Acute pancreatitis

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Acute Pancreatitis

Acute pancreatitis (AP) is a sudden inflammatory condition of the pancreas caused by enzymatic autodigestion of pancreatic tissue. It is the most common pancreatic disease worldwide and a leading cause of gastrointestinal hospitalization in the United States. Severity ranges from mild and self-limited to life-threatening necrotizing disease with multiorgan failure - overall mortality can reach 30% in severe cases, though the trend is improving.

Pancreatic anatomy (anterior view):

Etiology

The two dominant causes account for the vast majority of cases:

Gallstones: 40-70% of cases (most common cause overall)
Alcohol: 25-35% of cases

Other important causes include:

Category	Examples
Toxic-Metabolic	Hypertriglyceridemia (>1000 mg/dL), hypercalcemia, uremia, scorpion venom, drugs
Mechanical-Obstructive	Post-ERCP (5-10%), ampullary stenosis, pancreas divisum, annular pancreas, tumor
Infectious	Viral (mumps, coxsackievirus, HIV, CMV, EBV, varicella); bacterial (TB, Mycoplasma); parasitic (Ascaris)
Vascular	Vasculitis, embolism, hypoperfusion, hypercoagulability
Other	Idiopathic, hereditary, autoimmune, DKA

Note: Many "idiopathic" cases are thought to be caused by occult microlithiasis. Smoking and diabetes are independent risk factors.

In children, the distribution differs: trauma, systemic disease, medications (valproate, L-asparaginase, steroids, 6-mercaptopurine), and biliary disease are more prominent causes, with a genetic component (SPINK1, CFTR mutations) in recurrent cases.

Pathophysiology

Regardless of the trigger, AP begins with inappropriate intracellular activation of digestive enzymes - particularly trypsinogen converting to trypsin - within acinar cells. This leads to:

Autodigestion of pancreatic parenchyma
Local inflammatory response and microvascular damage
Release of inflammatory mediators (cytokines, phospholipase A2, elastase)
Progression to systemic inflammatory response syndrome (SIRS)
In severe disease: multiorgan failure, pancreatic necrosis, and sepsis

Classification (Revised Atlanta 2012)

By morphological type:

Interstitial edematous pancreatitis: The majority (~90-95%). Pancreatic edema with preserved perfusion. Usually resolves within the first week.
Necrotizing pancreatitis: ~5-10% of cases. Involves ischemic necrosis of pancreatic parenchyma and/or surrounding peripancreatic tissue. Necrosis may remain sterile or become infected; infected necrosis carries significantly higher morbidity.

By severity:

Mild: No organ failure, no local or systemic complications
Moderately severe: Transient organ failure (<48 hours) and/or local complications
Severe: Persistent organ failure (>48 hours), single or multiorgan

Local complications (by fluid collection type):

Type	Timing	Features
Acute peripancreatic fluid collection	<4 weeks	Homogeneous fluid adjacent to pancreas (interstitial)
Pancreatic pseudocyst	>4 weeks	Homogeneous with well-defined wall (interstitial)
Acute necrotic collection	<4 weeks	Heterogeneous fluid + necrosis (necrotizing)
Walled-off necrosis	>4 weeks	Heterogeneous with well-defined wall (necrotizing)

Clinical Features

Symptoms:

Persistent, moderate-to-severe epigastric or left upper quadrant pain
Radiation to the back, chest, or flanks (classic "boring" quality)
Pain may be relieved by leaning forward
Nausea, vomiting, and anorexia
Pain is exacerbated by oral intake

Signs:

Tachycardia, fever (inflammatory response)
Hypotension/shock in severe disease (fluid shifts, volume loss)
Epigastric tenderness ± guarding
Diminished or absent bowel sounds (paralytic ileus)
Jaundice suggests biliary/obstructive etiology
Cullen sign: Periumbilical bluish discoloration (hemoperitoneum) - rare, poor prognosis
Grey Turner sign: Reddish-brown flank discoloration (retroperitoneal hemorrhage) - rare, poor prognosis
Basilar crackles or decreased breath sounds (pulmonary complications)
Right upper quadrant tenderness + Murphy sign in gallstone pancreatitis

Systemic complications:

Pulmonary: pleural effusions (up to 50%, predominantly left-sided), ARDS, atelectasis
Cardiovascular: shock from fluid shifts and third-spacing
Renal failure: hypoperfusion + inflammatory mediators
Coagulopathy/DIC: cytokine-mediated coagulation cascade activation
Metabolic: hyperglycemia (decreased insulin), hypocalcemia (low albumin + magnesium)

Diagnosis

AP is diagnosed when at least 2 of 3 criteria are met:

Abdominal pain characteristic of AP
Serum lipase or amylase ≥3x upper limit of normal
Characteristic findings on imaging

Laboratory tests:

Test	Notes
Lipase	Preferred - more sensitive and specific than amylase. Peaks earlier, stays elevated ~1-2 weeks. Use this preferentially.
Amylase	Less specific (elevated in salivary disease, renal failure, appendicitis, cholecystitis, bowel obstruction). Stays elevated ~3-5 days. May be falsely normal in alcohol/hypertriglyceridemia-induced AP.
ALT	PPV ~95% for biliary pancreatitis when elevated
Bilirubin, AST	Evaluate for obstructive cause
Triglycerides	Check if no gallstones or alcohol history
Calcium	Elevated may be causative; low indicates severity
CBC, BMP	Evaluate SIRS, organ failure

Testing both lipase AND amylase does not improve diagnostic accuracy. Enzyme levels do NOT correlate with severity.

