• Pancreas – aetiology, clinical features, investigations, treatment & complications of acute & chronic pancreatitis
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Pancreatitis: Acute & Chronic - Complete Clinical Overview
ACUTE PANCREATITIS
Definition
Acute pancreatitis (AP) is a sudden inflammatory condition of the pancreas resulting from autodigestion by inappropriately activated pancreatic enzymes. The process ranges from mild interstitial oedema to severe haemorrhagic necrosis.
Aetiology
The mnemonic "GET SMASHED" covers the main causes:
| Category | Examples |
|---|---|
| Gallstones | Most common cause overall (40-60%); transient/sustained impaction at the ampulla of Vater |
| Ethanol | Second most common; direct acinar toxicity + sphincter of Oddi spasm |
| Trauma | Blunt abdominal injury; post-ERCP pancreatitis (1-3% of procedures) |
| Steroids | Corticosteroids, azathioprine, L-asparaginase, valproic acid |
| Mumps / viruses | EBV, coxsackievirus, HIV-related |
| Autoimmune | IgG4-associated (lymphocytic sclerosing pancreatitis) |
| Scorpion venom | Tityus trinitatis |
| Hyperlipidaemia / Hypercalcaemia | Hypertriglyceridaemia (chylomicron-induced ischaemia); hyperparathyroidism |
| ERCP | Duct disruption and enzyme extravasation |
| Drugs | Statins (weak link), gliptins, 6-mercaptopurine |
Hereditary pancreatitis - rare; mutations in the cationic trypsinogen gene (PRSS1); patients develop AP in teens, progress to chronic pancreatitis, and carry ~40% lifetime risk of pancreatic cancer.
Structural causes include pancreas divisum (most common anatomic aberration), ampullary tumours, and sphincter of Oddi dysfunction.
No more than 20% of cases should be classified as truly idiopathic after thorough workup. - Bailey and Love's Short Practice of Surgery, 28th Edition
Pathogenesis
Three converging pathways lead to acinar cell injury and enzyme activation:
FIG. 15.2 Proposed pathogenesis of acute pancreatitis - Robbins & Kumar Basic Pathology
- Pancreatic duct obstruction - gallstone/biliary sludge impaction raises intraductal pressure -> interstitial oedema -> vascular insufficiency -> ischaemic acinar injury
- Primary acinar cell injury - alcohol, hypertriglyceridaemia, ischaemia, drugs, and viruses directly injure acinar cells -> release of intracellular proenzymes and lysosomal hydrolases
- Defective intracellular transport - proenzymes co-package with lysosomal hydrolases -> intracellular trypsin activation -> lysosomal rupture -> enzyme cascade
Alcohol-specific mechanisms include: (a) transient increase in exocrine secretion + sphincter of Oddi contraction; (b) oxidative stress with direct acinar membrane damage; (c) delivery of proenzymes to lysosomal compartment with intracellular trypsin activation; (d) protein-rich secretions forming ductal plugs.
Once trypsin is activated, it triggers a cascade: trypsinogen -> trypsin activates all other proenzymes (chymotrypsin, elastase, phospholipase A2, kallikrein) -> proteolysis, haemorrhage, fat necrosis, and systemic inflammatory response syndrome (SIRS). - Robbins & Kumar Basic Pathology
Clinical Features
Symptoms:
- 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
Signs:
- 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
Both Grey Turner's and Cullen's signs indicate severe haemorrhagic necrotising pancreatitis and carry a poor prognosis.
Investigations
Three key questions to answer (Bailey & Love):
- Is the diagnosis of acute pancreatitis correct?
- How severe is the attack?
- What is the aetiology?
Biochemical:
- 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
Severity markers:
- CRP >150 mg/L at 48h = severe attack indicator
- FBC (WBC, haematocrit), U&E, LFTs, calcium, glucose, LDH, ABG, albumin, triglycerides
Imaging:
- 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
Severity Scoring:
Revised Atlanta Classification (2013):
| Grade | Criteria |
|---|---|
| Mild | No organ failure; no local/systemic complications |
| Moderately Severe | Transient organ failure (<48h) AND/OR local/systemic complications without persistent organ failure |
| Severe | Persistent organ failure (>48h); single or multiple organ failure |
Ranson Criteria (score ≥3 at 48h = severe):
| On Admission | Within 48 hours |
|---|---|
| Age >55 years | Haematocrit fall ≥10% |
| WBC >16×10⁹/L | BUN rise >5 mg/dL despite fluids |
| Blood glucose >11 mmol/L | PaO₂ <8 kPa (60 mmHg) |
| LDH >350 U/L | Serum calcium <2.0 mmol/L |
| AST >250 U/L | Base deficit >4 mmol/L |
| Fluid sequestration >6 litres |
Glasgow (Imrie) Criteria (score ≥3 within 48h = severe):
- 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
Mnemonic for Glasgow: PANCREAS - PaO₂, Age, Neutrophils, Calcium, Renal urea, Enzymes, Albumin, Sugar
Other systems: APACHE II, SOFA, SAPS, MODS, Modified Marshall. - Bailey and Love's Short Practice of Surgery, 28th Edition
Treatment
Mild AP - conservative management:
- 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
Severe AP - aggressive management:
- 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
Management of complications:
Infected pancreatic necrosis:
- 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)
Pseudocysts:
- 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
Abdominal compartment syndrome, ARDS, AKI, DIC - managed in ICU
Outcomes: Overall mortality remains 10-15%. Mortality in mild disease <1%; in severe necrotising disease with multi-organ failure up to 30-40%. Before discharge, aetiology must be determined to prevent recurrence. - Bailey and Love's Short Practice of Surgery, 28th Edition
