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Relationship between increases in pancreatic enzymes and cerebral events in children after traumatic brain injury

Joan Sanchez de Toledo¹, P David Adelson, R Scott Watson

¹Department of Critical Care Medicine, University of Pittsburgh, Pittsburgh, PA, USA. sanchezdetoledoj@upmc.edu

Neurocritical Care

|August 12, 2009

Insights

Increases in pancreatic enzymes (PE) are common in children after severe traumatic brain injury (TBI). Delayed PE increases are linked to intracranial events, suggesting a brain-gut connection.

Area of Science:

Pediatric critical care medicine
Neurotrauma research
Gastroenterology

Background:

Severe traumatic brain injury (TBI) in children can lead to various complications.
Pancreatic enzyme (PE) elevations are sometimes used to indicate pancreatitis in critically ill children.

Purpose of the Study:

To identify risk factors for early and delayed increases in pancreatic enzymes (PE) following severe TBI in children.
To investigate the association between cerebral events and PE elevations.

Main Methods:

Retrospective analysis of a prospectively collected Pediatric Neurotrauma Registry.
Inclusion of children with severe TBI (Glasgow Coma Scale ≤ 8).
Classification into normal PE, early PE (within 24h), and delayed PE (after 24h) groups.

Main Results:

57% of children experienced PE increases (18% early, 39% delayed).
Multisystem trauma was associated with early PE increases.
Delayed PE increases were linked to older age, intracranial hypertension, intracranial hemorrhage, and specific medications (pentobarbital, mannitol, vasoactive drugs).
Intracranial hypertension and hemorrhage independently predicted PE increases.

Conclusions:

Elevated pancreatic enzymes are frequent in children with severe TBI.
Delayed PE increases appear associated with intracranial events, indicating a potential brain-gut interaction.
Cerebral hemodynamic disturbances may contribute to pancreatic dysfunction in pediatric TBI.

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Abstract

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.

Design And Settings:

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.

Patients:

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)].

Measurements And Main 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.

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