Introduction to the Treatment of Portal Hypertension

Introduction to the Treatment of Portal Hypertension

Josef E. Fischer

The treatment of portal hypertension has become a critical issue in preserving lives of cirrhotic patients. Whereas previously in this country alcoholism was the principle reason for bleeding esophageal varices, the increased incidence of hepatitis B and hepatitis C have resulted in a reservoir of patients that may bleed from esophageal varices and ultimately are candidates for hepatic transplantation. In considering hepatic transplantation, it is important to carry out whatever therapy for portal hypertension one can and at least try to preserve the opportunity to carry out a liver transplant later. The principal anatomic necessity means that whatever mechanism one uses to carry out the control of bleeding esophageal varices, it should, whenever possible, leave the porta hepatis free of previous surgery.

For the most part, many centers of liver transplantation will also deal with patients with bleeding esophageal varices. This is done either by endoscopy, as detailed elsewhere in this section, either by injection or by rubber band obliteration of bleeding esophageal and gastric varices. When these techniques fail, a transjugular intrahepatic portosystemic shunt (TIPS) procedure is done, in which one provides an egress of high-pressure portal flow from the portal system into the systemic system by means of a shunt traversing the hepatic parenchyma. For the most part, in the present state of knowledge, TIPS cannot be used as definitive therapy for bleeding esophageal varices, but are used as a bridge in patients who must by necessity undergo liver transplantation in the finite future. The stenosis rate of the TIPS conduit is high, ranging between 30% and 50% or even higher at the end of 1 year. Thus, there are many techniques for actually dilating stenoses so that the patient can undergo subsequent hepatic transplant.

However, there remains a group of patients in whom cessation and arrest of bleeding esophageal varices and gastric varices cannot be accomplished with TIPS and other means of controlling the often-torrential hemorrhage. In these patients, shunt surgery then becomes a necessity.

In addition, there are a group of patients, mostly class A patients, in whom the state of hepatic function is such that it is thought they can survive for a long period of time without liver transplant. In these patients, some type of shunt surgery, which is described in the subsequent chapters, then becomes a necessity. The hypothetical equation in carrying out shunt surgery is to do enough to decrease portal pressure to a reasonable level so that bleeding from esophageal varices stops in this instance and can be prevented from happening again. The obverse of this equation is to provide enough forward portal pressure to allow hepatic perfusion so that hepatic failure is not the result of shunt surgery. In order to understand the complexities of this pressure equation, it is necessary to understand the basics.

The liver is supplied by two perfusion systems, the hepatic artery, a splanchnic artery that is usually responsible from between 20% and 25% of hepatic flow under normal circumstances. The portal vein is not generally oxygen-deprived; thus, the hepatic artery, rather than most organs supplying all of the essential oxygenation, supplies only 50% of the oxygen requirement of the liver. The portal vein, which normally supplies between 75% and 80% of the flow, also supplies 50% of the oxygen requirement of the liver, as well as the lion’s share of nutrients derived from the gut and its absorption of nutrients. The liver, sitting astride the portal vein, absorbs and processes and, in some cases, stores for release into the general circulation the nutrients, which appear in the portal vein. The liver probably processes nearly 100% of the carbohydrate presented to it. It also processes the majority of the amino acids presented to it, notably the aromatic amino acids, of which two in particular, phenylalanine and its hydroxylated product tyrosine, are principal components of hepatic protein synthesis, but also form the substrate for the sympathetic nervous system as well as many of the amines, which perform vital functions within the brain. Lipids are separately absorbed, and are usually absorbed in their triglyceride form in the lymphatics, which then enter the venous system through the thoracic duct and thus do not pass through the liver.

Only gold members can continue reading. Log In or Register to continue

Aug 2, 2016 | Posted by in GENERAL SURGERY | Comments Off on Introduction to the Treatment of Portal Hypertension

Full access? Get Clinical Tree

Get Clinical Tree app for offline access
%d bloggers like this: