It is now over fifty years since Guido Banti made his memorable declaration1 on the etiologic, pathologic and clinical features of the "disease" which bears his name. For many years, no serious challenge of his theories was advanced.
Not until well after the turn of the century did occasional reports appear showing that a variety of unrelated pathologic lesions, all located in the portal venous bed, could produce the clinical picture described by Warthin.2 In 1936, the initial report from the Spleen Clinic of the Presbyterian Hospital presented and supported a hypothesis at variance with the older, and then widely accepted, concept.3 This hypothesis has been reiterated in numerous communications.4
Continued experience has fortified the original position with a cumulative mass of supporting evidence. This material includes both clinical observations with long term follow-ups and postmortem confirmation of certain earlier cases in which, at the first reporting, there was
ROUSSELOT LM. COMBINED (ONE STAGE) SPLENECTOMY AND PORTACAVAL SHUNTS IN PORTAL HYPERTENSIONWith Observations on Venous Shunts in the Postsplenectomy Patient with Recurring Hemorrhage. JAMA. 1949;140(3):282–286. doi:10.1001/jama.1949.02900380022006
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