Critical care : the official journal of the Critical Care Forum
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Critical illness leads to increased endogenous production of carbon monoxide (CO) due to the induction of the stress-response enzyme, heme oxygenase-1 (HO-1). There is evidence for the cytoprotective and anti-inflammatory effects of CO based on animal studies. In critically ill patients after cardiothoracic surgery, low minimum and high maximum carboxyhemoglobin (COHb) levels were shown to be associated with increased mortality, which suggests that there is an 'optimal range' for HO-1 activity. Our study aimed to test whether this relationship between COHb and outcome exists in non-surgical ICU patients. ⋯ Critically ill patients surviving the admission to a medical ICU had slightly higher minimum and marginally higher average COHb levels when compared to non-survivors. Even though the observed differences are statistically significant, the minute margins would not qualify COHb as a predictive marker for ICU mortality.
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Editorial Comment
Respiratory variation in inferior vena cava diameter: surrogate of central venous pressure or parameter of fluid responsiveness? Let the physiology reply.
In the previous issue of Critical Care, Muller and colleagues investigated whether respiratory variation in inferior vena cava diameter (ΔIVC) could be a useful predictor of fluid responsiveness in spontaneously breathing patients. The study concludes that accuracy was not very good and therefore that this parameter should be used with caution in these patients. There is still confusion about the meaning of IVC respiratory variations, whether the patient is spontaneously breathing or mechanically ventilated. In this brief commentary, we try to summarize as clearly as possible the significance of IVC variation in different clinical settings.
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Editorial Comment
Please don't call me RI anymore; I may not be the one you think I am!
The previous issue of Critical Care reports new data on renal resistive index in critically ill patients. Although high renal resistive index may indeed be associated with acute kidney injury, the existence of several determinants of this index, of which renal resistance is only one among many, obscures the usefulness of this index in clinical practice.
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It is heavily debated whether or not treatment with hydroxyethyl starch 130/0.4 contributes to the development of acute kidney failure in patients with severe sepsis. In the previous issue of Critical Care, Muller and colleagues report no association between initial resuscitation with hydroxyethyl starch 130/0.4 and renal impairment in a cohort of septic patients. Can we then consider hydroxyethyl starch 130/0.4 a safe intervention? The answer is no - observational data should be interpreted with caution and should mainly be used to identify risks, while safety must be assessed in randomised clinical trials. With these factors in mind, Muller's data associate the use of vasopressors with poor outcome, underlining the need for further randomised clinical trials to assess the potential harmful effects of common interventions in the critically ill.