Traumatic brain injury in children with thoracic injury: clinical significance and impact on ventilatory management

Aims/Objectives/BackgroundIn the United Kingdom (UK), 20% of patients with severe traumatic brain injury (TBI) receive pre-hospital emergency anaesthesia (PHEA). Current guidance recommends an end-tidal carbon dioxide (ETCO2) of 4.0–4.5kPa to achieve a low-normal arterial partial pressure of CO2 (PaCO2), and reduce secondary brain injury. This recommendation assumes a 0.5kPa ETCO2-PaCO2 gradient. However, the gradient in the acute phase of TBI is unknown. Our primary aim was to report the ETCO2-PaCO2 gradient of TBI patients at hospital arrival.Methods/DesignA retrospective cohort study of adult patients with serious TBI, who received a PHEA by a pre-hospital critical care team in the East of England between 1st April 2015 to 31st December 2017. Linear regression was performed to test for correlation and reported as R-squared (R2). A Bland-Altman plot was used to test for paired ETCO2 and PaCO2 agreement and reported with 95% confidence intervals (95%CI). ETCO2-PaCO2 gradient data were compared with a two-tailed, unpaired, t-test.Results/Conclusions107 patients were eligible for inclusion. Sixty-seven patients did not receive a PaCO2 sample within 30 minutes of hospital arrival and were therefore excluded. Forty patients had complete data and were included in the final analysis; per protocol.The mean ETCO2-PaCO2 gradient was 1.7 (±1.0) kPa, with only moderate correlation of ETCO2 and PaCO2 at hospital arrival (R2=0.23, p=0.002). The Bland-Altman bias was 1.7 (95%CI 1.4–2.0) kPa with upper and lower limits of agreement of 3.6 (95%CI 3.0–4.1) kPa and -0.2 (95%CI -0.8–0.3) kPa respectively. There was no significant gradient correlation in patients with a co-existing serious thoracic injury (R2=0.13, p=0.10), and this cohort had a larger ETCO2-PaCO2 gradient, 2.0 (±1.1) kPa, p=0.01. Patients who underwent pre-hospital arterial blood sampling had an arrival PaCO2 of 4.7 (±0.2) kPa.Lower ETCO2 targets than previously recommended may be safe and appropriate. The use of pre-hospital PaCO2 measurement is advocated.

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The clinical significance of cerebral atrophy in traumatic brain injury

Archives of Clinical Neuropsychology ◽

10.1093/arclin/2.3.293 ◽

1987 ◽

Vol 2 (3) ◽

pp. 293-304 ◽

Cited By ~ 6

Author(s):

E. D. Bigler

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Clinical Significance ◽

Cerebral Atrophy

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Prospective Evaluation of Posttraumatic Vasospasm: Determining Its Clinical Significance after Traumatic Brain Injury

The American Surgeon ◽

10.1177/000313481408000330 ◽

2014 ◽

Vol 80 (3) ◽

pp. 310-312 ◽

Cited By ~ 1

Author(s):

Cherisse Berry ◽

Eric J. Ley ◽

Daniel R. Margulies ◽

Jessica Pruett ◽

Chad Miller ◽

...

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Clinical Significance ◽

Prospective Evaluation

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Profile of traumatic brain injury (TBI) in relation with maxillofacial and thoracic injury Dr. Hasan Sadikin General Hospital, Bandung

Journal of thee Medical Sciences (Berkala Ilmu Kedokteran) ◽

10.19106/jmedscie/005003201808 ◽

2018 ◽

Vol 50 (3) ◽

Author(s):

Padmini Laxmi Pathmanathan ◽

Gibran Tristan Alpharian ◽

Agung Budi Sutiono

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

General Hospital ◽

Thoracic Injury

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The Association of Early Electrocardiographic Abnormalities With Brain Injury Severity and Outcome in Severe Traumatic Brain Injury

Frontiers in Neurology ◽

10.3389/fneur.2020.597737 ◽

2021 ◽

Vol 11 ◽

Author(s):

Jelmer-Joost Lenstra ◽

Lidija Kuznecova-Keppel Hesselink ◽

Sacha la Bastide-van Gemert ◽

Bram Jacobs ◽

Maarten Willem Nicolaas Nijsten ◽

...

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Hospital Mortality ◽

Cardiac Arrhythmias ◽

Injury Severity ◽

Thoracic Injury ◽

Diffuse Brain Injury ◽

Severe Tbi ◽

Ecg Abnormalities ◽

Diffuse Brain

The aim of this study was to evaluate the frequency of electrocardiographic (ECG) abnormalities in the acute phase of severe traumatic brain injury (TBI) and the association with brain injury severity and outcome. In contrast to neurovascular diseases, sparse information is available on this issue. Data of adult patients with severe TBI admitted to the Intensive Care Unit (ICU) for intracranial pressure monitoring of a level-1 trauma center from 2002 till 2018 were analyzed. Patients with a cardiac history were excluded. An ECG recording was obtained within 24 h after ICU admission. Admission brain computerized tomography (CT)-scans were categorized by Marshall-criteria (diffuse vs. mass lesions) and for location of traumatic lesions. CT-characteristics and maximum Therapy Intensity Level (TILmax) were used as indicators for brain injury severity. We analyzed data of 198 patients, mean (SD) age of 40 ± 19 years, median GCS score 3 [interquartile range (IQR) 3–6], and 105 patients (53%) had thoracic injury. In-hospital mortality was 30%, with sudden death by cardiac arrest in four patients. The incidence of ECG abnormalities was 88% comprising ventricular repolarization disorders (57%) mostly with ST-segment abnormalities, conduction disorders (45%) mostly with QTc-prolongation, and arrhythmias (38%) mostly of supraventricular origin. More cardiac arrhythmias were observed with increased grading of diffuse brain injury (p = 0.042) or in patients treated with hyperosmolar therapy (TILmax) (65%, p = 0.022). No association was found between ECG abnormalities and location of brain lesions nor with thoracic injury. Multivariate analysis with baseline outcome predictors showed that cardiac arrhythmias were not independently associated with in-hospital mortality (p = 0.097). Only hypotension (p = 0.029) and diffuse brain injury (p = 0.017) were associated with in-hospital mortality. In conclusion, a high incidence of ECG abnormalities was observed in patients with severe TBI in the acute phase after injury. No association between ECG abnormalities and location of brain lesions or presence of thoracic injury was present. Cardiac arrhythmias were indicative for brain injury severity but not independently associated with in-hospital mortality. Therefore, our findings likely suggest that ECG abnormalities should be considered as cardiac mimicry representing the secondary effect of traumatic brain injury allowing for a more rationale use of neuroprotective measures.

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