Acute pancreatitis

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"acute pancreatitis"[MeSH Terms] AND management

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Acute Pancreatitis

A sudden inflammatory disease of the pancreas, acute pancreatitis (AP) ranges from a mild, self-limiting illness to a life-threatening emergency with multi-organ failure and mortality approaching 30% in severe cases.

Definition and Diagnosis

The diagnosis requires at least 2 of the following 3 criteria (Revised Atlanta Classification):
  1. Abdominal pain characteristic of acute pancreatitis
  2. Serum amylase and/or lipase ≥3x the upper limit of normal
  3. Characteristic findings on imaging (CT, MRI, or ultrasound)
  • Grainger & Allison's Diagnostic Radiology, p. 677
  • Textbook of Family Medicine 9e, p. 1136

Etiology

CauseApproximate Frequency
Gallstones / biliary sludge / microlithiasis>50% of cases
Alcohol~30%
Hypertriglyceridemia (TG >1000 mg/dL)<5%
Trauma (often blunt abdominal)<5%
Post-ERCP~3-5%
Medications<5% (valproate, L-asparaginase, 6-MP, corticosteroids, thiazides)
Infections (mumps, CMV, Coxsackievirus, EBV)Rare
Metabolic (hypercalcemia)Rare
Anatomic (pancreas divisum)Rare
Idiopathic (no identifiable cause)~5%
Pancreatic neoplasmConsider in any patient >40 years
Gallstones and alcohol together account for ~80% of all cases. When triglycerides are >1000 mg/dL with no evidence of gallstones or alcohol use, hypertriglyceridemia should be considered the etiology.
  • Textbook of Family Medicine 9e, p. 1136-1137

Pathophysiology

The central mechanism involves premature activation of pancreatic enzymes (particularly trypsinogen → trypsin) within acinar cells. This triggers a cascade of autodigestion:
  • In interstitial oedematous pancreatitis (70-80% of cases): proteolytic enzymes injure acinar cells causing edema and swelling, but the inflammatory response is not strong enough to cause necrosis. The gland remains perfused.
  • In necrotising pancreatitis: inflammation is sufficient to cause cell apoptosis and fat necrosis, which spreads to the parenchyma. Necrosis is the major determinant of morbidity and mortality.
Systemic effects arise from massive cytokine release (TNF-α, IL-1, IL-6), leading to SIRS, capillary leak, third-spacing of fluids, hypovolemia, and ultimately multi-organ failure (respiratory, renal, cardiovascular).
  • Grainger & Allison's Diagnostic Radiology, p. 681

Clinical Features

Symptoms:
  • Sudden-onset, severe, constant epigastric pain - classically described as "boring through to the back" or left scapular region
  • Nausea, vomiting, anorexia, fever
  • Patients are more comfortable sitting forward/leaning
Signs:
  • Tachycardia, tachypnea (reflecting SIRS)
  • Epigastric tenderness, guarding; hypoactive bowel sounds
  • Cool, cyanotic extremities (underperfusion)
  • Grey-Turner sign: flank ecchymosis (retroperitoneal hemorrhage)
  • Cullen sign: periumbilical ecchymosis
  • (Both signs indicate hemorrhagic necrosis and predict severe disease)
Lab findings:
  • WBC 12,000-20,000/mm³
  • Elevated serum amylase (rises within hours, clears faster) and lipase (more specific, persists longer)
  • Serum lipase is superior to amylase alone - relying on amylase alone is error-prone
  • Elevated bilirubin, transaminases, ALP suggest a biliary cause
  • Hemoconcentration (high hematocrit), elevated BUN/creatinine from third-spacing
  • Hypocalcemia, hyperglycemia in severe disease
  • Elevated CRP is a useful marker of pancreatic necrosis
  • Sleisenger & Fordtran's GI and Liver Disease, p. 174
  • Textbook of Family Medicine 9e, p. 1137

