Critical care : the official journal of the Critical Care Forum
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Carbon dioxide is a waste product of aerobic cellular respiration in all aerobic life forms. PaCO2 represents the balance between the carbon dioxide produced and that eliminated. Hypocapnia remains a common - and generally underappreciated - component of many disease states, including early asthma, high-altitude pulmonary edema, and acute lung injury. ⋯ Hypercapnia may play a beneficial role in the pathogenesis of inflammation and tissue injury, but may hinder the host response to sepsis and reduce repair. In contrast, hypocapnia may be a pathogenic entity in the setting of critical illness. The present paper reviews the current clinical status of low and high PaCO2 in the critically ill patient, discusses the insights gained to date from studies of carbon dioxide, identifies key concerns regarding hypocapnia and hypercapnia, and considers the potential clinical implications for the management of patients with acute lung injury.
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We summarize original research in the field of critical care nephrology accepted or published in 2009 in Critical Care or, when considered relevant or directly linked to this research, in other journals. Four main topics have been identified for a rapid overview: (a) post-surgical acute kidney injury (AKI); (b) timing of renal replacement therapy (RRT): different authors examined this critical issue of RRT in different settings (post-surgical patients, burned patients, and intensive care unit patients); (c) DoReMi (Dose Response Multicentre International) and other important surveys on dialysis dose and management; and (d) pediatric AKI and RRT: interest in this last topic is increasing, and studies on biomarkers, complications of pediatric dialysis, and application of RRT to extracorporeal membrane oxygenation are discussed.
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Comparative Study
Regulation and prognostic relevance of serum ghrelin concentrations in critical illness and sepsis.
Ghrelin has been recently identified as a mediator of various beneficial effects in animal models of sepsis. At present, no data are available concerning specific properties of ghrelin in critically ill patients from large cohorts. In order to identify possible pathogenic functions of ghrelin in critically ill patients and human sepsis from a clinical point of view, we aimed at analyzing ghrelin serum concentrations in a large cohort of well characterized patients with critical illness. ⋯ Ghrelin serum concentrations are elevated in all circumstances of critical disease, including sepsis and non-sepsis patients. High ghrelin levels are a positive predictor of ICU-survival in sepsis patients, matching previous results from animal models. Future experimental and clinical studies are needed to evaluate ghrelin as a novel prognostic tool in ICU patients and its potential therapeutic use in sepsis.
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Comparative Study
Interleukin-10 gene down-expression in circulating mononuclear cells during infusion of drotrecogin-α activated: a pilot study.
The purpose of this study was to investigate the gene expression of interferon-gamma (IFN-γ), tumor necrosis factor-alpha (TNF-α) and interleukin-10 (IL-10) in circulating mononuclear cells harvested from septic shock patients on drotrecogin-α activated (DAA) in order to determine whether this treatment has any effect on the inflammation phase. ⋯ In this study, lack of IL-10 gene down-expression despite a 36-hour infusion of DAA is an ominous sign in septic shock patients suggesting that DAA is not able to reverse the outcome. Our results suggest that DAA can decrease the expression of anti-inflammatory cytokines in septic shock patients. IL-10 or IFN-γ gene down-expression could represent markers of DAA response.
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Comment Review
Estimation of dead space fraction can be simplified in the acute respiratory distress syndrome.
Acute lung injury and acute respiratory distress syndrome are characterized by a non-cardiogenic pulmonary edema responsible for a significant impairment of gas exchange. The pulmonary dead space increase, which is due primarily to an alteration in pulmonary blood flow distribution, is largely responsible for carbon dioxide retention. Previous studies, computing the pulmonary dead space by measuring the expired carbon dioxide and the Enghoff equation, found that the dead space fraction was significantly higher in the non-survivors; it was even an independent risk of death. The computation of the dead space not by measuring the expired carbon dioxide but by applying a rearranged alveolar gas equation that takes into account only the weight, age, height, and temperature of the patient could lead to widespread clinical diffusion of this measurement at the bedside.