Liver dysfunction in the intensive care unit

Authors Aspasia Aspasia Soultati, S.P. Dourakis.


Liver dysfunction plays a significant role in the Intensive
Care Unit (ICU) patients morbidity and mortality.
Metabolic, hemodynamic and inflammatory factors
contribute in liver damage. Hemorrhagic shock, septic shock,
multiple organ dysfunction, acute respiratory dysfunction,
metabolic disorders, myocardial dysfunction, infection from
hepatitis virus, and therapeutic measures such as blood
transfusion, parenteral nutrition, immunosuppresion, and
drugs are all recognised as potential clinical situations on
the grounds of which liver dysfunction develops.
The liver suffers the consequences of shock- or sepsis-inducing
circumstances, which alter hepatic circulation parameters,
oxygen supply and inflammatory responses at the
cellular level. Moreover, the liver is an orchestrator of metabolic
arrangements which promote the clearance and production
of inflammatory mediators, the scavenging of bacteria,
and the synthesis of acute-phase proteins. This balance
defines the stage upon which the syndrome of shock
liver develops.
Ischemic hepatitis develops from shock and is characterised
by elevated plasma aminotransferase concentrations. ICU
jaundice emerges later in critical illness, mainly in
patients with trauma and sepsis. The commonly reported
biochemical abnormality is conjugated hyperbilirubinaemia.
The clinical setting suggests that hepatic ischemia
and hepatotoxic actions of inflammatory mediators are
the main aetiological factors. Cross-talk between hepatocytes,
Kupffer cells and endothelial cells, leading to an
inflammatory response mediated primarily by tumour necrosis
factor-alpha, is pivotal for the development of liver
injury at that stage.
Although determinations of aminotransferases, coagulation
studies, glucose, lactate and bilirubin can detect hepatic
injury, they only partially reflect the underlying pathophysiological
mechanisms. Both the presence and degree of jaundice
are associated with increased mortality in a number of
non hepatic ICU diseases.
Therapeutic approaches to shock liver focus on the
prevention of precipitating causes. Prompt resuscitation,
definitive treatment of sepsis, meticulous supportive care,
controlling of circulation parameters and metabolism, in
addition to the cautious monitoring of therapeutic measures
such as intravenous nutrition, mechanical ventilation and
catecholamine administration reduce the incidence and
severity of liver dysfunction. Only precocious measures can
be taken to prevent hepatitis in ICU.
Key words: shock liver, hypoxic hepatitis, ischemic hepatitis,
shock, multiple organs dysfunction.