---

Pancreatitis: Acute & Chronic - Complete Clinical Overview

---

ACUTE PANCREATITIS

Definition

---

Aetiology

---

Pathogenesis

1. Pancreatic duct obstruction - gallstone/biliary sludge impaction raises intraductal pressure -> interstitial oedema -> vascular insufficiency -> ischaemic acinar injury
2. Primary acinar cell injury - alcohol, hypertriglyceridaemia, ischaemia, drugs, and viruses directly injure acinar cells -> release of intracellular proenzymes and lysosomal hydrolases
3. Defective intracellular transport - proenzymes co-package with lysosomal hydrolases -> intracellular trypsin activation -> lysosomal rupture -> enzyme cascade

---

Clinical Features

• Pain - cardinal symptom; epigastric, severe, constant, reaching maximum within minutes; radiates to the back in ~50% of cases; some patients gain relief by leaning forward (classic "pancreatitis posture")
• Nausea and vomiting (does not relieve pain - distinguishes from peptic ulcer)
• Anorexia

• Epigastric tenderness and guarding
• Abdominal distension from ileus
• Fever, tachycardia
• Grey Turner's sign - bruising in the flanks (haemorrhagic pancreatitis; ~1-2 days after onset)
• Cullen's sign - periumbilical bruising (retroperitoneal haemorrhage tracking to umbilicus)
• Jaundice (if gallstone aetiology with CBD obstruction)
• Hypotension / shock in severe cases

---

Investigations

1. Is the diagnosis of acute pancreatitis correct?
2. How severe is the attack?
3. What is the aetiology?

• Serum amylase - >5× upper limit of normal is diagnostic; peaks within hours of onset; returns to near normal within 48h (may miss peak if bloods taken late); also elevated in peptic ulcer perforation, bowel obstruction, cholecystitis
• Serum lipase - more sensitive and specific than amylase; remains elevated longer (>3 days); preferred where available
• Urinary amylase:creatinine clearance ratio - useful if serum levels have normalised
• Peritoneal aspirate - prune-juice fluid with extremely high amylase (>10,000 units) in haemorrhagic necrosis

• CRP >150 mg/L at 48h = severe attack indicator
• FBC (WBC, haematocrit), U&E, LFTs, calcium, glucose, LDH, ABG, albumin, triglycerides

• Plain AXR - not diagnostic but shows: "sentinel loop" (gas-filled jejunal loop in upper abdomen - considered pathognomonic), "colon cut-off sign" (transverse colon gas abruptly stops), widened C-loop of duodenum
• CXR - pleural effusion (usually left-sided, indicates severity), ARDS pattern
• Ultrasound (within 24h of all admissions) - detects gallstones and CBD dilatation; pancreas may be oedematous; identifies peripancreatic fluid collections
• Contrast-enhanced CT - not needed in mild disease; indicated when: (a) diagnostic uncertainty; (b) severe attack to distinguish interstitial from necrotising pancreatitis; (c) suspected abscess (gas within fluid collection); (d) failure to improve within 72h. CT may underestimate necrosis extent in first 72h. Severity graded by the CT Severity Index (Balthazar grading A-E)
• MRCP/MRI - non-invasive assessment of CBD stones and pancreatic duct; avoids radiation
• EUS - detects microlithiasis and CBD stones; helps select patients for ERCP

• Age >55 years; WBC >15×10⁹/L; glucose >10 mmol/L; LDH >600 U/L or AST >200 U/L
• Urea >16 mmol/L (no response to fluids); PaO₂ <8 kPa; Ca²⁺ <2.0 mmol/L; albumin <32 g/L

---

Treatment

• Fluid resuscitation - aggressive IV crystalloid (Ringer's lactate preferred); guided by urine output, HR, CVP
• Analgesia - opiate analgesia (pethidine traditionally favoured; morphine now acceptable); NSAIDs adjunct
• Antiemetics
• Nutritional support - early oral/enteral feeding when tolerated; prolonged NBM not justified physiologically. Enteral > parenteral nutrition (fewer infections, lower cost). Nasogastric vs nasojejunal feeding is equivalent, though NJ preferred if gastric retention
• Antibiotics - NOT indicated prophylactically in mild disease; reserved for infected necrosis
• No drug therapy or CT needed in mild disease

• High-dependency / ICU admission with invasive monitoring
• Aggressive fluid resuscitation with close monitoring
• ERCP - for gallstone pancreatitis with cholangitis or biliary obstruction (urgent); early routine ERCP does not improve outcomes in the absence of obstruction
• Early laparoscopic cholecystectomy (within 3 days) in mild biliary pancreatitis improves outcomes
• Prophylactic antibiotics - controversial; no proven mortality benefit; currently NOT recommended routinely

