangiography) - access from above (liver) under imaging guidance

• Surgical biliary drainage - open common bile duct exploration + T-tube insertion (reserved for unstable patients where all other methods failed)

Step 4: Definitive Treatment

• After acute phase resolves → elective laparoscopic cholecystectomy (definitive; without this, risk of recurrent cholangitis is HIGH even after sphincterotomy)
• Early cholecystectomy during index admission is increasingly being studied and showing no increased complication rates

• Resectable: hepatic resection or Whipple's procedure (pancreaticoduodenectomy)
• Unresectable: palliative biliary bypass - Roux-en-Y hepaticojejunostomy (preferred) or choledochoduodenostomy

• Transduodenal sphincteroplasty - surgical incision of the ampulla; risk of pancreatic duct injury causing recurrent pancreatitis

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COMPLICATIONS OF ACUTE CHOLANGITIS

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OUTCOMES

• With improved ERCP techniques + antibiotics, mortality from acute cholangitis has fallen from 50% → ~10%
• 85% of cases resolve with antibiotics + non-surgical biliary drainage (ERCP)
• Mortality remains high in: elderly, immunocompromised, severe/Grade III cholangitis
• Without treatment of Reynolds pentad: mortality approaches 100%

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QUICK EXAM SUMMARY

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ASIATIC CHOLANGIOHEPATITIS (ACH)

---

DEFINITION

1. Intrahepatic and/or extrahepatic biliary calculi (brown pigment stones)
2. Biliary strictures (intrahepatic)
3. Recurrent episodes of bacterial cholangitis

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EPIDEMIOLOGY

• Endemic to East and Southeast Asia: China, Taiwan, Hong Kong, Korea, Japan, Vietnam, Philippines, Malaysia
• Prevalence >10% in parts of East Asia (especially Taiwan)
• Age: Predominantly 3rd-4th decade of life
• Sex: Males and females equally affected
• Risk factors: Low socioeconomic status; poor sanitation; areas where gastrointestinal parasitosis is endemic
• Now increasingly seen in Western countries due to migration from endemic areas

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AETIOLOGY & PATHOGENESIS

Causative Organisms:

Mechanism of Brown Pigment Stone Formation:

Parasites enter biliary tree
            ↓
Parasites + bacteria secrete β-glucuronidase enzyme
            ↓
β-glucuronidase hydrolyses water-soluble conjugated bilirubin glucuronides
            ↓
Free (unconjugated) bilirubin released → insoluble
            ↓
Free bilirubin precipitates with calcium
            ↓
CALCIUM BILIRUBINATE (brown pigment) stones form
            ↓
Stones + dead parasite fragments + bacteria accumulate in intrahepatic + CBD
            ↓
Partial/complete biliary obstruction → bile stasis
            ↓
Bacterial superinfection of stagnant bile (E. coli, Klebsiella most common)
            ↓
Recurrent episodes of acute cholangitis
            ↓ (chronic)
Intrahepatic strictures → segmental/lobar atrophy or hypertrophy
Pyogenic liver abscesses
Secondary biliary cirrhosis
Cholangiocarcinoma

It is still debated whether the primary event is infection causing inflammatory stricture, or inflammatory stricture causing infection of stagnant bile - likely a vicious cycle.

Key Stone Type:

• Brown pigment stones (soft, earthy, friable) - found in intrahepatic + extrahepatic ducts
• Distinct from cholesterol stones (Western; in gallbladder) and black pigment stones (haemolysis)

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DISTRIBUTION - ANATOMICAL PATTERN

• Predominantly involves intrahepatic bile ducts with focal strictures + dilations
• Left hepatic duct more commonly involved than right - due to its more acute angulation (the sharper bend predisposes to stasis and stone impaction)
• CBD may also be involved (choledocholithiasis)
• Disease may be unilateral (one lobe) or bilateral
• In chronic cases: lobar/segmental atrophy or hypertrophy due to longstanding ductal obstruction

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CLINICAL FEATURES

Acute Presentation:

• Charcot's Triad: RUQ/epigastric pain + fever/rigors + jaundice
• Nausea, vomiting
• Tender hepatomegaly
• Signs of sepsis if severe (Reynolds pentad in suppurative cases)
• Jaundice tends to be MILD (because stones are segmental/lobar, not causing complete obstruction of the whole biliary tree)

Chronic/Atypical Presentation:

• Recurrent attacks of RUQ pain + fever, often for months-years before diagnosis
• Symptoms may be subtle and go unrecognised for long periods
• Progressive weight loss
• Features of portal hypertension if cirrhosis develops (splenomegaly, varices, ascites)

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INVESTIGATIONS

Blood Tests:

Stool / Serology:

• Stool microscopy for ova and parasites (Ascaris, Clonorchis eggs)
• Serology for Clonorchis/Opisthorchis antibodies

Imaging:

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COMPLICATIONS

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MANAGEMENT

Phase 1: Acute Attack Management

• IV antibiotics (broad-spectrum: cover gram-negatives + anaerobes)
  • Piperacillin-tazobactam OR carbapenem (for severe)
  • Metronidazole for anaerobic cover
• IV fluids + resuscitation
• Analgesia
• If no response → urgent biliary drainage (ERCP or PTC)

Phase 2: Definitive/Elective Management

A. Endoscopic (ERCP-based) - preferred for CBD + main intrahepatic ducts

1. Biliary decompression - plastic stent or nasobiliary tube (NBT)
2. Cholangiogram to localise stones and strictures
3. Guidewire across stricture
4. Balloon dilation of strictures
5. Brush cytology of suspicious strictures (exclude cholangiocarcinoma)
6. Stone fragmentation: mechanical lithotripsy OR electrohydraulic lithotripsy (EHL) OR laser lithotripsy
7. Stone retrieval (balloon sweep / basket extraction)
8. Plastic stent placement if residual stones/strictures

Complete ductal clearance achieved in only ~32-67% of cases - multiple sessions often needed Limitations: Cannot reach peripheral intrahepatic ducts; high recurrence rate

