Acute pancreatitis

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"acute pancreatitis"[MeSH Terms] AND management

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Acute Pancreatitis

Pancreas Anatomy - Anterior View
Anatomy of the pancreas and surrounding vascular structures - Rosen's Emergency Medicine

Definition

Acute pancreatitis (AP) is a sudden inflammatory condition of the pancreas involving enzymatic autodigestion and destruction of pancreatic tissue. It ranges from a mild, self-limited illness to life-threatening multiorgan failure with sepsis. It is the most common pancreatic disease worldwide and one of the top reasons for GI-related hospitalization in the US. - Rosen's Emergency Medicine, p. 1265
Diagnosis requires 2 of 3:
  1. Abdominal pain strongly suggestive of AP (epigastric, radiating to back)
  2. Serum amylase and/or lipase ≥3× upper limit of normal
  3. Characteristic imaging findings
  • Grainger & Allison's Diagnostic Radiology, p. 677; Current Surgical Therapy 14e, p. 603

Etiology

CategoryCauses
Mechanical/ObstructiveGallstones (40-70%), post-ERCP, tumors, pancreas divisum, ampullary stenosis
Toxic/MetabolicAlcohol (25-35%), hypertriglyceridemia (TG >1000 mg/dL), hypercalcemia, uremia, scorpion venom
DrugsValproate, L-asparaginase, 6-mercaptopurine, steroids, thiazides, azathioprine
InfectiousMumps, coxsackievirus, HIV, CMV, EBV, Salmonella, Mycoplasma, ascariasis
TraumaBlunt abdominal trauma
Idiopathic~5-10% (many may be occult microlithiasis or genetic)
GeneticSPINK1, CFTR, PRSS1 mutations (consider in recurrent/pediatric cases)
  • Rosen's Emergency Medicine, Box 77.1, p. 1266
Smoking and diabetes are independent risk factors. ALT elevation (positive predictive value 95%) is particularly specific for biliary/gallstone pancreatitis.

Pathophysiology

The central mechanism is premature intracellular activation of digestive enzymes (primarily trypsinogen → trypsin) within the pancreas itself, triggering autodigestion. This leads to:
  • Local pancreatic inflammation and tissue destruction
  • Release of pro-inflammatory cytokines (IL-1, IL-6, TNF-α)
  • Systemic inflammatory response syndrome (SIRS)
  • Increased microvascular permeability → third-spacing of fluids
  • In severe cases: multiorgan dysfunction (lungs, kidneys, cardiovascular)
Enzymatic degradation of surfactant contributes to pulmonary sequelae. Coagulopathy results from cytokine-mediated activation of the coagulation cascade.

Classification (Revised 2012 Atlanta)

Morphological types:
  • Interstitial edematous pancreatitis - diffuse enlargement without necrosis; most common; usually resolves within first week
  • Necrotizing pancreatitis - affects ~5-10% of patients; may involve pancreatic parenchyma and peripancreatic tissue; necrosis may be sterile, liquefy, or become infected
Severity grades:
GradeFeaturesMortality
MildNo organ failure, no local/systemic complicationsVery rare (<5%)
Moderately severeTransient organ failure (<48h) OR local/systemic complications without persistent organ failure~15% of cases
SeverePersistent organ failure >48h (single or multi-organ)36-50%; higher with infected necrosis
  • Current Surgical Therapy 14e, p. 603-604
Organ failure (Modified Marshall score - any 1 of):
  • Cardiovascular: systolic BP <90 mmHg or HR >130 bpm
  • Pulmonary: PaO₂ <60 mmHg
  • Renal: creatinine >2.0 mg/dL

Clinical Features

Symptoms:
  • Persistent epigastric or LUQ pain, typically moderate-to-severe, radiating to the back, chest, or flanks
  • Pain relieved by sitting forward or leaning forward
  • Nausea, vomiting, anorexia
  • Note: pain intensity does NOT correlate with severity
Signs:
  • Vital signs: fever, tachycardia, and sometimes hypotension in severe disease
  • Jaundice suggests obstruction (gallstone or tumor)
  • Epigastric tenderness ± guarding; rebound less common
  • Absent bowel sounds if ileus present
  • Shallow respirations (pain splinting); basilar crackles or decreased breath sounds
  • Cullen sign - bluish periumbilical discoloration (hemoperitoneum) - rare, poor prognosis
  • Grey Turner sign - reddish-brown flank discoloration (retroperitoneal hemorrhage) - rare, poor prognosis
  • Murphy sign if gallstone etiology
Systemic complications:
  • ARDS, pleural effusions (up to 50% of patients, predominantly left-sided)
  • Cardiovascular collapse and shock (from fluid shifts)
  • Acute kidney injury (hypoperfusion + inflammatory mediators)
  • DIC/coagulopathy
  • Rosen's Emergency Medicine, p. 1265-1266

