Department of Anesthesia and Critical Care Medicine, University of California San Francisco, San Francisco General Hospital, 1001 Potrero Avenue, San Francisco, CA 94110, USA.
Neurocrit Care. 2011 Aug;15(1):175-81. doi: 10.1007/s12028-009-9315-8.
We report the effective use of dexmedetomidine in the treatment of a patient with a history of chronic alcohol abuse and an acute traumatic brain injury who developed agitation that was unresolved if from traumatic brain injury, or alcohol withdrawal or the combination of both. Treatment with benzodiazepines failed; lorazepam therapy obscured our ability to do reliable neurological testing to follow his brain injury and nearly resulted in intubation of the patient secondary to respiratory suppression. Upon admission to hospital, the patient was first treated with intermittent, prophylactic doses of lorazepam for potential alcohol withdrawal based upon our institution's standard of care. His neurological examinations including a motor score of 6 (obeying commands) on his Glasgow Coma Scale testing, laboratory studies, and repeat CT head imaging remained stable. For lack of published literature in diagnosing symptoms of patients with a history of both alcohol withdrawal and traumatic brain injury, a diagnosis of agitation secondary to presumed alcohol withdrawal was made when the patient developed acute onset of tachycardia, confusion, and extreme anxiety with tremor and attempts to climb out of bed requiring him to be restrained. Additional lorazepam doses were administered following a hospital-approved protocol for titration of benzodiazepine therapy for alcohol withdrawal. The patient's mental status and respiratory function deteriorated with the frequent lorazepam dosing needed to control his agitation. Dexmedetomidine IV infusion at a rate of 0.5 mcg/kg/h was then administered and was titrated ultimately to 1.5 mcg/kg/h. After 8 days of therapy with dexmedetomidine, the patient was transferred from the ICU to a step-down unit with an intact neurological examination and no evidence of alcohol withdrawal. Airway intubation was avoided during the patient's entire hospitalization. This case report highlights the intricate balance between the side effects of benzodiazepine sedation for treatment of agitation and the difficulties of monitoring the neurological status of non-intubated patients with traumatic brain injury.
Given the large numbers of alcohol-dependent patients who suffer a traumatic brain injury and subsequently develop agitation and alcohol withdrawal in hospital, dexmedetomidine offers a novel strategy to facilitate sedation without neurological or respiratory depression. As this case report demonstrates, dexmedetomidine is an emerging treatment option for agitation in patients who require reliable, serial neurological testing to monitor the course of their traumatic brain injury.
我们报告了使用右美托咪定治疗一位有慢性酒精滥用和急性创伤性脑损伤病史的患者的有效方法，该患者出现了激越症状，如果是由创伤性脑损伤、酒精戒断或两者共同引起的，这些症状无法得到解决。苯二氮䓬类药物治疗无效；劳拉西泮治疗掩盖了我们进行可靠的神经学测试来监测其脑损伤的能力，并几乎导致患者因呼吸抑制而需要插管。患者入院时，根据我们机构的标准护理，首先间歇性、预防性使用劳拉西泮治疗潜在的酒精戒断。他的神经系统检查，包括格拉斯哥昏迷量表测试中的运动评分 6 分（听从命令）、实验室研究和重复头部 CT 成像，均保持稳定。由于缺乏诊断既有酒精戒断又有创伤性脑损伤病史的患者症状的文献，当患者出现心动过速、意识混乱、极度焦虑、震颤和试图爬出床而需要被约束的急性发作时，诊断为假定的酒精戒断引起的激越。按照医院批准的苯二氮䓬类药物治疗酒精戒断的滴定方案，给予了额外的劳拉西泮剂量。由于需要频繁给予劳拉西泮来控制激越，患者的精神状态和呼吸功能恶化。然后给予右美托咪定静脉输注，速度为 0.5 mcg/kg/h，并最终滴定至 1.5 mcg/kg/h。在接受右美托咪定治疗 8 天后，患者从 ICU 转至降阶病房，神经学检查完整，无酒精戒断证据。患者整个住院期间均避免了气管插管。本病例报告强调了治疗激越时苯二氮䓬类药物镇静的副作用与监测非插管创伤性脑损伤患者神经状态的困难之间的微妙平衡。
鉴于大量患有酒精依赖的患者遭受创伤性脑损伤，随后在医院出现激越和酒精戒断，右美托咪定提供了一种新的策略，可在不引起神经或呼吸抑制的情况下促进镇静。正如本病例报告所示，对于需要进行可靠的、连续的神经学测试来监测其创伤性脑损伤过程的患者，右美托咪定是一种新的治疗激越的选择。