Imaging

Ultrasound

First-line for identifying gallstones as a cause. Sensitivity for pancreatitis itself is 62-95% (poor due to bowel gas obscuring the pancreas in up to 30% of cases). When the pancreas is visible, findings include diffuse enlargement, reduced reflectivity, and peripancreatic fluid.
Ultrasound in oedematous pancreatitis:
Ultrasound showing diffuse swelling of the pancreas with heterogeneous echogenicity and peripancreatic fluid (arrow)
Ultrasound shows diffuse swelling of the gland with reduced reflectivity and a small rim of peripancreatic fluid (arrow). - Grainger & Allison's Diagnostic Radiology

Contrast-Enhanced CT (CECT)

The gold standard for staging and assessing complications. Indications include:
  • Diagnostic uncertainty
  • Failure to improve clinically within 48-72 hours
  • Suspected complications (necrosis, abscess, vascular injury)
Important caveat: CT performed in the first 24 hours may underestimate the degree of necrosis, which can take 2-3 days to fully develop.
CT: Appropriate timing of imaging - early vs. day 3:
Coronal CT showing minimal signs at 12 hours vs. much more severe inflammation on day 3
(A) CT performed 12 hours after onset shows only minimal signs. (B) Follow-up CT on day 3 (prompted by clinical deterioration) reveals extensive inflammation. - Grainger & Allison's Diagnostic Radiology
CT: Axial section showing acute pancreatitis with peripancreatic inflammation:
Axial CT showing inflamed pancreas with surrounding fat stranding and peripancreatic changes
Axial CT demonstrating pancreatic body/tail with inflammatory changes. - Grainger & Allison's Diagnostic Radiology

MRI / MRCP

Preferred over CT when renal failure precludes IV contrast, or to evaluate the pancreatic duct and identify choledocholithiasis without ERCP. MRCP has largely replaced diagnostic ERCP.
  • Grainger & Allison's Diagnostic Radiology, pp. 677-681

Severity Classification (Revised Atlanta)

CategoryDefinition
MildNo organ failure, no local/systemic complications; self-limiting
Moderately SevereOrgan failure lasting <48 hours OR local/systemic complications without persistent organ failure
SeverePersistent organ failure (>48 hours), single or multi-organ
Severe AP is associated with mortality of ~29.5%, predominantly from organ failure (respiratory or hemodynamic) or infection.

Severity Scoring Systems

Ranson's Criteria (1974)

Assessed at admission (5 criteria) and at 48 hours (6 criteria). Score ≥3 predicts severe disease.
At AdmissionAt 48 Hours
Age >55 yearsHematocrit fall >10%
WBC >16,000/mm³BUN rise >5 mg/dL
Blood glucose >200 mg/dLCa²⁺ <8 mg/dL
LDH >350 IU/LPaO₂ <60 mmHg
AST >250 IU/LBase deficit >4 mEq/L
Fluid sequestration >6 L

BISAP Score

A simpler bedside tool - one point for each:
  • BUN >25 mg/dL
  • Impaired mental status
  • SIRS (≥2 of 4 criteria)
  • Age >60 years
  • Pleural effusion

CT Severity Index (CTSI) - Modified

Prognostic IndicatorPoints
Normal pancreas0
Intrinsic abnormalities ± peripancreatic fat changes2
Peripancreatic fluid collection or fat necrosis4
No pancreatic necrosis0
Necrosis ≤30%2
Necrosis >30%4
Extrapancreatic complications (pleural effusion, ascites, vascular, GI)2
Total 0-2 = Mild; 4-6 = Moderate; 8-10 = Severe
Note: CT scoring alone does not supersede clinical scoring systems for identifying severe pancreatitis.
  • Grainger & Allison's Diagnostic Radiology, p. 681
  • Sleisenger & Fordtran's GI and Liver Disease, p. 174

Management

1. Fluid Resuscitation (Most Important Step)

Aggressive IV fluid replacement is the single most important intervention:
  • 250-500 mL/hr of isotonic crystalloid (lactated Ringer's preferred by many guidelines)
  • Higher rates for patients with hypotension and tachycardia
  • Goal: decrease BUN; hematocrit may be elevated from hypovolemia due to third-spacing
  • Most beneficial in the first 12-24 hours - may minimize or prevent pancreatic necrosis
  • Avoid over-resuscitation (abdominal compartment syndrome risk)

2. Pain Management

Adequate analgesia is essential - IV opioids are standard. NSAIDs and metamizole are alternatives. Good analgesia may reduce the inflammatory response.

