TY - JOUR
T1 - Contrasting Patterns of Ascites Formation in Hepatic Cirrhosis
AU - Witte, Marlys Hearst
AU - Witte, Charles L.
AU - Cole, William R.
AU - Koehler, P. Ruben
PY - 1969/6/2
Y1 - 1969/6/2
N2 - In two patients with hepatic cirrhosis and massive ascites, the composition of lymph (thoracic duct, intestinal, and hepatic) and ascitic fluid pointed to a different pathogenesis of ascites and portal hypertension. Measurements of hepatic blood flow, splenoportography, selective arteriography, and laparotomy delineated the contrasting portal circulatory dynamics. The data suggest that in the first patient excess thoracic duct lymph and ascitic fluid originated primarily from the liver in response to increased resistance to hepatic venous outflow. In the second patient these fluids originated primarily from the extrahepatic portal bed in response to increased resistance to portal venous inflow. Portal hypertension in the first patient was due to moderately increased postsinusoidal resistance coupled with high portal blood flow, and in the second it was due to very high presinusoidal resistance but low portal blood flow. Surgical treatment was designed accordingly.
AB - In two patients with hepatic cirrhosis and massive ascites, the composition of lymph (thoracic duct, intestinal, and hepatic) and ascitic fluid pointed to a different pathogenesis of ascites and portal hypertension. Measurements of hepatic blood flow, splenoportography, selective arteriography, and laparotomy delineated the contrasting portal circulatory dynamics. The data suggest that in the first patient excess thoracic duct lymph and ascitic fluid originated primarily from the liver in response to increased resistance to hepatic venous outflow. In the second patient these fluids originated primarily from the extrahepatic portal bed in response to increased resistance to portal venous inflow. Portal hypertension in the first patient was due to moderately increased postsinusoidal resistance coupled with high portal blood flow, and in the second it was due to very high presinusoidal resistance but low portal blood flow. Surgical treatment was designed accordingly.
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U2 - 10.1001/jama.1969.03160090021005
DO - 10.1001/jama.1969.03160090021005
M3 - Article
C2 - 5818681
AN - SCOPUS:0014661281
SN - 0098-7484
VL - 208
SP - 1661
EP - 1666
JO - JAMA: The Journal of the American Medical Association
JF - JAMA: The Journal of the American Medical Association
IS - 9
ER -