Portal hypertension

Many advances in the management of portal hypertension and variceal hemorrhage have occurred during the last 10 years. Effective therapy for primary prevention of variceal hemorrhage is now available in the form of nonselective beta-blockers. Active bleeding should be managed with terlipressin, somatostatin or its analogues, and endoscopic therapy; TIPS and surgery are reserved as salvage therapy for patients who fail endoscopic treatment. Survivors of a variceal hemorrhage should be evaluated for liver transplantation. Specific treatment may be provided with EVL while these patients await transplantation. Patients who fail endoscopic treatment may be treated by TIPS or surgery.     

Portal hypertension

The time-course effects of portal hypertension on gastric secretory function, mucosal blood flow, vascular permeability, and ethanol-induced gastric mucosal damage were examined in anesthetized rats. Partial ligation of the portal vein effectively produced portal hypertension one to three days later but the raised pressure returned to normal on the sixth day after ligation. This time-course effect coincided with reduced pepsin secretion and mucosal blood flow and also with potentiated ethanol-induced mucosal damage during the first to third days. These effects started to tail off on the sixth day. However, gastric acid output was significantly reduced on the third day, and this was strongest on the sixth day after operation. Portal vein ligation also reduced basal vascular permeability, which was markedly potentiated after ethanol treatment. It is concluded that: (1) portal vein blood pressure changes are a time-dependent process following ligation; (2) changes in gastric mucosal blood flow (GMBF) and lesion formation are closely related to portal hypertension; (3) gastric mucosal injury is associated with vascular damage, as evidenced by increased in vascular permeability; and (4) pepsin but not acid secretion is closely related to the state of the GMBF.     

Portal hypertension

There are two types of shunts for the treatment of esophageal varices: total shunts or selective shunts. The various total shunts are designed to decompress both the portal and the variceal venous systems. In contrast, a selective shunt decompresses the varices only, and the portal pressure and presumably portal flow are not affected. The very purpose of the total shunt is the total or partial diversion of portal flow. This is the case no matter which branches of the portal and systemic venous systems are connected and whether the anastomosis is a direct one or is through a graft.In an ongoing prospective, randomized clinical trial, which now includes 46 patients, a total shunt (mesorenal H graft) and the selective distal splenorenal (Warren) shunt are compared. The operative mortality rate and the frequency of postoperative bleeding are the same. However, encephalopathy is more frequent after the total shunt (P<0.05), and a trend is developing which suggests a better long-term survival rate after the Warren shunt. If these trends continue, then the superiority of the Warren shunt is established in a selected group of patients who have bled at least once from their varices. If these patients continue to remain free of encephalopathy and hemorrhage will not recur, then it is probable that the Warren shunt could improve the chances of survival of cirrhotic patients with esophageal varices who did not bleed yet. The prophylactic value of the Warren shunt will require a multicenter, cooperative, controlled clinical trial.     

Portal circulation and portal hypertension.

During the last 25 years, there have been important developments in visualising the portal vein, in examining its contents, and in measuring the pressure of blood flowing within it. Radiologists have set the scene and now is the time of the scanner. These technical advances have been applied to the diagnosis and treatment of patients with portal hypertension, and many ingenious surgical techniques have been proposed. The problem of successful treatment of the patient with bleeding oesophageal varices and cirrhosis of the liver, however, has not yet been solved. This report discusses the portal vein in terms of pressure, flow, and regeneration factors. Portal hypertension is classified and methods of relief are discussed.     

Evidence-based guide to perioperative medicine

The discipline of perioperative medicine is assuming greater importance as increasing numbers of older patients with medical comorbidity undergo complex surgical procedures. If patient outcomes and use of limited hospital resources are to be optimized, physicians with skills and interest in perioperative risk assessment and therapeutic intervention are needed. This systematic review attempts to provide an evidence-based update in several key areas in the management of the perioperative patient.     

Portal hypertension syndrome

The clinical and laboratory manifestations of the following groups of patients were compared: 45 cases of schistosomal fibrosis, 30 cases of hepatic cirrhosis with schistosomiasis, and 40 cases of hepatic cirrhosis alone. The patients with schistosomal fibrosis had the following characteristics which distinguished them from those in the other two groups: (1) lower average age; (2) marked splenomegaly; (3) less frequent signs of liver failure and milder alterations in biochemical tests of liver function; (4) large gradients between intrasplenic pressure and wedged hepatic vein pressure; and (5) lower mortality of operations for portal hypertension.     

