尼莫地平对创伤性蛛网膜下腔出血的临床疗效评估
发布时间：2018-09-06 17:22
【摘要】：无论在平时或战时,颅脑创伤在全身各类创伤的发生率上居第2位,仅次于四肢伤,而其死亡率却居首位。在美国,颅脑创伤发生率为每10万人口就有200人患病,新发颅脑创伤病人每年大约50万,其中约有2万人死亡,3万人致残。而在我国,新发颅脑创伤病人每年大约60万人,其中死亡人数达10万之众,造成直接和间接经济损失达100亿元以上。而在临床上合并SAH的颅脑外伤占到39%-65%,故而在临床上将颅脑损伤后,脑组织挫裂伤,脑底部或脑表面皮层细小血管损伤出血,直接流入蛛网膜下腔的这一临床综合征定义为创伤性蛛网膜下腔出血。并根据其血液分布情况将其分为脑表面蛛网膜下腔型、颅底蛛网膜池型及脑表面和颅底蛛网膜池混合型三型。CVS的发生影响脑功能区的供血供氧,导致大脑相应功能部分或全部丧失,影响患者生活质量及预后。Graham等发现,在创伤性颅脑损伤死亡病人中,约有90%的病人脑组织有缺血性改变。而CVS的发生率在tSAH患者中高达67%。Hanlon等研究证实创伤性蛛网膜下腔出血是中、重型颅脑损伤病人较多发生的征象之一。有些文献认为颅脑损伤后伴有创伤性蛛网膜下腔出血者一般预后不良。尼莫地平是1、4-二氢吡啶类钙通道拮抗剂,脂溶性较高,能较为顺利通过血脑屏障,选择性阻滞细胞膜上钙离子通道开放,减少细胞外钙离子大量内流,抑制脑血管平滑肌的收缩,同时增强Ca2+—ATP酶活性,增加细胞内钙离子排出,减轻细胞内钙离子超载,保护神经细胞,并且尼莫地平对脑血管有高度选择性,改善脑动脉血流量的效果远大于外周血管,对大脑损伤区灌流不足部位灌注量的增加通常高于正常区域,故而不会产生脑内盗血现象。而以往的相关研究已证实,尼莫地平是目前唯一的,具有循证医学支持的,对aSAH后CVS有防治作用的有效药物。而对于tSAH引起的CVS有无相同疗效,医学界里尽管进行了很多研究,但目前尚无明确的定论。 目的 利用持续颅内压监测、TCD、GCS、GOS来分析尼莫地平在预防tSAH后CVS发生和改善tSAH预后方面的临床效果,从而为其临床应用提供理论依据。材料与方法 1.病例纳入和排除标准：(1)纳入标准：急性颅脑损伤,伤后6h内入院；头部CT显示蛛网膜下腔出血；320排头颅CT血管造影排除动脉瘤破裂出血；幕上血肿量30ml,幕下血肿10ml,中线移位5mmm；年龄18-65岁；入院GCS评分为6-12分。(2)排除标准：枪伤及开放性颅脑损伤；合并严重弥漫性轴索损伤、严重肝肾功能不全者；收缩压持续低于100mmHg达1h以上；孕妇；发病前两周或在临床试验中有尼卡地平或其他钙离子拮抗剂用药史的患者；中途病情变化需开颅手术或停止试验者。 2.病例采集及分组：2012年2月至2013年11月于广州军区武汉总医院神经外科共纳入符合上述标准tSAH患者62例,其中男性患者50例,女性患者12例；年龄最小者18岁,最大者65岁,平均年龄为(38±12.6)岁；入院时GCS评分6-8分23例,9-12分39例。按入院顺序分为治疗组和对照组,各31例。治疗组男性患者26例,女性患者5例；年龄18-62岁,平均年龄36岁。对照组男性患者24例,女性患者7例；年龄20-65岁,平均年龄40岁。 3.治疗方法：对照组给予促醒、营养神经、止血、预防消化道溃疡、脱水、预防感染、镇静等常规治疗；治疗组在对照组常规治疗的基础上于实行持续颅内压监测后开始用微量泵静脉推注尼莫地平注射液(德国拜耳公司,规格为50ml:10mg),具体剂量依体重而定(对于体重≤70kg者,初始剂量为0.5ml/h,如无颅内压急剧升高、低血压等不良反应,2h后改为lmg/h;体重70kg者,初始剂量为1mg/h,如耐受良好,2h后改为2mg/h),每天静脉给药剂量24-48mg,静脉用药14d后改为口服尼莫地平片(60mg,每日4次；德国拜耳公司,规格为30mg/片),一个疗程为7天,共用药3个疗程。 4.评价指标：入院后行持续颅内压监测14天,分别计取伤后1、3、5、7、10、14天的颅内压平均值；于伤后第1、3、5、7、10、14、21天分别对患者意识状态进行GCS评定；于伤后1、3、5、7、14、21天分别行大脑中动脉TCD检查监测大脑中动脉血流速度,血流速度大于120cm/s提示存在CVS；伤后3月随访,用GOS进行预后评定；预后评定分为良好、中度残疾、重度残疾、植物生存、死亡五个档次。其中持续植物生存壮态,即指对外界环境无任何反应,无任何意识和精神活动；重度致残即指由于神经功能障碍和精神异常,生活不能自理；中度致残,即指生活可以自理,但由于神经功能障碍或精神异常丧失正常工作能力；良好,即指恢复正常工作,可并发轻度神经功能异常或精神功能异常；而良好、中度残疾归为预后良好,其余情况为预后不良。试验结束后分别对GCS、大脑中动脉血流速度、颅内压及预后结果等相应指标进行统计学分析。 5.统计学分析：计量资料数据采用x±s表示,均采用SPSS13.0统计软件进行统计学分析,计量资料的比较采用重复测量方差分析(组间比较：方差齐采用LSD法,方差不齐采用Games-Howell法),计数资料及率的比较采用x2检验,以P0.05为差异有显著性的判定标准。 结果： 1.两组患者GCS评分比较：治疗组与对照组入院时的GCS值分别为9.03±1.89、8.97±1.91,两组患者治疗后GCS值均逐渐升高,治疗组治疗后第3、5、7、10、14、21天的GCS值分别为9.23±2.17、9.68±1.94、10.65±1.6211.87±1.78、12.55±1.52、14.52±0.89,对照组治疗后第3、5、7、10、14、21天的GCS值分别为9.10±1.97、9.35±1.89、9.42±1.95、10.35±1.94、11.58±1.82、13.58±1.46,两组GCS评分差异有统计学意义(F分组=5.612,P0.05),不同时间GCS评分的差异有统计学意义(F时间=73.383,P0.05),分组和时间的交互作用有统计学意义(F交互=2.246,P0.05),7天后治疗组明显高于对照组(P0.05)。 2.两组患者颅内压比较：在该试验中,对照组治疗前颅内压值为21.65±3.73mmHg,随后逐步上升,3天后达25.77±3.68mmHg,于治疗第5天左右达峰值(27.19±3.80mmHg),随后开始逐步下降,至2周时回复至15.74±1.71mmHg,但仍稍高于正常值,而治疗组颅内压从伤后23.65±3.37mmHg开始逐步上升,于伤后第3天时达峰值(26.61±3.68mmHg),后逐步下降,两周后恢复至正常范围(11.74±2.78mmHg)两组患者的颅内压先均有一定幅度上升,随后均呈下降趋势,但在时间上治疗组明显早于对照组；两组颅内压差异有统计学意义(F分组=60.597,P0.05),不同时间颅内压的差异有统计学意义(F时间=157.320,P0.05),分组和时间的交互作用有统计学意义(F交互=28.854,P0.05)。 3.