3. Nutrition

  • Mild AP: Oral feeding can restart immediately once nausea/vomiting have resolved and pain is controlled. A low-fat solid diet is as safe as a clear liquid diet.
  • Severe AP: Early enteral nutrition is preferred over parenteral nutrition - reduces infectious complications and cost.
    • Nasogastric (NG) feeding appears as effective as nasojejunal feeding, but nasojejunal tubes are preferred when gastric retention occurs from duodenal edema.
    • NPO >7 days requires nutritional support.

4. Antibiotics

  • Not started routinely - no benefit in sterile pancreatitis.
  • Indicated for extrapancreatic infections (e.g., cholangitis, pneumonia) or infected necrotizing pancreatitis.

5. ERCP

Reserved for specific indications only:
  • Concurrent cholangitis → ERCP within 24 hours
  • Biliary obstruction (elevated bilirubin) with suspected choledocholithiasis
  • Not indicated for routine uncomplicated gallstone pancreatitis
  • MRCP or EUS should be used first to screen for CBD stones - prevents unnecessary ERCP

6. Cholecystectomy (for Gallstone AP)

  • Laparoscopic cholecystectomy within 3 days of admission in mild biliary pancreatitis improves outcomes and decreases the need for ERCP.
  • Early cholecystectomy is the standard of care.
  • In patients not fit for surgery, ERCP with biliary sphincterotomy reduces risk of recurrent gallstone pancreatitis.
  • Sleisenger & Fordtran's GI and Liver Disease, Clinical GI Endoscopy, pp. 2783-2787
  • Textbook of Family Medicine 9e, pp. 1137-1138

Local Complications (Revised Atlanta Nomenclature)

ComplicationTimingDescription
Acute peripancreatic fluid collection<4 weeksNo defined wall; usually resolves spontaneously
Pancreatic pseudocyst>4 weeksEncapsulated fluid collection from ductal leak; no solid debris
Acute necrotic collection<4 weeksContains variable amounts of both fluid and necrotic tissue
Walled-off necrosis (WON)>4 weeksMature, encapsulated necrosis; may be sterile or infected
Endoscopic drainage is used for symptomatic and/or infected collections in close proximity to the gastric or duodenal wall.

Systemic Complications

  • Hypovolemia and shock
  • Acute renal failure
  • Hepatic dysfunction
  • Hypocalcemia (from saponification of fat)
  • ARDS / respiratory failure
  • Pleural effusion
  • Colonic infarction (due to thrombosis of middle or right colic artery) - may present as rapid hemodynamic collapse; requires emergent laparotomy

Special Populations: Pediatric AP

Etiology differs from adults - biliary tract disease (10-30%), medications (25%, especially valproate and L-asparaginase), systemic disease (33%, including hemolytic uremic syndrome, SLE), trauma (10-40%), and metabolic causes. Genetic mutations (SPINK1, CFTR combinations) are found in many "idiopathic" cases and should be tested after recurrent episodes.
  • Sleisenger & Fordtran's GI and Liver Disease, p. 14 (pediatric chapter)

Key Take-Aways

  • Most cases (80%) are mild and self-limiting; ~20% develop severe disease
  • Gallstones and alcohol account for ~80% of all etiologies - always get an abdominal ultrasound
  • Aggressive IV fluid resuscitation in the first 12-24 hours is the cornerstone of management
  • Antibiotics are not given prophylactically
  • Enteral nutrition is preferred over parenteral in severe disease
  • Early ERCP only for cholangitis or confirmed biliary obstruction; early cholecystectomy is standard for biliary AP
  • CT should be reserved for diagnostic uncertainty or clinical deterioration, ideally after 48-72 hours
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