· Mayank Kashyap  · 5 min read

Acute pancreatitis

According to Love and Bailey's "A Short Practice of Surgery", acute pancreatitis is defined as an acute inflammatory condition of the pancreas with varying involvement of other regional tissues or remote organ systems.

According to Love and Bailey's "A Short Practice of Surgery", acute pancreatitis is defined as an acute inflammatory condition of the pancreas with varying involvement of other regional tissues or remote organ systems.

Introduction to Acute Pancreatitis

According to Love and Bailey’s “A Short Practice of Surgery”, acute pancreatitis is defined as an acute inflammatory condition of the pancreas with varying involvement of other regional tissues or remote organ systems.

Key Epidemiological Facts

  • Incidence: 5-80 cases per 100,000 population annually

  • Mild edematous pancreatitis accounts for 80% of cases

  • Severe necrotizing pancreatitis occurs in 20% of cases

  • Overall mortality: 5-10% (higher in severe cases)

Etiology and Risk Factors

Common Causes (According to Love & Bailey)

EtiologyFrequencyRemarks
Gallstones40-50%Most common cause worldwide.
Alcohol25-35%More common in males, chronic consumption.
Idiopathic10-20%No identifiable cause after investigation.
Hypertriglyceridemia1-4%Triglycerides >1000 mg/dL
ERCP-induced3-5%Iatrogenic, usually mild.
Drug-induced1-2%Azathioprine, thiazides, steroids, etc.
Trauma1-2%Blunt abdominal trauma, surgical injury.

Less Common Causes

  • Infections (mumps, coxsackievirus, CMV)

  • Autoimmune pancreatitis

  • Hypercalcemia

  • Pancreatic duct obstruction

  • Hereditary pancreatitis

  • Scorpion venom (Tityus trinitatis)

Pathophysiology

Key Mechanisms According to Love & Bailey

1. Autodigestion Theory

The fundamental pathological process involves premature activation of pancreatic enzymes within the pancreas itself:

  • Trypsinogen → Trypsin (key activating enzyme)

  • Activation of other proenzymes (phospholipase A2, elastase)

  • Digestion of pancreatic parenchyma and peripancreatic tissues

  • Release of inflammatory mediators

2. Inflammatory Cascade

  • Activation of complement system

  • Release of cytokines (TNF-α, IL-1, IL-6, IL-8)

  • Activation of coagulation system

  • Systemic inflammatory response syndrome (SIRS)

3. Gallstone Pathogenesis

“Common channel” hypothesis:

  • Gallstone impacts at ampulla of Vater

  • Obstruction of pancreatic duct

  • Increased intraductal pressure

  • Activation of pancreatic enzymes

  • Pancreatic injury and inflammation

Clinical Features

Cardinal Symptoms

  • Abdominal pain: Severe, constant, epigastric radiating to back

  • Nausea and vomiting: Profuse, not relieving pain

  • Fever: Low-grade in mild cases, high in severe cases

  • Abdominal distension: Due to ileus

Physical Examination Findings

FindingDescriptionSignificance
Abdominal tendernessEpigastric with guardingLocalized or generalized peritonitis
Cullen’s signPeriumbilical bruisingIndicates hemorrhagic pancreatitis
Grey Turner’s signFlank bruisingIndicates hemorrhagic pancreatitis
HypotensionSystolic BP <90 mmHgSevere pancreatitis with third spacing
TachycardiaHeart rate >100/minSystemic inflammatory response
TachypneaRespiratory rate >20/minPleural effusion or ARDS

Diagnosis and Investigations

Diagnostic Criteria (Atlanta Classification)

Requires at least 2 of the following 3 features:

  1. Abdominal pain consistent with acute pancreatitis

  2. Serum amylase or lipase >3 times upper limit of normal

  3. Characteristic findings on imaging (CT, MRI, or US)

Laboratory Investigations

TestFindingsClinical Significance
Serum amylaseElevated (>3× normal)Rises in 2-12 hours, normalizes in 3-5 days
Serum lipaseElevated (>3× normal)More specific, remains elevated longer
Complete blood countLeukocytosisMarked elevation in severe cases
Liver function testsElevated bilirubin/ALPSuggests gallstone etiology
Serum calciumHypocalcemiaPrognostic marker, indicates severity
CRPElevatedBest laboratory marker of severity

Imaging Studies

  • Abdominal ultrasound: First-line for detecting gallstones, assessing biliary tree

  • Contrast-enhanced CT: Gold standard for diagnosis and assessing severity

  • MRI/MRCP: Excellent for detecting ductal abnormalities, subtle necrosis

  • Endoscopic ultrasound: For detecting microlithiasis, tumors

Severity Assessment

Ranson’s Criteria (at admission and 48 hours)

