Neurological injury markers in children with septic shock.
OBJECTIVE
To determine whether known serum markers of neurologic injury are increased in children with septic shock.


METHODS
Prospective, observational study.


METHODS
Tertiary-care, pediatric intensive care unit.


METHODS
Two cohorts of children (n = 24) with septic shock were prospectively enrolled within 24 hrs of their diagnosis. In cohort 1, serum markers (S100beta, neuron-specific enolase [NSE], and glial fibrillary acidic protein [GFAP]) were determined (n = 18). In cohort 2, in addition to serum markers, urine S100beta and GFAP were determined, and continuous electroencephalography (cEEG) was performed. Children who presented to the emergency room with a fever served as controls (n = 32). Children with known neurologic conditions were excluded.


METHODS
None.


RESULTS
Serum and urine were collected daily for up to 7 days or until pediatric intensive care unit discharge. Biomarker concentrations were determined by commercially available enzyme-linked immunosorbent assays. cEEG was performed on days 1, 2, 4, and 7 in a 16-channel montage for at least 6 hrs. Physical examinations did not reveal focal neurologic deficits. Children with septic shock demonstrated increased serum S100beta and NSE compared with controls (mean +/- SEM: 10.5 microg/L +/- 2.4 vs. .9 microg/L +/- .1, p < .001; 96.6 microg/L +/- 8.9 vs. 4.0 microg/L +/- 1.3, p < .001, respectively). Serum GFAP was detectable in five septic children and none of the controls. In cohort 2, urine of four patients demonstrated measurable S100beta levels, and GFAP was detected in one child (nonsurvivor). cEEG demonstrated moderate to severe encephalopathy in all children studied.


CONCLUSIONS
Markers of neurologic injuries are increased in children with septic shock. This may indicate subclinical injuries that are either transient or permanent. Studies that correlate the long-term neurologic outcome of children with these markers are needed to identify children at risk for neurologic injuries from septic shock.
Hsu
Angela A
AA
Division of Critical Care Medicine, Children's Research Institute, Children's National Medical Center, Washington, DC, USA. ahsu@cnmc.org
Fenton
Kimberly
K
Weinstein
Steven
S
Carpenter
Jessica
J
Dalton
Heidi
H
Bell
Michael J
MJ
D000293:Adolescent; D015415:Biomarkers / Q000097:blood*; D001930:Brain Injuries / Q000097:blood* / Q000209:etiology / Q000503:physiopathology; D016022:Case-Control Studies; D002648:Child; D002675:Child, Preschool; D004569:Electroencephalography; D004797:Enzyme-Linked Immunosorbent Assay; D005904:Glial Fibrillary Acidic Protein / Q000097:blood; D006801:Humans; D007223:Infant; D009414:Nerve Growth Factors / Q000097:blood; D010751:Phosphopyruvate Hydratase / Q000097:blood; D011446:Prospective Studies; D064568:S100 Calcium Binding Protein beta Subunit; D009418:S100 Proteins / Q000097:blood; D012772:Shock, Septic / Q000097:blood* / Q000150:complications / Q000503:physiopathology
D015415:Biomarkers; D005904:Glial Fibrillary Acidic Protein; D009414:Nerve Growth Factors; D064568:S100 Calcium Binding Protein beta Subunit; D009418:S100 Proteins; D010751:Phosphopyruvate Hydratase