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Acute Pancreatitis
A comprehensive review drawn from Sleisenger & Fordtran's GI and Liver Disease, Schwartz's Principles of Surgery, Current Surgical Therapy, Grainger & Allison's Diagnostic Radiology, and Rosen's Emergency Medicine.
Definition & Epidemiology
Acute pancreatitis (AP) is a sudden inflammatory disease of the pancreas triggered by premature activation of digestive enzymes within acinar cells, causing autodigestion. It accounts for approximately 111 hospitalizations per 100,000 persons/year (US data), and 80% of cases are mild and self-limiting. However, up to 20% are severe and life-threatening.
Etiology
The classic mnemonic is "I GET SMASHED":
| Cause | Notes |
|---|
| Gallstones | Most common overall (~40%). Stone/sludge impaction at the ampulla of Vater |
| Alcohol | Second most common (~30%). Chronic use more than acute binge |
| Hypertriglyceridemia | Triglycerides >1000 mg/dL; serum amylase may be falsely normal |
| Hypercalcemia | Any cause; activates trypsinogen |
| ERCP (post-procedure) | Most common iatrogenic cause |
| Trauma | Blunt abdominal injury; often missed in severely injured patients |
| Medications | Valproate, L-asparaginase, azathioprine/6-MP, thiazides, steroids, tetracyclines |
| Infections | Mumps, CMV, Coxsackievirus, Mycoplasma, Ascaris (in endemic areas) |
| Autoimmune / Structural | Pancreas divisum, autoimmune pancreatitis |
| Genetic | SPINK1, CFTR, PRSS1 mutations (esp. in recurrent/hereditary cases) |
| Idiopathic | ~5-15% of cases |
- Sleisenger & Fordtran's, p. 174; Grainger & Allison's, p. 677
Pathophysiology
The central event is premature activation of trypsinogen to trypsin within pancreatic acinar cells (normally a strictly extracellular event). This triggers a cascade:
- Acinar cell injury (oxidative stress, ductal obstruction, alcohol toxicity)
- Intracellular trypsin activation
- Trypsin activates other pro-enzymes: phospholipase A2, elastase, chymotrypsin
- Local inflammation, acinar cell necrosis, fat necrosis
- Systemic inflammatory response syndrome (SIRS) - cytokine release (IL-1, IL-6, TNF-a)
- Distant organ failure (ARDS, AKI, cardiovascular collapse)
Clinical Presentation
| Feature | Details |
|---|
| Pain | Acute onset, severe, constant epigastric pain radiating to the back/left scapula; described as "boring through to the back" |
| Nausea/Vomiting | Universal |
| Position | Patient leans forward to relieve pain (anteflexion position) |
| Fever | Usually low grade; high fever suggests infected necrosis |
| Tachycardia / Tachypnea | Reflect SIRS and third-space fluid losses |
| Abdominal exam | Hypoactive bowel sounds, epigastric tenderness, guarding/rigidity (variable) |
Rare but classic signs (indicate retroperitoneal hemorrhage/necrosis):
- Cullen's sign - periumbilical ecchymosis
- Grey Turner's sign - flank ecchymosis
Diagnosis
Diagnosis requires 2 of 3 of the following (Revised Atlanta Criteria):
- Abdominal pain strongly suggestive of AP
- Serum amylase and/or lipase ≥3x upper limit of normal
- Characteristic findings on imaging (CT/MRI)
Amylase: Rises within hours, peaks quickly, returns to normal in 3-5 days. No correlation between magnitude and severity. Can be falsely normal in hypertriglyceridemia or severe necrosis (burnt-out pancreas).
Lipase: More specific and remains elevated longer than amylase. Preferred enzyme.
Other labs: WBC 12,000-20,000, elevated BUN/creatinine (hemoconcentration), hyperglycemia, elevated LDH/AST, hypoalbuminemia, hypocalcemia (saponification).
