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目的观察乌司他汀治疗急性脑血管病伴神经源性肺水肿患者的临床效果。方法将80例急性脑血管病伴神经源性肺水肿患者随机分为治疗组与对照组各40例。2组患者均按照医学高等教育本科教材第8版对急性脑血管病给予规范治疗,对照组患者给予有创支气管插管术、呼吸机辅助通气,给予呋塞米减轻心脏负荷、少量糖皮质激素,给予抗生素预防控制感染,纠正水电解质酸碱失衡等综合治疗;治疗组在对照组治疗基础上给予加用乌司他汀治疗。治疗后比较2组患者血清中白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)、钠尿肽(BNP)水平差异。对比观察2组患者气管插管置管时间、3d内气管插管拔除率、ICU滞留时间、抗生素使用时间、病死率差异。结果治疗后治疗组IL-6、TNF-α、BNP水平均低于对照组,差异均有统计学意义(P<0.05)。治疗后,治疗组患者气管插管置管时间、ICU滞留时间和抗生素使用时间均短于对照组,3d内气管插管拔除率和病死率低于对照组,差异均有统计学意义(P<0.05)。结论乌司他汀治疗急性脑血管病伴神经源性肺水肿可以明显降低肺功能损害,减轻心脏负荷,提高临床疗效。分析其机制可能与乌司他汀降低患者血清中炎性反应水平有关。
Objective To observe the clinical effect of ulinastatin in patients with acute cerebrovascular disease and neurogenic pulmonary edema. Methods Eighty patients with acute cerebrovascular disease accompanied by neurogenic pulmonary edema were randomly divided into treatment group and control group of 40 cases. Patients in both groups were given standardized treatment of acute cerebrovascular disease according to the eighth edition of the medical undergraduate teaching materials. The patients in the control group were given invasive bronchial intubation, ventilator assisted ventilation, furosemide to reduce the heart load, a small amount of glucocorticoid , To give antibiotics to prevent and control infection, to correct the water and electrolyte acid-base imbalance and other comprehensive treatment; treatment group in the control group based on the treatment plus plus ulinastatin. The levels of interleukin-6, tumor necrosis factor-α (TNF-α) and natriuretic peptide (BNP) were compared between the two groups after treatment. The duration of endotracheal intubation, the rate of endotracheal intubation, ICU residence time, antibiotic use time and mortality were compared between the two groups. Results After treatment, the levels of IL-6, TNF-α and BNP in the treatment group were lower than those in the control group, with statistical significance (P <0.05). After treatment, intubation time, ICU residence time and antibiotic use time in treatment group were shorter than those in control group. The removal rate and mortality of tracheal intubation in 3d were lower than those in control group (P < 0.05). Conclusion Ulinastatin in patients with acute cerebrovascular disease accompanied by neurogenic pulmonary edema can significantly reduce pulmonary function damage, reduce cardiac load and improve clinical efficacy. Analysis of the mechanism may be related to the reduction of ulinastatin in patients with serum inflammatory response level.