This item is provided by the institution :

Repository :
Annals of Gastroenterology
see the original item page
in the repository's web site and access all digital files if the item*
share



Report (EN)

2007 (EN)
Liver dysfunction in the intensive care unit (EN)

Aspasia Soultati, S.P. Dourakis, Aspasia

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. (EN)

info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion

Ελληνική Γαστροεντερολογική Εταιρία (EL)
Hellenic Society of Gastroenterology (EN)

2007-03-19


Hellenic Society of Gastroenterology (EN)

1792-7463
1108-7471
Annals of Gastroenterology; Volume 18, No 1 (2005) (EN)



*Institutions are responsible for keeping their URLs functional (digital file, item page in repository site)