Define Acute Pancreatitis. Describe its causes, pathophysiology and clinical features.

The Concept — Autodigestion

Acute pancreatitis is acute inflammation of the pancreas caused by the premature activation of its own digestive enzymes within the gland, so that the pancreas begins to digest itself. This 'autodigestion' triggers inflammation, oedema and, in severe cases, necrosis, and can spill over into a systemic inflammatory response affecting the whole body. Understanding it as an enzyme-activation problem explains both the local and systemic effects.

Causes

The two dominant causes are gallstones and alcohol, which together account for most cases. The fuller list is remembered by 'get smashed': Gallstones, Ethanol, Trauma, Steroids, Mumps (and other infections), Autoimmune, Scorpion sting, Hyperlipidaemia/Hypercalcaemia, ERCP, and Drugs.

Pathophysiology

Whatever the trigger, there is premature intra-acinar activation of trypsinogen to trypsin, which then activates the other pancreatic enzymes. These digest the gland and surrounding tissue, causing inflammation, interstitial oedema, fat necrosis and, in severe disease, haemorrhagic necrosis. Released enzymes and inflammatory mediators drive a systemic inflammatory response (SIRS) and massive third-space fluid loss.

Clinical Features

The classic presentation is severe, constant epigastric pain radiating through to the back, relieved by sitting forward, with nausea and vomiting. Examination shows epigastric tenderness. In severe disease, tracking of haemorrhagic fluid produces the eponymous bruising signs: Cullen's sign (periumbilical) and Grey Turner's sign (flanks).

Investigation & Severity

Diagnosis rests on a serum amylase or lipase raised more than three times the upper limit of normal (lipase is more specific and stays elevated longer). Ultrasound looks for gallstones as the cause, and contrast CT (after 48–72 hours) assesses necrosis and complications. Severity scores — Glasgow, Ranson, APACHE II, with CRP — identify severe attacks needing intensive care.

Complications & Management

Local complications include necrosis, pseudocyst, abscess and haemorrhage; systemic complications include shock, ARDS, acute kidney injury, hypocalcaemia, DIC and multi-organ failure. Management is largely supportive: aggressive intravenous fluid resuscitation, analgesia, oxygen, careful monitoring (often in HDU/ICU for severe cases) and nutritional support. The cause is then treated — cholecystectomy for gallstone pancreatitis (or urgent ERCP if there is co-existing cholangitis) — and complications such as infected necrosis may need necrosectomy.

The Prognostic Scoring Systems

Because a minority of attacks are severe and life-threatening, early severity stratification is central to management. The Glasgow (Imrie) and Ranson criteria use parameters such as age, white cell count, glucose, urea, calcium, albumin, LDH and PaO2 measured over the first 48 hours, and APACHE II and serial CRP add to this. Identifying a predicted-severe attack triggers early transfer to a high-dependency or intensive-care setting, where aggressive support improves survival.

Local Complications & Their Timing

The local complications evolve over time, which guides when to image and intervene. Early there is peripancreatic fluid and necrosis; if necrosis becomes infected (usually after the first week) it is life-threatening and needs intervention (increasingly a 'step-up' approach of drainage then minimally invasive necrosectomy rather than early open surgery). Later, a pseudocyst may mature, and erosion into a vessel can cause haemorrhage or a pseudoaneurysm. Contrast CT after 48–72 hours is timed to detect necrosis reliably.

The Principle of Supportive Care

It is worth stressing that there is no drug that cures acute pancreatitis — outcome depends on excellent supportive care: aggressive early fluid resuscitation to counter the massive third-space loss, analgesia, oxygen, correction of electrolytes (including calcium), and early enteral nutrition where possible (which protects the gut barrier). Antibiotics are reserved for proven infection. Definitive treatment of the cause (cholecystectomy for gallstones, ideally on the same admission for mild disease) prevents recurrence.

Gallstone Pancreatitis — a Special Case

Gallstone pancreatitis deserves specific mention because it has a defined pathway. A stone passing through or impacted at the ampulla of Vater obstructs the pancreatic duct and triggers the attack. If it is accompanied by cholangitis or persistent obstruction, urgent ERCP with sphincterotomy relieves it; and once a mild attack settles, a cholecystectomy is performed on the same admission to prevent a further, possibly fatal, attack. This makes identifying gallstones as the cause (on ultrasound and LFTs) an early priority in every case of pancreatitis.

• Two main causes: gallstones and alcohol (full list = 'get smashed').
• Diagnosis: amylase or lipase >3× upper limit of normal (lipase more specific).
• Management is supportive (aggressive IV fluids, analgesia, organ support); score severity (Glasgow/Ranson/APACHE).

Gallstones and alcohol account for about 80% of cases.

• Acute pancreatitis = autodigestion from premature intra-acinar enzyme (trypsin) activation.
• Two main causes: gallstones and alcohol ('get smashed' for the rest).
• Severe constant epigastric pain radiating to back, relieved leaning forward, with vomiting; Cullen's/Grey Turner's signs if severe.
• Diagnose with amylase/lipase >3× normal; ultrasound for gallstones; CT (48–72 h) for necrosis; score severity (Glasgow/Ranson/APACHE, CRP).
• Treatment is supportive (aggressive fluids, analgesia, organ support); treat cause (cholecystectomy/ERCP); necrosectomy for infected necrosis.