• Diagnose by CT-guided fine-needle aspiration (FNA) for culture
• Treatment: step-up approach - percutaneous/endoscopic drainage first, then minimally invasive necrosectomy if drainage fails
• Surgical necrosectomy options: closed continuous lavage (Beger), closed drainage, open packing, or planned relaparotomy (Bradley)
• CT-guided percutaneous drainage + antibiotics (carbapenems penetrate pancreatic tissue well)

• Allow 4-6 weeks to mature and encapsulate
• Endoscopic transgastric or endoscopic ultrasound-guided cystgastrostomy (if in apposition to stomach wall)
• Percutaneous drainage or surgical cystgastrostomy/cystjejunostomy

---

Complications of Acute Pancreatitis

---

---

CHRONIC PANCREATITIS

Definition

---

Aetiology

---

Pathology / Morphology

• Parenchymal fibrosis
• Reduced acinar number and size (acinar loss - constant feature)
• Variable ductal dilatation; ductal epithelium atrophied, hyperplastic, or squamous metaplasia; ductal concretions
• Chronic inflammatory infiltrate around lobules and ducts
• Relative early sparing of islets of Langerhans, which eventually become embedded in sclerotic tissue, fuse, appear enlarged, and finally disappear

---

Clinical Features

• Continuous or episodic, often severe and refractory
• Epigastric, radiating to the back; accentuated by meals and alcohol
• May be so severe the patient becomes narcotic-dependent
• Later in disease, pain may actually diminish as gland "burns out"

• Steatorrhoea - bulky, foul-smelling, pale, floating stools with fat globules; fat malabsorption precedes carbohydrate malabsorption
• Weight loss and malnutrition
• Fat-soluble vitamin deficiency (A, D, E, K)

• Diabetes mellitus ("type 3c" or pancreatogenic diabetes) - islet destruction; may precede steatorrhoea

• Jaundice (biliary duct compression by fibrotic head)
• Repeated bouts mimicking acute pancreatitis
• Nausea, anorexia
• May be entirely silent until exocrine/endocrine failure develops

---

Investigations

• Serum amylase/lipase - often normal in established chronic disease (no functional acinar tissue)
• Glucose tolerance test - abnormal in >50% of patients with chronic pancreatitis/steatorrhoea
• Faecal elastase-1 (non-invasive exocrine function test; <200 µg/g = exocrine insufficiency)
• Lundh test meal - gold standard exocrine function test; reduced trypsin and amylase output post-meal
• Serum IgG4 - elevated in autoimmune pancreatitis
• Tumour markers - CA 19-9, CEA to exclude pancreatic carcinoma (important differential)
• Fat-soluble vitamin levels; vitamin B12

• Faecal fat (>7g/day = steatorrhoea)
• Faecal elastase-1 - practical first-line test

• Plain AXR - pancreatic calcification (pathognomonic when present, seen in ~30% of cases; especially in alcoholic CP and tropical pancreatitis)
• Ultrasound - ductal dilatation, calcification, pseudocysts, parenchymal changes
• CT scan - best for overall assessment; shows fibrosis, ductal dilatation, calcification, pseudocysts, vascular complications; excludes malignancy
• MRCP - non-invasive ductal imaging; shows "chain of lakes" appearance of irregular dilated main pancreatic duct
• ERCP - invasive; "chain of lakes" ductal morphology; allows therapeutic intervention (stenting, stone extraction); risk of post-ERCP pancreatitis
• EUS - most sensitive for parenchymal and ductal changes; allows FNA; detects early chronic pancreatitis
• CECT - staging; identifies mass lesions, vascular involvement

---

Treatment

• Abstinence from alcohol - essential; slows progression
• Cessation of smoking
• Analgesia - stepped approach; paracetamol -> weak opioids -> strong opioids (risk of dependence); adjuncts: pregabalin, duloxetine
• Pancreatic enzyme supplementation - with all meals and snacks (lipase-containing enteric-coated preparations); reduces steatorrhoea; may reduce pain (negative feedback on CCK)
• Diet - low-fat, high-protein, high-carbohydrate; small frequent meals; medium-chain triglycerides if severe fat malabsorption (absorbed directly without lipase)
• Fat-soluble vitamins supplementation (A, D, E, K) and vitamin B12
• Micronutrient therapy - methionine, vitamins C and E, selenium (may reduce pain and slow progression)
• PPI/H2 blocker - reduce gastric acid to optimise enzyme function
• Treat diabetes mellitus - insulin usually needed (brittle due to glucagon deficiency also)
• Steroids - only in autoimmune pancreatitis (Type 1 AIP responds dramatically to prednisolone)

• Stenting across dominant ductal stricture (leave ≤4-6 weeks before occlusion)
• Pancreatic duct stone extraction ± ESWL (extracorporeal shock wave lithotripsy)
• Pseudocyst drainage under EUS guidance
• Percutaneous or transgastric pseudocyst drainage

