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Liver Dysfunction in the Intensive Care Unit ANNALS of GASTROENTEROLOGY 2005, 18(1):35-4535

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Liver Dysfunction in the Intensive Care Unit ANNALS of GASTROENTEROLOGY 2005, 18(1):35-4535 Liver dysfunction in the intensive care unit ANNALS OF GASTROENTEROLOGY 2005, 18(1):35-4535 Review Liver dysfunction in the intensive care unit Aspasia Soultati, S.P. Dourakis SUMMARY crosis factor-alpha, is pivotal for the development of liver injury at that stage. Liver dysfunction plays a significant role in the Intensive Care Unit (ICU) patients morbidity and mortality. Although determinations of aminotransferases, coagulation Metabolic, hemodynamic and inflammatory factors studies, glucose, lactate and bilirubin can detect hepatic contribute in liver damage. Hemorrhagic shock, septic shock, injury, they only partially reflect the underlying pathophys- multiple organ dysfunction, acute respiratory dysfunction, iological mechanisms. Both the presence and degree of jaun- metabolic disorders, myocardial dysfunction, infection from dice are associated with increased mortality in a number of hepatitis virus, and therapeutic measures such as blood non hepatic ICU diseases. transfusion, parenteral nutrition, immunosuppresion, and Therapeutic approaches to shock liver focus on the drugs are all recognised as potential clinical situations on prevention of precipitating causes. Prompt resuscitation, the grounds of which liver dysfunction develops. definitive treatment of sepsis, meticulous supportive care, The liver suffers the consequences of shock- or sepsis-in- controlling of circulation parameters and metabolism, in ducing circumstances, which alter hepatic circulation pa- addition to the cautious monitoring of therapeutic measures rameters, oxygen supply and inflammatory responses at the such as intravenous nutrition, mechanical ventilation and cellular level. Moreover, the liver is an orchestrator of met- catecholamine administration reduce the incidence and abolic arrangements which promote the clearance and pro- severity of liver dysfunction. Only precocious measures can duction of inflammatory mediators, the scavenging of bac- be taken to prevent hepatitis in ICU. teria, and the synthesis of acute-phase proteins. This bal- Key words: shock liver, hypoxic hepatitis, ischemic hepati- ance defines the stage upon which the syndrome of shock tis, shock, multiple organs dysfunction. liver develops. Ischemic hepatitis develops from shock and is characterised 1. INTRODUCTION by elevated plasma aminotransferase concentrations. ICU jaundice emerges later in critical illness, mainly in Shock liver is a simplified term used to describe a patients with trauma and sepsis. The commonly reported complex critical ill patients liver syndrome whose biochemical abnormality is conjugated hyperbilirubi- pathophysiology includes haemodynamic, cellular, naemia. The clinical setting suggests that hepatic ischemia immunological and molecular mechanisms. Different and hepatotoxic actions of inflammatory mediators are grades of shock liver affect about 50% of all intensive- the main aetiological factors. Cross-talk between hepato- care patients.1 Although hepatic injury plays a significant cytes, Kupffer cells and endothelial cells, leading to an role in the Intensive Care Unit (ICU) patients morbidity 2 inflammatory response mediated primarily by tumour ne- and mortality, it is underdiagnosed. Shock liver is a consequences of shock- or sepsis- 2nd Department of Medicine, Medical School, Athens University, inducing circumstances. Liver dysfunction can also result Hippokration General Hospital, Athens from multiple organ dysfunction and acute respiratory Author for correspondence: distress syndrome or develop from myocardial dysfunction, S.P Dourakis, 28 Achaias st, 115 23 Athens, Greece, immunosuppresion, metabolic disorders, infection from Tel 210 6918464, 6932272477, FAX 210 6993693, hepatitis virus and therapeutic measures such as blood e-mail: [email protected] transfusion, parenteral nutrition and drugs.3 36 ASPASIA SOULTATI, S.P. DOURAKIS Shock liver is, on that ground, a practical term used flow for the decreased portal venous blood flow is in the to describe a pool of critically ill patients in whom the range of 2030%.10,11,12 Compensation in terms of oxy- elevation of liver function tests or overt hepatic gen delivery is substantially higher because of the much dysfunction is apparent. In most cases liver dysfunction greater oxygen content in the hepatic artery compared emerges without any noticeable changes in the patients to the portal vein. Thus liver oxygen supply is maintained clinical profile. ICU jaundice emerges later in critical until blood loss exceeds 30%.13 The hepatic artery buffer illness, mainly in patients with trauma and sepsis, whereas response is abolished early during endotoxaemia when the