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Acute Pancreatitis
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:
- Abdominal pain strongly suggestive of AP (epigastric, radiating to back)
- Serum amylase and/or lipase ≥3× upper limit of normal
- Characteristic imaging findings
- Grainger & Allison's Diagnostic Radiology, p. 677; Current Surgical Therapy 14e, p. 603
Etiology
| Category | Causes |
|---|
| Mechanical/Obstructive | Gallstones (40-70%), post-ERCP, tumors, pancreas divisum, ampullary stenosis |
| Toxic/Metabolic | Alcohol (25-35%), hypertriglyceridemia (TG >1000 mg/dL), hypercalcemia, uremia, scorpion venom |
| Drugs | Valproate, L-asparaginase, 6-mercaptopurine, steroids, thiazides, azathioprine |
| Infectious | Mumps, coxsackievirus, HIV, CMV, EBV, Salmonella, Mycoplasma, ascariasis |
| Trauma | Blunt abdominal trauma |
| Idiopathic | ~5-10% (many may be occult microlithiasis or genetic) |
| Genetic | SPINK1, 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:
| Grade | Features | Mortality |
|---|
| Mild | No organ failure, no local/systemic complications | Very rare (<5%) |
| Moderately severe | Transient organ failure (<48h) OR local/systemic complications without persistent organ failure | ~15% of cases |
| Severe | Persistent 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:
- Diagnostic uncertainty or normal enzymes with high clinical suspicion
- Ruling out other intra-abdominal pathology
- 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.
| Letter | Criteria |
|---|
| B | BUN >25 mg/dL |
| I | Impaired mental status (GCS <15) |
| S | SIRS (≥2 of 4 criteria present) |
| A | Age >60 years |
| P | Pleural 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
| Complication | Timing | Description |
|---|
| Acute Peripancreatic Fluid Collection (APFC) | <4 weeks | Homogenous, non-encapsulated, no necrosis; most resolve spontaneously |
| Pancreatic Pseudocyst | >4 weeks | Encapsulated collection with defined wall, without significant necrosis |
| Acute Necrotic Collection (ANC) | <4 weeks | Heterogeneous collection with necrotic debris |
| Walled-Off Necrosis (WON) | >4 weeks | Encapsulated necrotic collection |
| Vascular complications | Variable | Splenic/portal vein thrombosis, pseudoaneurysm |
| Bowel necrosis | Late | Rare, poor prognosis |
| Fistula | Variable | Pancreatico-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"):
- Percutaneous/endoscopic drainage first
- Video-assisted retroperitoneal debridement (VARD) or endoscopic necrosectomy if drainage fails
- 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