• Indicated for: intractable pain, ductal obstruction, mass lesion, complications
• Pancreatoduodenectomy (Whipple's) or Beger procedure (duodenum-preserving resection of pancreatic head) - for head mass
• Longitudinal pancreatojejunostomy (Puestow/Partington-Rochelle procedure) or Frey procedure (duct decompression + partial head resection) - for markedly dilated duct (>6mm); ~50% get long-term pain relief
• Distal pancreatectomy - for disease limited to the tail
• Total pancreatectomy ± islet autotransplantation - for intractable pain with diffuse disease; carries significant morbidity (brittle diabetes); ~1/3 get complete pain relief, 1/3 partial, 1/3 no benefit
• Celiac plexus neurolysis - for pain management (CT/EUS-guided)

---

Complications of Chronic Pancreatitis

---

Key Differentiating Features: Acute vs Chronic

---

• Bailey and Love's Short Practice of Surgery, 28th Edition
• Robbins & Kumar Basic Pathology
• Pye's Surgical Handicraft, 22nd Edition
• Sleisenger and Fordtran's Gastrointestinal and Liver Disease

---

Definitions

• Diverticulum - a hollow outpouching of the bowel wall
• Diverticulosis - the presence of diverticula without symptoms or inflammation (asymptomatic state)
• Diverticular disease - when diverticula cause symptoms or complications
• Diverticulitis - inflammation/infection of one or more diverticula

• True (congenital) diverticula: all three layers of bowel wall present (e.g. Meckel's diverticulum)
• False (acquired/pseudo) diverticula: only mucosa and submucosa herniate through the muscularis - NO muscularis propria in the wall; this is what colonic diverticular disease represents

---

Anatomy & Site

1. Bleeding from diverticula can be profuse (proximity of the vasa recta)
2. Diverticula are absent from the anti-mesenteric inter-taenial area

• Western countries: ~90% left-sided (sigmoid colon predominant); rectum almost never affected (complete muscle coat + wider lumen)
• South East Asia / East Asia: ~75-85% right-sided predominance
• Diverticula found in left colon in ~75% of those over 70 years in the Western world
• Typical size: 3-10 mm diameter; giant diverticula >4 cm (rare, up to 25 cm)

---

Aetiology

---

Pathogenesis

Diverticulosis Formation

Diverticulitis - How Inflammation Develops

1. The neck of a diverticulum becomes obstructed by inspissated stool (a faecalith)
2. The faecalith abrades the mucosal wall of the sac -> low-grade inflammation
3. Obstruction -> increased bacterial flora within the sac
4. Diminished venous outflow -> localised ischaemia
5. Altered mucosal defence mechanisms (defective CD2 pathway-induced apoptosis in lamina propria lymphocytes - similar to IBD)
6. Bacteria breach the mucosa and the process extends transmurally
7. Microperforation results - contained by pericolic fat/mesentery OR spreading to form:
   • Phlegmon (localised inflammatory mass)
   • Pericolic abscess
   • Pelvic/intra-abdominal abscess
   • Generalised purulent or faecal peritonitis

---

Clinical Features

Diverticulosis (Asymptomatic)

• Majority (70-80%) are completely asymptomatic
• Found incidentally on colonoscopy, CT, or barium enema
• No symptoms = no treatment beyond dietary advice

Symptomatic Uncomplicated Diverticular Disease (SUDD)

• Intermittent left iliac fossa (LIF) pain
• Bloating, flatulence, sensation of heaviness in the lower abdomen
• Altered bowel habit (constipation or diarrhoea)
• Symptoms overlap significantly with irritable bowel syndrome (IBS) and can be very difficult to distinguish

Acute Diverticulitis

• Persistent LIF pain (left-sided appendicitis" - "appendicitis of the left side")
• Fever, malaise, anorexia
• Nausea, vomiting
• Accompanying diarrhoea or constipation
• Urinary symptoms if bladder is adjacent and inflamed (frequency, dysuria)
• LIF tenderness on palpation; sigmoid colon may be thickened and tender
• Rectal examination may reveal a tender mass (abscess)
• Generalised peritonitis (free perforation): systemic upset, generalised tenderness and rigidity

Diverticular Haemorrhage

• Typically painless and profuse (the most common cause of significant lower GI haemorrhage in older patients)
• Bright red rectal bleeding (sigmoid) or darker blood (right-sided)
• 70-80% stop spontaneously; 10-15% have brisk, significant bleeds
• Often not painful - this distinguishes it from diverticulitis

Fistula Presentation

---

Investigations

Bloods

• FBC: leucocytosis in diverticulitis (WBC >11×10⁹/L); anaemia if chronic/acute bleeding
• CRP: elevated; useful for monitoring treatment response
• U&E, LFTs
• Blood cultures if septic