pivotal clinical case is that of mild elevation of liver gut blood flow decreases below a critical level and enzymes. Clinical suspicion of liver complications mainly partially recovers after several hours.14,15, 16, 17 depends upon abnormal laboratory tests. Regardless of the underlying mechanism, whenever Hyperbilirubinaemia, an increase in serum transaminas- hepatic microcirculation decreases below a critical es, alkaline phosphatase, lactate dehydrogenase, and ã threshold, cellular ischemia is induced, and this leads to gloutamyl-transpeptidase and a decrease in albumin and hepatic injury and dysfunction. At the same time, the coagulation factor levels are the pivotal laboratory parameters potent endothelin causes profound vasoconstriction in on which the diagnosis of hepatic dysfunction is based. vascular beds, including those of the liver, and its actions Although these parameters lack sensitivity and specificity, are antagonised by the synthesis of nitric oxide (NO) by they emerge as a result of hepatocellular or bile ducts injury, endothelial cells. NO acts as an inhibitor or agonist of cell and consequently they are widely used to detect hepatic signalling events in the liver. Constitutively generated, NO injury.4 Differential diagnosis between hepatocellular and maintains the hepatic microcirculation and endothelial cholestatic injury relies on aminotransferase (transaminases) integrity, while inducible NO synthase (iNOS)-governing and alkaline phosphatase levels.5,6,7 The incidence of liver NO production can be either beneficial or detrimental. Whether NO protects or injures is probably determined dysfunction is underestimated when traditional static mea- by the type of insult, the abundance of reactive oxygen sures such as serum-transaminases or bilirubin as opposed species, the source and amount of NO production, and to dynamic tests, such as clearance tests, are used to diag- the cellular redox status of liver.18 nose liver dysfunction. Dynamic tests, such as indocyanine green clearance, which is not available at the bed-side, are Sixty percent of the liver mass consists of hepatocytes, useful for the monitoring of perfusion and global liver with the remaining liver mass is composed of Kupffer cells, function.8 Finally, liver function is not affected by aging endothelial sinusoidal cells (dependent upon the state of processes.9 inflammation) and also neutrophils and mononuclear cells. The centrilobular liver cell necrosis observed in hy- 2. HYPOXIC HEPATITIS poxic hepatitis is generally attributed to failure of hepatic blood perfusion. Impaired oxygen availability following The liver benefits from double irrigation: one-third hemorrhage in ICU promotes liver injury and contrib- of the blood flow arising from the hepatic artery and two- utes to delayed mortality.19 ,20 Prolonged low flow/ thirds arise from the portal venous system. The portal hypoxia induces ATP depletion and pericentral necrosis venous system combines the effects of splanchnic vaso- and restoration of oxygen supply and ATP levels after constriction, bacterial translocation in the intestine, and shorter periods of low flow ischemia propagate pro- mesenteric arterial supply with the portal perfusion. Yet, grammed cell death or pericentral apoptosis.21 Accord- most of the regulation occurs at the level of the hepatic ingly, liver injury is commonly recognized under the terms artery, which has been designated the hepatic artery shock liver or ischemic hepatitis. In a recently buffer response. It is the inverse change of hepatic artery documented study, 142 episodes of hypoxic hepatitis were flow as a response to changes in portal venous blood flow identified and the role of the hemodynamic mechanisms that maintains a constant overall hepatic blood supply. of tissue hypoxia: ischemia, passive venous congestion, Hepatic flow during shock situations is regulated by the and hypoxemia were assessed.22 Four different hemo- hepatic artery buffer response, which is capable of dynamic mechanisms responsible for hypoxic hepatitis ensuring hepatic blood flow by dilatation of the hepatic were recognized: decompensated congestive heart fail- artery down to a systemic mean arterial pressure of 50 ure (80 cases), acute cardiac failure (20 cases), exacer- mmHg. When mesenteric and, consequently, portal bated chronic respiratory failure (19 cases), and toxic/ venous blood flow decreases, hepatic arterial blood flow septic shock (19 cases). In congestive heart failure and increases. The compensation of hepatic arterial blood acute heart failure, the hypoxia of the liver was attributed Liver dysfunction in the intensive care unit 37 to decreased hepatic blood flow (ischemia) due to left- In terms of cell dysfunction, liver in sepsis has two sided heart failure and to venous congestion secondary opposing roles: a source of inflammatory mediators and to right-sided heart
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