Acute pancreatitis

Epidemiology
1. Incidence - 100-400 cases per 1 million population
Pathology
1. Autodigestion by activated pancreatic enzymes
  1. 4 stage process
    1. 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. 2. Autodigestion of blood vessels - haemorrhage into extraperitoneal space. Blood staining causing bruising in flanks (Grey-Turners) and umbilical (Cullen's).
    3. 3. Inflammation proceeds to necrosis, which can become infected.
Causes
1. Gallstones - 60% cases, ethanol is second.
2. GET SMASH'N
  1. Gallstones, ethanol, Trauma, steroids (other drugs AZT), mumps (other viral infections e.g. coxsackie), AI e.g. SLE, scorpion bites, hyperlipidaemia (hyperPTH, hypothermia), neoplasia
Clinical features
1. Sudden onset, severe, epigastric pain, radiating to the back.
  1. ±N and V, may include the whole abdomen and lead to shock
    1. Diffusely tender abdomen with normal bowel sounds. But can resemble peritonitis in severe cases - px still, rigid abdomen, guarding, absent bowel sounds.
Investigations to diagnose
1. Serum AMY > 3 x ULN
  1. Urine AMY or lipase can be used if clinical suspicion but normal sAMY.
    Anmerkungen:
    - uAMY elevated for 24-48 hours longer. Degree of elevation not related to the severity of the condition.
    1. CT can show necrosis or tumour of the pancreas if given a few days.
Severity
1. Significance
  1. Closer monitoring, prophylactic abx, consider for urgent ERCP and endoscopic sphincterotomy.
    1. 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.
      Anmerkungen:
      - Infected necrosis most common cause of death in acute pancreatitis.
      1. Infected necrosis - high WCC, low density changes, positive blood culture.
        Open necrosectomy + cavity irrigation, retroperitoneal endoscopic necrosectomy using a modified nephroscope, transgastric endoscopic necrosectomy.
      2. Pseudocyst can develop - lesser peritoneal sac.
2. Systems
  1. Serial CRP measurements
  2. Ransons, Glasgow or APACHE II
    1. One point per item, >3 is severe
      1. At admission: >55 years, glucose >11, LDH>500, AST >200, WCC >16
      2. 48 hours later: HCT dropped >10%, urea >16, calcium <2, arterial pO2 < 8kPa, base deficit < 4mmol/L
Management
1. ABC
  1. ABGs, IVs + fluid, catheter - UO maintained > 30ml/hour, analgesia, fluid balance chart.
    1. NGT, NBM and antiemetics if V. May required antiemetics because opioids are going to be used.
    2. PPIs or H2R antagonists in first week
2. Poorer prognosis if AKI or ARDS develops.
3. Prophylactic abx if predicted severe - for 7 days, BS e.g. meropenem, ciprofloxacin
4. Aetiology
  1. Gallstones - USS and cholecystectomy to prevent further attacks
    1. Urgent sphincterotomy if biliary disease and severe acute pancreatitis.

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Acute pancreatitis

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