Imaging

• May show pneumoperitoneum (free perforation) on erect CXR/AXR
• Ileus pattern
• Not diagnostic of diverticulitis itself

• Excellent sensitivity and specificity
• Shows: bowel wall thickening, pericolic fat stranding, abscess, extraluminal gas/fluid, fistula
• Identifies Hinchey grade
• Guides CT-guided percutaneous drainage of abscesses
• CT angiography for diverticular haemorrhage (detects bleeding >1 mL/min as contrast "blush")

• Useful if CT not available; operator-dependent
• Can show thickened sigmoid wall and pericolic fluid

• NOT during acute attack (risk of perforation - avoid for 6 weeks after acute episode)
• Shows necks of diverticula within lumen; luminal narrowing
• Essential to exclude coexisting carcinoma (key differential diagnosis) - a cancer can mimic diverticular disease
• Right-sided diverticula appear as dark openings at endoscopy

• Shows diverticula ("saw-tooth" mucosal pattern), luminal narrowing, fistula tract
• Avoided in acute phase; used electively

---

Classification of Complicated Diverticulitis

Hinchey Classification (Original)

Modified Hinchey Classification

---

Complications Summary

---

Management

Diverticulosis (Asymptomatic)

• High-fibre diet and adequate fluid intake (evidence is "limited and conflicting" but low risk, conditional recommendation by AGA)
• Bulk-forming laxatives
• Avoid NSAIDs (increase bleeding/perforation risk)
• No surgical intervention indicated for asymptomatic disease
• Mesalazine: may reduce symptoms in SUDD; evidence modest

---

Acute Uncomplicated Diverticulitis (Hinchey 0/Ia)

• Bowel rest (liquid diet initially; not necessarily strict NBM)
• Antibiotics - increasingly selective use:
  • Immunocompetent patients with mild, uncomplicated diverticulitis and no systemic sepsis may not require antibiotics (self-limiting inflammatory process)
  • When used: broad-spectrum coverage of Gram-negative and anaerobic organisms
  • Options: co-amoxiclav; or ciprofloxacin + metronidazole; or cefuroxime + metronidazole
  • IV antibiotics for hospital admission
• Adequate analgesia (avoid opioids if possible; paracetamol/NSAIDs - caution with NSAIDs)
• Exclude perforation by CT before managing as outpatient

• Unable to tolerate oral fluids
• Severe pain
• Fever/leucocytosis
• Immunocompromised
• Diagnostic uncertainty
• Failure to improve after 48-72h outpatient treatment

---

Complicated Diverticulitis

• IV antibiotics + bowel rest
• Abscesses <3-4 cm may resolve with antibiotics alone
• Monitor carefully; if not improving -> escalate to drainage

• IV antibiotics
• CT-guided percutaneous drainage (success rate 74-80%): rapid sepsis control without anaesthesia; avoids multi-stage surgery; allows subsequent single-stage elective resection after 3-4 weeks
• If multiloculated, inaccessible, or not resolving -> emergency surgery
• ~20-25% require urgent surgery despite attempted drainage

• Generalised peritonitis
• Failure to respond to maximum medical management
• Haemodynamic instability

---

Diverticular Haemorrhage

1. Resuscitation - IV access, crossmatch, transfuse as needed; withhold anticoagulants
2. Localise the source:
   • CT angiography (first-line if active bleeding >1 mL/min) - shows "blush" of contrast; allows therapeutic embolisation (80-90% success)
   • Colonoscopy (after bowel prep/lavage) - directly identifies and allows treatment (coagulation, epinephrine injection, clips)
   • 99mTc-labelled red cell scan - for slow/intermittent bleeding
3. Interventional radiology embolisation - first-line therapeutic option for active bleeding
4. Surgery (sigmoid/subtotal colectomy) - if:
   • Bleeding continues despite interventional radiology
   • Haemodynamically unstable
   • Unable to localise source -> subtotal colectomy (removes ~80% of colonic mucosa but has higher morbidity)

---

Elective/Interval Surgery for Diverticular Disease

• Recurrent attacks of acute diverticulitis (traditionally after 2 episodes; now individualised)
• After complicated diverticulitis (abscess, perforation) once recovered
• Persistent/chronic symptoms not responding to conservative management
• Inability to exclude carcinoma
• Fistula (requires resection of diseased segment + repair of involved organ)
• Obstruction

---

Key Differentials

---

Summary Box

---

• Bailey and Love's Short Practice of Surgery, 28th Edition
• Sleisenger and Fordtran's Gastrointestinal and Liver Disease
• Fischer's Mastery of Surgery, 8th Edition
• Mulholland and Greenfield's Surgery, 7th Edition