Acute Pancreatitis

Acute pancreatitis (AP) is a sudden inflammation of the pancreas that can range from a mild, selflimiting episode to a severe, lifethreatening condition. It occurs when pancreatic enzymes become prematurely activated within the gland, leading to autodigestion, tissue injury, and a systemic inflammatory response.

Key Facts

• Incidence: Approximately 1345 cases per 100,000 adults per year in most developed countries.
• Age group: Most common between 30 and 60 years.
• Mortality: Overall 510%; rises to >30% in severe necrotizing pancreatitis.

Causes and Risk Factors

Primary Etiologies

• Gallstones obstruction of the pancreatic duct by biliary calculi accounts for 3540% of cases in Western populations.
• Alcohol abuse chronic heavy drinking is the leading cause in many Asian and European series.

Secondary Causes

• Hypertriglyceridaemia (1000mg/dL)
• Hypercalcaemia
• Postendoscopic retrograde cholangiopancreatography (ERCP)
• Trauma or abdominal surgery
• Medications (e.g., azathioprine, valproate, amoxicillinclavulanate)
• Infections (mumps, coxsackievirus, COVID19)
• Genetic mutations (e.g., PRSS1, SPINK1) rare, usually in hereditary pancreatitis.

Pathophysiology

In a healthy pancreas, digestive enzymes are synthesized as inactive zymogens and secreted into the duodenum where they are activated. In AP, premature intracellular activationmost notably of trypsintriggers a cascade of proteolysis, inflammatory cytokine release (IL1, IL6, TNF), and vascular leakage. The resulting edema can compress pancreatic ducts and blood vessels, worsening the injury. In severe disease, the inflammation spreads systemically, causing multiorgan dysfunction.

Clinical Presentation

• Sudden onset of epigastric or upper abdominal pain radiating to the back.
• Pain is typically constant, severe, and worsens after meals.
• Nausea and vomiting are common.
• Physical exam may reveal abdominal tenderness, guarding, or peritoneal signs in advanced cases.

Diagnosis

The diagnosis of acute pancreatitis requires (at least) two of the following three criteria:

1. Abdominal pain characteristic of pancreatitis.
2. Serum amylase or lipase 3 the upper limit of normal.
3. Imaging findings consistent with pancreatitis (typically contrastenhanced CT, MRI, or transabdominal ultrasound).

Laboratory Tests

• Serum lipase preferred over amylase because of greater specificity.
• Complete blood count leukocytosis may indicate severity.
• Comprehensive metabolic panel to assess electrolytes, renal function, and calcium.
• Triglyceride level important when hypertriglyceridaemia is suspected.
• Creactive protein (CRP) rises after 48h; values >150mg/L suggest severe disease.

Imaging

• Transabdominal ultrasound: Firstline to detect gallstones and biliary dilation.
• Contrastenhanced CT (CECT): Performed 4872h after admission to evaluate necrosis, fluid collections, and to stage severity (Balthazar CT severity index).
• MRCP: Helpful for delineating ductal anatomy, especially in recurrent cases.

Severity Assessment

Several scoring systems are used to predict outcomes and guide management:

• Ransons criteria uses admission and 48hour variables.
• Bedside Index for Severity in Acute Pancreatitis (BISAP) quick bedside tool (BUN, impaired mental status, SIRS, age>60, pleural effusion).
• Revised Atlanta Classification (2012) categorises AP as mild, moderately severe, or severe based on organ failure and local complications.

Management

Initial Care

1. Fluid resuscitation: Aggressive IV isotonic crystalloid (e.g., lactated Ringers) at 250500mL/h; goaldirected therapy to maintain MAP65mmHg and urine output>0.5mL/kg/h.
2. Pain control: Opioids (IV morphine, hydromorphone) titrated to pain relief; avoid NSAIDs if renal perfusion is compromised.
3. NPO (nil per os): Early fasting reduces pancreatic stimulation; enteral feeding is introduced once the patient stabilises.
4. Correct underlying cause: Early ERCP for cholangitis or obstructing stones; discontinue offending drugs; manage hypertriglyceridaemia with insulin infusion or apheresis.

Nutritional Support

Enteral feeding (nasogastric or nasojejunal) is preferred over parenteral nutrition and should start within 2448h when oral intake is not feasible. It reduces infectious complications and helps maintain gut barrier integrity.

Antibiotics

Prophylactic antibiotics are not recommended in sterile necrosis. They are indicated only when there is documented infected necrosis or extrapancreatic infection (e.g., cholangitis, pneumonia).

Management of Complications

• Pseudocysts & walledoff necrosis: Observe if asymptomatic; drainage (endoscopic, percutaneous, or surgical) if symptomatic, infected, or enlarging.
• Pancreatic necrosis: Minimally invasive stepup approachpercutaneous drainage followed by endoscopic necrosectomy if needed.
• Organ failure: ICU support for respiratory, renal, or cardiovascular failure (mechanical ventilation, renal replacement therapy, vasopressors).

Prevention of Recurrence

• Gallstone disease: Cholecystectomy during the same admission (after inflammation subsides) markedly reduces recurrence.
• Alcoholrelated AP: Complete abstinence; referral to addiction services, counseling, and medical therapy (e.g., naltrexone, acamprosate).
• Hypertriglyceridaemia: Lowfat diet, fibrates, omega3 fatty acids, and strict glycaemic control.
• Medication review: Avoid known offending agents when possible.

Prognosis

Most patients with mild acute pancreatitis recover fully within a week. However, severe disease carries a significant risk of mortality, especially when persistent organ failure (>48h) or infected necrosis develops. Early aggressive fluid therapy, timely source control, and a multidisciplinary approach improve outcomes.

Key TakeHome Points

• Acute pancreatitis is diagnosed by typical pain, elevated enzymes, and/or imaging.
• Gallstones and alcohol are the dominant causes; identify and treat the underlying etiology early.
• Fluid resuscitation and pain control are the cornerstones of early management.
• Severity scores (Ranson, BISAP, Atlanta classification) guide monitoring and escalation of care.
• Enteral nutrition is preferred over parenteral feeding.
• Antibiotics are reserved for proven infection.
• Timely cholecystectomy and lifestyle modifications prevent recurrence.

For further reading, reputable sources include the British Pancreatic Society, American College of Gastroenterology, and the latest guidelines from the World Health Organization.