THE DIVERSION OF portal venous blood into the systemic circulation through naturally occurring collateral vessels has long been recognized as a concomitant of processes which produce portal hypertension. Many of these vessel systems are familiar to the clinician as the hemorrhoidal, esophageal, and anterior abdominal wall plexuses. These various plexuses might be termed the normal porta-systemic communications, in that they are believed to be normally patent and respond to increased portal pressure by dilatation.
Splenoportography has enabled clinicians to recognize a second group of collateral pathways which have been designated the embryonal porta-systemic communications.1 Presumably, these are embryonic channels which are thought to be reopened or recanalized by the high pressures obtained in the portal system. Such pathways have been noted in approximately 14% of patients with portal hypertension in separate studies by Hamilton and Sullivan 1 and by Rousellot et al.2 These communications have most commonly been