B. Cholangioscopy (Peroral or Percutaneous)

• Direct visualisation of biliary tree beyond ERCP limits
• Allows targeted intraductal lithotripsy and biopsy of strictures
• Peroral cholangioscopy (POCS) for main ducts; percutaneous transhepatic cholangioscopy (PTCS) for peripheral disease

C. Percutaneous Transhepatic Approach (PTC/PTCS)

• When strictures/stones are in peripheral biliary ducts inaccessible by ERCP
• Allows progressively larger dilations + stone extraction over weeks-months

D. Surgical Management - almost always required eventually

• Predominantly left-sided disease with left lobe atrophy
• Intrahepatic strictures not amenable to endoscopy
• Risk of cholangiocarcinoma in a diseased lobe
• Failure of endoscopic/percutaneous clearance

1. Remove ALL stones (intraoperative choledochoscopy)
2. Bypass, enlarge, or resect strictures
3. Provide adequate long-term biliary drainage

Left hepatectomy is commonly required because the left hepatic duct is disproportionately affected

"Sump Roux limb" - when a Roux limb is exteriorised as a stoma - allows repeated endoscopic access to intrahepatic ducts postoperatively for residual/recurrent stone removal

Antiparasitic Treatment

• Praziquantel - for Clonorchis sinensis and Opisthorchis viverrini (drug of choice)
• Albendazole/Mebendazole - for Ascaris lumbricoides

---

SURVEILLANCE FOR CHOLANGIOCARCINOMA

• All patients require long-term follow-up
• Annual or biannual MRCP or CT to monitor for malignant transformation
• Suspicious strictures → ERCP with brush cytology/cholangioscopy biopsy
• Disease predominantly in one lobe = resect (to remove at-risk tissue)
• Serum CA 19-9 as tumour marker (limited specificity)

---

QUICK SUMMARY TABLE

---

CHOLELITHIASIS - COMPLETE GUIDE

---

DEFINITION

---

EPIDEMIOLOGY

• Affects ~15-20% of adults in Western countries
• Second most common cause of surgical admission
• ~80% remain asymptomatic throughout life
• Women affected 2-3x more than men (oestrogen effect)
• Incidence increases with age

---

TYPES OF GALLSTONES

Comparison of Stone Types

---

PATHOGENESIS

Cholesterol Stone Formation - 3 Key Steps:

Step 1: SUPERSATURATION
Cholesterol hypersecretion into bile
→ cholesterol concentration exceeds capacity of bile salts 
  and phospholipids (lecithin) to keep it in solution
→ bile becomes LITHOGENIC (supersaturated)

Step 2: NUCLEATION
Cholesterol crystals precipitate out of supersaturated bile
→ enhanced by mucin glycoproteins (pronucleating agents)
→ inhibited by apolipoproteins A1 and A2

Step 3: STONE GROWTH / GALLBLADDER STASIS
Crystals aggregate and grow
→ impaired gallbladder motility = stasis → stone enlargement

• Cholesterol
• Bile salts (bile acids)
• Lecithin (phospholipid)

Black Pigment Stone Formation:

• Excess unconjugated bilirubin (from haemolysis) in bile
• Deconjugation of bilirubin → free bilirubin precipitates with calcium
• Occurs in: haemolytic anaemias (sickle cell, hereditary spherocytosis, thalassaemia), cirrhosis, prolonged TPN, ileal disease (Crohn's - impaired bile salt reabsorption), vagotomy

Brown Pigment Stone Formation:

• Bacterial β-glucuronidase hydrolyses conjugated bilirubin → free bilirubin + calcium bilirubinate = soft brown stones
• Associated with biliary stasis + infection (E. coli, Klebsiella) and parasites (Ascaris, Clonorchis)
• Form in bile DUCTS (not just gallbladder)

---

RISK FACTORS - "THE Fs" (for cholesterol stones)

---

CLINICAL PRESENTATIONS

Asymptomatic (silent) gallstones  →  80%
         ↓
Biliary colic (symptomatic cholelithiasis)
         ↓
Acute cholecystitis (cystic duct obstruction + inflammation)
         ↓
Complications:
  ├── Empyema of gallbladder
  ├── Perforation → bile peritonitis
  ├── Mucocele/Hydrops of gallbladder
  ├── Mirizzi syndrome
  ├── Choledocholithiasis (CBD stone) → obstructive jaundice
  │         ↓
  │     Acute cholangitis / Gallstone pancreatitis
  ├── Gallstone ileus (Bouveret syndrome)
  └── Gallbladder carcinoma (long-term, rare)

---

1. Asymptomatic (Silent) Cholelithiasis

• ~80% of gallstone carriers
• Found incidentally on USS for other reasons
• Do NOT require cholecystectomy routinely
• Exceptions: porcelain gallbladder (calcified wall - controversial), immunocompromised patients, very large stones (>3 cm - increased CA risk)

---

2. Biliary Colic (Symptomatic Cholelithiasis)

• Pain: Constant (not truly "colic") - RUQ or epigastric, severe, rapid onset
• Radiation: To right scapula or between the shoulder blades (infrascapular)
• Duration: 1-5 hours, then resolves spontaneously
• Triggers: Fatty meal (CCK release → gallbladder contraction), often wakes patient at night
• Associated: Nausea, vomiting; may have mild RUQ tenderness
• Between attacks: Patient is completely well; normal WBC + LFTs
• Association with meals: only ~50% of patients
• If pain lasts >24 hours → suspect acute cholecystitis or impacted stone

---

3. Acute Cholecystitis

• Severe RUQ pain, constant, lasting >24 hours (unlike biliary colic)
• Fever, nausea, vomiting
• Murphy's sign - inspiratory arrest on deep palpation of RUQ (patient catches breath when inflamed GB hits examiner's fingers)
• Ultrasonographic Murphy's sign - tenderness directly over GB on USS probe pressure
• Guarding and rigidity if perforation
• Lab: Leukocytosis; mild ↑ bilirubin, ALP; ↑ CRP

• Empyema - gallbladder fills with pus; septic patient
• Gangrenous cholecystitis - ischaemia → wall necrosis; risk of perforation
• Perforation → biliary peritonitis or pericholecystic abscess
• Emphysematous cholecystitis - gas-forming organisms (Clostridium, E. coli) - seen in diabetics; surgical emergency

