Effectiveness of ketamine in decreasing intracranial pressure in children with intracranial hypertension Clinical article
Effectiveness of ketamine in decreasing intracranial pressure in children with intracranial hypertension Clinical article
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DOI：
10.3171/2009.1.peds08319
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发表时间：
2009-07-01
影响因子：
1.9
通讯作者：
Guilburd, Joseph N.
中科院分区：
文献类型：
--
作者：
Bar-Joseph, Gad;Guilburd, Yoav;Guilburd, Joseph N.
对象。颅内高压患者通常需要深度镇静。所有广泛使用的镇静和麻醉剂（阿片类药物、苯二氮卓类药物、异丙酚和巴比妥类药物）都能降低血压，从而降低脑灌注压（CPP）。氯胺酮是一种有效、安全、快速起效的麻醉剂，不会降低血压。然而，氯胺酮在外伤性脑损伤和颅内高压患者中的使用被排除，因为它被广泛认为会增加颅内压（ICP）。基于临床经验，作者推测氯胺酮不会增加-而可能会降低- icp。作者进行了一项前瞻性，对照，临床试验的数据获得在儿科重症监护病房的区域创伤中心。所有患者在纳入研究前均给予镇静和机械通气。持续升高的ICP （> 18 mm Hg）对一线治疗有耐药性的儿童接受单剂量氯胺酮（1-1.5 mg/kg），以防止在潜在的痛苦干预期间ICP进一步增加（组1）或作为降低ICP的额外措施（组2）。在氯胺酮给药前记录血流动力学、ICP和CPP值，并采用重复测量方差分析将这些值与氯胺酮给药后每分钟记录的值进行比较。对30例患者82次氯胺酮给药结果进行分析。总体而言，氯胺酮给药后，ICP下降了30%（从25.8 +/- 8.4降至18.0 +/- 8.5 mm Hg） （p < 0.001）， CPP从54.4 +/- 11.7上升至58.3 +/- 13.4 mm Hg （p < 0.005）。在第1组中，氯胺酮给药后ICP显著降低，在17个事件中只有1个在痛苦干预期间ICP升高bb0.2 mm Hg。在第二组中，当氯胺酮用于降低持续性颅内高压时，使用氯胺酮后，颅内压下降33%（从26.0 +/- 9.1降至17.5 +/- 9.1 mm Hg） （p < 0.0001）。在接受通气治疗的颅内高压患者中，氯胺酮可以有效降低ICP，并在潜在的痛苦干预中防止ICP升高，而不会降低血压和CPP。这些结果驳斥了氯胺酮增加ICP的观点。氯胺酮是一种安全有效的治疗创伤性脑损伤合并颅内压增高的药物，可安全用于创伤急诊。(DOI: 10.3171 / 2009.1.peds08319)
Object. Deepening sedation is often needed in patients with intracranial hypertension. All widely used sedative and anesthetic agents (opioids, benzodiazepines, propofol, and barbiturates) decrease blood pressure and may therefore decrease cerebral perfusion pressure (CPP). Ketamine is a potent, safe, rapid-onset anesthetic agent that does not decrease blood pressure. However, ketamine's use in patients with traumatic brain injury and intracranial hypertension is precluded because it is widely stated that it increases intracranial pressure (ICP). Based on anecdotal clinical experience, the authors hypothesized that ketamine does not increase-but may rather decrease-ICP.Methods. The authors conducted a prospective, controlled, clinical trial of data obtained in a pediatric intensive care unit of a regional trauma center. All patients were sedated and mechanically ventilated prior to inclusion in the study. Children with sustained, elevated ICP (> 18 mm Hg) resistant to first-tier therapies received a single ketamine dose (1-1.5 mg/kg) either to prevent further ICP increase during a potentially distressing intervention (Group 1) or as an additional measure to lower ICP (Group 2). Hemodynamic, ICP, and CPP values were recorded before ketamine administration, and repeated-measures analysis of variance was used to compare these values with those recorded every minute for 10 minutes following ketamine administration.Results. The results of 82 ketamine administrations in 30 patients were analyzed. Overall, following ketamine administration, ICP decreased by 30% (from 25.8 +/- 8.4 to 18.0 +/- 8.5 mm Hg) (p < 0.001) and CPP increased from 54.4 +/- 11.7 to 58.3 +/- 13.4 mm Hg (p < 0.005). In Group 1, ICP decreased significantly following ketamine administration and increased by > 2 mm Hg during the distressing intervention in only 1 of 17 events. In Group 2, when ketamine was administered to lower persistent intracranial hypertension, ICP decreased by 33% (from 26.0 +/- 9.1 to 17.5 +/- 9.1 mm Hg) (p < 0.0001) following ketamine administration.Conclusions. In ventilation-treated patients with intracranial hypertension, ketamine effectively decreased ICP and prevented untoward ICP elevations during potentially distressing interventions, without lowering blood pressure and CPP. These results refute the notion that ketamine increases ICP. Ketamine is a safe and effective drug for patients with traumatic brain injury and intracranial hypertension, and it can possibly be used safely in trauma emergency situations. (DOI: 10.3171/2009.1.PEDS08319)