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  • Portal hypertension, resulting from increased intrahepatic resistance to portal flow and increased portal inflow, marks the transition from compensated to decompensated cirrhosis.

  • The sequelae of portal hypertension affect each organ system, requiring multi-disciplinary management.

  • Grades III and IV hepatic encephalopathy require immediate ICU transfer and elective intubation for airway protection.

  • Pulmonary derangements resulting from portal hypertension may be severe and include hepatopulmonary syndrome, portopulmonary hypertension, and hepatic hydrothorax.

  • Hepatorenal syndrome is a diagnosis of exclusion and is characterized by renal impairment in the setting of advanced liver disease, circulatory dysfunction, and increased activity of the renin-angiotensin system.

  • SBP is a known precipitant of HRS, which is a cause of increased mortality in cirrhotic patients; therefore empiric antibiotic treatment is warranted in patients in whom the suspicion for SBP is high.

  • Aggressive intravenous resuscitation, airway protection, and early endoscopic management of cirrhotic patients presenting with suspected variceal bleed is critical.


Hepatic decompensation in the critical care setting can present in two distinct contexts, which include acute liver failure and acute on chronic liver failure. In this chapter, we discuss the critical care approach to acute on chronic liver failure. In the intensive care setting, severe cases of acute on chronic liver failure require a systematic multiorgan system approach to management in order to address hepatic and extrahepatic organ dysfunction. An optimization of hepatic and extrahepatic derangements, including cardiopulmonary, neurologic and renal dysfunction, is essential for the successful management of the critically ill cirrhotic patient.


The pathophysiology and sequelae of chronic liver disease warrant a unique approach to ICU management and treatment of disease. Namely, portal hypertension marks the transition from compensated to decompensated cirrhosis, resulting in life-threatening conditions including gastrointestinal variceal bleeding, hepatorenal syndrome, pulmonary complications, and hepatic encephalopathy.1

Portal hypertension in cirrhosis is a result of the combined effect of intrahepatic resistance to portal flow and increased portal inflow. The resistance to portal flow consists of both fixed and functional components. The fixed component occurs from sinusoidal fibrosis and compression by regenerative nodules. The functional component is secondary to vasoconstriction, resulting from both decreased intrahepatic nitric oxide and enhanced intrahepatic vasoconstrictor activity. The paradoxical decreased intrahepatic nitric oxide and overproduction of extrahepatic nitric oxide produces splanchnic vasodilation and increased portal inflow. Combined, the effects of the intrahepatic resistance to flow and increased portal inflow result in a portal hypertensive state.2 In addition, the pathologic splanchnic vasodilation results in a shunting of the cardiac output to the splanchnic circulation, and an associated decrease in effective systemic arterial blood volume perfusing other organ systems. These hemodynamic derangements in the splanchnic and systemic circulation form the basis for current management strategies in decompensated cirrhosis. An organ-system-based review of the management of specific disease manifestations in acute on chronic liver failure follows.


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