Fevers and leukocytosis after pediatric craniotomy trigger diagnostic evaluation and antimicrobial therapy for possible brain infection. This study determined the incidence and predictors of infection in infants and children undergoing epilepsy neurosurgery.
We reviewed the postoperative course of 100 consecutive surgeries for pediatric epilepsy, comparing those with and without infections for clinical variables and daily maximum temperatures, blood white blood cell (WBC) and differential and cerebrospinal fluid (CSF) studies.
Infections were the most common adverse events after these surgeries. Four patients (4%) had CSF infections and 12 had non-CSF infections (including 1 with distinct CSF and bloodstream infections). Most (88%) infections occurred before postoperative day 12 and were associated with larger resections involving ventriculostomies. Fevers (T ≥ 38.5°C) were observed in the first 12 days postsurgery in 43% of cases, and were associated with patients undergoing hemispherectomy and multilobar resections. Fevers in the first 3 days postsurgery identified infections with 73% sensitivity, 69% specificity and 70% accuracy; 2 (13%) patients with infections never developed fevers. Peripheral blood WBC >15,000 was found in 49% of patients and 5 cases of infections never had elevated WBC counts. WBC differential, CSF protein, red blood cell, WBC and red blood cell/WBC ratios were poor predictors of infections. Longer hospital stays were associated with infections and hemispherectomy and multilobar resections. Patients with and without infections were equally likely to be seizure free after surgery.
Fevers and elevated blood WBC counts were common after pediatric epilepsy surgery, but CSF infections were uncommon. Positive cultures and other confirmatory microbiologic tests should drive changes in antimicrobial therapy after surgery.
From the Departments of *Neurosurgery and Psychiatry & Biobehavioral Medicine, †Pediatrics, ‡Molecular and Medical Pharmacology, §The Intellectual and Developmental Disabilities Research Center, and ¶The Brain Research Institute, ‖David Geffen School of Medicine, University of California, Los Angeles, CA.
This work was supported by grants from the National Institutes of Health [R01 NS38992] to G.W.M. and the Short Term Training Program at David Geffen School of Medicine at UCLA to J.P. The authors have no other funding or conflicts of interest to disclose.
Address for correspondence: Paul Krogstad, MD, Department of Pediatrics, David Geffen School of Medicine at UCLA, 615 Charles E. Young Drive South, BSRB 173, Los Angeles, CA 90095. E-mail: firstname.lastname@example.org.