Current Concepts in Fluid Resuscitation and Vasopressor Use in Cirrhosis

Critically ill patients with cirrhosis and liver failure do not uncommonly have hypotension due to multifactorial reasons, which include a hyperdynamic state with increased cardiac index (CI), low systemic vascular resistance (SVR) 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. Haemodynamic assessment includes measuring inferior vena cava indices, cardiac output (CO), and SVR using point-of-care ultrasound (POCUS), arterial waveform analysis, pulmonary artery pressures, and lactate clearance to guide fluid resuscitation. Fluid responsiveness reflects the ability of fluid bolus to increase the CO and is assessed effectively by POCUS, passive leg raises manoeuvre, and dynamic tests such as pulse pressure and stroke volume variation in spontaneously breathing and mechanically ventilated patients. Albumin has pleiotropic benefits through anti-inflammatory properties besides its standard action on oncotic pressure and volume expansion in patients with cirrhosis but has the potential for precipitating pulmonary oedema. In conclusion, fluid therapy in critically ill patients with liver disease is a complex and dynamic process that requires individualized management protocols to optimize patient outcomes.