Investigations

Bloods:
  • Lipase - preferred over amylase; more sensitive and specific; elevated for 1-2 weeks (amylase 3-5 days)
  • Both begin rising within hours of onset; degree of elevation does NOT correlate with severity
  • Amylase falsely negative in alcohol and hypertriglyceridemia-induced AP
  • LFTs (ALT, AST, bilirubin) - evaluate for biliary etiology; ALT >3× ULN has PPV of 95% for gallstone pancreatitis
  • FBC, BMP - assess for SIRS, organ failure
  • Calcium, triglycerides - if no obvious etiology
  • CRP >100 mg/L - useful marker of severity during hospitalization
  • BUN - rising BUN associated with inadequate hydration and higher mortality
Imaging: CT/MRI not routinely indicated for diagnosis. CT recommended only in:
  1. Diagnostic uncertainty or normal enzymes with high clinical suspicion
  2. Ruling out other intra-abdominal pathology
  3. Assessing complications when patient fails to improve after 48-72 hours
Best done 3-7 days after presentation for complication assessment (earlier CT may underestimate necrosis).
Ultrasound: first-line to assess for gallstones/biliary dilation.

Severity Scoring Systems

BISAP Score (Bedside Index of Severity in Acute Pancreatitis)

Used within first 24h. Score ≥3 = substantially increased mortality risk.
LetterCriteria
BBUN >25 mg/dL
IImpaired mental status (GCS <15)
SSIRS (≥2 of 4 criteria present)
AAge >60 years
PPleural effusion on imaging

Ranson Criteria

At admission (non-biliary):
  • Age >55 years
  • WBC >16,000/mm³
  • Glucose >200 mg/dL
  • AST >250 IU/L
  • LDH >350 IU/L
At 48 hours:
  • Hematocrit drop >10%
  • BUN rise >5 mg/dL
  • Calcium <8 mg/dL
  • PaO₂ <60 mmHg
  • Base deficit >4 mEq/L
  • Fluid needs >6 L
Score ≥3 = severe disease.

Other Systems

  • APACHE II - can be calculated at any time; PPV 43%, NPV 89% for critically ill
  • CT Severity Index (CTSI/Modified CTSI) - based on degree of necrosis, inflammation, and fluid collections on CT
  • PASS (Pancreatitis Activity Scoring System) - dynamic, continuous monitoring throughout illness course
CT scoring does NOT supersede clinical scoring systems for identifying severe disease. - Grainger & Allison's, p. 685
  • Rosen's Emergency Medicine, Table 77.1, p. 1267; Harrison's 22e, p. 2791; Current Surgical Therapy 14e, p. 604

Management

1. Fluid Resuscitation (cornerstone of treatment)

  • Aggressive IV fluid replacement - Lactated Ringer's preferred over normal saline (lower incidence of SIRS)
  • Typical rate: 250-500 mL/hr initially
  • Target: urine output >0.5 mL/kg/hr, decreasing BUN and hematocrit
  • A decrease in hematocrit and BUN within 12-24h confirms adequate resuscitation
  • Less aggressive strategy may be sufficient for milder disease; adjust for cardiac/pulmonary/renal comorbidities

2. Pain Management

  • IV opioids are safe and recommended
  • Hydromorphone or morphine; meperidine no longer preferred
  • NSAIDs and patient-controlled analgesia can supplement

3. Nutrition

  • Mild AP: low-fat solid diet once patient can tolerate oral intake
  • Severe AP: enteral nutrition preferred over TPN - initiated within 2-3 days of admission
    • Enteral feeding maintains gut barrier integrity, limits bacterial translocation, lower cost, fewer complications than TPN
    • Gastric feeding (nasogastric) is safe; jejunal (nasojejunal) has possible physiologic advantages but not proven superior
  • Nil-by-mouth has no benefit and worsens outcomes in most cases

