Portal pressure, presence of gastroesophageal varices and variceal bleeding
Article first published online: 6 DEC 2005
Copyright © 1985 American Association for the Study of Liver Diseases
Volume 5, Issue 3, pages 419–424, May/June 1985
How to Cite
Garcia-Tsao, G., Groszmann, R. J., Fisher, R. L., Conn, H. O., Atterbury, C. E. and Glickman, M. (1985), Portal pressure, presence of gastroesophageal varices and variceal bleeding. Hepatology, 5: 419–424. doi: 10.1002/hep.1840050313
- Issue published online: 6 DEC 2005
- Article first published online: 6 DEC 2005
- Manuscript Accepted: 28 JAN 1985
- Manuscript Received: 17 OCT 1984
- Medical Research Service
This study was performed to examine the relationships between portal pressure measurements and the presence of esophagogastric varices, the size of varices and the occurrence of hemorrhage from varices in 93 patients with alcoholic cirrhosis, using standardized measurements of portal pressure by hepatic vein catheterization.
The mean hepatic vein pressure gradient (HVPG) was significantly higher in 49 patients who had bled from varices than in 44 cirrhotic patients who had not (20.4 ± 5.1 vs. 16.0 ° 5. 2; p < 0.001). None of the 49 patients who had bled from varices had an HVPG <12 mm Hg. Among the 87 patients who had been examined by endoscopy for varices, all 72 with varices had an HVPG > 12 mm Hg. Six of 15 cirrhotic patients without varices had HVPG < 12 mm Hg.
The mean HVPG in the 15 patients without varices (15.1 ± 6.8 mm Hg) was lower than the 72 patients with varices (19.3 ± 4.8 mm Hg; p < 0.01).
Of the 72 patients with varices, 40 had large varices, 28 had small varices, and in four patients variceal size coukt not be assessed adequately. The mean HVPG was similar in the patients with large or small varices (19.8 ± 4.8 vs. 18.3 ± 5.0 mm Hg; p < 0.10).
There was a positive relationship between the presence of large varices and the occurrence of bleeding from varices. Thirty-three of the 46 patients who had bled from varices had large varices (72%) compared to 7 of the 22 who had not bled from varices (32%) (p < 0.01).
The mean HVPG was similar in groups with large varices who had bled (20.3 ± 4.9) and in the group with small varices who had bled (20.2 ± 6.2 mm Hg) (p > 0.10). The mean HVPG in the groups of patients with large varices who had not bled was similar to those with small varices who had not bled (17.3 ± 3.1 vs. 16.7 ± 3.2 mm Hg) (p > 0.10). In both groups, the pressure was lower in those who had not bled.
We confirm previous observations that an HVPG > 12 mm Hg is necessary for the occurrence of variceal hemorrhage. We note in addition that this pressure gradient is necessary for the appearance of gastroesophageal varices. Elevated portal pressure plays a major role in the development of esophageal varices, but other factors contribute to the precipitation of hemorrhage from varices. All of these factors, which include size of the varix, thickness of the wall and transmural pressure are integrated in the wall stress formula, which is based on the LaPlace formula. Risk factors are multiple and variable and may interact in the individual patient to precipitate variceal hemorrhage.