William F. Panke

Portal blood flow in cirrhosis of the liver.

Direct measurements of portal flow and pressure in a relatively large number of patients with cirrhosis show a marked reduction in flow associated with a nearly constant plateau of portal pressure. This lack of correlation indicates the complex relationships of resistances in the splanchnic, collateral, and hepatic circuits determining the division of the available splanchnic flow between the portal vein and the collateral pathways. Subtracting the measured portal flow from well-established estimates of total hepatic blood flow in cirrhosis suggests that the hepatic artery contributes more than one-half of the blood perfusing the cirrhotic liver. There was no instance of retrograde portal flow during the preshunt measurements, although such reversal was frequent after side-to-side portacaval anastomosis. Attempting to explain the plateau of portal pressure in the face of an increasing outflow resistance presumably associated with progress of the disease, we postulate that an augmented inflow resistance to the splanchnic chamber reduces splanchnic flow in cirrhosis. End-to-side portacaval anastomosis did not return normal portal flow, although it decreased pressure to accepted control levels. The assumption is that most of the splanchnic blood was flowing through the shunt, leading to a high splanchnic resistance in the immediate postshunt status. If this resistance was previously elevated, as suggested by the plateau of portal pressure, the mechanism responsible for the elevation was not immediately deactivated after the shunt, and the true effect of the operation upon splanchnic flow may not be measurable at such time. Respiratory oscillations were a significant component of portal flow in cirrhosis before and after portacaval anastomosis, indicating the limitations of any steady state analysis of the circulatory derangement in cirrhosis.

Hepatic artery flow improvement after portacaval shunt: a single hemodynamic clinical correlate.

We have documented a highly significant increment in hepatic arterial flow following a portacaval shunt in patients with cirrhosis of the liver and portal hypertension. In contrast with other hemodynamic variables, the increment in arterial flow was directly related to morbidity, hospital mortality, and long term survival. Patients with increments smaller than 100 ml/min had the worst clinical results. They accounted for all of the hospital mortality, the largest incidence of encephalopathy, and the worst long term cumulative survival rates. The extent of the increment was not related directly to the type of shunt but, rather, to some intrinsic capability of the cirrhotic liver to increase its arterial flow in response to the relief of sinusoidal hypertension produced by the shunt. This capability appears related to the degree of entrapment of the hepatic arterioles by the fibrous tissues of cirrhosis. This encasement of arterioles should change the elastic properties of the hepatic arterial bed and we propose to measure these properties by determining the characteristic input impedance of the arterial bed.

Experiences with portacaval anastomosis: Analysis of 104 elective end-to-side shunts for the prevention of recurrent hemorrhage from esophagogastric varices (1952 through 1961)

H EMORRHAGE from esophagogastric varices is probably the most lethal complication of portal hypertension secondary to cirrhosis of the liver. Because of the often progressive nature of the cirrhotic process, and because long-term results from large, carefully controlled series have only recently been available [7-71, the value of surgical corrective measures for portal hypertension and associated varices is still questioned by some internists and surgeons. Objections to surgical portal decompression are frequently based on an allegedly prohibitive operative mortality ascribed to portacaval surgery, doubts as to its efficacy in preventing recurrent bleeding from varices, the disabling side effects that are said to be incurred, and its questioned ability to alter in any significant way the course set by the natural history of the primary underlying disease. Our interest in the surgical correction of portal hypertension extends over a period of twenty-five years, and it is freely admitted that some of these disquieting thoughts have entered the minds of members of our group from time to time. Prior to 1952 one of us (L. M. R.) advocated the splenorenal shunt as the preferred method of portal decompression, but we became discouraged by a 33 per cent incidence of failure in attaining our main objective of preventing recurrent bleeding from varices. This failure resulted either from late closure or thrombosis of the anastomosis, or from inability to provide adequate decompression of the congested splanchnic bed by this means, due to small vessel and stoma1 size. These discouraging results led to adoption of the direct end-to-side portacaval shunt as the method of choice in attempting surgical prevention of recurrent variceal hemorrhage. In the ten year period from 1952 through 1961 we have performed this operation on an elective basis in 104 patients with well documented varices, portal hypertension and cirrhosis of the liver. The primary purpose of the surgical therapy was to prevent recurrence of hemorrhage from ruptured esophagogastric varices. No patient surviving variceal hemorrhage was denied surgery unless progressive, irreversible hepatic failure followed the bleeding episode. Emergency and so-called prophylactic shunts, as well as side-to-side, splenorenal and caval mesenteric shunts and resections performed as alternative procedures, are not included in this report. Reports of others [1-71 frequently include various types of shunts (portacaval, splenorenal, makeshift, etc.) thus adding to the complexity of evaluation. In this respect our series represents a homogeneous group. Since complete follow-up studies are available in 103 of the 104 patients in this series a careful objective analysis of the results so far obtained may shed some light on the many questions

Angiographic Localization of Pheochromocytoma

In the study of hypertension, renal vascular lesions were the only indication for angiography until recently, when clear radiographic demonstrations of pheochromocytoma were obtained following the injection of contrast medium into the aorta, or after selective renal artery catheterization (1, 3, 7, 8, 10, 12, 16, 19, 21, 22a). In the past, hypertensive patients in whom pheochromocytoma was suspected were examined by conventional radiographic technics only, mainly intravenous pyelography and retroperitoneal pneumography (20–24). Although pheochromocytomas may arise in the chromaffin tissue anywhere in the body (9, 17, 18), the overwhelming majority arise in the adrenal glands. Our main concern in arteriography for their diagnosis, then, is the visualization of the vessels leading to these glands. Usually three arteries supply the suprarenal gland (13): the superior, the middle, and the inferior suprarenal. The superior suprarenal artery arises from the inferior diaphragmatic artery, the middle directly fro...

Endocardial fibroelastosis occurring in the adult

Abstract A brief review of the concept of fibroelastosis is presented and a case in a young adult is reported similar to that seen in infants. This case probably represente an extremely rare case of a patient with this disease maintaining sufficient cardiac reserve to carry her into adult life.