Management of varices and variceal hemorrhage in liver cirrhosis: a recent update

Abstract

Cirrhosis consists of two main stages: compensated (asymptomatic) and decompensated, the latter with a higher mortality. Variceal hemorrhage, together with ascites or encephalopathy, or both, are events that define cirrhosis decompensation and are driven by portal hypertension. The approach and management of patients with compensated cirrhosis has been mostly focused on preventing variceal hemorrhage in those who have high-risk varices on endoscopy. Recent studies suggest a paradigm shift aimed at preventing all decompensating events, not only variceal hemorrhage, in patients with cirrhosis and clinically significant portal hypertension identified via noninvasive measures such as liver stiffness and platelet count. In these patients, nonselective beta-blockers have been shown to prevent ascites (the most common decompensating event) and variceal growth. Variceal hemorrhage has a high mortality rate and even though advances in diagnostic approach and standard of care over the past decades have led to a decrease in mortality, it is still high with a 6-week mortality rate of 15-20%. Survival has improved with the preemptive placement of the transjugular intrahepatic portosystemic shunt in patients at high risk of failing standard therapy. In this review, we provide an overview of the pathophysiology and bases for therapy of portal hypertension and varices, the diagnostic approach and management of compensated cirrhosis with clinically significant portal hypertension, and the management of acute variceal hemorrhage as well as prevention strategies for variceal hemorrhage recurrence.

Keywords: Clinically significant portal hypertension; nonselective beta-blockers; portal hypertension; transjugular intrahepatic portosystemic shunt; variceal hemorrhage; varices.

Figure 1.

Pathophysiology of portal hypertension and mechanism of action of various therapies used in the management of portal hypertension and variceal hemorrhage. CSPH: clinical significant portal hypertension; EVL: endoscopic variceal ligation; HVPG: hepatic venous portal gradient; NSBB: nonselective beta-blockers; PH: portal hypertension; TIPS: transjugular intrahepatic portosystemic shunt; VH: variceal hemorrhage. *Carvedilol has additional α-1 blockade effect. Source: Created with BioRender.com.

Figure 2.

(a) and (b) Approach to compensated cirrhosis relying on less invasive strategies to identify patients with and without clinical significant portal hypertension (CSPH). Goal of patient with clinical significant portal hypertension now is the prevention of any decompensation. (c) Approach to patient presenting with ascites and no history of variceal hemorrhage. CSPH, clinical significant portal hypertension; EVL, esophageal varices ligation; KPa, kilopascals; LVP, large-volume paracentesis; NSBB, nonselective beta-blocker; plt, platelets. ^aSmall (<5 mm), no red signs, no CTP-C. ^bLarge (>5 mm), red spot signs, CTP-C LSM: liver stiffness measurement. *Based on the PREDISCI trial carvedilol outperformed propranolol. Source: Created with BioRender.com.

Figure 3.

Acute variceal hemorrhage management algorithm. CTP, Child–Turcotte–Pugh; FFP, fresh frozen plasma; NSBB, nonselective beta-blockers; PRBC, packed red blood cells; TIPS, transjugular intrahepatic portosystemic shunt. ^aBefore starting prophylactic antibiotic ideally perform diagnostic paracentesis to increase yield in the case of spontaneous bacterial peritonitis.