4. Antibiotics

  • No role for prophylactic antibiotics in necrotizing pancreatitis - does not improve survival and may promote opportunistic fungal infections
  • Empiric antibiotics indicated for: clinical decompensation, suspected infected necrosis, confirmed infection
  • Drug-induced pancreatitis: discontinue offending agent

5. Addressing Etiology

  • Gallstone pancreatitis: cholecystectomy (same admission for mild AP; after resolution for severe)
  • Post-ERCP: rectal indomethacin and/or pancreatic duct stenting for prophylaxis
  • Hypertriglyceridemia: insulin infusion, fibrates; adjuncts include heparin or plasmapheresis (limited evidence); outpatient lipid-lowering therapy
  • Hypercalcemia: treat underlying hyperparathyroidism or malignancy

6. ICU Triage

  • Lower BISAP, normal hematocrit, low BUN → regular ward
  • Persistent SIRS at 24h or significant comorbidities → step-down unit
  • Higher BISAP, elevated hematocrit and BUN, respiratory failure, organ failure → ICU
  • Harrison's 22e, p. 2791-2792; Rosen's Emergency Medicine, p. 1268-1270

Local Complications

ComplicationTimingDescription
Acute Peripancreatic Fluid Collection (APFC)<4 weeksHomogenous, non-encapsulated, no necrosis; most resolve spontaneously
Pancreatic Pseudocyst>4 weeksEncapsulated collection with defined wall, without significant necrosis
Acute Necrotic Collection (ANC)<4 weeksHeterogeneous collection with necrotic debris
Walled-Off Necrosis (WON)>4 weeksEncapsulated necrotic collection
Vascular complicationsVariableSplenic/portal vein thrombosis, pseudoaneurysm
Bowel necrosisLateRare, poor prognosis
FistulaVariablePancreatico-pleural fistula (↑ pleural amylase)
Suspect local complications in: prolonged/worsening symptoms, secondary rise in enzymes, fever, leukocytosis, sepsis.

Management of Necrosis

  • Sterile necrosis: managed conservatively unless complications arise
  • Infected necrosis (suspected): empiric broad-spectrum antibiotics (carbapenems penetrate necrosis well)
  • Fine-needle aspiration (FNA) of necrosis for Gram stain/culture is no longer universally recommended - risk of contaminating sterile collections
  • Drainage/debridement ("step-up approach"):
    1. Percutaneous/endoscopic drainage first
    2. Video-assisted retroperitoneal debridement (VARD) or endoscopic necrosectomy if drainage fails
    3. Open surgical necrosectomy (last resort - high morbidity/mortality)
  • Interventions delayed until necrosis is walled off (typically >4 weeks) for better outcomes
Multidisciplinary team (gastroenterology, surgery, interventional radiology, ICU) is recommended; transfer to tertiary pancreas center if specialized services unavailable.
  • Harrison's 22e, p. 2792; Current Surgical Therapy 14e, p. 604-605

Prognosis

  • Overall mortality ~5% (declining over time despite rising incidence)
  • Severe AP: 36-50% mortality
  • Infected pancreatic necrosis: extremely high mortality
  • Rising BUN during hospitalization = inadequate hydration + higher in-hospital mortality
  • Persistent SIRS at 24h = predictor of organ failure and necrosis
  • CRP >100 mg/L during hospitalization = marker of severity

Key Pearls

  • Lipase is preferred over amylase (more sensitive, specific, and remains elevated longer)
  • Degree of enzyme elevation does NOT predict severity
  • CT should NOT be routine - wait 48-72h (ideally 3-7 days) to assess complications
  • No role for prophylactic antibiotics in necrotizing pancreatitis
  • Enteral nutrition over TPN in severe AP
  • Lactated Ringer's over normal saline for fluid resuscitation
  • Delay intervention on necrosis until it is walled off (>4 weeks)
  • ALT >3× ULN has 95% PPV for biliary pancreatitis

Sources: Rosen's Emergency Medicine 10e | Harrison's Principles of Internal Medicine 22e (2025) | Current Surgical Therapy 14e | Sleisenger & Fordtran's GI & Liver Disease | Grainger & Allison's Diagnostic Radiology
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