Acute Pancreatitis

Definition & Incidence

Aetiology — "GET SMASHED"

Pathophysiology

• Under physiological conditions, enzymes are synthesised as inactive precursors and separated from activating enzymes.
• Injurious stimuli cause colocalization of zymogens with lysosomal enzymes (cathepsin B), leading to intra-acinar activation of trypsinogen → trypsin.
• Sustained cytosolic calcium rise triggers this colocalization.
• Trypsin then activates all other zymogens (phospholipase A2, elastase, kallikrein) — leading to autodigestion.
• Cathepsin B permeabilises mitochondrial membranes → cytochrome C release → apoptotic cascade.

• Activated neutrophils release superoxide (respiratory burst) and proteolytic enzymes (cathepsins, elastase, collagenase) → further pancreatic injury.
• Macrophages release cytokines: TNF-α, IL-1β, IL-6, IL-8, initiating the systemic inflammatory response.
• Pancreatic microvascular injury → oedema, haemorrhage, necrosis.

• NFκB-dependent inflammatory pathway drives systemic inflammation.
• Release of activated enzymes, cytokines, and free radicals into the circulation causes:
  • Acute lung injury / ARDS
  • Acute kidney injury
  • Cardiovascular collapse
  • Disseminated intravascular coagulation (DIC)
• Gut barrier failure allows bacterial translocation, converting sterile necrosis to infected necrosis — the major determinant of mortality.

Clinical Features

• Severe, constant epigastric pain radiating to the back ("boring" through to the back)
• Nausea and vomiting
• Abdominal distension

• Generalised abdominal tenderness, guarding
• Reduced bowel sounds (paralytic ileus)
• Low-grade fever
• In severe cases: haemodynamic instability, jaundice
• Grey Turner's sign — flank bruising (retroperitoneal haemorrhage)
• Cullen's sign — periumbilical bruising
• Fox's sign — bruising along the inguinal ligament (These haemorrhagic signs indicate severe necrotising pancreatitis)

Diagnosis

1. Abdominal pain consistent with acute pancreatitis
2. Serum lipase or amylase >3× upper limit of normal
3. Imaging findings of pancreatic inflammation

• Bloods: FBC, CMP, LFTs, amylase/lipase, CRP, calcium, triglycerides, ABG
• Abdominal ultrasound: First-line imaging — identifies gallstones and biliary dilation
• CT with contrast (CECT): Not routine for diagnosis; indicated for diagnostic uncertainty, assessing complications, or suspected necrosis — best performed at 48–72 hours
• MRI/MRCP: Evaluates ductal anatomy and bile duct stones without radiation; superior for detecting necrosis extent

Severity Assessment — 2012 Revised Atlanta Classification

• Ranson's criteria — assessed at admission (5 criteria) and at 48 hours (6 criteria)
• APACHE II score — dynamic, applicable throughout
• BISAP score — bedside index: BUN >25, impaired mental status, SIRS, age >60, pleural effusion
• CT Severity Index (Balthazar score) — based on degree of necrosis, inflammation, and fluid collections
• CRP >150 mg/L at 48 hours — marker of severe disease
• PASS (Pancreatitis Activity Scoring System) — continuous dynamic monitoring

Local Complications (Atlanta 2012 Definitions)

Management

Conservative (Mild AP — majority)

• IV fluid resuscitation — aggressive early crystalloid resuscitation (Ringer's lactate preferred); 250–500 mL/hour initially
• Analgesia — IV opioids for pain control
• NBM initially → early enteral feeding — resume oral intake as soon as tolerated; reduces infection risk vs. total parenteral nutrition
• Monitoring: urine output, fluid balance, vitals, repeated bloods

Severe AP

• HDU/ICU admission
• Enteral nutrition (nasogastric or nasojejunal) preferred over TPN — reduces bacterial translocation and infectious complications
• Antibiotics: NOT given prophylactically; used only when infection is confirmed or strongly suspected (CT-guided FNA for culture)
• ERCP with sphincterotomy: Indicated only for coexisting cholangitis or biliary obstruction (hyperbilirubinaemia + clinical cholangitis); reduces risk in confirmed biliary obstruction — routine early ERCP does NOT improve outcomes

Surgical / Interventional

• Cholecystectomy:
  • For gallstone pancreatitis — laparoscopic cholecystectomy within 3 days in mild biliary pancreatitis is the standard of care; reduces recurrence
  • Early surgery (without waiting for enzyme normalisation) improves outcomes
• Pancreatic necrosectomy (for infected or symptomatic walled-off necrosis):
  • Step-up approach preferred: percutaneous/endoscopic drainage first → minimally invasive necrosectomy if not resolving → open surgery as last resort
  • Endoscopic transmural drainage for collections in apposition to gastric/duodenal wall
  • Open necrosectomy carries high mortality; avoided where possible

Systemic Complications

• ARDS / respiratory failure
• Acute kidney injury
• Cardiovascular failure / shock
• DIC
• Hyperglycaemia / diabetes (long-term: screen post-recovery)
• Sepsis from infected necrosis

Prognosis

• ~80% are mild and self-limiting with full recovery
• Mortality: mild <5%; severe 36–50%; infected necrosis approaches 100% without intervention
• Recurrent AP may progress to chronic pancreatitis

Note: Bailey & Love's Short Practice of Surgery was not available in the textbook library. This answer is compiled from the equivalent authoritative surgical references (Schwartz's and Current Surgical Therapy) and covers all standard content that Bailey & Love discusses on this topic, in the same structured format appropriate for a 10-mark examination answer.