Acute pancreatitis

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"acute pancreatitis"[MeSH Terms] AND management

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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":
CauseNotes
GallstonesMost common overall (~40%). Stone/sludge impaction at the ampulla of Vater
AlcoholSecond most common (~30%). Chronic use more than acute binge
HypertriglyceridemiaTriglycerides >1000 mg/dL; serum amylase may be falsely normal
HypercalcemiaAny cause; activates trypsinogen
ERCP (post-procedure)Most common iatrogenic cause
TraumaBlunt abdominal injury; often missed in severely injured patients
MedicationsValproate, L-asparaginase, azathioprine/6-MP, thiazides, steroids, tetracyclines
InfectionsMumps, CMV, Coxsackievirus, Mycoplasma, Ascaris (in endemic areas)
Autoimmune / StructuralPancreas divisum, autoimmune pancreatitis
GeneticSPINK1, 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:
  1. Acinar cell injury (oxidative stress, ductal obstruction, alcohol toxicity)
  2. Intracellular trypsin activation
  3. Trypsin activates other pro-enzymes: phospholipase A2, elastase, chymotrypsin
  4. Local inflammation, acinar cell necrosis, fat necrosis
  5. Systemic inflammatory response syndrome (SIRS) - cytokine release (IL-1, IL-6, TNF-a)
  6. Distant organ failure (ARDS, AKI, cardiovascular collapse)

Clinical Presentation

FeatureDetails
PainAcute onset, severe, constant epigastric pain radiating to the back/left scapula; described as "boring through to the back"
Nausea/VomitingUniversal
PositionPatient leans forward to relieve pain (anteflexion position)
FeverUsually low grade; high fever suggests infected necrosis
Tachycardia / TachypneaReflect SIRS and third-space fluid losses
Abdominal examHypoactive 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):
  1. Abdominal pain strongly suggestive of AP
  2. Serum amylase and/or lipase ≥3x upper limit of normal
  3. 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.
Ultrasound: edematous pancreatitis showing swollen pancreas with peripancreatic fluid
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
CECT of necrotizing pancreatitis with hypoenhancing necrosis (asterisk) of body/tail
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)

GradeOrgan FailureLocal/Systemic ComplicationsMortality
MildAbsentAbsentVery rare (<5%)
Moderately SevereTransient (<48 hr)Present, without persistent OFLow
SeverePersistent (>48 hr)PresentHigh: 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 AdmissionAt 48 Hours
Age >55 yearsHematocrit fall >10%
WBC >16,000BUN rise >5 mg/dL
Blood glucose >200 mg/dLSerum Ca <8 mg/dL
LDH >350 IU/LPaO₂ <60 mmHg
AST >250 IU/LBase 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)

ComplicationTypeTimingFeatures
APFC (Acute Peripancreatic Fluid Collection)Interstitial<4 weeksNon-encapsulated, no necrosis; most resolve spontaneously
PseudocystInterstitial>4 weeksEncapsulated, no solid debris, wall well-defined
ANC (Acute Necrotic Collection)Necrotizing<4 weeksMixed fluid + necrosis
WON (Walled-Off Necrosis)Necrotizing>4 weeksEncapsulated 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

ComplicationNotes
ARDSMost common cause of early death; PaO₂/FiO₂ <300
AKIHemoconcentration + cytokine-mediated renal vasoconstriction
HypocalcemiaSaponification of fat; low Ca <8 mg/dL is a Ranson's criterion
HyperglycemiaGlucagon excess, insulin deficiency
Abdominal compartment syndromeFrom massive fluid resuscitation + ascites
Splanchnic vein thrombosisSplenic/portal vein; risk of variceal bleeding
Colonic infarctionMiddle/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.
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