From the Department of Anesthesiology (N.L., R.H.) and Department of Critical Care Medicine (J.Z.), Beijing Tiantan Hospital, Capital Medical University, Beijing, China; Department of Anesthesia and Perioperative Care, University of California San Francisco, San Francisco, California (A.W.G.).
Anesthesiology. 2016 Mar;124(3):598-607. doi: 10.1097/ALN.0000000000000994.
Sedation is commonly used in neurosurgical patients but has been reported to produce transient focal neurologic dysfunction. The authors hypothesized that in patients with frontal-parietal-temporal brain tumors, focal neurologic deficits are unmasked or exacerbated by nonspecific sedation independent of the drug used.
This was a prospective, randomized, single-blind, self-controlled design with parallel arms. With institutional approval, patients were randomly assigned to one of the four groups: "propofol," "midazolam," "fentanyl," and "dexmedetomidine." The sedatives were titrated by ladder administration to mild sedation but fully cooperative, equivalent to Observer's Assessment of Alertness and Sedation score = 4. National Institutes of Health Stroke Scale (NIHSS) was used to evaluate the neurologic function before and after sedation. The study's primary outcome was the proportion of NIHSS-positive change in patients after sedation to Observer's Assessment of Alertness and Sedation = 4.
One hundred twenty-four patients were included. Ninety had no neurologic deficits at baseline. The proportion of NIHSS-positive change was midazolam 72%, propofol 52%, fentanyl 27%, and dexmedetomidine 23% (P less than 0.001 among groups). No statistical difference existed between propofol and midazolam groups (P = 0.108) or between fentanyl and dexmedetomidine groups (P = 0.542). Midazolam and propofol produced more sedative-induced focal neurologic deficits compared with fentanyl and dexmedetomidine. The neurologic function deficits were mainly limb motor weakness and ataxia. Patients with high-grade gliomas were more susceptible to the induced neurologic dysfunction regardless of the sedative.
Midazolam and propofol augmented or revealed neurologic dysfunction more frequently than fentanyl and dexmedetomidine at equivalent sedation levels. Patients with high-grade gliomas were more susceptible than those with low-grade gliomas.
镇静在神经外科患者中很常见,但有报道称其会导致短暂的局灶性神经功能障碍。作者假设,在额顶颞部脑肿瘤患者中,局灶性神经功能缺损是由非特异性镇静引起的,而与所使用的药物无关。
这是一项前瞻性、随机、单盲、自身对照的平行分组设计。经机构批准,患者被随机分配到四组中的一组:“异丙酚”、“咪达唑仑”、“芬太尼”和“右美托咪定”。通过阶梯给药将镇静剂滴定至轻度镇静但完全合作,相当于观察者警觉和镇静评分=4。使用国立卫生研究院卒中量表(NIHSS)评估镇静前后的神经功能。该研究的主要结局是镇静后 NIHSS 阳性变化的患者比例,观察者警觉和镇静评分=4。
共纳入 124 例患者。90 例患者基线时无神经功能缺损。NIHSS 阳性变化的比例分别为咪达唑仑 72%、异丙酚 52%、芬太尼 27%和右美托咪定 23%(组间比较 P<0.001)。异丙酚和咪达唑仑组之间(P=0.108)或芬太尼和右美托咪定组之间(P=0.542)无统计学差异。咪达唑仑和异丙酚与芬太尼和右美托咪定相比,产生更多的镇静诱导局灶性神经功能缺损。神经功能缺损主要为肢体运动无力和共济失调。无论使用何种镇静剂,高级别胶质瘤患者更容易发生诱导性神经功能障碍。
在等效镇静水平下,咪达唑仑和异丙酚比芬太尼和右美托咪定更频繁地增强或揭示神经功能障碍。高级别胶质瘤患者比低级别胶质瘤患者更敏感。