Serum procalcitonin, C-reactive protein and white blood cell levels following hypothermia after cardiac arrest: a retrospective cohort study

Authors


Philipp Schuetz, MD, Beth Israel Deaconess Medical Center, Department of Emergency Medicine, 330 Brookline Ave., Boston, MA 02215, USA. Tel.: 0041 61 265 65 65; fax: 0041 61 265 51 00; e-mail: pschuetz@hsph.harvard.edu

Abstract

Eur J Clin Invest 2010; 40 (4): 376–381

Abstract

Introduction  The 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.

Methods  We 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).

Results  From 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.

Conclusion  High 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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