Acute pancreatitis

Acute pancreatitis

1. Epidemiology

   • Incidence - 100-400 cases per 1 million population

2. Pathology

   • Autodigestion by activated pancreatic enzymes
     • 4 stage process
       • 1. oedema and fluid shift, which can cause shock. Vomiting compounds this. Fluid and enzymes into the peritoneal cavity, causing fat necrosis in the peritoneal cavity.
       • 2. Autodigestion of blood vessels - haemorrhage into extraperitoneal space. Blood staining causing bruising in flanks (Grey-Turners) and umbilical (Cullen's).
       • 3. Inflammation proceeds to necrosis, which can become infected.

3. Causes

   • Gallstones - 60% cases, ethanol is second.
   • GET SMASH'N
     • Gallstones, ethanol, Trauma, steroids (other drugs AZT), mumps (other viral infections e.g. coxsackie), AI e.g. SLE, scorpion bites, hyperlipidaemia (hyperPTH, hypothermia), neoplasia

4. Clinical features

   • Sudden onset, severe, epigastric pain, radiating to the back.
     • ±N and V, may include the whole abdomen and lead to shock
       • Diffusely tender abdomen with normal bowel sounds. But can resemble peritonitis in severe cases - px still, rigid abdomen, guarding, absent bowel sounds.

5. Investigations to diagnose

   • Serum AMY > 3 x ULN
     • Urine AMY or lipase can be used if clinical suspicion but normal sAMY.
       • uAMY elevated for 24-48 hours longer. Degree of elevation not related to the severity of the condition.
       • CT can show necrosis or tumour of the pancreas if given a few days.

6. Severity

   • Significance
     • Closer monitoring, prophylactic abx, consider for urgent ERCP and endoscopic sphincterotomy.
       • Most patients get better but severe acute cases - MOF sometimes. If they overcome acute phase then infected necrosis is possibility. CT aspiration confirms the diagnosis.
         • Infected necrosis most common cause of death in acute pancreatitis.
         • Infected necrosis - high WCC, low density changes, positive blood culture.
           • Open necrosectomy + cavity irrigation, retroperitoneal endoscopic necrosectomy using a modified nephroscope, transgastric endoscopic necrosectomy.
         • Pseudocyst can develop - lesser peritoneal sac.
   • Systems
     • Serial CRP measurements
     • Ransons, Glasgow or APACHE II
       • One point per item, >3 is severe
         • At admission: >55 years, glucose >11, LDH>500, AST >200, WCC >16
         • 48 hours later: HCT dropped >10%, urea >16, calcium <2, arterial pO2 < 8kPa, base deficit < 4mmol/L

7. Management

   • ABC
     • ABGs, IVs + fluid, catheter - UO maintained > 30ml/hour, analgesia, fluid balance chart.
       • NGT, NBM and antiemetics if V. May required antiemetics because opioids are going to be used.
       • PPIs or H2R antagonists in first week
   • Poorer prognosis if AKI or ARDS develops.
   • Prophylactic abx if predicted severe - for 7 days, BS e.g. meropenem, ciprofloxacin
   • Aetiology
     • Gallstones - USS and cholecystectomy to prevent further attacks
       • Urgent sphincterotomy if biliary disease and severe acute pancreatitis.