• Occurs in critically ill patients (ICU, burns, trauma, post-op, TPN)
• Mechanism: gallbladder ischaemia + stasis + infection
• Higher mortality than calculous cholecystitis

---

4. Choledocholithiasis (CBD Stones)

• Stones pass from gallbladder into CBD (secondary stones) or form in CBD (primary brown stones)
• Presents with: obstructive jaundice, dark urine, pale stools, pruritus
• ↑ bilirubin (conjugated), ↑ ALP, ↑ GGT; ± ↑ amylase
• Complications: acute cholangitis (Charcot's triad), gallstone pancreatitis
• Treatment: ERCP + sphincterotomy + stone extraction; then cholecystectomy

---

5. Mirizzi Syndrome

• Large stone in Hartmann's pouch or cystic duct extrinsically compresses the adjacent common hepatic duct
• Causes obstructive jaundice from OUTSIDE the duct (not choledocholithiasis)
• Can erode through and form a cholecystocholedochal fistula
• Difficult cholecystectomy; risk of bile duct injury

---

6. Gallstone Ileus

• Large gallstone erodes through GB wall into adjacent duodenum (cholecystoduodenal fistula) → passes into small bowel → obstructs at the terminal ileum (narrowest point)
• Classic plain AXR: Rigler's triad = (1) bowel obstruction, (2) ectopic gallstone, (3) pneumobilia (air in biliary tree from fistula)
• Treatment: enterotomy + stone extraction; fistula may be dealt with later

---

INVESTIGATIONS

Blood Tests

Imaging

---

MANAGEMENT

Asymptomatic Gallstones

• Watchful waiting - no treatment for most
• Annual incidence of developing symptoms: ~1-2%
• Prophylactic cholecystectomy considered for: porcelain gallbladder (debated), very large stones (>3 cm), immunocompromised, transplant patients, patients in remote areas

Biliary Colic (Symptomatic, Uncomplicated)

• Elective laparoscopic cholecystectomy - definitive treatment
• Analgesia: diclofenac (NSAID) or opioids for acute attacks
• Low-fat diet while awaiting surgery
• Ursodeoxycholic acid (UDCA) - medical dissolution of small cholesterol stones; only works in ~50%; stones recur after stopping; rarely used now given widespread laparoscopic cholecystectomy

Acute Cholecystitis

• NBM, IV fluids
• IV antibiotics (cephalosporin + metronidazole OR piperacillin-tazobactam)
• Analgesia (NSAIDs + opioids)

• Early laparoscopic cholecystectomy within 24-72 hours of symptoms = gold standard
  • Shorter hospital stay, lower complication rate vs delayed surgery
  • Morbidity 2-3%, mortality 0.1-0.5%
  • Tokyo Guidelines recommend early lap cholecystectomy for Grade I (mild) and Grade II (moderate) cholecystitis in fit patients
• Percutaneous cholecystostomy (USS-guided drainage) for Grade III severe cholecystitis in unfit/unstable patients as a bridge to surgery
• Convert to open if critical view of safety not achieved, excessive bleeding, bile duct injury

Laparoscopic Cholecystectomy - Key Technical Points

• 4 ports: 12 mm umbilical (specimen extraction) + 3 × 5 mm (subxiphoid, RMC, RAAI)
• Triangle of Calot dissection: CBD (medially) + cystic duct (inferiorly) + inferior surface of liver (superiorly)
• Critical view of safety (CVS): Two and ONLY two structures entering GB, lower third of GB dissected off liver, cleared hepatocystic triangle - MUST be achieved before clipping
• Calot's node (Lund's node): Lymph node overlying cystic artery - useful landmark
• Intraoperative cholangiogram (IOC) if CBD stones suspected
• Clip cystic duct + cystic artery → divide → remove GB from liver bed

Choledocholithiasis

• ERCP + sphincterotomy + stone extraction - then cholecystectomy (ideally same admission or within 6 weeks)
• If ERCP fails: PTC or open CBD exploration + T-tube
• Retained CBD stones (post-cholecystectomy): ERCP first; if T-tube in situ, can extract through T-tube tract at 4 weeks

---

COMPLICATIONS OF CHOLECYSTECTOMY

---

GALLBLADDER CARCINOMA (Association with Gallstones)

• Found in ~1% of cholecystectomy specimens
• Risk: long-standing gallstones (large stones >3 cm; porcelain GB), females, Native American
• Often presents late with advanced disease
• Prognosis poor if invasion beyond mucosa

---

QUICK SUMMARY TABLE

---

BREAST CANCER 101 - COMPLETE GUIDE

---

EPIDEMIOLOGY

• Most common cancer in women worldwide - ~2.3 million new cases in 2020 (~25% of all cancers in women)
• In Western Europe: 1 in 9 women will develop breast cancer in their lifetime
• Accounts for 3-5% of all deaths in women in high-income countries
• In resource-poor countries: 1 in 28 women affected; for every 2 diagnosed, 1 dies
• Median age of presentation: ~60 years (West); ~48 years in low/middle-income countries
• Male breast cancer: 0.5-1% of all breast cancers

---

RISK FACTORS

Modifiable Risk Factors

Non-Modifiable Risk Factors

• BRCA1 - mostly triple-negative breast cancers
• BRCA2 - associated with cancers of prostate, colon, gallbladder, bile duct, stomach, pancreas

---

PATHOLOGY - TYPES OF BREAST CANCER

In Situ Carcinomas (pre-invasive)

Invasive Carcinomas

---

PATHOGENESIS - WHY SIGNS OCCUR

Tumour mass enlarges in breast parenchyma
            ↓
Releases growth factors:
  - FGF (fibroblast growth factor)
  - TGFα / TGFβ
  - VEGF
            ↓
FGF stimulates adjacent fibrocytes → fibroblasts → collagen
(DESMOPLASTIC REACTION = hard, irregular mass)
            ↓
Collagen contracts → SHORTENS COOPER'S LIGAMENTS
            ↓
Pulls skin inwards:
  Single ligament → DIMPLING
  Many ligaments → PUCKERING / TETHERING
  Nipple ligaments → NIPPLE RETRACTION
            ↓
Tumour obstructs dermal lymphatics → PEAU D'ORANGE
(skin oedema - skin over lymphatic pores looks like orange peel)

