UNTIL the cause of atrophic cirrhosis is known, palliative measures will be necessary to prevent or control the complications which are known to be fatal within a relatively short time. The ultimate goal is the restoration of normal hepatic physiology. The atrophic cirrhotic liver is an inelastic fibrotic and shrunken organ which can neither adjust to changes in blood flow nor permit a sufficient amount of portal blood to reach its ischemic parenchyma. Under these conditions the liver and the entire splanchnic bed may harbor huge networks of abnormal arteriovenous and venovenous communications which bypass the sinusoids. These auxiliary passages or shunts may become inordinate, leading to vascular and lymphatic decompensation with resultant esophageal and other varices and ascites. It was our hope that ligations of the arterial components of this network would reduce the high pressure in the portal system, decrease the competition between venous and arterial constituents for
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Jacob K. Berman (1954) studied this question.
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