1969Annual Review of MedicineRequires access

Hemodynamic Studies in Portal Hypertension

John J. Fomon, W. Dean Warren

Open publisher page 18 citations

Abstract

The hemodynamic alterations occurring in portal hypertension are com­ plex and difficult to evaluate. Investigation and understanding of the vas­ cular pathophysiology assume clinical importance because operative treat­ ment very often alters splanchnic blood flow suddenly and dramatically. I t is generally conceded that hepatic function is a major determinant in the degree of well being of patients with portal hypertension, especially after complications of portal hypertension are treated by portosystemic shunt. The concept that hepatic function is not the sole determining factor is em­ phasized by a number of clinical studies. Callow et al. (I), Conn & Linden­ muth (2) and Jackson et al. (3) have analyzed the results of shunt therapy in controlled, randomized studies. Survival rates in the surgical groups are not superior to those in the groups treated medically. In a review of the subject, Grace et al. (4) came to the same conclusion. Although survival rates were similar, modes of death differed. In the medically treated control group, hemorrhage from esophageal varices was the major cause while in patients undergoing portacaval shunt, liver failure was the most common cause of death. Johnson et al. (S) reported the results of nonshunting procedures in the control of esophageal varices. None of the long-term survivors were troubled with hepatic encephalopathy or liver failure. In bilharzial cirrhosis hepato­ cellular function usually remains good but Hassab (6) found that 20.6 per cent of such patients undergoing portacaval shunt developed encephalopathy. After nonshunting operations on 3SS patients with the same disease only one patient developed encephalopathy in the absence of bleeding. Mikkelsen et al. (7) reported on 36 patients, in 17 of whom the portal vein was patent, liver function was excellent and there was no evidence of liver disease on gross examination. Following portacaval shunts, 10 developed signs of encephalopathy and five died of liver failure. In those patients with spon­ taneously occluded portal veins these complications were infrequent. The foregoing clinical observations suggest that the sudden complete diversion of portal blood flow, as occurs following an end-to-side or side-to­ side (8, 9) portacaval shunt, may be detrimental to the liver under certain circumstances. This detrimental effect has been observed in dogs (10), spider monkeys (11), and man (12). Warren et al. (13, 14) studied hemo-

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The hemodynamic alterations occurring in portal hypertension are com­ plex and difficult to evaluate. Investigation and understanding of the vas­ cular pathophysiology assume clinical importance because operative treat­ ment very often alters splanchnic blood flow suddenly and dramatically. I t is generally conceded that hepatic function is a major determinant in the degree of well being of patients with portal hypertension, especially after complications of portal hypertension are treated by portosystemic shunt. The concept that hepatic function is not the sole determining factor is em­ phasized by a number of clinical studies. Callow et al. (I), Conn & Linden­ muth (2) and Jackson et al. (3) have analyzed the results of shunt therapy in controlled, randomized studies. Survival rates in the surgical groups are not superior to those in the groups treated medically. In a review of the subject, Grace et al. (4) came to the same conclusion. Although survival rates were similar, modes of death differed. In the medically treated control group, hemorrhage from esophageal varices was the major cause while in patients undergoing portacaval shunt, liver failure was the most common cause of death. Johnson et al. (S) reported the results of nonshunting procedures in the control of esophageal varices. None of the long-term survivors were troubled with hepatic encephalopathy or liver failure. In bilharzial cirrhosis hepato­ cellular function usually remains good but Hassab (6) found that 20.6 per cent of such patients undergoing portacaval shunt developed encephalopathy. After nonshunting operations on 3SS patients with the same disease only one patient developed encephalopathy in the absence of bleeding. Mikkelsen et al. (7) reported on 36 patients, in 17 of whom the portal vein was patent, liver function was excellent and there was no evidence of liver disease on gross examination. Following portacaval shunts, 10 developed signs of encephalopathy and five died of liver failure. In those patients with spon­ taneously occluded portal veins these complications were infrequent. The foregoing clinical observations suggest that the sudden complete diversion of portal blood flow, as occurs following an end-to-side or side-to­ side (8, 9) portacaval shunt, may be detrimental to the liver under certain circumstances. This detrimental effect has been observed in dogs (10), spider monkeys (11), and man (12). Warren et al. (13, 14) studied hemo-

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Available abstract

The hemodynamic alterations occurring in portal hypertension are com­ plex and difficult to evaluate. Investigation and understanding of the vas­ cular pathophysiology assume clinical importance because operative treat­ ment very often alters splanchnic blood flow suddenly and dramatically. I t is generally conceded that hepatic function is a major determinant in the degree of well being of patients with portal hypertension, especially after complications of portal hypertension are treated by portosystemic shunt. The concept that hepatic function is not the sole determining factor is em­ phasized by a number of clinical studies. Callow et al. (I), Conn & Linden­ muth (2) and Jackson et al. (3) have analyzed the results of shunt therapy in controlled, randomized studies. Survival rates in the surgical groups are not superior to those in the groups treated medically. In a review of the subject, Grace et al. (4) came to the same conclusion. Although survival rates were similar, modes of death differed. In the medically treated control group, hemorrhage from esophageal varices was the major cause while in patients undergoing portacaval shunt, liver failure was the most common cause of death. Johnson et al. (S) reported the results of nonshunting procedures in the control of esophageal varices. None of the long-term survivors were troubled with hepatic encephalopathy or liver failure. In bilharzial cirrhosis hepato­ cellular function usually remains good but Hassab (6) found that 20.6 per cent of such patients undergoing portacaval shunt developed encephalopathy. After nonshunting operations on 3SS patients with the same disease only one patient developed encephalopathy in the absence of bleeding. Mikkelsen et al. (7) reported on 36 patients, in 17 of whom the portal vein was patent, liver function was excellent and there was no evidence of liver disease on gross examination. Following portacaval shunts, 10 developed signs of encephalopathy and five died of liver failure. In those patients with spon­ taneously occluded portal veins these complications were infrequent. The foregoing clinical observations suggest that the sudden complete diversion of portal blood flow, as occurs following an end-to-side or side-to­ side (8, 9) portacaval shunt, may be detrimental to the liver under certain circumstances. This detrimental effect has been observed in dogs (10), spider monkeys (11), and man (12). Warren et al. (13, 14) studied hemo-

Key concepts: Medicine, Portal hypertension, Portacaval shunt, Esophageal varices, Encephalopathy, Cirrhosis, Hepatic encephalopathy, Varices

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