Current Concepts in Fluid Resuscitation and Vasopressor Use in Cirrhosis.

Abstract

Critically ill patients with cirrhosis and liver failure not uncommonly have hypotension due to multifactorial reasons, that include hyperdynamic state with increased cardiac index, low systemic vascular resistance due to portal hypertension, following the use of beta blocker or diuretic therapy, and severe sepsis. These changes are mediated by microvascular alterations in the liver, systemic inflammation, activation of renin angiotensin aldosterone system, and vasodilatation due to endothelial dysfunction. Hemodynamic assessment includes measuring inferior vena cava indices, cardiac output and systemic vascular resistance using point-of-care ultrasound (POCUS), in addition to arterial waveform analysis, or pulmonary artery pressures, and lactate clearance to guide fluid resuscitation. Fluid responsiveness reflects the ability of fluid bolus to increase the cardiac output and is assessed effectively by POCUS, passive leg raise manoeuvre, and dynamic tests such as pulse pressure and stroke volume variation both in spontaneously breathing and mechanically ventilated patients. Albumin has pleotropic benefits through anti-inflammatory properties besides its standard action on oncotic pressure and volume expansion in patients with cirrhosis but has potential for precipitating pulmonary edema. In conclusion, fluid therapy in critically ill patients with liver disease is a complex and dynamic process that requires individualised management protocols to optimise patient outcomes.