Ketamine, an N-methyl-D-aspartate (NMDA) receptor antagonist, is widely used in trauma and emergency medicine for its rapid analgesic and sedative properties. While its efficacy in acute pain management is well established, concerns persist regarding its long-term psychological effects, particularly its potential role in the development of posttraumatic stress disorder (PTSD). Some studies indicate that ketamine may provide rapid symptom relief in PTSD, whereas others raise concerns about its contribution to dissociative states and maladaptive memory consolidation. This narrative review examines existing literature on ketamine’s influence on PTSD symptomatology in trauma-exposed populations. A comprehensive assessment of randomized controlled trials and observational studies was undertaken to explore ketamine’s effects on dissociation, memory processing, and long-term psychiatric outcomes. Relevant studies were identified from major medical databases, and findings were synthesized to present an integrated overview of ketamine’s psychological impact in trauma care settings. Clinical trials suggest that a single intravenous infusion of ketamine (0.5 mg/kg) may significantly reduce PTSD symptoms within 24 hours compared to midazolam, with improvements in overall clinical presentation and no lasting dissociative effects. Conversely, some observational studies have linked ketamine use in acute trauma care to heightened dissociation, hyperarousal, and stress symptoms during early follow-up. Research on burn patients receiving intraoperative ketamine suggests a possible reduction in PTSD incidence, although a later study reported no significant difference compared with non-ketamine controls. The relationship between ketamine and PTSD is complex, with effects appearing to depend on dose and timing of administration. While perioperative ketamine may confer protective benefits against long-term psychiatric sequelae, immediate post-trauma administration may worsen dissociative symptoms and acute stress responses. Further well-controlled clinical trials are needed to refine dosing protocols and identify patient-specific risk factors, including preexisting psychiatric conditions, to better guide its use.
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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PURPOSE The aim of this study was to assess the clinical efficacy of combined treatment with local anesthesia and ketamine procedural sedation for pediatric facial laceration repair in the Emergency Department (ED). METHODS Patients aged 1 to 5 years receiving ketamine for facial laceration repair were prospectively enrolled in a double-blind, randomized, and controlled study at an ED. All patients were to receive intravenous ketamine (2 mg/kg). The local anesthesia group (LA group) received a local anesthetic along with ketamine, whereas the no local anesthesia group (NLA group) received only ketamine. The total time of sedation, the patients' movements and groans, adverse events, and the satisfaction ratings of physicians, nurses, and parents were recorded. RESULTS A total of 186 patients were randomized (NLA group: 90, LA group: 96). The total time of sedation (30.5 minutes for the NLA group, 32.6 minutes for the LA group; p=0.660), patients' groans (26 (28.9%) versus 23 (24.0%); 0.446) and movements (27 (30%) versus 35 (36.5%); p=0.350) was not affected by the addition of local anesthesia. Other adverse events were similar between the two groups. Also, the satisfaction ratings of physicians (median 4 for the NLA group versus 4 for the LA group (p=0.796)), nurses (2 versus 2.5 (p=0.400)), and parents (4 versus 4 (p=0.199)) were equivalent between the two groups. CONCLUSION In this study, we found that local anesthesia was not required along with ketamine sedation for pediatric facial laceration repair.