Discuss the aetiology, clinical features, severity assessment, complications and management of acute pancreatitis.

Definition and Diagnosis

Acute pancreatitis is an acute inflammatory process of the pancreas with variable involvement of peripancreatic tissue and remote organ systems. Diagnosis requires two of the following three (revised Atlanta criteria):

1. Characteristic abdominal pain — acute, severe, epigastric, radiating to the back

2. Serum amylase or lipase ≥ 3 times the upper limit of normal

3. Characteristic findings on cross-sectional imaging (CECT, MRI or ultrasound)

Aetiology — "i Get Smashed"

Pathophysiology

Whatever the trigger, the common pathway is premature intracellular activation of trypsinogen to trypsin, which activates the entire cascade of pancreatic enzymes within the gland — causing autodigestion, acinar necrosis, and a local inflammatory response. In severe disease this becomes a systemic inflammatory response syndrome (SIRS) with capillary leak, third-space fluid sequestration, distributive shock and multi-organ failure — which is why fluid resuscitation is central to management.

Clinical Features

• Severe, constant epigastric pain radiating to the back, relieved by sitting forward and worsened by lying flat.
• Nausea and persistent vomiting that does not relieve the pain.
• Fever, tachycardia, hypotension; shock in severe disease.
• Abdominal tenderness with guarding; reduced or absent bowel sounds (ileus); abdominal distension.
• Jaundice — suggests a gallstone aetiology with biliary obstruction.
• Retroperitoneal haemorrhage signs (uncommon but classic): Cullen's sign (periumbilical ecchymosis) and Grey Turner's sign (flank ecchymosis) — both indicate severe necrotising disease.
• Fox's sign (inguinal ecchymosis); tetany from hypocalcaemia; subcutaneous fat necrosis (panniculitis).
• Pleural effusion (usually left-sided) and basal atelectasis.

Investigations

• Serum lipase — more sensitive and specific than amylase, and remains raised longer; amylase falls within 3–5 days and may be normal in late presentation, in alcoholic pancreatitis and in hypertriglyceridaemia.
• Note that the DEGREE of enzyme elevation does NOT correlate with severity — a common misconception.
• Assess severity and organ function: CBC (haematocrit — haemoconcentration indicates third-space loss), urea and creatinine, calcium (low), glucose (high), LDH, AST, albumin, arterial blood gas, CRP at 48 hours (a useful severity marker), and coagulation profile.
• Triglycerides and calcium — to identify a metabolic cause; liver function tests (a raised ALT strongly suggests gallstones).
• Ultrasound abdomen in every patient — to identify gallstones and biliary dilatation; this determines definitive management.
• CECT abdomen — best performed after 72 hours, when necrosis has declared itself; earlier scans underestimate necrosis. Reserve for diagnostic uncertainty, suspected complications, or failure to improve.
• MRCP or endoscopic ultrasound for suspected choledocholithiasis; IgG4 for autoimmune pancreatitis.

Severity Assessment

Revised Atlanta classification:

• Mild — no organ failure, no local or systemic complications
• Moderately severe — transient organ failure (< 48 hours) and/or local complications
• Severe — persistent organ failure (> 48 hours), with mortality of 30% or more

Scoring systems: Ranson's criteria (assessed at admission and 48 hours), APACHE II, BISAP, modified Glasgow (Imrie) score, and the CT severity index (Balthazar). Persistent organ failure is the single strongest predictor of death.

Complications

Local:

• Acute peripancreatic fluid collection and pseudocyst (a collection with a defined wall, after 4 weeks; may become infected, bleed or obstruct).
• Pancreatic necrosis — sterile or INFECTED; infected necrosis is the leading cause of late death.
• Walled-off necrosis; pancreatic abscess.
• Splenic and portal vein thrombosis; pseudoaneurysm (splenic artery) with haemorrhage.
• Gastric outlet obstruction; pancreatic ascites and fistula.

Systemic: ARDS, acute kidney injury, shock, DIC, sepsis and multi-organ failure, hyperglycaemia, hypocalcaemia, and pancreatic encephalopathy.

Late: chronic pancreatitis, exocrine insufficiency with steatorrhoea, and endocrine insufficiency (diabetes).

Management

1. Aggressive but controlled fluid resuscitation — the single most important early intervention

Give balanced crystalloid (Ringer's lactate is preferred over normal saline), guided by heart rate, blood pressure, urine output (target 0.5 mL/kg/hour), haematocrit and blood urea. The first 24 hours matter most. Note that recent evidence has moved away from very aggressive fluid loading, which increases fluid overload and respiratory complications — the aim is goal-directed moderate resuscitation, not maximal volume.

2. Analgesia — give adequate opioid analgesia; the old teaching that morphine is contraindicated because of sphincter of Oddi spasm is not supported by evidence and should not lead to under-treatment of pain.

3. Nutrition — early enteral feeding

• Start oral or enteral feeding EARLY (within 24–72 hours) as tolerated — this maintains gut mucosal integrity, reduces bacterial translocation and infective complications, and improves outcome.
• "Pancreatic rest" with prolonged nil-by-mouth is obsolete. Use a nasogastric or nasojejunal tube if oral intake is not tolerated
• parenteral nutrition only if enteral feeding fails.

4. Antibiotics — NOT routinely

Prophylactic antibiotics are not recommended, even in necrotising pancreatitis. They are given only for proven or strongly suspected infection — infected necrosis (suggested by clinical deterioration, gas in the necrosis on CT, or positive FNA culture), cholangitis, or extrapancreatic infection.

5. Treat the cause

• Gallstone pancreatitis: urgent ERCP with sphincterotomy within 24 hours ONLY if there is concurrent cholangitis or persistent biliary obstruction — not for all gallstone pancreatitis. Cholecystectomy during the same admission for mild disease, and after resolution of collections in severe disease — delaying it results in a high rate of recurrence.
• Alcohol: abstinence with structured support.
• Hypertriglyceridaemia: insulin infusion, fibrates, and plasmapheresis in severe cases.
• Hypercalcaemia: treat the underlying cause.
• Stop implicated drugs.

6. Management of complications

• Infected necrosis: the modern approach is a "step-up" strategy — percutaneous or endoscopic drainage first, escalating to minimally invasive necrosectomy if needed, with open surgery as a last resort; and delaying intervention beyond 4 weeks where possible, which markedly improves survival compared with early open necrosectomy.
• Pseudocyst: most resolve spontaneously; drain (endoscopically) if symptomatic, infected, bleeding or enlarging.
• Organ support in intensive care for respiratory and renal failure.