Acute Pancreatitis
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Direct answer
Acute pancreatitis is autodigestion of the gland by its own prematurely activated enzymes — trypsin at the centre of the cascade — triggered most often by gallstones or alcohol, and ranging from mild interstitial oedematous disease that settles in days to necrotising haemorrhagic pancreatitis with multi-organ failure. Lipase risen to three times the upper limit supports the diagnosis, severity is staged by the revised Atlanta classification (mild, moderately severe with transient organ failure, severe with persistent organ failure beyond 48 hours), and the local complications follow a fixed timeline — acute peripancreatic fluid collection in the first weeks, pseudocyst or walled-off necrosis after week four. In Indian practice gallstones have overtaken alcohol as the leading cause in most series, and the disease strikes a decade younger than in Western reports.
What you must remember
- Two-hit aetiology: duct obstruction (gallstone migration, the commonest Indian cause) and toxic-metabolic injury (alcohol, the second) — together explaining most cases; the remainder include endoscopic retrograde cholangiopancreatography, hypertriglyceridaemia (over about 1000 milligrams per decilitre), hypercalcaemia, drugs and viruses such as mumps.
- Enzyme cascade: trypsin activated within the acinar cell activates phospholipase A, elastase and lipase; phospholipase damages membranes and surfactant (lung injury), elastase digests vessel walls (haemorrhage), lipase fat-nercrosis with calcium soap formation — the chalky-white foci that explain hypocalcaemia.
- Morphology: interstitial oedematous pancreatitis — swollen gland, oedema, neutrophils, usually recovers; necrotising — grey-yellow necrosis of parenchyma and fat with haemorrhage; Grey-Turner (flank) and Cullen (periumbilical) ecchymoses signal the haemorrhagic form.
- Revised Atlanta timeline: sterile acute peripancreatic fluid collection and acute necrotic collection before four weeks; pseudocyst (fluid only) and walled-off necrosis after four weeks, each readable on contrast computed tomography best performed after about 72 hours.
- Severity scores: Ranson criteria (11 variables; three or more predict severe disease) and the modified Glasgow score at 48 hours; persistent organ failure — respiratory, renal, cardiovascular — beyond 48 hours defines severe pancreatitis.
- Infection question: fever with gas in necrosis raises infected necrosis; the step-up approach — percutaneous drainage first, minimally invasive necrosectomy if needed, and ideally delayed beyond four weeks — has replaced early open surgery.
- Distant complications: acute respiratory distress syndrome from phospholipase-damaged surfactant, disseminated intravascular coagulation, acute kidney injury and hypocalcaemia.
Forty-eight hours that decide the course
A 34-year-old woman presents with sudden, constant, transfixing epigastric pain boring through to the back, vomiting and tenderness with guarding; serum lipase is four times normal. The first decision is cause: an ultrasound looking for gallstones and a dilated common duct, because a stone impacted at the ampulla changes management to urgent endoscopic retrograde cholangiopancreatography, and a sliding-scale search for alcohol, drugs and triglycerides follows. The second decision is severity. At 48 hours she has a respiratory rate of 30, a falling urine output and a rising creatinine — organ failure. If these persist beyond 48 hours she is severe by Atlanta definitions and goes to intensive care; if they reverse, she is moderately severe; and if her pain settles with fluids alone, mild.
The third phase is anatomical. A contrast scan at day five shows a collection without enhancement of the gland periphery — necrosis developing; by week six a thick-walled walled-off necrosis has organised. Should fever and deterioration supervene, drainage is attempted percutaneously, with necrosectomy deferred — because early open debridement of inflamed necrosis carried prohibitive mortality, the lesson the step-up trials taught. Walking the same patient from enzyme release to organ failure to organised collection is how theory papers and clinical vivas both want this chapter told.
Where students slip
Amylase habits mislead twice over: it normalises within days (a late presenter may have a normal amylase with a rising lipase), and it rises in parotitis, ectopic pregnancy and diabetic ketoacidosis without pancreatitis — quoting lipase specificity recovers both marks. The pseudocyst definition must include "no epithelial lining"; examiners specifically hunt for the word pseudo being explained. And severe disease is equated with a high enzyme level — severity is defined by organ failure and necrosis, not by the height of lipase, a distinction that separates memorised answers from understood ones.
Frequently asked questions
Which two mechanisms initiate acute pancreatic enzyme injury?
Duct obstruction (classically a migrating gallstone) and direct toxic-metabolic acinar injury (classically alcohol), converging on premature intracellular trypsin activation.
Why does acute pancreatitis cause hypocalcaemia?
Lipase-split fatty acids combine with calcium to form insoluble soaps in areas of fat necrosis, along with a component of parathyroid hormone resistance in severe disease.
What distinguishes a pseudocyst from walled-off necrosis?
Both mature after about four weeks; a pseudocyst contains fluid with a granulation-tissue wall and no epithelium, while walled-off necrosis contains necrotic pancreatic tissue and needs debridement if infected.
Which Atlanta category applies when organ failure persists beyond 48 hours?
Severe acute pancreatitis — persistent respiratory, renal or cardiovascular failure; failure reversing within 48 hours is moderately severe disease.
When is contrast computed tomography most informative?
After about 72 hours, when necrosis becomes demarcated; early scans underestimate the extent of injury.
What is the step-up approach to infected necrosis?
Percutaneous or endoscopic catheter drainage first, reserving minimally invasive necrosectomy for non-resolving sepsis and delaying intervention beyond four weeks where possible.