To investigate day-by-day changes in procalcitonin and maximum obtained levels as predictors of mortality in critically ill patients.
Prospective observational cohort study.
Multidisciplinary intensive care unit at Rigshospitalet, Copenhagen University Hospital, a tertiary reference hospital in Denmark.
Four hundred seventy-two patients with diverse comorbidity and age admitted to this intensive care unit.
Equal in all patient groups: antimicrobial treatment adjusted according to the procalcitonin level.
Daily procalcitonin measurements were carried out during the study period as well as measurements of white blood cell count and C-reactive protein and registration of comorbidity. The primary end point was all-cause mortality in a 90-day follow-up period. Secondary end points were mortality during the stay in the intensive care unit and in a 30-day follow-up period. A total of 3,642 procalcitonin measurements were evaluated in 472 critically ill patients. We found that a high maximum procalcitonin level and a procalcitonin increase for 1 day were independent predictors of 90-day all-cause mortality in the multivariate Cox regression analysis model. C-reactive protein and leukocyte increases did not show these qualities. The adjusted hazard ratio for procalcitonin increase for 1 day was 1.8 (95% confidence interval 1.3–2.7). The relative risk for mortality in the intensive care unit for patients with an increasing procalcitonin was as follows: after 1 day increase, 1.8 (95% confidence interval 1.4–2.4); after 2 days increase, 2.2 (95% confidence interval 1.6–3.0); and after 3 days increase: 2.8 (95% confidence interval 2.0–3.8).
A high maximum procalcitonin level and a procalcitonin increase for 1 day are early independent predictors of all-cause mortality in a 90-day follow-up period after intensive care unit admission. Mortality risk increases for every day that procalcitonin increases. Levels or increases of C-reactive protein and white blood cell count do not seem to predict mortality.
From the Department of Clinical Microbiology (JUJ, MT) and Department of Critical Intensive Care (LH, THJ, KE), Rigshospitalet, Copenhagen University Hospital, Denmark; and SAS Institute, Denmark (PS).
Supported by Rigshospitalet, Copenhagen University Hospital, Blegdamsvej, Denmark.
The authors have not disclosed any potential conflicts of interest.
Address requests for reprints to: Jens Ulrik Jensen, MD, Department of Clinical Microbiology, Rigshospitalet, Copenhagen University Hospital, Blegdamsvej 9, DK-2100, Denmark. E-mail: email@example.com.