At AdmissionDuring Initial 48 Hours
Age >55 yearsHct decrease >10%
WBC >16,000/mm³BUN increase >5 mg/dL
Blood glucose >200 mg/dLSerum calcium <8 mg/dL
LDH >350 IU/LArterial PO₂ <60 mmHg
AST >250 IU/LBase deficit >4 mEq/L
Fluid sequestration >6 L

Interpretation: Mortality: 0-2 criteria = 2%, 3-4 criteria = 15%, 5-6 criteria = 40%, >6 criteria = 100%

Management Principles

Initial Management (According to Love & Bailey)

  1. Resuscitation:

    • Aggressive IV fluid therapy (crystalloids)

    • Monitor urine output (target >0.5 mL/kg/hr)

    • Correct electrolyte abnormalities

  2. Pain Management:

    • Opioids (preferably patient-controlled analgesia)

    • Avoid morphine (may cause sphincter of Oddi spasm)

  3. Nutritional Support:

    • Mild cases: NPO initially, advance as tolerated

    • Severe cases: Enteral nutrition (nasojejunal preferred)

    • Parenteral nutrition if enteral route not feasible

  4. Monitoring:

    • Vital signs, fluid balance, organ function

    • Serial clinical assessment and laboratory tests

Specific Treatments

Gallstone Pancreatitis

  • Early ERCP (within 72 hours) for cholangitis or persistent biliary obstruction

  • Cholecystectomy during same admission for mild cases

  • Delayed cholecystectomy (after resolution) for severe cases

Severe Acute Pancreatitis

  • ICU admission for monitoring and organ support

  • Antibiotics for infected necrosis (proven or suspected)

  • Minimally invasive or open necrosectomy for infected necrosis not responding to antibiotics

Complications of Acute Pancreatitis

Local Complications

ComplicationTimingManagement
Acute peripancreatic fluid collection<4 weeksConservative, drainage if symptomatic
Pancreatic pseudocyst>4 weeksDrainage if >6cm or symptomatic
Acute necrotic collection<4 weeksAntibiotics if infected, drainage
Walled-off necrosis>4 weeksDrainage if infected or symptomatic
Pancreatic abscess>4 weeksPercutaneous or surgical drainage

Systemic Complications

  • Respiratory: Pleural effusion, ARDS, atelectasis

  • Cardiovascular: Hypotension, arrhythmias, myocardial depression

  • Renal: Acute kidney injury, renal failure

  • Hematological: DIC, thrombocytopenia

  • Metabolic: Hypocalcemia, hyperglycemia, hypertriglyceridemia

  • Gastrointestinal: Ileus, portal vein thrombosis, colonic necrosis

References

  • Love, R. J. M., & Bailey, H. (Latest Edition). A Short Practice of Surgery. London: Edward Arnold.

  • Chapter on Pancreatic Diseases in Love & Bailey’s textbook

  • American Gastroenterological Association Guidelines on Acute Pancreatitis

  • International Association of Pancreatology Guidelines

  • Atlanta Classification of Acute Pancreatitis (Revised)

Key Learning Points from Love & Bailey

“The management of acute pancreatitis requires a multidisciplinary approach with careful monitoring, aggressive fluid resuscitation, and timely intervention for complications.”

- Love & Bailey, A Short Practice of Surgery

Important Clinical Pearls

  • Early aggressive fluid resuscitation improves outcomes

  • Contrast-enhanced CT is the gold standard for diagnosis and staging

  • Enteral nutrition is preferred over parenteral nutrition

  • Infected pancreatic necrosis requires drainage and/or debridement

  • Cholecystectomy should be performed during the same admission for gallstone pancreatitis

This educational blog is based on the surgical textbook “A Short Practice of Surgery” by Love and Bailey.

For medical professionals and students only. Always consult current guidelines and local protocols.

© Medical Education Blog

  • Most common cause of acute pancreatitis is gall stones.

  • 2nd most common cause is alcohol.

  • Other cause include Secondary to trauma.

  • Iatrogenic causes e.g. post-ERCP(Endoscopic Retrograde CholangioPancreaticography).

  • Pathogenesis is Explained by Co-localisation theory, In which enzymes of pancreas activate inside it and start causing damage to pancreas.

  • Clinical features include pain in epigastric region, which relieves on bending.

  • Signs include grey turner sign, cullen sign and fox sign.

  • Diagnostic criteria involves any 2 positive out of imaging suggestive, three fold rise in serum amylase and pain in right epigastric region associated with acute pancreatitis.

  • Investigation of choice is (CECT)Contrast Enhanced Computed Tomography.

  • For chronic pancreatitis there is TIGARO classification where T stands for Toxins, I stands for Idiopathic, G stands for Genetic, A stands for Autoimmune, R stands for Recurrent, O stands for Obstructive.

  • Investigation of choice is MRCP.

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