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EDUCATION EXHIBIT |
Department of Hepatology, Baylor Regional Transplant Institute, Baylor University Medical Center, Dallas, Texas
Creation of TIPS represents a total shunt through the liver, with reversal of flow in the intrahepatic portal veins, and use of these shunts has become an essential part of treating patients with liver disease. Significant portal hypertension responsible for ascites, bleeding, and inanition, often with associated renal dysfunction, is a cause of substantial morbidity and mortality (1). A 25%–50% 1-year mortality in patients whose ascites cannot be controlled has been previously reported (2,3). In addition, surgical shunts whose creation involves use of general anesthetics are reported to have a 10%–15% operative mortality (4,5). Thus, the development of TIPS has been a major advancement in the treatment of liver disease. Uncontrolled ascites and bleeding can be stabilized and more easily managed with TIPS, but with costs in some cases. Hepatic encephalopathy (also known as portosystemic encephalopathy), worsening of hepatic function, and deepening cholestasis all occur. Fortunately, mortality and morbidity from TIPS is low (6); thus, use of these stents has proliferated, and our understanding of their problems and limitations has increased (7,8). The preceding article by Madoff et al represents the next logical step in attempting to manage portal venous pressure to maintain hepatocellular profusion and to prevent hepatic encephalopathy.
Hepatic encephalopathy is a major, all-too-frequent complication resulting from TIPS. Its prevalence has been reported to be as high as 20%–31%, although in most cases, hepatic encephalopathy can be controlled with nonabsorbable antibiotics and disaccharides. The prevalence of TIPS reversal because of severe hepatic encephalopathy is not known, but it is likely less than 5% (9). Hepatic atrophy is another complication from TIPS. Shunting of venous blood is thought to divert hepatotrophic factors and cause hepatic atrophy (10). "Shunt hyperbilirubinemia" also occurs and may add to morbidity. In addition, use of TIPS has not been proved to have an impact on survival (11–13), which should not be surprising, since it treats only one aspect of hepatic dysfunction. Mortality rates after TIPS range from 3% to 58% (14). Patient status before the procedure is likely the major determinant of mortality. Total bilirubin level, APACHE score, Child-Pugh class, the presence of alcoholic versus nonalcoholic liver disease, bleeding status, and age all play a role in patient outcome (15).
Hepatic encephalopathy may be a predictor of patient outcome, but defining encephalopathy is far from uniform. A broad spectrum of signs and symptoms of hepatic encephalopathy from mild confusion to coma has been observed after TIPS placement. A recent article in Hepatology addresses the challenge of designing trials to study the treatment of hepatic encephalopathy (16). Studies that address the subtleties of hepatic encephalopathy before TIPS placement need to be formulated. The ability of a stent to cause or prevent encephalopathy depends on the definition of the clinical syndrome and its severity.
Can we clinically determine who will be significantly affected by TIPS? Chalasani et al (14) looked at 21 clinical and biochemical factors in patients before TIPS placement. These authors identified variceal hemorrhage, bilirubin levels greater than 3 mg/dL, levels of alanine aminotransferase greater than 100 U/L, and pre-TIPS hepatic encephalopathy as being predicative of death during a 2
-year follow-up (17). Other investigators have discovered similar trends (18). Perhaps development of criteria predictive of patient outcome before TIPS placement may eventually be useful in determining what type of stent, constrained versus unconstrained, to place.
Some investigators believe that the maintenance of portal venous blood flow after TIPS is predictive of patient outcome. This appealing hypothesis is a foundation for creating constrained stents. Sarfeh et al (19) looked at portal H-graft diameter in 68 patients with portacaval shunts. They observed that use of large grafts caused loss of prograde portal flow and therefore hepatic encephalopathy (19). Small grafts (10 mm and 8 mm) caused less hepatic encephalopathy (19% and 9%, respectively). In their study, all grafts were effective at preventing recurrent bleeding from esophageal varices. They concluded that preserving prograde portal venous flow prevented hepatic encephalopathy. Interestingly, no patient experienced recurrent bleeding, yet the 8-mm stent must have kept portal venous pressure high.
Sanyal et al (20) noted that in 100 patients with esophageal hemorrhage who underwent TIPS with unconstrained stents that a PSG of 12–18 was associated with disappearance of esophageal varices. Traditionally, PSG of less than 12 is thought to be the goal in portal venous decompression and disappearance of esophageal varices. These observations make placement of constrained stents attractive, and studies will be needed to explore the impact of partial portal venous decompression on bleeding.
Use of constrained stents is new. All investigators to date have used homemade stents for the most part and have achieved varying degrees of success in "restraining" portal blood flow. One of the problems has been the lack of uniformity in the effect that these shunts have on reducing the PSG. One hopes that this deficiency can be overcome by the creation of a standard stent. Use of a standard stent will allow the evaluation of pre- and post-TIPS variables that affect the natural history and survival of patients with portal hypertension. The future looks bright as we take the next step in dealing with portal hypertension. The work by Madoff et al holds promise as we take these next steps toward the future.
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