---

CLINICAL EXAMINATION OF THE BREAST

Step 1 - History Taking

• Onset, duration, change of lump
• Relationship to menstrual cycle (cyclical = likely benign)
• Nipple discharge (colour: bloody/serous/green/milky)
• Skin changes; pain
• Menstrual history: age at menarche, LMP, regularity
• Reproductive history: parity, age at first birth, breastfeeding
• Hormonal history: OCP use, HRT
• Family history: breast/ovarian/other cancers, affected relatives + age of onset
• Previous biopsies (histological result)

---

Step 2 - INSPECTION (Patient seated, arms by sides)

1. Arms raised - better view of lower breast and inframammary fold
2. Hands on hips + pectoral muscle contraction - accentuates skin retraction/dimpling from deep tumours attached to Cooper's ligaments

---

Step 3 - PALPATION OF LYMPH NODES (still seated)

• Axillary nodes - with patient's ipsilateral arm supported by examiner to relax muscles
  • Anterior (pectoral): palpate anterior axillary fold
  • Posterior (subscapular): posterior axillary fold
  • Lateral (humeral): medial arm
  • Central: high axilla
  • Apical: apex of axilla below clavicle
• Supraclavicular nodes - from behind patient, palpate above clavicle
• Infraclavicular nodes - below clavicle
• Cervical nodes

---

Step 4 - PALPATION OF BREASTS (patient supine)

• Use flat of the finger pads (not fingertips) in a systematic pattern
• Methods: concentric circles OR radial spokes from nipple OR grid/strip method
• Palpate all 4 quadrants + axillary tail of Spence
• Include the subareolar region (retroareolar area)
• Note: normal breasts have nodularity in the upper outer quadrant, inframammary ridge, and subareolar region - this is NORMAL

---

Step 5 - NIPPLE EXAMINATION

• Inversion: Present? Lifelong or new onset?
• Discharge: Elicit by gentle pressure around areola
  • Unilateral, single-duct, bloody/serous discharge = HIGH SUSPICION for malignancy or duct ectasia/intraductal papilloma
  • Bilateral multiduct milky = galactorrhoea (prolactinoma)
  • Green/brown discharge = fibrocystic disease/duct ectasia

---

Summary: Signs of Malignancy on Examination

---

INVESTIGATIONS - TRIPLE ASSESSMENT

Imaging

• Views: Cranio-caudal (CC) + Mediolateral oblique (MLO)
• Features suggesting malignancy:
  • Spiculated/stellate mass (irregular radiating margins)
  • Microcalcifications (clustered/pleomorphic = DCIS)
  • Asymmetric density
  • Architectural distortion

• Women <35 = dense breasts → start with USS rather than mammography

• For younger women (<35-40), pregnant women, or to characterise mammographic lesions
• Distinguishes solid from cystic lesions
• Features suggesting malignancy: irregular hypoechoic mass, spiculated margins, posterior acoustic shadowing, taller-than-wide shape

• For BRCA1/2 carriers (annual screening from age 30)
• Pre-operative staging: multifocal/multicentric disease assessment
• Post-lumpectomy - assess margins
• NOT first-line for all patients

• Core needle biopsy (CNB) - preferred; provides histology, receptor status (ER, PR, HER2), grade
• FNAC - cytology only; quicker but no architecture
• Vacuum-assisted biopsy for microcalcifications

---

MOLECULAR SUBTYPES (Receptor Status)

---

STAGING - AJCC TNM 8TH EDITION

T - Primary Tumour

N - Lymph Nodes

M - Metastases

• M0 = No distant mets
• M1 = Distant mets

Overall Stage Groups

---

METASTATIC SPREAD

• Axillary nodes - main pathway (lateral and upper outer tumours)
• Internal mammary nodes - inner half tumours
• Supraclavicular nodes - N3 disease
• Contralateral axilla (via subdermal or retrosternal lymphatics)

1. Bone - lumbar vertebrae > neck of femur > thoracic vertebrae > ribs > skull
   • Mostly osteolytic (can be osteosclerotic or mixed)
   • In limbs: only above elbow and above knee (haematopoietic marrow distribution)
2. Liver
3. Lungs
4. Brain
5. Adrenal glands, ovaries

At tumour size 1-2 mm (10⁵ cells), neoangiogenesis begins - marks onset of rapid growth and metastatic potential

---

TREATMENT

Multimodal Approach - MDT Including:

Neoadjuvant Systemic Therapy (NAST) - before surgery

• Locally advanced cancer (T3, T4, N2/N3) - to downsize
• Early cancer: to enable BCS; HER2+ tumours; TNBC; premenopausal; node-positive

• NACT (neoadjuvant chemotherapy)
• Neoadjuvant targeted therapy - Trastuzumab + Pertuzumab for HER2+ >5 mm
• Neoadjuvant hormonal therapy - elderly/frail ER+/PR+ patients (takes 3-6 months for response)

Surgical Options

A. Breast Surgery

B. Axillary Surgery

Adjuvant Therapy (after surgery)

Metastatic Disease (Stage IV) - Palliative Intent

• Endocrine therapy preferred for ER+ with bone mets + limited visceral involvement
• Chemotherapy for HR-negative, hormone-refractory, visceral crisis
• Palliative radiotherapy for painful bony mets (weight-bearing: vertebrae, femur)
• Bisphosphonates (zoledronic acid) for bone mets
• Pleural effusions: drain + pleurodesis
• Surgical resection only for solitary visceral mets in fit patients with favourable biology

---

SCREENING

---

HEREDITARY MANAGEMENT

• Bilateral risk-reducing mastectomy → reduces risk by 90%
• Chemoprophylaxis: Tamoxifen or anastrozole → reduces risk by ~50%
• Bilateral salpingo-oophorectomy at 35-40 years (after completing family) → reduces ovarian CA risk

---

QUICK EXAM SUMMARY

---

HEMATEMESIS 101 - COMPREHENSIVE GUIDE

---

DEFINITIONS

• UPPER GI = proximal to the Ligament of Treitz (duodenojejunal flexure)
• LOWER GI = distal to the Ligament of Treitz

---

EPIDEMIOLOGY

• Incidence: >100 per 100,000 population/year in Western countries; increases with age
• In-hospital mortality: 5-10%; rises to 33% when bleeding first occurs in patients already hospitalised for another condition
• Strongly associated with NSAID use
• UGIB accounts for up to 150 hospital admissions per 100,000 per year

---

CAUSES OF UPPER GI BLEEDING

Frequency Table (Bailey and Love)

Full Causes List - Mnemonic: "PEPTIC VOMIT"

---

PATHOPHYSIOLOGY OF KEY CAUSES

1. Peptic Ulcer Bleeding

• H. pylori (prevalence 80%+ developing countries; 20-50% industrialised) → antral-predominant gastritis → duodenal ulcers
• NSAIDs → inhibit COX-mediated prostaglandin synthesis → impaired mucosal protection
• Pathology: 96% of surgically resected bleeding ulcers have an underlying artery (50% protruding above ulcer surface, 50% clot overlying breach in vessel wall)
• Deep posterior duodenal ulcer → erodes into gastroduodenal artery → exsanguinating haemorrhage

2. Mallory-Weiss Tear

• Mucosal (NOT full thickness) tear at the gastro-oesophageal junction
• Caused by sudden increase in intra-abdominal pressure: forceful retching/vomiting, coughing, lifting, pregnancy, trauma, bowel prep
• Extends distally into hiatal hernia sac (if present)
• Usually single tear, starts at GEJ
• Bleeding is typically self-limiting in 90% of cases
• Heals within 24-48 hours
• Contrast with Boerhaave's syndrome (full-thickness oesophageal rupture) - surgical emergency

3. Oesophageal Varices

• Portal hypertension (most commonly from liver cirrhosis) → portosystemic shunting → oesophageal submucosal veins dilate
• Variceal rupture triggered by: increased portal pressure, variceal size, bacterial infection (spontaneous bacterial peritonitis)
• High mortality - each bleed: 20-30% mortality

---

CLINICAL PRESENTATION

History

• Character of vomit: Bright red (active, brisk) vs coffee-ground (slower/stopped bleeding)
• Amount and frequency
• NSAID / aspirin / anticoagulant / steroid use
• Alcohol use / liver disease (suggests varices)
• Preceding nausea and retching before haematemesis (suggests Mallory-Weiss)
• History of peptic ulcer disease (PUD), heartburn, epigastric pain
• Previous similar episodes, previous endoscopy
• Melaena (suggests upper GI source; blood in GI tract >6 hours)
• Dysphagia, weight loss, anorexia (malignancy)
• Family history of GI cancer or polyposis

Symptoms of Haemodynamic Compromise (blood loss)

---

EXAMINATION

General

• Pallor (anaemia)
• Jaundice / stigmata of chronic liver disease - if varices suspected: spider naevi, palmar erythema, gynaecomastia, caput medusae, hepatosplenomegaly, asterixis (hepatic encephalopathy), parotid enlargement, Dupuytren's contracture, leukonychia
• Alcohol smell
• Peripheral access availability

Vital Signs (Shock Assessment)

• Pulse rate (tachycardia >100 bpm = significant blood loss)
• Blood pressure (systolic <100 = haemodynamic compromise)
• Postural hypotension - BP drop >20 mmHg on standing = significant haemorrhage
• Respiratory rate, GCS, urine output (oliguria = end-organ hypoperfusion)

Abdomen

• Epigastric tenderness - peptic ulcer
• Hepatomegaly/splenomegaly - portal hypertension
• Ascites - cirrhosis
• Rectal examination - confirm melaena vs haematochezia; assess for anorectal sources

---

INVESTIGATIONS

Immediate (A-E assessment simultaneously)

Definitive Investigation

• Diagnostic AND therapeutic
• Timing:
  • Severe/ongoing bleeding: immediate OGD
  • Stabilised patients with mild bleeding: next morning (guided by local policy)
  • No evidence for IV PPI prior to endoscopy (does not improve outcomes)

---

RISK STRATIFICATION SCORES

A. Glasgow-Blatchford Score (GBS) - PRE-ENDOSCOPY

• GBS = 0 → safe for outpatient management (very low risk)
• GBS ≥6 → 50% likelihood of requiring treatment (high risk)
• Range: 0-23; higher = higher risk

B. Rockall Score - PRE + POST-ENDOSCOPY - Predicts rebleeding and mortality

• Clinical Rockall score = Age + Shock + Comorbidity (pre-endoscopy)
• Clinical Rockall 0 = 0% mortality
• Complete Rockall ≤2 = low risk; safe early discharge
• Complete Rockall 5 = ~10% mortality
• Complete Rockall ≥8 = ~40% mortality

C. Forrest Classification - Endoscopic stigmata of bleeding peptic ulcer

---

MANAGEMENT

Step 1 - RESUSCITATION (ABCDE - simultaneous with assessment)

1. Airway - protect airway in obtunded/actively vomiting patients; consider intubation before OGD if haematemesis with altered GCS
2. 2 large-bore IV cannulae (≥16G) or central venous access
3. IV fluids - isotonic crystalloid (NS or Hartmann's) for immediate resuscitation
4. Blood transfusion - trigger: Hb <7 g/dL (target Hb 7-9 g/dL); higher threshold (Hb <8-9) in patients with coronary artery disease; >30% blood volume loss is a transfusion indication
   • RESTRICTED transfusion strategy in variceal bleeding reduces rebleeding and mortality (Harrison's)
5. Correct coagulopathy - FFP for elevated PT/INR (especially liver disease, anticoagulants); platelets if <50
6. Urinary catheter - monitor urine output (target >0.5 mL/kg/hr)
7. CVP monitoring - for severe bleeding

Step 2 - PHARMACOLOGICAL THERAPY

Step 3 - ENDOSCOPIC THERAPY (OGD)

• Immediate OGD for: haemodynamic instability, suspected varices, ongoing active bleeding
• Within 24 hours for stable patients

