HPB
1. Acute Pancreatitis
Overview
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Definition: Inflammation of the exocrine pancreas, ranging from mild oedema to severe necrosis and systemic inflammation.
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Incidence:
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UK: 15–42 cases/100,000/year, rising by 2.7% annually.
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Mortality: 1–7% (up to 20% in necrosis).
Aetiology
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Primary causes:
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UK: Gallstones (75%) > Alcohol.
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Global: Alcohol most common.
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Other causes: Drugs (e.g., corticosteroids, azathioprine), trauma, hypercalcemia, hypertriglyceridemia, infections, autoimmune conditions.
Pathophysiology
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Key mechanisms:
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Acinar cell injury → Premature trypsin activation.
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Ethanol increases pancreatic ductal pressure and enzymatic activation.
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Calcium transients potentiate enzymatic activity.
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Complications: Pancreatic necrosis, vascular leakage, systemic inflammatory response.
Diagnostic Approach
Criteria (2 of 3 required):
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Typical abdominal pain.
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Serum amylase/lipase > 3× upper limit of normal.
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Imaging (CT/MRI/US) consistent with AP.
Laboratory Investigations
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Markers:
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Elevated lipase/amylase (supportive, not definitive).
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Elevated ALT > 150 IU/L indicates gallstone pancreatitis.
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C-reactive protein: Inflammation severity.
Imaging
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Preferred initial test: Ultrasound for gallstones.
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CT:
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After 48 hours if clinical deterioration.
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Identifies necrosis, abscesses.
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MRI/MRCP: Better for biliary obstructions and soft tissue resolution.
Prognostication in Acute Pancreatitis (AP)
Prognostication is critical to determine severity, predict complications, and guide management.
Systemic Inflammatory Response Syndrome (SIRS)
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Definition:
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Criteria: ≥2 of the following:
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Temperature <36°C or >38°C.
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Heart rate >90 bpm.
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Respiratory rate >20 breaths/min or PaCO₂ <32 mmHg.
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WBC count <4×10⁹/L or >12×10⁹/L.
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Persistent SIRS (>48 hours) is associated with:
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Mortality: ~25%.
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Higher risk of organ failure.
APACHE II (Acute Physiology and Chronic Health Evaluation II)
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Parameters:
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Physiological variables: Temperature, heart rate, MAP, pH, sodium, potassium, creatinine, hematocrit, WBC count.
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Age.
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Chronic health points (e.g., comorbidities).
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Scoring:
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8 indicates severe AP with a high risk of mortality.
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Strengths:
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Applicable at admission.
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Limitations:
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Complexity; requires detailed data.
Ranson’s Criteria
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Parameters: Separate for admission and 48 hours.
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At Admission:
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Age >55 years.
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WBC count >16×10⁹/L.
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Glucose >200 mg/dL (11.1 mmol/L).
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LDH >350 IU/L.
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AST >250 IU/L.
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At 48 Hours:
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Hematocrit drop >10%.
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BUN increase >5 mg/dL.
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Calcium <8 mg/dL.
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PO₂ <60 mmHg.
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Base deficit >4 mEq/L.
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Fluid sequestration >6 L.
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Scoring:
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≥3 criteria = severe AP.
Modified Glasgow Score (Imrie Score)
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Parameters (PANCREAS mnemonic):
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PaO₂ <8 kPa.
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Age >55 years.
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Neutrophilia: WBC count >15×10⁹/L.
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Calcium <2 mmol/L.
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Renal function: Urea >16 mmol/L.
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Enzymes: LDH >600 IU/L, AST >200 IU/L.
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Albumin <32 g/L.
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Sugar: Glucose >10 mmol/L.
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Scoring:
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≥3 indicates severe AP.
Bedside Index for Severity in Acute Pancreatitis (BISAP)
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Parameters:
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BUN >25 mg/dL.
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Impaired mental status (GCS <15).
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SIRS present.
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Age >60 years.
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Pleural effusion.
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Scoring:
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Each criterion = 1 point; total score out of 5.
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≥3 indicates high mortality risk.
Management
Initial Treatment
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Resuscitation:
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IV fluids (e.g., Ringer’s lactate) at 5–10 mL/kg/hour.
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Analgesics (opiates).
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Antiemetics.
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Monitoring:
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Blood glucose, arterial oxygenation, and acid-base status.
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Urine output to guide fluid therapy.
Severe Pancreatitis
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Supportive Care:
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High-dependency unit admission.
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Insulin for strict glucose control.
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Correction of hypocalcemia and hypomagnesemia.
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Antibiotics:
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Not recommended in non-infected pancreatitis.
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Indicated for proven infection of necrosis.
Collections in Severe Pancreatitis
Types of Collections
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Acute Peripancreatic Fluid Collections (APFCs):
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Develop <4 weeks after onset.
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Typically contain only fluid and lack a defined capsule.
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Often resolve spontaneously without intervention.
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Acute Necrotic Collections (ANCs):
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Contain both liquid and necrotic debris.
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Develop <4 weeks after onset.
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Walled-Off Necrosis (WON):
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Develops >4 weeks post-onset as a mature encapsulated collection.
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Contains necrotic debris and fluid.
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Pancreatic Pseudocysts:
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Encapsulated, fluid-only collections.
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Occur >4 weeks post-onset and lack solid necrotic debris.
Indications for Intervention
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Symptomatic collections causing pain, infection, or obstruction.
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Infected necrosis diagnosed by imaging or clinical signs (e.g., fever, leukocytosis).
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Persistent unresolving collections.
Management Approaches
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Observation:
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Asymptomatic collections can be monitored without immediate intervention.
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Drainage Techniques:
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Endoscopic drainage:
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Preferred for WON and pseudocysts when anatomically accessible.
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Use of lumen-apposing metal stents (LAMS) is common.
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Percutaneous drainage:
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Suitable for collections not accessible endoscopically.
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Can serve as a bridge to surgical management if needed.
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Surgical necrosectomy:
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Reserved for severe, refractory cases where other methods fail.
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Minimally invasive approaches are preferred over open surgery.
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Mild AP:
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Reintroduce diet as pain subsides.
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Severe AP:
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Early enteral feeding (nasogastric or nasojejunal).
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Avoid parenteral feeding unless enteral goals unmet.
Special Considerations
Alcohol-Induced Pancreatitis
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Prophylaxis for Withdrawal:
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Benzodiazepines, thiamine, folic acid.
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Prevention:
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Outpatient follow-up to reduce recurrence.
Gallstone Pancreatitis
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Cholecystectomy:
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Mild AP: Within the same admission or 2 weeks post-discharge.
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Severe AP: Delayed until inflammation resolves.
References
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Goodchild G, et al. Practical Guide to the Management of Acute Pancreatitis. Frontline Gastroenterology, 2019. Read Full Text
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Roberts SE, Akbari A, et al. The incidence of acute pancreatitis. Aliment Pharmacol Ther, 2013.
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Banks PA, Bollen TL, et al. Classification of acute pancreatitis--2012. Gut, 2013.