Saidala 24: Acute pancreatitis

Introduction

Acute pancreatitis is a sudden inflammation of the pancreas, a gland located in the upper abdomen behind the stomach that plays a vital role in digestion (by producing digestive enzymes) and metabolism (by secreting hormones such as insulin and glucagon). The condition ranges in severity from mild, self-limiting inflammation to severe, life-threatening disease associated with systemic inflammatory response syndrome (SIRS), organ failure, and local complications such as pancreatic necrosis.

It is a major cause of acute abdominal pain requiring hospitalization. The incidence varies worldwide but is estimated to affect 13–45 cases per 100,000 population annually. The two most common causes are gallstones and chronic alcohol consumption.

Pathophysiology

Acute pancreatitis occurs due to premature activation of digestive enzymes, particularly trypsinogen, within the pancreas. Normally, these enzymes are secreted in an inactive form and activated only in the duodenum. In pancreatitis, intra-pancreatic activation causes autodigestion, inflammation, and tissue necrosis.

The inflammatory cascade involves:

Acinar cell injury → premature activation of trypsinogen to trypsin.
Cytokine release → local and systemic inflammation.
Microvascular dysfunction → edema, ischemia, and necrosis.
Immune cell infiltration → amplification of injury.

Severe cases may progress to multiorgan failure due to systemic inflammatory mediator release.

Causes and Risk Factors

Gallstones – Obstruction of the common bile duct increases pancreatic ductal pressure and triggers inflammation.
Alcohol abuse – Direct toxic effects on pancreatic acinar cells.
Hypertriglyceridemia (>1000 mg/dL).
Medications – e.g., azathioprine, didanosine, valproate, tetracycline, furosemide, corticosteroids.
Post-ERCP (Endoscopic Retrograde Cholangiopancreatography).
Infections – Mumps, Coxsackievirus, Mycoplasma.
Genetic mutations – PRSS1, SPINK1, CFTR.
Autoimmune pancreatitis.
Trauma or surgery.

Clinical Presentation

Acute onset of severe epigastric pain (often radiating to the back, worsened by lying flat, relieved by leaning forward).
Nausea and vomiting.
Abdominal distension and tenderness.
Fever, tachycardia, hypotension in severe cases.
Jaundice if associated with biliary obstruction.
Grey Turner’s sign (flank ecchymosis) and Cullen’s sign (periumbilical ecchymosis) may appear in severe necrotizing pancreatitis.

Diagnosis

Laboratory Findings

Serum amylase: Elevated (>3× normal) in most cases but not specific.
Serum lipase: More sensitive and specific, elevated earlier and longer than amylase.
Liver enzymes: ALT and AST elevated in gallstone pancreatitis.
Triglycerides: Elevated in hyperlipidemic pancreatitis.
CRP: Elevated in severe cases, marker of inflammation.
Calcium: Hypocalcemia due to fat necrosis binding calcium.

Imaging

Ultrasound: Detects gallstones, biliary dilation.
CT scan with contrast: Best modality for severity assessment, necrosis, pseudocyst, or abscess.
MRI/MRCP: Alternative imaging for ductal evaluation.

Severity Classification

Acute pancreatitis is classified by the Revised Atlanta Classification (2012):

Mild: No organ failure or local complications.
Moderately severe: Transient organ failure (<48 hrs) or local complications.
Severe: Persistent organ failure (>48 hrs), often multi-organ.

Complications

Local Complications

Acute fluid collections.
Pancreatic pseudocyst.
Pancreatic necrosis (sterile or infected).
Abscess formation.

Systemic Complications

Acute respiratory distress syndrome (ARDS).
Shock due to hypovolemia and vasodilation.
Acute kidney injury.
Sepsis and multi-organ failure.

Treatment

There is no specific curative therapy; management is supportive and focuses on controlling inflammation, preventing complications, and treating the underlying cause.

1. Hospitalization and Monitoring

Most patients require hospital admission.
Severe cases are managed in intensive care units.

2. Fluid Resuscitation

Aggressive IV fluids are essential in the first 24–48 hours to prevent hypovolemia and organ failure.
Preferred fluid: Ringer’s lactate (better outcomes compared to normal saline).
Monitoring of urine output, hematocrit, and vital signs is required.

3. Pain Management

Severe abdominal pain requires opioid analgesics.
Morphine (2.5–5 mg IV every 4 hours as needed).
Hydromorphone or fentanyl as alternatives.
NSAIDs (e.g., ibuprofen 400 mg every 6–8 hrs) may be used in mild cases.

4. Nutritional Support

Early oral feeding is encouraged once nausea resolves and pain improves.
In severe cases, enteral nutrition via nasojejunal tube is preferred over total parenteral nutrition (TPN) to maintain gut integrity.

5. Antibiotics

Not routinely recommended in acute pancreatitis unless there is evidence of infection (e.g., infected necrosis, cholangitis).
If indicated:
- Meropenem 1 g IV every 8 hours.
- Imipenem/cilastatin 500 mg IV every 6 hours.
- Ciprofloxacin 400 mg IV every 12 hours plus metronidazole 500 mg IV every 8 hours as an alternative.

6. Management of Underlying Cause

Gallstones:
- ERCP with sphincterotomy if cholangitis or persistent biliary obstruction.
- Cholecystectomy recommended after recovery.
Alcohol-induced: Abstinence and counseling.
Hypertriglyceridemia:
- Insulin infusion (to lower triglycerides).
- Plasmapheresis in severe cases.
Drug-induced: Discontinue offending agent.

7. Treatment of Complications

Pseudocyst: Often resolves spontaneously; drainage if symptomatic or infected.
Infected necrosis: Requires antibiotics and often percutaneous or surgical drainage.
Severe necrotizing pancreatitis: May require debridement.

Prognosis and Outcomes

Mild acute pancreatitis: Most patients recover within a week.
Severe acute pancreatitis: Associated with 15–30% mortality, especially if infected necrosis develops.
Prognosis can be assessed with scoring systems such as Ranson’s criteria, APACHE II, or BISAP score.

Prevention and Lifestyle Modifications

Gallstone prevention: Cholecystectomy when indicated.
Alcohol-related: Complete abstinence.
Hypertriglyceridemia: Dietary modification, fibrates (fenofibrate 145 mg orally daily) or omega-3 fatty acids.
Avoid high-fat diets.
Regular monitoring for patients with recurrent episodes.

Saidala 24

الصفحات

Saturday, August 16, 2025

Acute pancreatitis