Clinical outcomes of ketamine in patients with traumatic brain injury: A systematic review.

A systematic review of 21 studies involving 886 patients with traumatic brain injury (TBI) found inconsistent effects of ketamine-induced anesthesia on key brain measures. Some studies showed a significant decrease in intracranial pressure (ICP) with ketamine sedation, while others showed a significant increase. Several studies found no link between ketamine dose and ICP changes. Cerebral perfusion pressure (CPP) increased significantly in some studies but decreased in one study using ketamine-midazolam; most studies found no effect. Other measures like brain electrical activity, neurologic outcomes, and side effects also varied. The review concludes that ketamine anesthesia inconsistently improves or worsens TBI outcomes and calls for research into the factors behind these mixed results.

Study at a glance

Abstract

The current literature provides contradictory results concerning the impact of ketamine-induced anesthesia on traumatic brain injury (TBI) outcomes. This study aimed to investigate the potential of ketamine boluses to influence the brain pathophysiology in TBI patients. Twenty-one studies (n = 886) were extracted from PubMed, Web of Science, Scopus, CINAHL, and Cochrane Library. The primary endpoints included intracranial pressure (ICP) and cerebral perfusion pressure (CPP). The secondary endpoints were mean arterial pressure (MAP), heart rate (HR), electroencephalography (EEG), mean cerebral blood flow velocity, jugular oxygen saturation, ventilation, neurological outcomes, mortality, and overall efficacy and side-effects of ketamine-induced anesthesia. Four studies indicated a statistically significant decline in ICP in TBI patients, with ketamine sedation. Contrastingly, two studies revealed statistically significant ICP elevations, after ketamine-induced anesthesia, in TBI patients. Five studies negated any correlation between ketamine dosages and ICP changes. Three studies indicated a statistically significant increase in CPP after ketamine-induced anesthesia in TBI patients. One study revealed CPP decline after the administration of ketamine-midazolam treatment to TBI patients. Five studies revealed no noticeable influence of ketamine bolus on CPP in TBI patients. Similarly, inconsistent variations were observed in most of the secondary endpoints, including electroencephalography, neurologic outcomes, and ketamine-related side effects (all P <0.05). This systematic review emphasizes the role of ketamine-induced anesthesia in inconsistently improving or deteriorating clinical outcomes in patients with TBI. Future studies should evaluate the predominant causes (i.e., factors and attributes) of ketamine-related clinical outcomes in the TBI setting.