Acute Pancreatitis

Acute pancreatitis is a medical emergency with a wide range of severity, from mild self-limiting inflammation to life-threatening multiorgan failure and pancreatic necrosis. In the UK, the most common causes are gallstones (migrating into the common bile duct) and alcohol excess. Other causes include hypertriglyceridaemia, hypercalcaemia, and ERCP-induced injury. The core symptom is sudden-onset, severe epigastric pain that typically radiates through to the back and is partially relieved by leaning forward. Diagnosis requires two of the following: 1. Characteristic abdominal pain, 2. Serum amylase or lipase >3x the upper limit of normal, 3. Radiological evidence on CT or MRI. Serum amylase rises quickly but stays elevated for only 24-48 hours, whereas lipase is more sensitive and stays elevated longer. Severity is assessed using the Glasgow Score (PANCREAS) or APACHE II. Management is primarily supportive: intensive IV fluid resuscitation (titrated to urine output), supplemental oxygen, and effective analgesia (often IV opioids). Routine antibiotics are not recommended unless there is evidence of infection (e.g., infected necrosis). Significant complications include acute respiratory distress syndrome (ARDS), acute kidney injury (AKI), and the later development of pancreatic pseudocysts or necrosis.

The central mechanism is the premature activation of pancreatic pro-enzymes (especially trypsinogen) within the pancreatic acinar cells. Normally, these enzymes are only activated in the duodenum. Intracellular activation leads to autodigestion of the pancreatic parenchyma and surrounding adipose tissue (fat necrosis). This triggers a massive release of inflammatory mediators (cytokines) into the systemic circulation, leading to systemic inflammatory response syndrome (SIRS). Increased capillary permeability results in 'third-spacing' of fluid, leading to hypovolaemia, hypotension, and organ failure. Pathologically, it is divided into interstitial oedematous pancreatitis and necrotising pancreatitis, the latter of which has a much higher mortality rate due to the risk of secondary infection.

Patients appear acutely unwell, often with tachycardia and tachypnoea. Abdominal examination shows epigastric tenderness with guarding; in severe cases, there may be paralytic ileus (absent bowel sounds). Rare signs of haemorrhagic pancreatitis include Cullen's sign (periumbilical bruising) and Grey-Turner's sign (flank bruising). Evaluation of severity using the 'PANCREAS' (Glasgow) score is vital: P-PaO2 <8kPa, A-Age >55, N-Neutrophils (WBC >15), C-Calcium <2mmol/L, R-Renal (Urea >16), E-Enzymes (LDH >600 or AST >200), A-Albumin <32g/L, S-Sugar (Glucose >10). A score of 3 or more indicates severe pancreatitis and warrants high-dependency care. Complications can be early (ARDS, AKI, shock) or late (pancreatic pseudocyst 4-6 weeks later, or abscess). Chronic pancreatitis may follow recurrent acute episodes, leading to exocrine and endocrine insufficiency (diabetes).

Bloods: Serum Amylase (immediate) or Lipase (more specific); FBC, U&Es, LFTs (high ALT suggests gallstones), CRP, Glucose, Calcium, Arterial Blood Gas (for PaO2). Imaging: Transabdominal Ultrasound (to look for gallstones/biliary dilatation). Chest X-ray (to rule out perforated viscus). CT Abdomen with contrast (indicated if the diagnosis is uncertain or if symptoms persist/worsen after 72 hours to assess for necrosis).

Acute: ABCDE approach. Aggressive IV fluid resuscitation (e.g., 250–500 mL/h of isotonic crystalloid initially). High-flow oxygen. Analgesia (IV Morphine or Pethidine). Nutrition: Enteral nutrition is preferred over TPN if the patient can tolerate it. Treatment of Cause: If gallstone-induced and the patient has cholangitis or jaundice, urgent ERCP (within 24-72 hours) is indicated. Laparoscopic cholecystectomy should be performed during the same admission for gallstone pancreatitis. Antibiotics: Only for proven infection (e.g., infected necrosis), usually Carbapenems.