Imaging

Abdominal Ultrasound - should be performed in all patients:

Limited direct pancreatic visualization (bowel gas obstruction)
First-line to evaluate for biliary etiology (gallstones, ductal dilation)
Normal ultrasound does NOT exclude AP

Contrast-Enhanced CT (CECT) - gold standard for severity assessment:

90% sensitivity and specificity
Indicated when diagnosis is uncertain, or to assess severity/complications
Best done 48-72 hours after onset (early CT may underestimate necrosis)
Normal CT in 15-30% of mild cases

CT findings of interstitial edematous pancreatitis (peripancreatic fat stranding, mild fluid):

CT - Acute Interstitial Pancreatitis with peripancreatic fat stranding and fluid (arrows)

CT findings of necrotizing pancreatitis (area of non-enhancement, arrow):

CT - Necrotizing Pancreatitis showing non-enhancing area (arrow)

MRI/MRCP: Superior for biliary tract imaging, equal diagnostic value to CT; preferred when contrast is contraindicated or for duct evaluation. MRCP has largely replaced diagnostic ERCP.

CT Severity Index (CTSI / Balthazar score): Grades from A-E based on pancreatic inflammation + degree of necrosis. Scores ≥7 carry ~17% mortality and 92% morbidity.

Severity Scoring Systems

Several scoring systems predict disease severity, though no single system is ideal for ED use:

Score	Parameters	Notes
BISAP (Bedside Index for Severity in AP)	BUN >25, impaired mental status, SIRS, age >60, pleural effusion	Simpler, ED-friendly; score ≥3 predicts severe AP
Ranson criteria	11 parameters over 48 hours	Classic but requires 48-hr assessment
APACHE II	Multiple physiologic variables	Validated, used in ICU
Revised Atlanta	Clinical + radiologic	Current standard classification

Management

Initial resuscitation

IV fluid resuscitation is the cornerstone of initial therapy
- Lactated Ringer's solution preferred over normal saline (NS associated with hyperchloremic acidosis and worse outcomes in some studies)
- Goal-directed: 250-500 mL/hr initially; reassess at 6 hours
- Avoid aggressive over-resuscitation (worsens pulmonary complications)
Continuous monitoring: urine output, BUN, hematocrit, vital signs

Pain management

Aggressive analgesia required - IV opioids (morphine, hydromorphone, fentanyl) are acceptable and do not worsen outcomes
NSAIDs/ketorolac useful adjuncts
Avoid withholding analgesia out of concern for masking symptoms

Nutrition

Mild AP: Oral feeding as tolerated - initiate early (within 24-48 hours when pain improves and tolerated)
Severe AP: Enteral feeding preferred over parenteral (maintains gut barrier, reduces infectious complications)
- Nasojejunal or nasogastric tube feeding if oral route not possible
- Total parenteral nutrition (TPN) is a last resort
NPO is no longer recommended as standard practice for mild AP; early refeeding improves outcomes

Antibiotics

NOT indicated prophylactically in sterile necrosis
Indicated only for proven or strongly suspected infected pancreatic necrosis or concurrent infection (cholangitis, etc.)
Agents: carbapenems, fluoroquinolones, or metronidazole combinations (good pancreatic penetration)

Biliary pancreatitis - specific interventions

ERCP with sphincterotomy: Indicated within 24-48 hours if concurrent acute cholangitis or biliary obstruction (NOT for uncomplicated gallstone pancreatitis)
Cholecystectomy: Should be performed during the same admission in mild biliary AP (reduces recurrence risk); can be deferred in severe AP

Necrotizing pancreatitis

Sterile necrosis: Conservative management; antibiotics NOT indicated
Infected necrosis (suspected when clinical deterioration after day 7-10, fever, leukocytosis):
- CT-guided fine needle aspiration (FNA) for culture (though diagnosis increasingly made clinically)
- Step-up approach is now standard:
  1. Percutaneous or endoscopic drainage first
  2. Video-assisted retroperitoneal debridement (VARD) or endoscopic necrosectomy if drainage fails
  3. Open surgical necrosectomy (last resort - high mortality)
- Surgery delayed at least 4 weeks to allow "walled-off necrosis" to mature

ICU care

Patients with severe AP (persistent organ failure) require ICU-level monitoring for:

Respiratory: supplemental O2, may need mechanical ventilation for ARDS
Cardiovascular: vasopressors for shock refractory to fluids
Renal: renal replacement therapy for AKI

Differential Diagnosis

Peptic ulcer disease / perforated viscus
Cholecystitis, cholangitis, choledocholithiasis
Mesenteric ischemia
Bowel obstruction
Myocardial infarction (especially inferior MI)
Aortic dissection / AAA
Pericarditis
Diabetic ketoacidosis
Sickle cell crisis

Prognosis & Complications

Majority (~80%) have mild disease and recover within 1-2 weeks
~20% develop severe AP; mortality ~30% in this group
Overall mortality has decreased despite rising hospitalization rates

Late complications:

Pancreatic pseudocyst (most common fluid complication)
Walled-off necrosis
Splenic or portal vein thrombosis
Gastrointestinal bleeding
Gastric outlet obstruction
Exocrine insufficiency and endocrine insufficiency (diabetes) - especially after recurrent or necrotizing disease
Recurrent AP can progress to chronic pancreatitis (fibrosis, ductal changes, exocrine/endocrine failure)

Sources: Rosen's Emergency Medicine, 9e (Ch. 77); Sleisenger and Fordtran's Gastrointestinal and Liver Disease; Grainger & Allison's Diagnostic Radiology, 6e (Ch. 25)

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