Non-neurologic organ dysfunction plays a major role in predicting outcomes in pediatric traumatic brain injury.


Journal

Journal of pediatric surgery
ISSN: 1531-5037
Titre abrégé: J Pediatr Surg
Pays: United States
ID NLM: 0052631

Informations de publication

Date de publication:
Aug 2020
Historique:
received: 11 06 2019
revised: 02 12 2019
accepted: 24 01 2020
pubmed: 23 2 2020
medline: 5 1 2021
entrez: 22 2 2020
Statut: ppublish

Résumé

Nonneurological organ dysfunction (NNOD) occurs after traumatic brain injury (TBI) and is associated with mortality. The aim of our study was to evaluate the prevalence of NNOD and its association with outcomes in pediatric patients with TBI. We hypothesized that NNOD is associated with worse outcomes in pediatric patients with severe TBI. We performed a 4-year (2013-16) analysis of our prospectively maintained TBI database. All patients (age < 18) with an isolated-severe TBI (head-abbreviated injury scale: AIS ≥ 3 & extracranial-AIS < 3) were included. NNOD was measured using the pediatric multiple organ dysfunction (P-MOD) score. Outcomes were in-hospital mortality, Glasgow Outcome Scale-Extended (GOS-E), and adverse discharge disposition: rehabilitation or skilled nursing facility (SNF). Regression analysis was performed. We analyzed 292 patients. Mean age was 11 ± 6 years, 57% were male and the mortality rate was 18.1%. The incidence of NNOD was 35%. The most common dysfunctional organ system was the respiratory (25%) followed by the cardiovascular (12%). On regression analysis, the presence of at least one NNOD was independently associated with in-hospital mortality (OR 2.1 [1.7-2.9]; p < 0.01), low GOS-E (OR 1.8 [1.5-2.3]; p < 0.01), and SNF disposition (OR 1.7 [1.2-2.1]; p < 0.01). NNOD develops in one of every three severe TBI pediatric patients and is independently associated with adverse outcomes. Identification of NNOD in pediatric TBI and focusing on management of NNOD could improve outcomes. III Prognostic.

Sections du résumé

BACKGROUND BACKGROUND
Nonneurological organ dysfunction (NNOD) occurs after traumatic brain injury (TBI) and is associated with mortality. The aim of our study was to evaluate the prevalence of NNOD and its association with outcomes in pediatric patients with TBI. We hypothesized that NNOD is associated with worse outcomes in pediatric patients with severe TBI.
METHODS METHODS
We performed a 4-year (2013-16) analysis of our prospectively maintained TBI database. All patients (age < 18) with an isolated-severe TBI (head-abbreviated injury scale: AIS ≥ 3 & extracranial-AIS < 3) were included. NNOD was measured using the pediatric multiple organ dysfunction (P-MOD) score. Outcomes were in-hospital mortality, Glasgow Outcome Scale-Extended (GOS-E), and adverse discharge disposition: rehabilitation or skilled nursing facility (SNF). Regression analysis was performed.
RESULTS RESULTS
We analyzed 292 patients. Mean age was 11 ± 6 years, 57% were male and the mortality rate was 18.1%. The incidence of NNOD was 35%. The most common dysfunctional organ system was the respiratory (25%) followed by the cardiovascular (12%). On regression analysis, the presence of at least one NNOD was independently associated with in-hospital mortality (OR 2.1 [1.7-2.9]; p < 0.01), low GOS-E (OR 1.8 [1.5-2.3]; p < 0.01), and SNF disposition (OR 1.7 [1.2-2.1]; p < 0.01).
CONCLUSION CONCLUSIONS
NNOD develops in one of every three severe TBI pediatric patients and is independently associated with adverse outcomes. Identification of NNOD in pediatric TBI and focusing on management of NNOD could improve outcomes.
LEVEL OF EVIDENCE METHODS
III Prognostic.

Identifiants

pubmed: 32081358
pii: S0022-3468(20)30094-4
doi: 10.1016/j.jpedsurg.2020.01.051
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1590-1595

Informations de copyright

Copyright © 2020 Elsevier Inc. All rights reserved.

Auteurs

Kamil Hanna (K)

Division of Trauma, Critical Care, Emergency Surgery, and Burns, Department of Surgery, College of Medicine, University of Arizona, Tucson, AZ. Electronic address: kamilhanna@surgery.arizona.edu.

Mohammad Hamidi (M)

Division of Trauma, Critical Care, Emergency Surgery, and Burns, Department of Surgery, College of Medicine, University of Arizona, Tucson, AZ. Electronic address: hamidi@surgery.arizona.edu.

Phillip Vartanyan (P)

Division of Trauma, Critical Care, Emergency Surgery, and Burns, Department of Surgery, College of Medicine, University of Arizona, Tucson, AZ. Electronic address: pvartanyan@email.arizona.edu.

Marion Henry (M)

Division of Trauma, Critical Care, Emergency Surgery, and Burns, Department of Surgery, College of Medicine, University of Arizona, Tucson, AZ. Electronic address: mcwhenry@surgery.arizona.edu.

Lourdes Castanon (L)

Division of Trauma, Critical Care, Emergency Surgery, and Burns, Department of Surgery, College of Medicine, University of Arizona, Tucson, AZ. Electronic address: lourdes.castanon@ahn.org.

Andrew Tang (A)

Division of Trauma, Critical Care, Emergency Surgery, and Burns, Department of Surgery, College of Medicine, University of Arizona, Tucson, AZ. Electronic address: atang@surgery.arizona.edu.

Muhammad Zeeshan (M)

Division of Trauma, Critical Care, Emergency Surgery, and Burns, Department of Surgery, College of Medicine, University of Arizona, Tucson, AZ. Electronic address: mzeeshan@surgery.arizona.edu.

Narong Kulvatunyou (N)

Division of Trauma, Critical Care, Emergency Surgery, and Burns, Department of Surgery, College of Medicine, University of Arizona, Tucson, AZ. Electronic address: nkulvatunyou@surgery.arizona.edu.

Bellal Joseph (B)

Division of Trauma, Critical Care, Emergency Surgery, and Burns, Department of Surgery, College of Medicine, University of Arizona, Tucson, AZ. Electronic address: bjoseph@surgery.arizona.edu.

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Classifications MeSH