阻塞性睡眠呼吸暂停低通气综合征与高血压性脑出血血肿周围水肿的相关性

A study on correlation of obstructive sleep apnea-hypopnea syndrome and perihematoma edema of hypertensive cerebral hemorrhage

目的分析阻塞性睡眠呼吸暂停低通气综合征（obstructivesleepapnea—hypopneasyndrome，OSAHS）与高血压性脑出血血肿周围水肿的相关性。方法收集高血压性脑出血患者144例，其中合并OSAHS患者78例。不合并OSAHS的高血压性脑出血患者66例，作为空白对照组，两组患者均接受常规脱水降颅压、降压、保护脑细胞治疗。在入院时行头CT检查并于24h内行夜间多导睡眠图（polymonography，PSG）监测。入院后24h及第4天均复查CT，测量脑血肿体积和血肿周围水肿体积，动态观察脑血肿及血肿周围水肿变化。结果伴或不伴OSAHS两组在年龄、性别组成、体重指数、血糖、血脂等方面差异均无统计学意义。两组患者的相对水肿体积指数（relativeedemaindex，REI）在人院时和24h后差异均无统计学意义；入院第4天，OSAHS组水肿体积变化指数为0．96±1．35，明显高于对照组（0．40±0．45，t=4．149，P=0．000）。不同程度OSAHS患者的水肿体积及水肿变化的分析结果表明，入院时不同程度OSAHS的脑出血患者的脑水肿程度差异无统计学意义（无OSAHS组和轻、中、重组分别为1．05±0．65、0．84±0．48、1．20±0．54、1．10±0．40，F=1．061，P=0．374）；入院24h和第4天时，随着OSAHS严重程度的增加，脑出血患者的脑水肿程度增加。水肿体积变化差异性分析显示，重度OSAHS合并症的患者，水肿体积增加更明显。水肿变化指数与OSAHS程度指标呼吸暂停低通气指数呈明显正相关，Pearson相关系数为0．652（P=0．000）。结论OSAHS可加重高血压性脑出血患者的水肿恶化程度，且恶化程度与OSAHS严重程度呈正相关。

Objective To analysis the correlation of obstructive sleep apnea-hypopnea syndrome （OSAHS） and perihematoma edema of hypertensive cerebral hemorrhage. Methods One hundred and forty-four patients with hypertensive cerebral hemorrhage were collected and 78 of these patients were suffered from OSAHS. The patients were divided into two groups, control and OSAHS group, according to whether were accompanied by OSAHS or not. Both of the groups received the routine treatments including dehydration, reducing blood press, protecting the cerebral cells and so on. Cerebral CT scan was taken on admission. Night polymonography （PSG） was done within 24 hours of admission. Twenty-four hours and 4 days after admission, cerebral CT scan was taken again. The volumes of cephalophyma and perihematoma edema were calculated according to the results of CT scan. The changes of cephalophyma and perihematoma edema were dynamic observed. Results No difference in patients＇ age, sex, body mass index, serum glucose, blood lipid and so on, was observed between the two groups. The relative edema index became significantly different until 4 days after admission （0. 40 ± 0. 45, 0. 96 ± 1.35 in control and OSAHS group respectively, t = 4. 149, P = 0. 000）. Similarly, the alternation edema index of OSAHS was obviously higher than that of control group only in 4 days after admission. While the analysis of the correlation between different degree OSAHS groups and edema indexes showed that at 24 hours after admission the edema volumes for different degree OSAHS groups were consistent （ 1.05 ±0. 65, 0. 84± 0.48, 1.20 ± 0. 54,1. 10±0. 40 in control, slight, moderate and severe groups respectively, F = 1. 061, P = 0. 374）. At 24 hours arid 4 days after admission, the edema volumes were positively correlated with the degree of OSAHS. Alternation edema index was significantly correlated with apnea hypopnea index according to the result of Pearson＇ s correlation analysis （ r = 0. 652, P = 0. 000）. Conclusion OSAHS complication can promote the progression of perihematoma edema of hypertensive cerebral hemorrhage, and the degree of edema aggravation is positive correlated to the degree of OSAHS.