两组MCA血流速度比较：在试验中共有38例患者(61.3%)MCA至少经历了一次CVS,而在时间上绝大多数发生于伤后5天内,持续时间一般不超过14天；治疗组CVS发生率(35.5%,11/31)明显低于对照组(61.3%,19/31),差异有统计学意义(χ2=4.473,P0.05)。在该设计试验中,对照组伤后治疗前MCA血流速度为128.45±20.07cm/s,明显高于正常,3天后达到峰值(132.97±21.28cm/s),治疗第5天较前略有下降(129.16±17.42cm/s),但仍处于较高水平,治疗第7天显示血流速度继续下降(118.35±14.54cm/s),两个星期后恢复至正常范围(112.13±8.70cm/s),而治疗组MCA血流速度从开始治疗后并未出现明显上升,反而呈逐步下降趋势,并于一周后恢复至正常范围(106.90±11.34cm/s),治疗组治疗3天后伤侧MCA血流速度明显低于对照组；两组患者MCA血流速度差异有统计学意义(F分组=9.762,P0.05),不同时间Vp的差异有统计学意义(F时间=76.580,0.05),分组和时间的交互作用有统计学意义(F交互=3.257,P0.05)。 4.两组患者预后比较：伤后3月对所有患者采用GOS评分进行随访,其中治疗组恢复良好19例(61.3%),中度残疾7例(22.6%),重度残疾5例(16.1%)；对照组恢复良好16例(51.6%),中度残残2例(6.5%),重度残疾13例(41.9%)；治疗组预后良好率(83.9%,26/31)明显高于对照组(58.1%,18/31)。差异有统计学意义(χ2=5.010,P0.05)。 结论 本实验结果显示创伤性蛛网膜下腔出血患者早期脑血管痉挛发生率比较高,其中,对照组明显高于尼莫地平治疗组；尼莫地平治疗组预后良好率明显高于对照组。这一结果表明,尼莫地平有助于防治创伤性蛛网膜下腔出血脑血管痉挛的发生,明显改善tSAH患者预后。
[Abstract]:No matter in peacetime or wartime, craniocerebral trauma ranks second in the incidence of all kinds of trauma, second only to limb trauma, and its mortality rate ranks first. In the United States, the incidence of craniocerebral trauma is 200 people per 100,000 population, about 500,000 new cases of craniocerebral trauma every year, of which about 20,000 people die and 30,000 people become disabled. About 600,000 patients suffer from craniocerebral trauma each year, of which 100,000 are dead, resulting in direct and indirect economic losses of more than 10 billion yuan. In clinical cases, 39% - 65% of the patients suffer from craniocerebral trauma combined with SAH. Therefore, after craniocerebral trauma, brain tissue contusion and laceration, small blood vessel injury and hemorrhage in the cerebral basal or surface cortex are directly influxed into the brain. This clinical syndrome of subarachnoid space is defined as traumatic subarachnoid hemorrhage. According to its blood distribution, it can be divided into three types: subarachnoid hemorrhage on brain surface, subarachnoid cistern on skull base and mixed type of arachnoid cistern on brain surface and skull base. Graham et al found that about 90% of the patients died of traumatic brain injury had ischemic changes in brain tissue, while the incidence of CVS was as high as 67% in patients with tSAH. Hanlon et al. confirmed that traumatic subarachnoid hemorrhage was one of the most common symptoms in patients with severe brain injury. Nimodipine is a 1,4-dihydropyridine calcium channel antagonist with high liposolubility, which can smoothly cross the blood-brain barrier, selectively block the opening of calcium channel on the cell membrane, reduce the influx of extracellular calcium ions, and inhibit cerebrovascular diseases. Smooth muscle contraction, while enhancing the activity of Ca2+-ATPase, increasing intracellular calcium excretion, reducing intracellular calcium overload, protecting nerve cells, and nimodipine is highly selective to cerebrovascular, improve cerebral artery blood flow is far greater than the effect of peripheral blood vessels, the brain injury area perfusion of insufficient parts of the increase is usually high. Previous studies have confirmed that nimodipine is the only effective drug with evidence-based medical support that has preventive and therapeutic effects on CVS after aSAH. However, there is no definite evidence that nimodipine has the same effect on CVS caused by tSAH. The conclusion is made.