- Schwartz's Surgery, p. 1471-1472
Imaging
Ultrasound (first-line initial study)
Best for identifying gallstones as etiology. In edematous pancreatitis: diffuse pancreatic enlargement with reduced reflectivity and peripancreatic fluid (below). US cannot reliably detect necrosis.
US of oedematous pancreatitis: (A) diffuse swelling, heterogeneous echogenicity, small rim of peripancreatic fluid; (B) contrast-enhanced US showing homogeneous hyperenhancement - Grainger & Allison's
Contrast-Enhanced CT (CECT) - gold standard for severity
- Indicated when: diagnosis is uncertain, or severe/complicated disease
- NOT routinely needed in mild AP
- Best done 48-72 hours after onset (severity may underestimate early)
- Distinguishes interstitial edematous from necrotizing pancreatitis
Necrotizing pancreatitis: hypoenhancing necrosis (asterisk) of body/tail; small enhancing parenchyma at head (arrow) - Current Surgical Therapy
Gas within a necrotic collection = infected necrosis (surgical emergency indicator).
MRI/MRCP
Preferred over CT for: pregnant patients, renal impairment, evaluating ductal anatomy, detecting bile duct stones without ERCP.
Severity Classification (2012 Revised Atlanta Classification)
| Grade | Organ Failure | Local/Systemic Complications | Mortality |
|---|
| Mild | Absent | Absent | Very rare (<5%) |
| Moderately Severe | Transient (<48 hr) | Present, without persistent OF | Low |
| Severe | Persistent (>48 hr) | Present | High: 36-50%; extremely high with infected necrosis |
- Current Surgical Therapy, Table 1; Schwartz's, p. 1472
Scoring Systems
Ranson's Criteria
Scored over 48 hours. ≥3 criteria = severe disease.
| On Admission | At 48 Hours |
|---|
| Age >55 years | Hematocrit fall >10% |
| WBC >16,000 | BUN rise >5 mg/dL |
| Blood glucose >200 mg/dL | Serum Ca <8 mg/dL |
| LDH >350 IU/L | PaO₂ <60 mmHg |
| AST >250 IU/L | Base deficit >4 mEq/L |
| Fluid sequestration >6 L |
Score ≥6: mortality ~50%.
BISAP Score (within 24 hours)
BUN >25 mg/dL | Impaired mental status (GCS <15) | SIRS | Age >60 | Pleural effusion
Score ≥3 = high mortality risk. Simpler but comparable accuracy.
APACHE II
Score ≥8 at 24h has similar accuracy to Ranson's.
CT Severity Index (CTSI)
Balthazar grade (A-E) + % necrosis score. Correlates with morbidity and mortality.
Local Complications (Revised Atlanta Nomenclature)
| Complication | Type | Timing | Features |
|---|
| APFC (Acute Peripancreatic Fluid Collection) | Interstitial | <4 weeks | Non-encapsulated, no necrosis; most resolve spontaneously |
| Pseudocyst | Interstitial | >4 weeks | Encapsulated, no solid debris, wall well-defined |
| ANC (Acute Necrotic Collection) | Necrotizing | <4 weeks | Mixed fluid + necrosis |
| WON (Walled-Off Necrosis) | Necrotizing | >4 weeks | Encapsulated necrosis; may become infected |
Other local complications: hemorrhagic pancreatitis, splenic/portal vein thrombosis, pseudoaneurysms, gastric outlet obstruction, colonic infarction (middle/right colic artery - presents as rapid hemodynamic collapse; requires emergent laparotomy).
Management
General Principles
Accurate diagnosis, appropriate triage, high-quality supportive care, and monitoring for/treatment of complications.
