Management of Acute Pancreatitis
Mechanism and Pathophysiology
Acute pancreatitis results from pancreatic enzyme activation causing autodigestion, leading to local inflammation, third-space fluid losses, and systemic inflammatory response that can progress to multi-organ failure. 1, 2 The inflammatory cascade causes significant intravascular volume depletion, making aggressive early fluid resuscitation the single most critical intervention to prevent organ failure and reduce mortality. 2
Initial Assessment and Diagnosis
Diagnose acute pancreatitis when two of three criteria are present: 2
- Upper abdominal pain
- Serum amylase or lipase elevation (typically >3× upper limit of normal)
- Characteristic imaging findings
Immediately assess severity to determine appropriate level of care and monitoring intensity. 1, 2
Severity Stratification and Triage
Mild Acute Pancreatitis (80% of cases)
- Manage on general medical ward with basic monitoring 3
- Monitor temperature, pulse, blood pressure, and urine output 3
- Peripheral IV access and possibly nasogastric tube; urinary catheter rarely needed 3
Severe Acute Pancreatitis (20% of cases, 95% of deaths)
All patients with severe acute pancreatitis must be managed in ICU or HDU with full monitoring and systems support. 1, 2 Required monitoring includes: 1
- Peripheral venous access and central venous line (for fluid administration and CVP monitoring)
- Urinary catheter with hourly urine output measurement
- Nasogastric tube
- Hourly vital signs: pulse, blood pressure, CVP, respiratory rate, oxygen saturation, temperature
- Regular arterial blood gas analysis (hypoxia and acidosis may be detected late clinically) 3
- Swan-Ganz catheter if cardiocirculatory compromise exists or initial resuscitation fails 3
Fluid Resuscitation: The Cornerstone of Management
Aggressive fluid resuscitation within the first 12-24 hours is the most critical intervention to prevent organ failure and reduce mortality. 2 However, recent evidence has challenged the "more is better" approach. 4, 5
Fluid Type
Lactated Ringer's solution is superior to normal saline and should be the preferred crystalloid. 6, 7 LRS reduces systemic inflammatory response syndrome (SIRS) at 24 hours (84% reduction vs 0% with normal saline, P=0.035) and decreases C-reactive protein levels (51.5 vs 104 mg/dL, P=0.02). 7
Fluid Rate and Volume
Use goal-directed moderate fluid resuscitation rather than aggressive high-rate infusion. 4, 5 Recent evidence shows high fluid rate infusion is associated with increased mortality and severe adverse events compared to moderate rates. 5 Early aggressive fluid therapy appears most beneficial in predicted mild severity, whereas aggressive resuscitation in predicted severe disease may be futile and deleterious. 4
Resuscitation Goals
Target urine output >0.5 ml/kg body weight. 1, 2 Monitor frequently: 2, 8
- Central venous pressure to guide fluid rate
- Hematocrit, blood urea nitrogen, creatinine (elevated values should prompt more intensive resuscitation)
- Lactate levels to assess tissue perfusion 1
Oxygen Supplementation
Administer supplemental oxygen to maintain arterial saturation >95% with continuous monitoring. 2
Pain Management
Pain control is a clinical priority requiring a multimodal approach. 1, 2
Preferred analgesic strategy: 1
- Dilaudid is preferred over morphine or fentanyl in non-intubated patients
- Patient-controlled analgesia (PCA) should be integrated with every pain management strategy
- Epidural analgesia should be considered as alternative or adjunct to IV analgesia
- Avoid NSAIDs in acute kidney injury 1
Nutritional Support
Enteral nutrition is superior to total parenteral nutrition and should be initiated early, even in severe cases. 1, 2 Enteral feeding prevents gut failure and infectious complications. 1, 2
Feeding Route
Both gastric and jejunal feeding can be delivered safely. 1, 2 Start early enteral nutrition regardless of severity. 1
When to Consider Parenteral Nutrition
- Avoid TPN when possible 1
