GI Bleeding in Patient with Known Cirrhosis
- Differential diagnosis:
- Variceal (50-90% of bleeds in pts with cirrhosis)
- Epidemiology:
- 50% stop spontaneously (vs 90% of all other UGIB)
- High rate of re-bleed within 6 weeks
- Two-year survival of 40% after first bleed
- Pathophysiology:
- Ohm's law: Portal pressure = portal flow x outflow resistance
- Portal HTN results from increased flow from splanchnic vasodilatation and increased resistance from distorted hepatic sinusoids
- Varices form to relieve portal HTN and shunt portal drainage into systemic circulation
- Occur when hepatic venous pressure gradient (portal pressure - hepatic vein pressure) is greater than 10mm Hg
- Ohm's law: Portal pressure = portal flow x outflow resistance
- Epidemiology:
- Portal hypertensive gastropathy (snakeskin stomach)
- Results form increased gastric mucosal blood flow, and presents as oozing
- Treatment involves decreasing portal pressure: propranolol, TIPS, portocaval shunt, transplantation
- Gastric antral vascular ectasia (watermelon stomach)
- Ectatic mucosal vessels, presents as episodic bleeding
- Treat with endoscopic coagulation (e.g. Argon)
- Peptic ulcer disease/gastritis/esophagitis
- Mallory-Weiss tear
- Variceal (50-90% of bleeds in pts with cirrhosis)
- Management:
- As in all UGIB, initial step is stabilization and evaluation of ABCs
- NG lavage should be performed to confirm diagnosis and determine if high risk bleed is present (i.e. fresh blood)
- However, can yield false negative if pylorus is closed - presence of bilious aspirate indicates that duodenum has been interrogated
- Stool should be examined, but is not a reliable discriminator between upper and lower sources, as rapid UGIB can result in hematochezia
- NG lavage should be performed to confirm diagnosis and determine if high risk bleed is present (i.e. fresh blood)
- Medical therapy:
- Octreotide: inhibits vasodilatory hormones such as glucagon, resulting in splanchnic vasoconstriction and decreased portal flow
- Effective in controlling bleeding, but no mortality benefit
- Acid suppression: promotes clot formation
- Only studied in PUD, but should be used given that cause of bleed unclear until EGD, and same hemostatic principles apply
- Antibiotics: bacterial superinfection present in 20% of UGIB in cirrhotics, probably from translocation
- Optimal antibiotic unknown, but should cover GNRs (3rd gen cephalosporin, fluoroquinolone)
- Should treat for short course (e.g. 7d) barring identification of another infection (e.g. pneumonia, bacteremia)
- Octreotide: inhibits vasodilatory hormones such as glucagon, resulting in splanchnic vasoconstriction and decreased portal flow
- Endoscopic therapy:
- Sclerotherapy
- Band ligation: shown to be superior to sclerotherapy (see attached NEJM article)
- Rescue therapy:
- Balloon tamponade
- Surgery (shunt, transection, devascularization)
- TIPS
- Prophylaxis
- Beta blockers: attenuate vasodilatory tone of mesenteric arterioles, thus decreasing portal flow
- Nitrates: may increase mortality, so should not be used routinely
- As in all UGIB, initial step is stabilization and evaluation of ABCs
(Christopher Woo MD, 9/10/10)