1. Pain Control
- Mild pain: NSAIDs (e.g., metamizole 2 g IV q8h)
- Severe pain: Opioids IV (buprenorphine, pentazocine, meperidine)
- Avoid morphine - may cause sphincter of Oddi spasm
2. Fluid Resuscitation
- Most important early intervention
- Ringer's Lactate is preferred - has anti-inflammatory effects, reduces metabolic acidosis compared to normal saline
- Rate: 5-10 mL/kg/hour, titrated to goals
- Targets: HR normalization, MAP, urine output >0.5 mL/kg/hr
- Severe AP: target CVP 8-12 mmHg, mixed venous O₂ sat ≥70%
- Monitor for volume overload (tachypnea, hypoxia, edema, pleural effusion)
3. Nutrition
- Early enteral nutrition is preferred over parenteral (fewer infectious complications, lower cost)
- Nasogastric (NG) feeding is as effective as nasojejunal in most patients
- Nasojejunal preferred if gastric retention from duodenal edema
- TPN only if enteral feeding is not tolerated
- Prior practice of "pancreatic rest"/NPO is no longer recommended
4. Antibiotics
- Prophylactic antibiotics are NOT recommended - necrosis is initially sterile, and prophylaxis promotes resistant organisms
- Indicated when infected necrosis is documented (CT gas, positive culture)
- Preferred: Carbapenems (best pancreatic penetration vs. cephalosporins/fluoroquinolones)
- Aim to stabilize, defer intervention for at least 4 weeks to allow WON maturation
5. Role of ERCP
- NOT routinely recommended in acute biliary pancreatitis
- Indicated for: cholangitis or biliary obstruction (hyperbilirubinemia + clinical cholangitis)
- Use MRCP/EUS first to identify CBD stones - prevents unnecessary ERCP
- Early laparoscopic cholecystectomy (within 3 days in mild disease) is standard of care for gallstone pancreatitis
6. Intervention for Pancreatic Necrosis
- Sterile necrosis - conservative management; surgery/drainage not indicated
- Infected necrosis - drainage required; ideally deferred until WON is mature (≥4 weeks)
- Drainage options (step-up approach preferred):
- Percutaneous drainage (CT or US-guided) - first step
- Endoscopic transmural drainage (EUS-guided) - if collection in apposition to stomach/duodenum
- Surgical necrosectomy - minimally invasive video-assisted retroperitoneal debridement (VARD) or open - reserved for failures of minimally invasive approaches
ICU Admission
Transfer to ICU when: persistent tachycardia/hypotension, oliguria, SOFA score deteriorating, multi-organ failure. Target CVP 8-12 mmHg, MVO₂ ≥70%.
Systemic Complications
| Complication | Notes |
|---|
| ARDS | Most common cause of early death; PaO₂/FiO₂ <300 |
| AKI | Hemoconcentration + cytokine-mediated renal vasoconstriction |
| Hypocalcemia | Saponification of fat; low Ca <8 mg/dL is a Ranson's criterion |
| Hyperglycemia | Glucagon excess, insulin deficiency |
| Abdominal compartment syndrome | From massive fluid resuscitation + ascites |
| Splanchnic vein thrombosis | Splenic/portal vein; risk of variceal bleeding |
| Colonic infarction | Middle/right colic artery - rare but catastrophic |
Summary of Key Management Points
- Most AP is mild and self-limiting - supportive care, early enteral feeding, Ringer's lactate
- Severity scoring (Ranson's, BISAP, APACHE-II) guides triage to ICU vs. ward
- CECT is the standard for severity assessment but not needed in obvious mild disease
- ERCP only in cholangitis or biliary obstruction - not routine
- Early laparoscopic cholecystectomy for gallstone pancreatitis
- No prophylactic antibiotics - carbapenems only for documented infected necrosis
- Step-up approach for necrosis intervention: percutaneous/endoscopic before surgery
- Morphine avoided due to sphincter of Oddi spasm
Sources: Sleisenger & Fordtran's Gastrointestinal and Liver Disease; Schwartz's Principles of Surgery, 11th ed.; Current Surgical Therapy, 14th ed.; Grainger & Allison's Diagnostic Radiology; Rosen's Emergency Medicine.