Abstract
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.
Keywords
POCUS - point-of-care ultrasound - albumin in cirrhosis - sepsis and septic shock
- fluid resuscitation - vasopressors
