Peters Austin J, Khan Saad A, Koike Seiji, Rowell Susan, Schreiber Martin
Department of Anesthesiology and Perioperative Medicine, Oregon Health & Science University, Portland, OR, USA.
Creighton University School of Medicine, Omaha, NE, USA.
J Trauma Inj. 2023 Dec;36(4):354-361. doi: 10.20408/jti.2023.0034. Epub 2023 Nov 7.
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.
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.
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.
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.
由于担心氯胺酮会升高颅内压，过去一直将其列为创伤性脑损伤（TBI）的禁忌药物。然而，鉴于其良好的呼吸和血流动力学特性，它在TBI治疗中的应用越来越多。迄今为止，尚无研究评估TBI患者使用氯胺酮是否与患者生存或残疾相关。
我们对多中心创伤性脑损伤院前氨甲环酸使用试验的数据进行了回顾性分析，比较了使用氯胺酮和未使用氯胺酮的TBI患者，以确定氯胺酮给药与死亡率以及次要结局指标之间是否存在关联。
我们分析了原始研究中的841名合格受试者，其中131名（15.5%）接受了氯胺酮治疗。使用氯胺酮的受试者更年轻（37.3±16.9岁 vs. 42.0±18.6岁，P = 0.037），初始格拉斯哥昏迷量表评分更差（7±3 vs. 8±4，P = 0.003），且与未使用氯胺酮的受试者相比，更有可能接受气管插管（88.5% vs. 44.2%，P < 0.001）。总体而言，两组之间的死亡率（12.2% vs. 15.5%，P = 0.391）或残疾指标没有差异。与未使用氯胺酮的受试者相比，使用氯胺酮的受试者颅内压（ICP）升高的情况明显更少（56.3% vs. 82.3%，P = 0.048）。在非常罕见的心脏事件和癫痫发作结局中，使用氯胺酮的受试者癫痫发作在统计学上更有可能发生（3.1% vs. 1.0%，P = 0.010）。在颅内出血亚组中，使用氯胺酮的受试者心脏事件更有可能发生（2.3% vs. 0.2%，P = 0.025）。氯胺酮暴露与TBI蛋白生物标志物浓度的较小升高相关。
尽管氯胺酮用于伤势更严重的受试者，但它与更差的生存或残疾无关。氯胺酮暴露与ICP升高减少、癫痫发作次数增加以及TBI蛋白生物标志物浓度降低相关。
