Depressive DisordersPTSDChronic PainTraumatic Brain Injury (TBI)Neurological InjuryKetamine

Outcomes and physiologic responses associated with ketamine administration after traumatic brain injury in the United States and Canada: a retrospective analysis

Ketamine administration after traumatic brain injury was not associated with increased mortality or greater disability despite being given to more severely injured patients. Ketamine exposure correlated with fewer episodes of elevated intracranial pressure and smaller rises in TBI protein biomarkers, but a higher incidence of seizures and, in the intracranial haemorrhage subgroup, more cardiac events.

Authors

  • Peters, A. J.
  • Khan, S. A.
  • Koike, S.

Published

Journal of Trauma Injury Infection and Critical Care
individual Study

Abstract

Purpose

Ketamine has historically been contraindicated in traumatic brain injury (TBI) due to concern for raising intracranial pressure. However, it is increasingly being used in TBI due to the favorable respiratory and hemodynamic properties. To date, no studies have evaluated whether ketamine administered in subjects with TBI is associated with patient survival or disability.

Methods

We performed a retrospective analysis of data from the multicenter Prehospital Tranexamic Acid Use for Traumatic Brain Injury trial, comparing ketamine-exposed and ketamine-unexposed TBI subjects to determine whether an association exists between ketamine administration and mortality, as well as secondary outcome measures.

Results

We analyzed 841 eligible subjects from the original study, of which 131 (15.5%) received ketamine. Ketamine-exposed subjects were younger (37.3±16.9 years vs. 42.0±18.6 years, P=0.037), had a worse initial Glasgow Coma Scale score (7±3 vs. 8±4, P=0.003), and were more likely to be intubated than ketamine-unexposed subjects (88.5% vs. 44.2%, P<0.001). Overall, there was no difference in mortality (12.2% vs. 15.5%, P=0.391) or disability measures between groups. Ketamine-exposed subjects had significantly fewer instances of elevated intracranial pressure (ICP) compared to ketamine-unexposed subjects (56.3% vs. 82.3%, P=0.048). In the very rare outcomes of cardiac events and seizure activity, seizure activity was statistically more likely in ketamine-exposed subjects (3.1% vs. 1.0%, P=0.010). In the intracranial hemorrhage subgroup, cardiac events were more likely in ketamine-exposed subjects (2.3% vs. 0.2%, P=0.025). Ketamine exposure was associated with a smaller increase in TBI protein biomarker concentrations.

Conclusions

Ketamine administration was not associated with worse survival or disability despite being administered to more severely injured subjects. Ketamine exposure was associated with reduced elevations of ICP, more instances of seizure activity, and lower concentrations of TBI protein biomarkers.

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Research Summary of 'Outcomes and physiologic responses associated with ketamine administration after traumatic brain injury in the United States and Canada: a retrospective analysis'

Introduction

The authors contextualise ketamine as a dissociative anaesthetic historically avoided in traumatic brain injury (TBI) because early reports suggested it could raise intracranial pressure (ICP), cerebral blood flow and metabolic rate. More recent clinical practice has increasingly used ketamine in trauma because of its haemodynamic stability, analgesic properties and respiratory-sparing effects. Small-scale prospective studies in TBI have reported either no increase or a reduction in ICP after ketamine, and preclinical mechanisms (e.g. reduction of glutamate toxicity and inhibition of cortical spreading depression) have suggested possible neuroprotective effects. However, earlier work did not examine patient-centred outcomes such as survival or disability, leaving uncertainty about the overall safety and outcome implications of ketamine use after TBI. Using the dataset from the multicentre Prehospital Tranexamic Acid Use for Traumatic Brain Injury (TXA for TBI) trial, the researchers set out to examine whether prehospital ketamine administration is associated with mortality, disability and physiologic responses in subjects with moderate-to-severe TBI. They also investigated ketamine's association with longitudinal trajectories of circulating TBI protein biomarkers (GFAP, MAP2, UCHL1) and performed a predefined subgroup analysis in patients with intracranial haemorrhage (ICH). The a priori hypothesis was that ketamine exposure would not be associated with worse survival or disability and would not produce different physiologic or biomarker responses compared with no ketamine exposure.

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