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Critical Care 2008
Towards goal-directed therapy of hepatorenal syndrome: we have the tools but we need the trialsDOI: 10.1186/cc6804 Abstract: Decompensated cirrhosis is characterized by severe circulatory derangements including progressive splanchnic vasodilatation and portal hypertension. These derangements result in several of the complications of advanced cirrhosis, such as increasing ascites and hepatorenal syndrome (HRS). The splanchnic vasodilatation in turn results in relative arterial underfilling [1], with consequent activation of the neurohumoral system, leading to vasoconstriction of numerous vascular beds including the liver, the kidney and the brain [2]. The more advanced the disease, the greater the activation of these neurohumoral factors, most maximal in the state of HRS [3]. Management of tense ascites in the context of evolving HRS has been debated with the concern that a large-volume paracentesis may evoke paracentesis-induced circulatory dysfunction despite volume replacement, thereby further potentiating HRS.The study reported by Umgelter and colleagues in the previous edition of Critical Care describes the single and combined effects on haemodynamics and renal function of plasma expansion with albumin and paracentesis in patients with tense ascites and HRS [4]. Maintenance of the global end-diastolic volume was achieved by invasive monitoring of the central volume. The study's key findings were a demonstration that the cardiac index in HRS patients was fluid responsive despite a normal central venous pressure, and that the reduction in intra-abdominal pressure following paracentesis was associated with an improvement in renal function in the context of fluid substitution guided by assessment of the global end-diastolic volume. In their uncontrolled study, a transpulmonary thermodilution technique (the PiCCO system, Pulsion Medical Systems, AG) facilitated measurement of both cardiac output as well as intrathoracic and pulmonary blood volumes. A subtraction of the pulmonary blood volume from the intrathoracic blood volume enabled an estimate of the 'central' blood volume, referred to
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