الفهرس 
Physiology of LiverOnly 14 pages are availabe for public view
 |  | from | 119 |  |  |
| | | from | 119 | | |
Abstract
Hepatic dysfunction and jaundice are traditionally viewed as late features of sepsis and other critical illnesses. Identifying true cholestatic liver dysfunction is difficult given the lack of specificity of standard laboratory tests, especially in the context of a complex systemic condition as critical illness during sepsis and other critical illnesses.
The liver is a fundamental player in the host defense mechanisms as it regulates a wide range of metabolic, endocrine and immunological processes. However, inflammation and hypoxemia severely challenge the hepatic microcirculation and function.
Elevated circulating levels of ALT, AST, ALP and γ-GT can further indicate liver injury and cholestasis. Inflammation-induced alterations in the transport of bile acids appear to drive bile acids and bilirubin towards the systemic circulation.
In daily clinical practice, the most often used diagnostic criterion for critical illness-induced cholestasis is a total plasma bilirubin concentration higher than 2 or 3 mg/dl often combined with a maximally two or threefold increase in ALP and γ-GT levels. As to date, no specific liver test for critical illness-induced cholestasis is available; it remains a “diagnosis of exclusion”.
In absence of an obstruction or pre-existing liver disease, abnormal liver tests more likely indicate critical illness-induced cholestasis.
Because cholestasis induced by critical illness is primarily a result of functional alterations at the hepatocyte and bile duct levels, it is usually reversible, and there is no clear argument for attempting to treat this condition. There still is no treatment available for cholestasis induced by critical illness, and the general treatment of patients in the ICU focuses on avoiding additional inflammatory stimuli and hypoxia to the liver.
Prevention, however, appears possible to a certain extent. Optimizing supportive care and reducing risk factors that could provoke severe cholestasis, such as the excessive use of antibiotics and other drugs, preventing hyperglycemia, and not using parenteral nutrition during the first week of critical illness have been shown to prevent cholestatic features observed during critical illness.
The use of enteral nutrition rather than parenteral nutrition has been associated with fewer infections and reduced occurrence of metabolic complications in patients with liver disease and after liver transplant. Adequately optimizing hemodynamic perfusion is an essential step in preventing liver dysfunction.