We bring up to date our series of direct measurements of portal flow and pressure in patients with cirrhosis of the liver. In 153 patients the portal flow averaged 447 plus or minus 350 ml. Hg per minute and the portal pressure 28.5 plus or minus 4 mm. Hg (approximately 387 mm. H2O). Both quantities compare favorably with our previous measurements in smaller groups of patients. In 80 of our patients we had also measurements of pressure on the hepatic and splanchnic sides of a clamp occluding the portal vein. Nine of these patients had an hepatic occluded portal pressure higher than either or both the free portal pressure and the splanchnic occluded portal pressure. Of these nine patients with reversed pressure differences, two had stagnant portal flow and the remaining seven had forward flow into the liver measuring from 80 to 1,116 ml. Hg per minute.

Because of its presumed serious clinical significance, we made an analysis of the evidence for and against the occurrence of spontaneous reversal of portal flow in cirrhosis of the liver. We examined the evidence obtained from manometric studies, radioactive tracer studies, radiologic studies, and actual measurements of magnitude and direction of portal blood flow. Concerning manometric studies, we introduced a physical analysis, based on first principles, which demonstrates that the occluded portal pressures cannot be used to construct a hydraulic gradient for portal flow. Similarly, we examined the weakness of the evidence derived from radioactive tracer and radiologic studies and, in the latter, the drastically opposite results reported by different investigators. Finally, we found that actual measurements of magnitude and direction of portal flow provide impressive evidence against the occurrence of spontaneous reversal of portal flow in cirrhosis. We conclude that unless new and convincing evidence is provided, it may not serve the best interests of medicine and of our patients to continue accepting spontaneous reversal of portal flow in cirrhosis as if it were a proven phenomenon.

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.

The study of the outflow tracts of the liver has remained, for the most part, in the realm of anatomical investigations. Plastic casts obtained by injection-corrosion technics have provided information on the configuration and structural changes of the hepatic vein system in health and disease (5, 13). Postmortem perfusion experiments have added some insight into the complex nature of the phenomena that, in life, may regulate the flow of blood through the liver (8, 14). In the living subject, hepatic vein manometries have been used in an effort to obtain data concerning the physiological and physiopathological behavior of hepatic outflow tracts (10–12, 22). From the radiologic point of view, two primary approaches to the visualization of the hepatic vein system have been explored, both consisting in the intraluminal injection of contrast medium into an hepatic vein branch. By the first approach, where a catheter is advanced into an hepatic vein, the contrast material is injected in a retrograde manner against the normal direction of the flow of blood (3, 19, 24, 25). With the second approach, which uses the percutaneous trans-hepatic route, an hepatic vein branch is directly injected (2, 20). In an attempt to find a more physiological approach to the study of the hepatic outflow tracts, the method of intraparenchymal deposition of contrast medium was developed by this group. Its use in small (15) and large (16, 17) laboratory animals has been previously reported. In essence, the procedure consists of the radiologic study of the vascular structures that remove an intraparenchymal deposit of medium. It is presumed that by observation of these vascular structures as they perform their intended role of draining the liver tissue, a better understanding of the function of the normal and pathologic hepatic outflow tracts may be gained. The purpose of this paper is to present the results derived from the intraparenchymal deposition of contrast medium in normal human subjects as well as in patients with hepatic and cardiac disorders. These results also include what is believed to be the first direct visual demonstration of two unusual phenomena: the role of the portal vein as an accessory outflow tract following side-to-side portacaval anastomosis and the increased transport of lymph in the efferent lymphatic system of the cirrhotic liver. An Addendum incorporates findings in the experimental animal related to a new working hypothesis concerning the etiopathogenesis of cirrhotic and cardiac ascites. Materials and Methods The method of intraparenchymal deposition of contrast medium was used in 87 instances in 62 patients. Sixteen of the 62 patients had normal liver function and served as controls. The remaining 46 had either cirrhosis of the liver or congestive heart failure. Thirty cirrhotic patients had associated ascites. Eleven patients were studied at varying intervals after the establishment of a portacaval anastomosis.

MORENO, AUGUSTO H. M.D.; ROUSSELOT, LOUIS M. M.D.; BURCHELL, ALBERT R. M.D.; BONO, RUDOLPH F. M.D.; BURKE, JEAN HOPE A.B. Author Information