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pancreatitis

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pancreatitis

aetiology or contributing factors:

  • cholelithiasis (gallstones) / choledocholithiasis
  • others (<10%):
    • trauma - penetrating or blunt
    • pregnancy - any trimester, post-partum
    • post-ERCP
    • hypercalcaemia
    • penetrating peptic ulcer
    • drugs, toxins - oestrogen, phenformin, steroids, rifampicin, tetracyclines, isoniazid, thiazides, frusemide / furosemide / Lasix, salicylates, indomethacin, warfarin, paracetamol (acetaminophen), ethacrynic acid, glucagon-like peptide-1 (GLP-1) peptide analogs (eg. Ozempic), gabapentinoids
    • obstruction - neoplasms, diverticula, roundworms, benign
    • viral infection - mumps, hep A,B,C, IM, Coxsackie Gp B, Rubella, CMV, EBV, Varicella, Echo, Adenovirus
    • bacterial infection - typhoid, paratyphoid, scarlet fever, strept. food poisoning, dysentery, TB, mycoplasma, MAIS, legionella, leptospirosis, campylobacter
    • other infection - ascariasis, clonorchiasis
    • cystic fibrosis
    • with prominent eosinophilia:
      • drug induced pancreatitis
        • esp. NSAIDs, metronidazole, sulfonamides, ACE inhibitors, diuretics, immunosuppressants
      • parasitic infections (usually from tropical regions):
        • invasive helminth or protozoal infections (such as Strongyloides or Schistosoma)
      • autoimmune pancreatitis (AIP) and vasculitis
        • eosinophilic granulomatosis with polyangiitis (EGPA / Churg-Strauss syndrome)
      • severe food allergies (rarely cause pancreatitis)
      • incidental concurrent allergic event unrelated to the pancreatitis
      • hypereosinophilic syndrome (HES)

clinical features:

  • mid-epigastric or LUQ pain:
    • usually constant, boring, often radiates to back as well as flanks, chest or lower abdomen
    • variable intensity
    • worse supine & relieved by sitting with trunk & knees flexed
  • nausea & vomiting are common
  • abdominal bloating due to GIT hypomotility frequent
  • examination:
    • epigastric tenderness
    • may have low grade fevers, tachycardia, and hypotension
    • 10% have resp. symptoms due to atelectasis, pleural effusion (usually left sided) & rarely, ARDS
    • peritonitis is a late finding
    • rarely, haemorrhagic pancreatitis occurs which may cause Cullen sign & Grey Turner sign as bruising tracks to flanks & around umbilicus.
    • hypotension may result from fluid third-spacing, increased vascular permeability, vasodilatation, cardiac depression & vomiting.

investigation:

  • serum lipase rise early & are reasonably sensitive (90%) but not totally specific (75% for amylase, 90% for lipase)
  • erect CXR, AXR useful to exclude other pathology such as perforated viscus & may show a pleural effusion
    • calcification suggests chronic pancreatitis
  • biliary US may show cholelithiasis (gallstones), pancreatic oedema & pseudocysts, but is insensitive in Dx of acute pancreatitis
  • CT abdomen is insensitive in early or mild disease

prognostic markers:

  • Ranson criteria for predicting mortality risk from acute pancreatitis:
    • on admission:
      • age > 55yrs
      • blood sugar > 11mM
      • WCC > 16,000
      • AST > 250
      • LDH > 400
    • 48hrs later:
      • haematocrit fall > 10%
      • BUN rise > 1.8mM
      • fall in Ca to < 1.9mM
      • fall in PaO2 below 60mmHg 
      • rapid fluid sequestration > 6L
      • base deficit > 4 meq/L
  • criteria interpretation:
    • < 3 markers = <1% mortality
    • 3-4 markers = 16% mortality
    • 5-6 markers = 40% mortality
    • 6 markers = 100% mortality

management:

  • 90% recover with supportive care of “resting” the pancreas:
    • nil oral or clear fluids (some advocate NG tube but no evidence to support benefit)
    • IV fluid resuscitation to ensure urine output 100ml/h
    • unstable patients may require invasive monitoring
    • parenteral narcotics & antiemetics
    • if severe, IV imipenem decreases sepsis rate but not mortality
  • in biliary pancreatitis:
    • urgent decompression is indicated if there is persistent biliary obstruction
    • transient obstruction only, then elective cholecystectomy once inflammation subsides
  • see acute severe hypertriglyceridaemia (SHTG) for emergent Mx of this cause including possible plasmapheresis
  • acute fluid collections are rarely symptomatic & frequently resolve spontaneously
  • laparatomy is indicated for haemorrhage control & abscess drainage

disposition:

  • home if:
    • mild alcoholic pancreatitis with no evidence of systemic complications and,
    • able to tolerate oral fluids, and,
    • pain is well controlled
    • follow up in 24-48hrs
  • otherwise, admit under general surgery unit.
  • ALL patients with pancreatitis due to biliary causes should be admitted.
  • high risk patients should be admitted to a hospital with ICU capabilities
  • NB. a 2024 study suggests ~1/3rd of patients will develop exocrine pancreas insufficiency (EPI) by 12 months as assessed by measuring fecal elastase 1 (FE-1) levels 1)
pancreatitis.1781686222.txt.gz · Last modified: 2026/06/17 08:50 by gary1

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