GI Bleeding, Upper

• Differential:
  • Ulcerations/erosions:
    • Infectious: H pylori, HSV, CMV, candida
    • Drugs: NSAIDs, ASA, pill-induced
  • Portal hypertensive: varices, portal hypertensive gastropathy
  • Vascular malformations: AVM, GAVE, Dieulafoy’s lesion
  • Traumatic: Mallory-Weiss, foreign body
  • Tumor
• Initial treatment:
  • NGT is specific, but not sensitive for detection of active upper GI bleed
    • If clear contents return, one cannot be certain that the duodenum has been interrogated
    • Bilious return indicates that there is no post-pyloric bleeding
  • Acid suppression: increase in gastric pH to >6 facilitates platelet aggregation
    • High dose PPI (IV bolus + continuous infusion) has been most rigorously studied (NEJM 2007) and reduces the need for endoscopic intervention, but not the risk of rebleed, need for surgical intervention, or mortality
  • Reversal of coagulopathy: in this patient, given her AKI, she is at risk for uremic platelet dysfunction
    • dDAVP (desmopressin): stimulates release of vWF-factor VIII from endothelium
    • Estrogen: mechanism unknown
    • Cryoprecipitate (approved by most Jehovah’s Witnesses): includes fibrinogen, vWF-VIII, and XIII
• Endoscopic findings of PUD: key is differentiating patients at high risk of rebleed
  • Active bleeding: 90%
  • Non-bleeding visible vessel: 50%
  • Adherent clot: 25%
  • Ooozing: 20%
  • Flat spot: 10%
  • Clean base: 5%

(Christopher Woo MD, 2/15/11)