To determine whether hypothermia within 24 hours of sepsis diagnosis is associated with development of persistent lymphopenia, a feature of sepsis-induced immunosuppression.
Retrospective cohort study.
A 1,200-bed university-affiliated tertiary care hospital.
Adult patients diagnosed with bacteremia and sepsis within 5 days of hospital admission between January 1, 2010, and July 31, 2012.
Leukocyte counts were recorded during the first 4 days following sepsis diagnosis. Persistent lymphopenia was defined as an absolute lymphocyte count less than 1.2 cells/μL × 103 present on the fourth day after diagnosis. Of the 445 patients with sepsis included, hypothermia developed in 64 patients (14.4%) (defined as a body temperature < 36.0°C) within 24 hours of sepsis diagnosis. Hypothermia was a significant independent predictor of persistent lymphopenia (adjusted odds ratio, 2.70 [95% CI, 1.10, 6.60]; p = 0.03) after accounting for age, disease severity, comorbidities, source of bacteremia, and type of organism. Compared with the nonhypothermic patients, hypothermic patients had higher 28-day (50.0% vs 24.9%, p < 0.001) and 1-year mortality (60.9% vs 47.0%, p = 0.001).
Hypothermia is associated with higher mortality and an increased risk of persistent lymphopenia in patients with sepsis, and it may be an early clinical predictor of sepsis-induced immunosuppression.
1Department of Anesthesiology, Washington University School of Medicine, St. Louis, MO.
2Department of Emergency Medicine, Washington University School of Medicine, St. Louis, MO.
3Department of Pharmacy, Barnes-Jewish Hospital, St. Louis, MO.
4Department of Surgery, Washington University School of Medicine, St. Louis, MO.
* See also p. 1327.
This study was performed at Washington University School of Medicine and Barnes-Jewish Hospital, St. Louis, MO.
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Dr. Drewry was supported by the Foundation for Anesthesia Education and Research and the Washington University Institute of Clinical and Translational Sciences (grant UL1 TR000448) from the National Center for Advancing Translational Sciences. She received support for article research from the National Institutes of Health (NIH). Dr. Fuller received support for article research from the NIH and was supported by the Washington University Institute of Clinical and Translational Sciences (grant UL1 TR00448 and KL2 TR000450). Dr. Skrupky received support for article research from the NIH. His institution received grant support from the NIH/National Center for Advancing Translational Sciences, Clinical and Translational Science Awards grant UL1TR000448. Dr. Hotchkiss consulted for Glaxo and received support for article research from the NIH (grants GM 44118 and GM 55194). He receives grant support from MedImmune, Bristol-Myers Squibb, Agennix, and Aurigene. His institution received grant support from the NIH.
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