To determine the relationship between cerebrospinal fluid procalcitonin concentration and severe traumatic brain injury in children.
Prospective, observational clinical study.
A multidisciplinary, tertiary-care pediatric intensive care unit.
Twenty-eight patients who required external ventricular drainage for management of severe traumatic brain injury (Glasgow Coma Scale score of <8) and 22 control patients for whom lumbar cerebrospinal fluid evaluation excluded possible meningitis.
Standard intracranial pressure-directed neurointensive care, including intraventricular catheter placement and continuous cerebrospinal fluid drainage, was used to manage patients with severe traumatic brain injury.
Demographic data including age, mechanism of injury, time of injury, initial Glasgow Coma Scale score, and outcome were collected. Cerebrospinal fluid procalcitonin concentration was determined by immunoluminometric assay. Initial cerebrospinal fluid procalcitonin concentration (median [range]) in patients with severe traumatic brain injury was increased greater than three-fold vs. controls (0.41 ng/mL [0.15–2.14] vs. 0.12 ng/mL [0.00–0.24], p < .001). Initial cerebrospinal fluid procalcitonin concentration among patients with abusive head trauma (0.31 ng/mL [0.29–0.50]) also was increased vs. controls (p < .05), although this increase was less robust than patients with accidental trauma (0.41 ng/mL [0.15–2.14], p < .001 vs. controls).
Additional examination of key demographic and outcome variables with a generalized linear regression model was performed for patients with severe traumatic brain injury. Univariate analysis revealed that both time after injury (p < .01) and abusive head trauma as a mechanism of injury (p < .001) were associated with attenuation of the increased cerebrospinal fluid procalcitonin response after traumatic brain injury.
Cerebrospinal fluid procalcitonin concentration is increased in children after traumatic brain injury. The attenuated increase in cerebrospinal fluid procalcitonin among victims of abusive head trauma warrants further study because it may reflect impairment of endogenous neuroprotective mechanisms or delay in seeking medical attention. The significance of these observations remains to be determined as future studies elucidate the physiologic and mechanistic properties of procalcitonin.
From the Departments of Anesthesiology and Critical Care Medicine (YYH, JAC, RAR, MJB, PMK), Pediatrics (JAC, PMK), and Neurosurgery (PDA, DWM), University of Pittsburgh School of Medicine; the Department of Epidemiology (SRW), Graduate School of Public Health, University of Pittsburgh; the Safar Center for Resuscitation Research (RAR, MJB, KLJ, PMK), University of Pittsburgh Medical Center; and the Children‘s Hospital of Pittsburgh (YYH, JAC, RAR, PDA, PMK), Pittsburgh, PA.
Address requests for reprints to: Patrick M. Kochanek, MD, Safar Center for Resuscitation Research, 3434 Fifth Avenue, Pittsburgh, PA 15260. E-mail: Kochanekpccm@anes.upmc.edu
Supported, in part, by University of Pittsburgh Center for Injury Research and Control/Centers for Disease Control and Prevention T32-HD40686 from NICHD of the National Institutes of Health grant 3M01RR56GCRC, and Brahms Diagnostica GmbH.
Presented, in part, at the 29th Educational and Scientific Symposium of the Society of Critical Care Medicine, Orlando, FL, February 11–15, 2000, and the Pediatric Academic Societies Annual Meeting, Boston, MA, May 12–16, 2000.