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
- Ulcerations/erosions:
- 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
- NGT is specific, but not sensitive for detection of active upper GI bleed
- 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)