Portal hypertension and primary biliary cirrhosis.

Portal hypertension has been regarded as an uncommon and late complication of primary biliary cirrhosis (PBC). 24 patients with PBC were investigated for portal hypertension. Esophageal varices were present in 20, 50, and 90% of the patients 1, 3, and 9 years, respectively, after the onset of pruritus and/or jaundice. Portal hypertension was responsible for gastrointestinal bleedings in 11 patients; bleeding was the first clinical manifestation of PBC in two of them. Wedged hepatic venous pressure was increased in all the patients with portal hypertension whether regenerative nodules were present or absent. Portacaval shunt was performed in five patients and was well tolerated in three of them. It is concluded that (a) portal hypertension is common in PBC; (b) the intrahepatic block is of the so-called postsinusoidal type, even in patients without regenerative nodules; (c) gastro-intestinal bleeding due to portal hypertension occurs in about half of the patients and may be the first manifestation of PBC; (d) portacaval shunt seems to be indicated when gastro-intestinal bleeding occurs in earlier stage of the disease.     

Portal hypertension in acute liver failure.

Twenty five patients with acute liver failure were measured for hepatic venous pressure gradient as an index of portal pressure during the course of a transjugular liver biopsy. Hepatic venous pressure gradient ranged from 4 to 24.5 mm Hg with a mean of 12.8 (5.3) mm Hg (normal values less than 5 mm Hg). All patients but one had increased portal pressure gradient. Portal hypertension correlated with the degree of architectural distortion of the liver, as suggested by a direct correlation between hepatic venous pressure gradient and the area of reticulin collapse, evaluated by means of a morphometric analysis on Sirius red stained liver slides (r = 0.43, p less than 0.05). Hepatic venous pressure gradient was significantly higher in patients with ascites (15.1 (5) mm Hg, n = 15) or renal failure (14.4 (5.3) mm Hg, n = 16) than in those without (9.3 (3.4) mm Hg and 10.1 (4) mm Hg, respectively; p less than 0.05). Portal hypertension was associated with systemic vasodilation and a hyperkinetic circulatory state, with decreased arterial pressure, and peripheral resistance and increased cardiac output.     

Portal hypertension in fulminant viral hepatitis.

The gradient between wedged and free hepatic venous pressures were measured in 10 unselected adult patients suffering from fulminant viral hepatitis. The gradient was increased in all the studied patients, ranging from 0.9 to 2.1 kPa; this finding indicates that portal hypertension was present in all these cases. Ascites was present in all the five patients having a gradient about 1.5 kPa and affected only two of the five patients having a gradient below 1.5 kPa; this observation suggests that portal hypertension plays a role in the mechanism of ascites in fulminant viral hepatitis. Portal hypertension in fulminant viral hepatitis is likely to be the consequence of an intrahepatic block due to massive necrosis of the liver cells.     

Evidence-based medicine and hypertension

BACKGROUND: Evidence-based medicine (EBM) has been propagated as a revolutionary development which will improve the quality of clinical decision-making and guideline development Historically it follows an early 19th-century French attempt to introduce mathematical analysis into clinical practice. This met with resistance from both clinicians and scientists and was only accepted in more recent times with the development of clinical epidemiology and clinical trials. NATURE OF EBM: EMB claims to utilize the best available evidence to reach scientific conclusions, rejecting the appeal to expert authority. This involves a hierarchy of sources which places large controlled trials at the apex. Less value is attributed to arguments from clinical observation or pathophysiology. Systematic reviews and meta-analyses of trials therefore provide the strongest evidence for clinical decisions. THE CONCEPT OF EVIDENCE: The approach advocated in EBM is an over-simplification of the process of clinical thinking which involves interpretation and synthesis of relevant evidence from all sources and extrapolation to the clinical situation. In this process, there is no hierarchy of evidence. The relative value given to any particular evidence depends more upon its relevance and persuasiveness than the category to which it belongs. Discussion and debate amongst informed 'experts' is an integral feature of this process at each stage. IMPACT OF EBM: Although advocates of EBM acknowledge the contribution of all forms of evidence, the differential value attached to different sources has led to na?ve and simplistic attempts to omit the traditional processes of interpretation, synthesis and extrapolation and to draw wide-ranging conclusions from trial data without adequate scientific discussion.