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目的:观察鼠神经生长因子联合高压氧治疗急性一氧化碳中毒(ACOP)的临床疗效。方法:选择急性ACOP 46例,随机分为观察组和对照组各23例。对照组给予吸氧、防止脑水肿、补液等常规治疗和高压氧治疗,高压氧治疗采用压力1.5MPa,每次60min,每天1次,7天为1个疗程,一般2～4个疗程,平均治疗21次。观察组在对照组基础上,加用鼠神经生长因子治疗,每次30μg,肌内注射,每天1次,疗程4周。观察两组好转时间、治愈时间,随访迟发性脑病发生、脑电图恢复、出院时智能精神状态评分(MMSE)及日常生活能力评分(ADL)等指标。结果:观察组好转和治愈时间分别为(5.04±0.31)天、(13.21±1.74)天,对照组分别为(7.39±0.62)天、(22.35±2.89)天;两组比较,差异显著(P<0.05)。观察组发生迟发性脑病1例,占4.3%;对照组发生6例,占26.1%。两组比较,差异显著(P<0.05)。观察组脑电图恢复情况显著优于对照组(P<0.05),MMSE及ADL评分显著优于对照组(P<0.05)。结论:鼠神经生长因子联合高压氧治疗能够显著改善ACOP神经功能受损,减少迟发性脑病的发生。
Objective: To observe the clinical effect of nerve growth factor combined with hyperbaric oxygen on acute carbon monoxide poisoning (ACOP). Methods: Acute ACOP 46 cases were randomly divided into observation group and control group of 23 cases. Control group was given oxygen, to prevent cerebral edema, rehydration and other conventional treatment and hyperbaric oxygen therapy, hyperbaric oxygen therapy using pressure 1.5MPa, each 60min, day 1, 7 days for a course of treatment, usually 2 to 4 courses, the average Treatment 21 times. The observation group on the basis of the control group, plus mouse nerve growth factor treatment, each 30μg, intramuscular injection once a day for 4 weeks. The improvement time, the healing time, the incidence of delayed encephalopathy at follow-up, EEG recovery, MMSE and ADL at discharge were observed. Results: The improvement and the healing time in the observation group were (5.04 ± 0.31) days and (13.21 ± 1.74) days respectively, which were (7.39 ± 0.62) days and (22.35 ± 2.89) days in the control group respectively <0.05). The observation group had delayed encephalopathy in 1 case, accounting for 4.3%; in the control group, 6 cases occurred, accounting for 26.1%. The difference between the two groups was significant (P <0.05). EEG recovery in the observation group was significantly better than that in the control group (P <0.05), MMSE and ADL scores were significantly better than the control group (P <0.05). Conclusion: NGF and hyperbaric oxygen therapy can significantly improve the neurological deficits of ACOP and reduce the incidence of delayed encephalopathy.