Complications of Acute Pancreatitis
Local:
| Complication | Features |
|---|---|
| Peripancreatic fluid collections | Early (<4 weeks); usually resolve spontaneously |
| Acute pancreatic necrosis | Sterile or infected; identified on contrast CT (non-enhancing areas) |
| Pancreatic abscess | Gas within fluid collection on CT; requires drainage |
| Pseudocyst | After >4 weeks; fluid collection with defined wall; devoid of solid debris; result of ductal leak or liquefied fat necrosis |
| Walled-off necrosis (WON) | After >4 weeks; encapsulated necrotic collection; sterile or infected |
| Splenic vein thrombosis | Left-sided (sinistral) portal hypertension |
| Haemorrhage | Erosion of vessels; pseudoaneurysm formation |
Systemic:
| System | Complication |
|---|---|
| Respiratory | Pleural effusion (left-sided), atelectasis, ARDS |
| Renal | Acute tubular necrosis, AKI |
| Cardiovascular | Hypotension, shock, pericardial effusion |
| Metabolic | Hypocalcaemia (calcium saponification in fat necrosis), hyperglycaemia, hypoalbuminaemia |
| Coagulation | DIC |
| GI | Paralytic ileus, stress ulcers, bowel ischaemia |
| Endocrine | Transient or permanent diabetes (islet destruction) |
CHRONIC PANCREATITIS
Definition
Chronic pancreatitis is a progressive inflammatory disease characterised by irreversible destruction of pancreatic tissue, leading to loss of exocrine function (malabsorption) and, eventually, endocrine function (diabetes mellitus). - Bailey and Love's Short Practice of Surgery, 28th Edition
Incidence: 2-10 new cases per 100,000/year (higher in parts of southern India: 100-200/100,000). Male:female ratio 4:1. Mean age of onset ~40 years.
Aetiology
The TIGAR-O classification organises causes:
| Category | Examples |
|---|---|
| Toxic-metabolic | Alcohol (most common; 60-70% of cases in the West), smoking, hypercalcaemia, hyperlipidaemia, drugs |
| Idiopathic | Early-onset (<20yr), late-onset (>50yr), tropical (southern India/Africa) |
| Genetic | PRSS1 (cationic trypsinogen), SPINK1 (trypsin inhibitor), CFTR mutations - hereditary pancreatitis |
| Autoimmune | IgG4-associated (Type 1); ISGP4/AIP criteria; responds to steroids |
| Recurrent acute pancreatitis | Post-necrotic, recurrent biliary |
| Obstructive | Pancreas divisum, sphincter of Oddi dysfunction, ductal stricture, tumour |
Only 5-10% of alcoholics develop chronic pancreatitis (suggesting additional genetic/metabolic susceptibility). - Robbins & Kumar Basic Pathology
Pathology / Morphology
Gross: Hard, fibrotic gland; extremely dilated ducts; visible calcific concretions (ductal stones); may have a mass in the head mimicking carcinoma.
Microscopic:
- 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
Autoimmune pancreatitis (AIP): Dense lymphocyte and IgG4+ plasma cell infiltrate; "swirling" periductal fibrosis; venulitis (lymphocytic sclerosing pancreatitis). - Robbins & Kumar Basic Pathology
Clinical Features
Pain - most common and dominant symptom:
- 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"
Exocrine insufficiency (develops after >90% gland destruction):
- 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)
Endocrine insufficiency:
- Diabetes mellitus ("type 3c" or pancreatogenic diabetes) - islet destruction; may precede steatorrhoea
Other features:
- Jaundice (biliary duct compression by fibrotic head)
- Repeated bouts mimicking acute pancreatitis
- Nausea, anorexia
- May be entirely silent until exocrine/endocrine failure develops
Investigations
Biochemistry:
- 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 studies:
- Faecal fat (>7g/day = steatorrhoea)
- Faecal elastase-1 - practical first-line test
Imaging:
- 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
Medical (conservative):
- 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)
Endoscopic (ERCP-based):
- 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
Surgical:
- 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
| Complication | Details |
|---|---|
| Exocrine insufficiency | Steatorrhoea, malnutrition, fat-soluble vitamin deficiency |
| Diabetes mellitus | Type 3c; both insulin and glucagon deficiency; brittle |
| Pseudocyst | Common; may cause pain, obstruction, bleeding, infection |
| CBD stricture | Obstructive jaundice; biliary cirrhosis if untreated |
| Duodenal obstruction | Fibrotic mass compresses duodenum |
| Pancreatic fistula | Internal (pancreatic ascites, pleural effusion) or external |
| Splenic vein thrombosis | Left-sided portal hypertension, gastric varices |
| Pseudoaneurysm | Splenic artery most common; life-threatening haemorrhage |
| Pancreatic carcinoma | ~4-5% lifetime risk (20-year follow-up); highest in hereditary pancreatitis (~40% by age 70) |
| Narcotic addiction | From chronic analgesic use |
| Osteoporosis | Fat-soluble vitamin D malabsorption |
Key Differentiating Features: Acute vs Chronic
| Feature | Acute | Chronic |
|---|---|---|
| Reversibility | Potentially reversible | Irreversible |
| Amylase | Markedly elevated | May be normal |
| Pain | Sudden onset, very severe | Chronic, meal-related |
| Calcification | Absent | Pathognomonic when present |
| Steatorrhoea | Absent | Cardinal feature |
| Diabetes | Transient | Permanent |
| Ductal changes | Oedema | "Chain of lakes" on MRCP |
Sources consulted:
- 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
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