• Adrenaline injection (1:10,000) - slows bleeding; never used alone (high re-bleed rate)
• Thermal coagulation - heater probe, multipolar electrocoagulation (MPEC)
• Haemoclip - mechanical occlusion of vessel
• Best evidence: Combination of adrenaline injection + haemoclip and/or heater probe
• Therapeutic endoscopy achieves haemostasis in ~70% of cases

• Endoscopic Variceal Ligation (EVL) / Band ligation - first-line for oesophageal varices
• Endoscopic sclerotherapy - injection of sclerosant (ethanolamine oleate) - second-line
• Gastric varices: tissue glue (cyanoacrylate) injection or thrombin

• Active bleeders: haemoclips (first-line) or adrenaline injection + MPEC
• Spontaneously stops in ~90%

Step 4 - ANGIOGRAPHIC INTERVENTION (if endoscopy fails)

• Mesenteric angiography → selective catheterisation → transcatheter arterial embolisation (TAE)
• Valuable alternative to surgery in expert centres
• Celiac axis + SMA angiograms (with CO2 or iodinated contrast)
• Can identify bleeding at rates >0.5 mL/min
• Prophylactic embolisation of gastroduodenal artery for duodenal ulcer bleeding

Step 5 - SURGICAL INTERVENTION

• Persistent bleeding despite 2 attempts at endoscopic haemostasis
• Haemodynamic instability with ongoing bleeding
• Rebleeding after endoscopy
• Transfusion requirement >6 units of RBC
• Frail/elderly patients should have EARLY surgery (paradox: they are more likely to die from bleeding, not surgery)

1. Oversewing/underrunning alone - emergency damage control; ligate GDA with 3-point U-stitch (superior, inferior, pancreatic branch)
2. Oversewing + vagotomy and pyloroplasty (V+D) - reduces acid secretion
3. Vagotomy and antrectomy (V+A) - lowest rebleed rate but higher morbidity

Kocher manoeuvre is performed FIRST at surgery - mobilises duodenum to allow posterior approach and manual compression of GDA from behind.

• Longitudinal duodenotomy/pyloroduodenotomy
• Expose ulcer (usually posterior/superior)
• Under-run the bleeding vessel with heavy sutures (U-stitch/figure-of-8) in ulcer base
• Close pylorotomy transversely (Heineke-Mikulicz)
• If large ulcer destroys first part of duodenum: distal gastrectomy with Roux-en-Y

• Anterior gastrotomy → underrun vessel → biopsy ulcer margins (exclude malignancy) → local excision if feasible

• TIPS (Transjugular Intrahepatic Portosystemic Shunt) - decompresses portal system
  • Complication: encephalopathy in up to 20%
  • Used as bridge to transplantation
• Balloon tamponade (Sengstaken-Blakemore tube or Minnesota tube) - temporary bridge to definitive therapy
  • Inflates oesophageal + gastric balloons to compress varices
  • MAX 24 hours (risk of oesophageal necrosis/rupture)
• Surgical shunts (Warren selective splenorenal shunt) - rarely used

---

SPECIFIC CONDITIONS IN DETAIL

Stress Ulceration

• ICU patients with major illness/injury/surgery
• Incidence reduced by enteral nutrition and prophylactic PPI/H2 blockers
• Curling's ulcer = burns; Cushing's ulcer = raised ICP/head injury (vagal stimulation)

Dieulafoy's Lesion

• Large, tortuous submucosal artery (usually left gastric artery branch) erodes through mucosa
• Tiny mucosal defect with MASSIVE, recurrent, arterial bleeding
• Location: within 6 cm of GEJ, on lesser curve
• Diagnosis: endoscopy (may be missed if not actively bleeding); can require repeated OGDs or angiography
• Treatment: endoscopic haemoclip or band ligation

Aortoenteric Fistula

• After aortic graft surgery → fistula between aortic graft and duodenum (3rd/4th part)
• Presents with herald bleed (small self-limiting haematemesis/melaena) before catastrophic exsanguinating haemorrhage
• Diagnosis: CT angiography; OGD (blood in D3/D4)
• Treatment: emergency vascular surgery

Haemobilia

• Bleeding into biliary tract → blood exits via ampulla of Vater
• Causes: trauma (most common - hepatic artery pseudoaneurysm), liver biopsy, ERCP, hepatic artery aneurysm
• Quincke's triad: haemobilia + obstructive jaundice + RUQ colic
• Diagnosis: OGD (blood from ampulla); angiography
• Treatment: hepatic artery embolisation

---

VARICEAL BLEEDING ALGORITHM

Acute variceal bleed
        ↓
Resuscitate:
- Hb target 7-9 g/dL (RESTRICTED strategy)
- FFP only if evidence of coagulopathy
- DO NOT correct PT with FFP routinely
        ↓
Pharmacology (BEFORE endoscopy):
- Octreotide / Terlipressin IV
- Prophylactic antibiotics (ceftriaxone IV)
        ↓
Urgent OGD + Band ligation (EVL)
        ↓
     ┌──────────────────────┐
Controlled                Failed
     ↓                        ↓
Prevention:         Balloon tamponade
- Repeated EVL          (Sengstaken-Blakemore)
  until obliterated          ↓
- Non-selective BB      TIPS
  (propranolol/         ↓
  carvedilol)       Consider transplant
                    evaluation (Child's B/C)

---

PEPTIC ULCER DISEASE - MANAGEMENT OVERVIEW

Medical (Non-bleeding)

• H. pylori eradication - Triple therapy: PPI + amoxicillin + clarithromycin x 7-14 days
• PPI (omeprazole, lansoprazole) - long-term if NSAID cannot be stopped
• Stop NSAIDs if possible

Surgical Indications for PUD (4 Cs):

1. Continuous/persistent bleeding despite medical and endoscopic therapy
2. Complications - perforation, obstruction
3. Cancer exclusion for gastric ulcer
4. Can't comply with medical therapy / recurrent despite treatment

