Journal of hepatology · 1996
The impact of endoscopic variceal ligation on the pressure of the portal venous system.
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Lo G H, Liang H L, Lai K H, Chang C F, Hwu J H, Chen S M, Lin C K, Chiang H T
Аннотация
BACKGROUND/AIMS: Endoscopic variceal ligation is a viable substitute for injection sclerotherapy. It is still not known how endoscopic variceal ligation may influence the portal venous system. To clarify this issue we investigated the impact of endoscopic variceal ligation on the pressure of the portal venous system.
METHODS: Twenty-nine patients with a history of esophageal variceal bleeding but without ascites were enrolled. All had cirrhosis; 63% of them were post-hepatitic. Ligation was performed at intervals of 2-3 weeks until all the varices were obliterated. Portal venograms were performed before institution of ligation and after variceal obliteration to assess venographic findings and pressure changes. The pressures of the main portal vein, splenic vein and superior mesenteric vein were recorded.
RESULTS: Twenty-five patients completed the study. A mean of 4.4 sessions (range: 2-7) of ligation over a period of 2 months was needed. Seventeen (68%) patients experienced elevated pressure and eight (32%) patients reduced pressure after ligation. Mean (median) pressure changes were as follows: portal venous pressure, 26.5 +/- 4.7 (25.0) mmHg vs. 28.2 +/- 7.2 (28.0) mmHg (p > 0.05); splenic venous pressure, 28.2 +/- 4.9 (26.0) mmHg vs. 29.0 +/- 6.8 (29.0) mmHg (p > 0.05); superior mesenteric venous pressure, 28.4 +/- 6.0 (27.0) mmHg vs. 29.5 +/- 7.0 (29.0) mmHg (p > 0.05). Five patients (20%) experienced rebleeding before variceal obliteration; all of them presented elevated portal pressures after variceal obliteration. Among the eight patients with decreased portal pressure, seven (87%) had other major collaterals apart from esophageal varices, compared to three out of the 17 (18%) patients with elevated portal pressure who had other major collaterals (p < 0.01).
CONCLUSIONS: Among patients receiving endoscopic variceal ligation, 68% experienced elevated portal pressure, while 32% had decreased portal pressure. Elevation of portal pressure after variceal ligation may be an important factor in variceal rebleeding. The presence of other major collaterals apart from esophageal varices may be responsible for the decrease in portal pressure after obliteration of esophagel varices.
METHODS: Twenty-nine patients with a history of esophageal variceal bleeding but without ascites were enrolled. All had cirrhosis; 63% of them were post-hepatitic. Ligation was performed at intervals of 2-3 weeks until all the varices were obliterated. Portal venograms were performed before institution of ligation and after variceal obliteration to assess venographic findings and pressure changes. The pressures of the main portal vein, splenic vein and superior mesenteric vein were recorded.
RESULTS: Twenty-five patients completed the study. A mean of 4.4 sessions (range: 2-7) of ligation over a period of 2 months was needed. Seventeen (68%) patients experienced elevated pressure and eight (32%) patients reduced pressure after ligation. Mean (median) pressure changes were as follows: portal venous pressure, 26.5 +/- 4.7 (25.0) mmHg vs. 28.2 +/- 7.2 (28.0) mmHg (p > 0.05); splenic venous pressure, 28.2 +/- 4.9 (26.0) mmHg vs. 29.0 +/- 6.8 (29.0) mmHg (p > 0.05); superior mesenteric venous pressure, 28.4 +/- 6.0 (27.0) mmHg vs. 29.5 +/- 7.0 (29.0) mmHg (p > 0.05). Five patients (20%) experienced rebleeding before variceal obliteration; all of them presented elevated portal pressures after variceal obliteration. Among the eight patients with decreased portal pressure, seven (87%) had other major collaterals apart from esophageal varices, compared to three out of the 17 (18%) patients with elevated portal pressure who had other major collaterals (p < 0.01).
CONCLUSIONS: Among patients receiving endoscopic variceal ligation, 68% experienced elevated portal pressure, while 32% had decreased portal pressure. Elevation of portal pressure after variceal ligation may be an important factor in variceal rebleeding. The presence of other major collaterals apart from esophageal varices may be responsible for the decrease in portal pressure after obliteration of esophagel varices.