Relationship between increases in pancreatic enzymes and cerebral events in children after traumatic brain injury.
OBJECTIVE
To describe the risk factors of early and delayed increases in pancreatic enzymes (PE) in children after severe traumatic brain injury (TBI) and to determine if cerebral events (such as intracranial hemorrhage or intracranial hypertension) are associated with increases in PE.


METHODS
Retrospective analysis of prospectively collected Pediatric Neurotrauma Registry for children with severe TBI (GCS ≤ 8). We assessed the association of clinical characteristics with the development of increases in PE using regression analyses.


METHODS
Fifty-one children with severe TBI were classified into three groups [normal PE; early PE (PE increases within first 24 h); delayed PE (PE increases after 24 h)].


RESULTS
Increases in PE were observed in 29/51 children [57% total; n = 9 (18%) early; n = 20 (39%) delayed]. Multisystem trauma was more prevalent in patients with early increases in PE compared to those without increases in PE (70 vs. 30%, RR = 2.8, 95% CI 1.1-7) but not different between delayed PE and normal PE groups. In the bivariate analyses, increasing age (odds ratios, [95% CI]; 1.2, [1.05-1.4]), intracranial hypertension (14.6, [2.6-80.5]), intracranial hemorrhage (6.2, [1.15-33.7]), receipt of pentobarbital (9.3, [2.1-39.9]), mannitol (13.2, [2.7-62.2]), and vasoactive medications (6.9, [1.5-31.3]) were associated with the development of delayed increases in PE, whereas sex, initial Glasgow Coma Scale, severity of injury (PRISM, Injury Severity Score), therapeutic hypothermia, morphine and furosemide were not associated. Both intracranial hypertension and intracranial hemorrhage independently predicted the development of increases in PE (14.6, [2.6-80.5], and 9.1, [1.31-63.3], respectively).


CONCLUSIONS
Increases in PE, often used as the only measures of pancreatitis in children with other severe injuries, are common in children after severe TBI and delayed presentation appears related to intracranial events. This suggests a possible interaction between the brain and the gastrointestinal system, implying that disturbances in cerebral hemodynamics may lead to pancreatic dysfunction.
de Toledo
Joan Sanchez
JS
Department of Critical Care Medicine, University of Pittsburgh, Pittsburgh, PA, USA. sanchezdetoledoj@upmc.edu
Adelson
P David
PD
Watson
R Scott
RS
Gaines
Barbara
B
Brown
S Danielle
SD
Kochanek
Patrick M
PM
Wisniewski
Stephen R
SR
Fink
Ericka
E
Bayir
Hülya
H
Clark
Robert S B
RS
Bell
Michael J
MJ
D000681:Amylases / Q000097:blood*; D015415:Biomarkers / Q000097:blood; D001930:Brain Injuries / Q000453:epidemiology* / Q000378:metabolism*; D002648:Child; D002675:Child, Preschool; D005260:Female; D015600:Glasgow Coma Scale; D006801:Humans; D008049:Lipase / Q000097:blood*; D008297:Male; D046790:Pancreas, Exocrine / Q000378:metabolism; D015995:Prevalence; D012042:Registries; D012044:Regression Analysis; D012189:Retrospective Studies; D012307:Risk Factors
D015415:Biomarkers; D008049:Lipase; D000681:Amylases