---

SUMMARY TABLE - QUICK EXAM POINTS

• ✅ Definition + anatomical landmark (Ligament of Treitz)
• ✅ Epidemiology (>100/100,000/year, 5-10% mortality)
• ✅ Full causes table with frequencies (PUD 60%, erosions 26%, Mallory-Weiss 4%, varices 4%)
• ✅ Pathophysiology of PUD, Mallory-Weiss, oesophageal varices
• ✅ Clinical presentation + haemodynamic shock classification
• ✅ Examination (stigmata of liver disease, postural hypotension)
• ✅ Investigations (Urea:Creatinine ratio, FBC, coags, crossmatch)
• ✅ Glasgow-Blatchford Score (pre-endoscopy triage)
• ✅ Rockall Score (complete with table + mortality thresholds)
• ✅ Forrest Classification (Ia → III with rebleed % and management)
• ✅ Management stepwise: Resuscitation → Pharmacology → OGD → Angioembolisation → Surgery
• ✅ Surgical technique for bleeding DU (Kocher, pyloroduodenotomy, U-stitch, Heineke-Mikulicz)
• ✅ Variceal algorithm (octreotide/terlipressin + ceftriaxone → EVL → TIPS → transplant evaluation)
• ✅ Special conditions: Dieulafoy's, aortoenteric fistula, haemobilia, stress ulcers

1. Non-variceal vs variceal UGIB - side-by-side comparison
2. H. pylori - pathogenesis, diagnosis and eradication regimens in depth
3. Portal hypertension - pathophysiology, Child-Pugh/MELD scoring, TIPS procedure
4. Acute management OSCE/exam station - step-by-step clinical approach script
5. Lower GI bleeding - as the complementary topic

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BURNS 101 - COMPREHENSIVE GUIDE

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DEFINITION AND EPIDEMIOLOGY

• Burns are a leading cause of accidental death worldwide
• Scald injuries (hot liquids) are most common in children <2 years (accidental or non-accidental)
• Flame burns are more common in teenagers and adults
• Children have thinner skin → more severe burns from same thermal exposure; larger BSA-to-mass ratio → greater insensible fluid losses
• Inhalation injury has now become the main cause of mortality in burn patients as resuscitation has improved

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TYPES OF BURNS BY AETIOLOGY

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BURN DEPTH CLASSIFICATION

Depth of injury = Temperature × Duration
                  ─────────────────────
                       Blood Flow

• Superficial burns = NOT included in TBSA% calculation (only partial + full thickness)
• Scalds → usually partial thickness
• Clothes catching fire → usually full thickness
• Wounds healing in <14 days = no significant scar
• Wounds healing in 14-21 days = some scarring
• Wounds taking >21 days = deep dermal/full thickness → unacceptable scarring → surgery

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ESTIMATION OF BURN SIZE - % TBSA

Rule of Nines (Adults)

Why different in children? Head is proportionately larger; lower limbs proportionately smaller.

Lund and Browder Chart

• More accurate than Rule of Nines, especially in children
• Accounts for age-related body proportion changes (Berkow formula)

Palm Method

• Patient's palm (fingers together) = approximately 1% TBSA in all ages
• Useful for scattered/irregular burns

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INITIAL ASSESSMENT - ATLS APPROACH

Primary Survey

• Signs of inhalation injury requiring immediate intubation:
  1. Full-thickness burns of face/perioral area
  2. Circumferential neck burns
  3. Acute respiratory distress / stridor
  4. Progressive hoarseness or air hunger
  5. Carbonaceous (sooty) sputum
  6. Supraglottic oedema on bronchoscopy
  7. Respiratory depression / altered GCS
• Delay leads to progressive oedema → loss of airway → cannot intubate
• Fibreoptic bronchoscopy = gold standard if uncertain
• Cover burn with DRY sheet during primary survey; defer debridement

• 100% humidified oxygen by non-rebreather mask for ALL suspected inhalation injury
• CO poisoning falsely elevates SpO2 on pulse oximetry → ABG with carboxyhaemoglobin mandatory
• Circumferential chest burns → restrict chest wall expansion → may need escharotomy

• 2 large-bore IV cannulae (ideally through unburnt skin - but can be placed through burns if necessary)
• Urinary catheter (monitor urine output)
  • Target UO: 0.5 mL/kg/hr (adults and children >30 kg)
  • Target UO: 1 mL/kg/hr (children <30 kg)
• Check for circumferential limb burns → compartment syndrome

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INHALATION INJURY

• Closed-space fires
• Decreased mentation (alcohol, drugs, head injury, overdose)

Three Components of Inhalation Injury

CO Poisoning

• SpO2 probe CANNOT detect CO - always get ABG
• Treatment: 100% oxygen (displaces CO from haemoglobin - half-life reduced from 5h → 60-90 min)
• Consider hyperbaric oxygen for severe CO poisoning (GCS <8, pregnant patients, cardiac involvement)

Cyanide Poisoning

• From combustion of nitrogen-containing polymers: wool, silk, polyurethane, vinyl
• Binds cytochrome oxidase → uncouples oxidative phosphorylation → histotoxic hypoxia
• Suspect when: profound metabolic acidosis + high lactate + low response to O2
• Treatment: hydroxocobalamin (Cyanokit) IV; sodium thiosulfate

Diagnosis of Inhalation Injury

• History: enclosed-space fire, LOC at scene
• Signs: facial burns, singed nasal hair, soot in mouth/nose, hoarseness, carbonaceous sputum, expiratory wheeze
• ABG + carboxyhaemoglobin levels
• CXR (may be normal initially)
• Bronchoscopy - direct visualisation (gold standard)

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FLUID RESUSCITATION - PARKLAND FORMULA

When to start?

• Burns >15-20% TBSA in adults, >10% TBSA in children

Parkland Formula (Baxter Formula)

Total 24-hour fluid = 4 mL × Weight (kg) × %TBSA burned

• Fluid used: Hartmann's solution (Lactated Ringer's) - crystalloid
• Count only 2nd and 3rd degree burns (not superficial/1st degree burns) in TBSA calculation

Administration Schedule

Critical point: the 8 hours is counted from time of injury, not from time of arrival at hospital. If a patient arrives 3 hours after the burn, the first 8 hours worth of fluid must be delivered in the remaining 5 hours.

