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Donovan C. Browne, M.D.; George E. Welch, M.D.
JAMA. 1955;158(2):106-109. doi:10.1001/jama.1955.02960020012004.
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Portal hypertension and its relation to liver disease, the development of ascites, and upper gastrointestinal hemorrhage has increasingly engaged the interest of the physician and laboratory worker in recent years. The impetus of this renewed study is due to a great degree to the work of such men as Whipple,1 and Blakemore and Lord2 on portal shunt for the relief of portal hypertension. Although substantial progress has been made in answering some of the perplexing questions, the understanding of the pathological physiology of these conditions remains to some extent theoretical and confusing at the present time. It is well accepted that portal hypertension may clinically and anatomically be divided into two groups. The first is the extrahepatic group in which the basis for the increased portal pressure arises from obstruction in the extrahepatic portal vein. A number of pathological states may contribute to this, such as post-traumatic thrombosis


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