Abstract
In Response We agree with Vos et al.1 that the absence of liver enzyme measurements in some of our patients may be a drawback in our study. However, biochemical hepatic function testing may not offer the key information on hepatocellular dysfunction2 as Vos et al. suggest. Hultcrantz et al.3 described that chronically elevated liver enzymes without symptoms or physical signs of liver disease correspond with various forms of liver disease preferably in the presence of a positive history on alcohol consumption, drug abuse, hepatitis, or obesity. All patients displaying these factors were excluded from our study population, thus removing those patients that may exhibit elevated hepatic enzymes in the absence of physical signs or symptoms of liver disease. Regarding the importance of hemodynamics and indocyanine green plasma disappearance rate (ICG-PDR), we originally intended to use the noninvasive method of ICG measurement, pulse dye densitometry, to measure cardiac output in our study population. To validate the transcutaneous method versus intraarterial measurement of ICG, we performed simultaneous measurements in a subpopulation. In this subpopulation, we had to conclude that, for individual measurement of cardiac output, the transcutaneous measurement of ICG by pulse dye densitometry is not accurate enough.4 For the purpose of this discussion, the measurements of cardiac output versus the ICG-PDR value in the patients in whom we performed arterial blood sampling is shown in Figure 1. The open diamonds represent the patients receiving a propofol induction. Inspection of Figure 1 leads to the conclusion that the absence or presence of propofol did not induce significant hemodynamic changes in this otherwise healthy population nor did it affect ICG-PDR.Figure 1: Representation of cardiac output measurements based on arterial blood indocyanine green (ICG) concentrations versus ICG– plasma disappearance rate (PDR) values determined in patients who underwent simultaneous arterial ICG sampling. The circles represent the measurements in awake subjects; the diamonds represent the measurements during propofol induction.We thus maintain our conclusion4 that ICG-PDR values in a population without clinical signs of liver failure range well below 18% min−1, cited as the cutoff value for hepatic failure and propagated as criterion for clinical intervention. This cutoff value needs to be reconsidered as has been suggested elsewhere.5 We agree with the reviewers that further studies are needed and that the final word on this subject has not yet been written.
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