Worked Example

• 70 kg adult with 40% TBSA burns
• Total = 4 × 70 × 40 = 11,200 mL
• First 8 hours = 5,600 mL (700 mL/hr)
• Next 16 hours = 5,600 mL (350 mL/hr)

Monitoring Adequacy

• Urine output (primary guide): 0.5 mL/kg/hr adults; 1 mL/kg/hr children
• Heart rate, blood pressure, mental status
• Serum lactate (tissue perfusion)

Pitfalls

• Parkland formula = estimate only; titrate to urine output
• Can lead to over-resuscitation ("fluid creep") → abdominal compartment syndrome, pulmonary oedema
• Do NOT forget to add maintenance fluids (especially in children)
• Children also need dextrose-containing maintenance fluid alongside Parkland resuscitation (to prevent hypoglycaemia)

Modified Brooke Formula (alternative)

2 mL × Weight (kg) × %TBSA = 24-hour crystalloid

Paediatric addition

• Add 5% dextrose in 0.45% NaCl at maintenance rate alongside Parkland formula
• Monitor glucose closely

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BURN CENTRE REFERRAL CRITERIA (American Burn Association)

1. Partial-thickness burns >10% TBSA
2. Burns involving face, hands, feet, genitalia, perineum, or major joints
3. Full-thickness burns of any age
4. Electrical burns
5. Chemical burns
6. Inhalation injury
7. Burns with preexisting medical comorbidities
8. Burns with concomitant trauma where burn poses greater risk
9. Burned children in hospitals without appropriate paediatric facilities
10. Burns requiring specialised social/emotional/rehabilitative intervention

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WOUND MANAGEMENT

Topical Antimicrobial Agents

Dressings

• Small superficial burns → moist non-adherent dressings (e.g. Mepitel, Mepilex)
• Larger partial thickness → silver-containing foam dressings; change every 3-5 days
• For transfer → large wounds: dry dressings (limit heat loss); small wounds: clean moist dressings

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ESCHAROTOMY AND FASCIOTOMY

Escharotomy

• Indicated for circumferential full-thickness burns of limb or chest
• Circumferential burns create a rigid, non-compliant eschar → tourniquet effect → compartment syndrome
• Chest escharotomy: bilateral mid-axillary line incisions ± transverse incision = improves chest wall excursion + ventilation

• Increasing pain / paresthesia / pallor / pulselessness
• Compartment pressure >30 mmHg (or within 30 mmHg of diastolic BP)
• Doppler signals absent in digits

• Incision through eschar to fat (NOT fascia) in medial and lateral mid-axial lines of limb
• Extend across involved joints
• Digit escharotomies in lateral mid-axial lines

Fasciotomy

• For high-voltage electrical burns and crush injuries → myonecrosis + compartment syndrome despite escharotomy
• Can be performed through the bed of the escharotomy incision

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SURGICAL MANAGEMENT OF BURN WOUNDS

Goals of Surgery (three interdependent goals):

1. Closure - wound closure (life-saving for large burns)
2. Function - preserve/restore range of movement
3. Cosmesis - acceptable appearance

Timing of Excision

• Early excision and grafting = proven to improve survival in large burns and improve cosmesis in smaller burns
• Wounds that will take >21 days to heal → benefit from excision and grafting
• Wounds estimated to heal within 17 days → observe in most patients
• Burns >40% TBSA → rapid closure is life-saving (best defence against sepsis + catabolism)

Tangential Excision (most common method)

• Sequential shaving of burned tissue until viable bleeding dermis/fat is reached
• Signs of viability at surgery:
  • Healthy dermis: pearly white appearance after exsanguination under tourniquet
  • Healthy fat: bright yellow
  • Nonviable dermis: red-to-purple staining after exsanguination
  • Compromised fat: dull yellow-to-orange/brown
• Extremity burns excised under tourniquet (minimises blood loss)

Fascial Excision

• Burns of great depth over large area → excise to fascial level
• Greater blood loss reduction + efficiency, but marked functional and cosmetic impact

Wound Coverage Options

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SYSTEMIC COMPLICATIONS OF MAJOR BURNS

Early (<48 hours) - Burn Shock Phase

Late (>48 hours) - Hyperdynamic/Septic Phase

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ELECTRICAL BURNS

• High-voltage (>1000V): entry wound + exit wound; internal damage far exceeds external appearance
• Current follows path of least resistance: nerves, blood vessels, muscle
• Complications:
  • Cardiac arrhythmias (ECG monitoring mandatory for 24 hours in high-voltage)
  • Rhabdomyolysis → myoglobinuria → acute renal failure
  • Compartment syndrome (may require fasciotomy even without visible burn)
  • Cataracts (if current passes through head)
  • Neurological injury, spinal cord injury
• Management: aggressive fluid resuscitation to maintain UO 1-1.5 mL/kg/hr to flush myoglobin; consider mannitol

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CHEMICAL BURNS

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PROGNOSTIC SCORING

Baux Score

Baux Score = Age + %TBSA burned

• Scores >100-120 historically associated with ~50% mortality
• Revised Baux Score = Age + %TBSA + 17 (if inhalation injury present)
• Simple bedside predictor of mortality

Rule for Lethal Burns (50% mortality - LD50)

• Varies with age and burn centre
• Modern burn centres: LD50 ≈ 60-70% TBSA in healthy adults

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NON-ACCIDENTAL INJURY (NAI) IN BURNS - RED FLAGS

• Stocking/glove distribution of scald injury (immersion burns - bilateral, sharply demarcated)
• Halo of spared buttocks skin (child held down during forced immersion)
• Delay in seeking medical attention
• History inconsistent with burn pattern or developmental stage
• Previous history of burn injury
• Unburned adults present at time of injury
• Bilateral/symmetric burns

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NUTRITION IN BURNS

• Burns induce the highest metabolic rate of any injury (hypermetabolism)
• Early enteral nutrition (within 6 hours of burn) is preferred:
  • Maintains gut mucosal integrity
  • Reduces bacterial translocation
  • Reduces catabolism
• Formulas used: Curreri formula for caloric requirements
  • Adults: 25 kcal/kg/day + 40 kcal × %TBSA/day
• High protein requirement: 2-3 g/kg/day
• Glutamine supplementation has shown benefit in major burns
• Parenteral nutrition only if enteral route is unavailable

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QUICK SUMMARY TABLE