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Eur. J. Clin. Invest. · Apr 2010
Serum procalcitonin, C-reactive protein and white blood cell levels following hypothermia after cardiac arrest: a retrospective cohort study.
- Philipp Schuetz, Barbara Affolter, Sabina Hunziker, Clemens Winterhalder, Michael Fischer, Gianmarco M Balestra, Patrick Hunziker, and Stephan Marsch.
- Department of Emergency Medicine, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA. pschuetz@hsph.harvard.edu
- Eur. J. Clin. Invest. 2010 Apr 1;40(4):376-81.
IntroductionThe aim of this study was to investigate time course of procalcitonin (PCT), C-reactive protein (CRP) and white blood cell (WBC) levels in patients with therapeutic hypothermia after cardiac arrest.MethodsWe retrospectively assessed laboratory and clinical data in a consecutive cohort of patients admitted to the medical intensive-care-unit of the University Hospital in Basel, Switzerland, in whom therapeutic hypothermia was induced because of cardiac arrest between December 2007 and January 2009. Infection was considered based on microbiological evidence (restricted definition) and/or clinical evidence of infection with prescription of antibiotics (extended definition).ResultsFrom 34 included patients, 25 had respiratory tract infection based on the clinical judgment and in 18 microbiological cultures turned positive (restricted definition). PCT concentrations were highest on the first day after hypothermia and showed a steady decrease until day 7 without differences in patients with and without presumed infection. CRP concentrations increased to a peak level at days 3-4 followed by a steady decrease; CRP concentrations were higher in patients with clinical diagnosis of infection on day 4 (P = 0.02); and in patients with evidence of bacterial growth in cultures on days 4 and 5 (P = 0.01 and P = 0.006). WBC remained unchanged after hypothermia without differences between patients with and without infection.ConclusionHigh initial values of PCT and high peak levels after 3-4 days of CRP were found in patients with induction of hypothermia after cardiac arrest. This increase was unspecific and mirrors rather an inflammatory reaction than true underlying infection, limiting the diagnostic potential for early antibiotic stewardship in these patients.
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