氯胺酮丸与颅内压降低和脑灌注压升高有关:重型颅脑损伤患者的回顾性观察研究

IF 1.8 Q3 CRITICAL CARE MEDICINE
Bradley A Dengler, O. Karam, Colleen A Barthol, Aaron B. Chance, Laura E. Snider, Clare M. Mundy, M. Bounajem, W. C. Johnson, M. Maita, Paola M. Mendez-Gomez, A. Seifi, Shaheryar Hafeez
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Methods We conducted a retrospective review of all patients admitted to the neurointensive care unit at a single tertiary referral center who had a severe traumatic brain injury with indwelling intracranial pressure monitors. We identified those patients with refractory intracranial pressure who received boluses of ketamine. We defined refractory as any sustained ICP greater than 20 mmHg after the patient was adequately sedated, serum Na was at goal, and CO2 was maintained between 35 and 40 mmHg. The primary outcome was a reduction in ICP with a subsequent increase in CPP. Results The patient cohort consisted of 44 patients with a median age of 30 years and a median presenting Glasgow Coma Scale (GCS) of 5. The median reduction in ICP after administration of a ketamine bolus was −3.5 mmHg (IQR −9 to +1), and the postketamine ICP was significantly different from baseline (p < 0.001). 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引用次数: 7

摘要

背景长期以来,颅内压(ICP)升高和低血压已被证明会导致严重创伤性脑损伤(TBI)人群的预后恶化。充分镇静是TBI护理的基本原则,氯胺酮是一种有吸引力的镇静选择,因为它通常不会引起全身性低血压,而大多数其他镇静药物都会引起全身性降压。我们评估了氯胺酮推注对严重TBI和难治性ICP患者的ICP和脑灌注压(CPP)的影响。方法我们对在一个三级转诊中心入住神经重症监护室的所有患者进行了回顾性审查,这些患者患有严重创伤性脑损伤,并使用了内置颅内压监测仪。我们确定了那些接受氯胺酮推注的难治性颅内压患者。我们将难治性定义为任何持续ICP大于20 患者充分镇静后mmHg,血清Na达到目标,CO2保持在35-40之间 mmHg。主要结果是ICP减少,随后CPP增加。结果患者队列包括44名患者,中位年龄为30岁,格拉斯哥昏迷量表(GCS)中位值为5。氯胺酮推注给药后ICP的中位降低为−3.5 mmHg(IQR−9至+1),氯胺酮后的ICP与基线有显著差异(p<0.001)。氯胺酮推注导致CPP增加2 mmHg(IQR−5至+12),与基线相比也有显著差异(p<0.001)。结论在这项针对严重颅脑损伤患者的单一机构研究中,氯胺酮推注与ICP降低和CPP增加有关。这是对43名患者的回顾性审查,因此在性质上是有限的,但应进行进一步的随机对照试验来证实这一发现。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Ketamine Boluses Are Associated with a Reduction in Intracranial Pressure and an Increase in Cerebral Perfusion Pressure: A Retrospective Observational Study of Patients with Severe Traumatic Brain Injury
Background Increased intracranial pressure (ICP) and hypotension have long been shown to lead to worse outcomes in the severe traumatic brain injury (TBI) population. Adequate sedation is a fundamental principle in TBI care, and ketamine is an attractive option for sedation since it does not commonly cause systemic hypotension, whereas most other sedative medications do. We evaluated the effects of ketamine boluses on both ICP and cerebral perfusion pressure (CPP) in patients with severe TBI and refractory ICP. Methods We conducted a retrospective review of all patients admitted to the neurointensive care unit at a single tertiary referral center who had a severe traumatic brain injury with indwelling intracranial pressure monitors. We identified those patients with refractory intracranial pressure who received boluses of ketamine. We defined refractory as any sustained ICP greater than 20 mmHg after the patient was adequately sedated, serum Na was at goal, and CO2 was maintained between 35 and 40 mmHg. The primary outcome was a reduction in ICP with a subsequent increase in CPP. Results The patient cohort consisted of 44 patients with a median age of 30 years and a median presenting Glasgow Coma Scale (GCS) of 5. The median reduction in ICP after administration of a ketamine bolus was −3.5 mmHg (IQR −9 to +1), and the postketamine ICP was significantly different from baseline (p < 0.001). Ketamine boluses led to an increase in CPP by 2 mmHg (IQR −5 to +12), which was also significantly different from baseline (p < 0.001). Conclusion In this single-institution study of patients with severe traumatic brain injury, ketamine boluses were associated with a reduction in ICP and an increase in CPP. This was a retrospective review of 43 patients and is therefore limited in nature, but further randomized controlled trials should be performed to confirm the findings.
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来源期刊
Critical Care Research and Practice
Critical Care Research and Practice CRITICAL CARE MEDICINE-
CiteScore
3.60
自引率
0.00%
发文量
34
审稿时长
14 weeks
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