Elevated serum creatine phosphokinase is associated with mortality and inotropic requirement in critically injured adults |
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| Affiliation: | 1. Division of Trauma and Surgical Critical Care, Vanderbilt University School of Medicine, United States;2. Department of Biostatistics, Vanderbilt University School of Medicine, United States;3. Division of Allergy, Pulmonary, and Critical Care Medicine, Department of Medicine, Vanderbilt University School of Medicine, United States;4. Department of Pathology, Microbiology and Immunology, Vanderbilt University School of Medicine, United States;5. Department of Pharmacology, Vanderbilt University School of Medicine, United States;1. Orthopaedic Hand and Upper Extremity Service, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA;2. University of Amsterdam Orthopaedic Residency Program (PGY 4), Academic Medical Center, Amsterdam, The Netherlands;1. Leicester Royal Infirmary, Leicester, UK;2. University Hospitals of North Tees, Stockton-On-Tees, UK;3. Northampton General Hospital, Northampton, UK;4. University Hospitals of Coventry and Warwickshire, UK;5. Harcourt Building, 8 Harcourt Crescent, Sheffield, UK;1. Universitat de Vic – Universitat Central de Catalunya (UVic-UCC), Vic, Spain;2. Universitat Pompeu Fabra (UPF), Barcelona, Spain;3. Agència de Salut Pública de Barcelona (ASPB), Barcelona, Spain;4. CIBER Epidemiologia y Salud Pública (CIBERESP), Spain;5. Institut d’Investigació Biomèdica (IIB Sant Pau), Barcelona, Spain;1. Universidad Autónoma Metropolitana-Iztapalapa, Departamento de Química, Área de Química Analítica, San Rafael Atlixco 186, Col. Vicentina, Del. Iztapalapa, C.P. 09340 México DF, Mexico;2. Universidad Autónoma Metropolitana-Azcapotzalco, Área Ingeniería de Materiales, Departamento de Materiales, Av. San Pablo 180, Col. Reynosa-Tamaulipas, C.P. 02200 México DF, Mexico |
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| Abstract: | BackgroundHemeproteins such as free myoglobin can undergo autoxidation and catalyse lipid peroxidation, increasing oxidative stress. Creatine phosphokinase (CPK) elevation is a marker for free myoglobin after myocyte damage. Since oxidative injury is a key mechanism of injury-related organ dysfunction, we hypothesised that serum CPK levels correlate with mortality and need for inotropic medication and duration of inotropic support, i.e. shock, among critically injured patients.MethodsWe conducted a retrospective review of 17,847 patients admitted to a single Trauma Intensive Care Unit over 9 years. 2583 patients with serum CPK levels were included in the analysis. Patient data were collected continuously into an electronic ICU repository. Univariate analysis was accomplished using Spearman correlation and the Mann–Whitney U test. Propensity score adjustment models accounting for potential confounders were used to assess the independent effect of CPK level on mortality, need for inotropic support, and duration of inotropic support.ResultsMedian CPK was significantly higher in patients who died (916 [IQR 332, 2472] vs. 711 [253, 1971], p = 0.004) and in those who required inotropic medications (950 [353, 2525] vs. 469 [188, 1220], p < 0.001). After adjusting for propensity score and potential confounders the odds of mortality increased by 1.10 (95% CI 1.02–1.19, p = 0.020) and the odds of inotropic medication use increased by 1.30 (95% CI 1.22–1.38, p < 0.001) per natural log unit increase in CPK. There was a significant association between CPK level and duration of inotropic support (Spearman's rho .237, p < 0.001) that remained significant in a propensity score-adjusted model.ConclusionIn critically injured patients, elevated serum CPK level is independently associated with mortality, need for inotropic medication, and duration of inotropic support. This study is the first to evaluate the relationship of CPK level and mortality in addition to surrogate measures of shock in a population of critically injured patients. If these associations are verified prospectively, there may be a role for treatment with hemeprotein reductants, such as paracetamol, to mitigate the effects of shock and end-organ dysfunction. |
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| Keywords: | Shock Mortality Hemeprotein-mediated Creatine phosphokinase Oxidative injury |
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