TY - JOUR
T1 - Treatment of bleeding from portal hypertensive gastropathy by portacaval shunt
AU - Orloff, Marshall J.
AU - Orloff, Mark S.
AU - Orloff, Susan L.
AU - Haynes, Kevin S.
N1 - Funding Information:
Abbreviations: PHG, portal hypertensive gastropathy; PCS, portacaval shunt; PV, portal vein; 1VC, inferior vena cava; PSE, portal-systemic encephalopathy. From the 1Department of Surgery and 2Division of Gastroenterology, University of California, San Diego, Medical Center, San Diego, CA. Received April 29, 1994; accepted November 16, 1994. Supported in part by the National Institutes of Hea\]th, Bethesda, MD, grant no. DK41920. Presented in preliminary form at the annual meeting of the American Asso-clarion for the Study of Liver Diseases, at Digestive Disease Week, May 15, 1994, New Orleans, LA. Dr Mark S. Orloffs present address is Department of Surgery, University of Rochester Medical Center, Rochester, NY. Dr Susan L. Orloffs present address is Department of Surgery, University of California, San Francisco, Medical Center, San Francisco, CA. Address reprint requests to: Marshall J. Orloff, MD, Department of Surgery, UCSD Medical Center, 200 West Arbor Dr, San Diego, CA 92103-8999. Copyright © 1995 by the American Association for the Study of Liver Diseases. 9270-9139/95/2104-001853.00/0
PY - 1995/4
Y1 - 1995/4
N2 - Portal hypertensive gastropathy is a vascular disorder of the gastric mucosa distinguished by ectasia of the mucosal capillaries and submucosal veins without inflammation. During 1988 to 1993,12 patients with biopsy-proven cirrhosis (10 alcoholic, 2 posthepatitic) were evaluated and treated prospectively by portacaval shunt for active bleeding from severe portal hypertensive gastropathy. Eleven patients had been hospitalized for bleeding three to nine times previously, and one was bleeding uncontrollably for the first time. Requirement for blood transfusions ranged from 11 to 39 units cumulatively, of which 8 to 30 units were required specifically to replace blood lost from portal hypertensive gastropathy. Admission findings were ascites in 9 patients, jaundice in 8, severe muscle wasting in 10, hyperdynamic state in 9. Child's risk class was C in 7, B in 4, A in 1. Ten of the 12 patients had previously received repetitive endoscopic sclerotherapy for esophageal varices, which has been reported to precipitate portal hypertensive gastropathy. Eight patients had failed propranolol therapy for bleeding. Portacaval shunt was performed emergently in 11 patients and electively in 1, and permanently stopped bleeding in all by reducing the mean portal vein-inferior vena cava pressure gradient from 251 to 16 mm saline. There were no operative deaths, and two unrelated late deaths after 13 and 24 months. During 1 to 6.75 years of follow-up, all shunts remained patent by ultrasonography, the gastric mucosa reverted to normal on serial endoscopy, and there was no gastrointestinal bleeding. Recurrent portal-systemic encephalopathy developed in only 8% of patients. Quality of life was generally good. It is concluded that portacaval shunt provides definitive treatment of bleeding portal hypertensive gastropathy by eliminating the underlying cause, and makes possible prolonged survival with an acceptable quality of life.
AB - Portal hypertensive gastropathy is a vascular disorder of the gastric mucosa distinguished by ectasia of the mucosal capillaries and submucosal veins without inflammation. During 1988 to 1993,12 patients with biopsy-proven cirrhosis (10 alcoholic, 2 posthepatitic) were evaluated and treated prospectively by portacaval shunt for active bleeding from severe portal hypertensive gastropathy. Eleven patients had been hospitalized for bleeding three to nine times previously, and one was bleeding uncontrollably for the first time. Requirement for blood transfusions ranged from 11 to 39 units cumulatively, of which 8 to 30 units were required specifically to replace blood lost from portal hypertensive gastropathy. Admission findings were ascites in 9 patients, jaundice in 8, severe muscle wasting in 10, hyperdynamic state in 9. Child's risk class was C in 7, B in 4, A in 1. Ten of the 12 patients had previously received repetitive endoscopic sclerotherapy for esophageal varices, which has been reported to precipitate portal hypertensive gastropathy. Eight patients had failed propranolol therapy for bleeding. Portacaval shunt was performed emergently in 11 patients and electively in 1, and permanently stopped bleeding in all by reducing the mean portal vein-inferior vena cava pressure gradient from 251 to 16 mm saline. There were no operative deaths, and two unrelated late deaths after 13 and 24 months. During 1 to 6.75 years of follow-up, all shunts remained patent by ultrasonography, the gastric mucosa reverted to normal on serial endoscopy, and there was no gastrointestinal bleeding. Recurrent portal-systemic encephalopathy developed in only 8% of patients. Quality of life was generally good. It is concluded that portacaval shunt provides definitive treatment of bleeding portal hypertensive gastropathy by eliminating the underlying cause, and makes possible prolonged survival with an acceptable quality of life.
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U2 - 10.1016/0270-9139(95)90248-1
DO - 10.1016/0270-9139(95)90248-1
M3 - Article
C2 - 7705773
AN - SCOPUS:0028964198
SN - 0270-9139
VL - 21
SP - 1011
EP - 1017
JO - Hepatology
JF - Hepatology
IS - 4
ER -