- If ileus persists >5 days, parenteral nutrition will be required 1
- Partial parenteral nutrition integration can be considered if enteral route is not completely tolerated 1
Antibiotic Therapy
Do not administer prophylactic antibiotics routinely in mild acute pancreatitis. 3, 1, 2 There is no evidence that antibiotics affect outcome or reduce septic complications in mild cases. 3
Severe Acute Pancreatitis with Necrosis
In severe acute pancreatitis with evidence of pancreatic necrosis, prophylactic antibiotics may reduce complications and deaths. 1 If used: 1, 2
- Intravenous cefuroxime provides reasonable balance between efficacy and cost
- Maximum duration should be 14 days
- Antibiotics are warranted when specific infections occur (chest, urine, bile, or cannula-related) 3, 1
Maintain strict asepsis with invasive monitoring equipment as these may serve as sources of subsequent sepsis in the presence of pancreatic necrosis. 3
Imaging Strategy
Mild Pancreatitis
Routine CT scanning is unnecessary unless there are clinical signs of deterioration. 3, 1
Severe Pancreatitis
Obtain dynamic CT with IV contrast within 3-10 days to identify pancreatic necrosis and guide management. 1, 2 Use CT severity index scoring to assess severity. 2
Follow-up CT is recommended only if clinical status deteriorates or fails to show continued improvement. 1, 2
Management of Biliary Acute Pancreatitis
Urgent therapeutic ERCP should be performed within 24-72 hours in patients with acute pancreatitis of suspected or proven gallstone etiology who have: 1, 2
- Severe pancreatitis with cholangitis
- Jaundice
- Dilated common bile duct
All patients undergoing early ERCP for severe gallstone pancreatitis require endoscopic sphincterotomy whether or not stones are found in the bile duct. 1
Cholecystectomy should be performed during the same hospital admission, or a clear plan for definitive treatment should be made within 2 weeks. 2
Etiologic Investigation
The etiology should be determined in 75-80% of cases; no more than 20-25% should be classified as "idiopathic." 3 Consider endoscopic ultrasound, bile sampling for microlithiasis, or sphincter of Oddi manometry in patients with repeated attacks and no identified cause. 3
Management of Infected Necrosis
Infected necrosis is the most serious local complication with 40% mortality. 1 Two-thirds of deaths occur after the first week from infected necrosis. 2
Use a step-up approach: 2
- Start with percutaneous or endoscopic drainage
- Consider minimally invasive surgical strategies if drainage fails
- Open surgical necrosectomy as last resort
Delay surgical, radiologic, or endoscopic drainage for 4 weeks when possible to allow wall formation around necrosis, which reduces mortality. 2
Pharmacological Treatments Without Proven Benefit
No specific pharmacological treatment except for organ support and nutrition has proven effective. 1 The following have no proven value and cannot be recommended: 3, 1
- Aprotinin
- Glucagon
- Somatostatin/octreotide
- Fresh frozen plasma
- Peritoneal lavage
- Antiproteases (gabexate)
- Anti-inflammatory agents
Organizational Requirements
Every hospital receiving acute admissions should have: 1, 2
- Single nominated clinical team to manage all acute pancreatitis patients
- Facilities for 24-hour ERCP with sphincterotomy and stone extraction/stenting
- Access to ICU/HDU for severe cases
Refer to specialist unit for: 1, 2
- Extensive necrotizing pancreatitis (>30% necrosis)
- Other complications requiring multidisciplinary specialist pancreatic team
- Each case should be managed in an individualized way by this team 1
Expected Outcomes
Overall mortality for acute pancreatitis should be <10%, and severe disease mortality should be <30%. 2 One-third of deaths occur in the first week from multiple organ failure, and two-thirds occur after the first week from infected necrosis. 2 With proper initial resuscitation and monitoring, the proportion of early deaths from circulatory, respiratory, and renal failure can be reduced. 3