Abstract

Portal hypertension is one cause and a part of a dynamic process triggered by chronic liver disease, mostly induced by alcohol or incorrect nutrition and less often by viral infections and autoimmune or genetic disease. Adequate staging - continuously modified by current knowledge - should guide the prevention and treatment of portal hypertension with defined endpoints. The main goals are interruption of etiology and prevention of complications followed, if necessary, by treatment of these. For the past few decades, shunts, mostly as intrahepatic stent bypass between portal and hepatic vein branches, have played an important role in the prevention of recurrent bleeding and ascites formation, although their impact on survival remains ambiguous. Systemic drugs, such as non-selective beta-blockers, statins, or antibiotics, reduce portal hypertension by decreasing intrahepatic resistance or portal tributary blood flow or by blunting inflammatory stimuli inside and outside the liver. Here, the interactions among the gut, liver, and brain are increasingly examined for new therapeutic options. There is no general panacea. The interruption of initiating factors is key. If not possible or if not possible in a timely manner, combined approaches should receive more attention before considering liver transplantation.

Highlights

  • Portal hypertension is defined as the pathological increase of portal venous pressure, mainly due to chronic end-stage liver disease, leading to augmented hepatic vascular resistance and congestion of the blood in the portal venous system

  • This review focuses on portal hypertension in patients with advanced liver disease

  • If there are no signs of jaundice, ascites, or encephalopathy, the patient has a good chance of being in a compensated stage of cirrhosis with a 10-year survival of above 50%, while clinical signs of decompensation indicate a mortality of more than 75% within the 5 years[9]

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Summary

Introduction

Portal hypertension is defined as the pathological increase of portal venous pressure, mainly due to chronic end-stage liver disease, leading to augmented hepatic vascular resistance and congestion of the blood in the portal venous system. TIPS insertion is the most efficient method to reduce portal hypertension and to prevent bleeding in patients with liver cirrhosis, it does not improve survival as compared to patients receiving a non-shunt approach[71], at least in the elective situation This holds true for the most recent trials comparing non-selective beta-blockers (NSBB) with or without ligation to TIPS with covered stents[36,73,79]. Trials suggest that pre-emptive or “early” TIPS insertion is beneficial in high-risk patients, mainly those with active bleeding, decompensated liver cirrhosis, and/or HVPG >20 mmHg62,80,81, with respect to hemostasis and early rebleeding and long-term survival This strategy still needs to be established and proven in broad clinical practice. Combining small lumen TIPS with modulation of the systemic inflammatory response could be a possible approach

Conclusion
18. Castera L
PubMed Abstract
38. Boyer TD
58. Trebicka J
70. Rössle M: TIPS
84. Trebicka J: Emergency TIPS in a Child-Pugh B patient
88. Sanyal AJ
Findings
96. Vaillant GE
Full Text
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