objective
Continuous intracranial pressure monitoring, TCD, GCS, GOS were used to analyze the clinical effect of nimodipine in preventing CVS after tSAH and improving the prognosis of tSAH, so as to provide theoretical basis for its clinical application.
1. Inclusion and exclusion criteria: (1) Inclusion criteria: acute craniocerebral injury, admission within 6 hours after injury; head CT showed subarachnoid hemorrhage; 320 row head CT angiography excluded aneurysm rupture and hemorrhage; supratentorial hematoma volume 30 ml, subtentorial hematoma 10 ml, midline shift 5 mm; age 18-65 years; admission GCS score 6-12 points. (2) Exclusion criteria Gunshot injury and open craniocerebral injury; severe diffuse axonal injury with severe hepatorenal insufficiency; systolic blood pressure below 100 mmHg for more than 1 hour; pregnant women; patients with a history of nicardipine or other calcium antagonists used in clinical trials two weeks prior to onset of the disease; and patients whose condition changes halfway require craniotomy or discontinuation of the trial A person.
2. Case collection and grouping: From February 2012 to November 2013 in Wuhan General Hospital of Guangzhou Military Region, 62 patients with tSAH were enrolled, including 50 males and 12 females; the youngest was 18 years old, the oldest was 65 years old, with an average age of (38 + 12.6); the GCS score at admission was 6-8 in 23 cases, and 9-12 in 39 cases. The treatment group consisted of 26 males and 5 females, aged 18-62 with an average age of 36. The control group consisted of 24 males and 7 females, aged 20-65 with an average age of 40.
3. Treatment: The control group was given routine treatment such as wake-up stimulation, nerve nutrition, hemostasis, prevention of gastrointestinal ulcer, dehydration, prevention of infection, sedation, etc. The treatment group was given Nimodipine Injection by micro-pump after continuous intracranial pressure monitoring on the basis of routine treatment in the control group (German Bayer Company, specifications 50ml:10mg). Body dose depends on body weight (for those with body weight less than 70 kg, the initial dose is 0.5 ml/h, if no adverse reactions such as rapid increase of intracranial pressure, hypotension, etc., and then changed to lmg/h after 2 hours; for those with body weight of 70 kg, the initial dose is 1 mg/h, if tolerated well, changed to 2 mg/h after 2 hours), the daily intravenous dose is 24-48 mg, and nimodipine tablets are orally taken after 14 days (60 mg, daily). The 4 time; Bayer company in Germany, specifications for 30mg/ tablets), a course of treatment for 7 days, sharing drugs 3 courses.
4. Evaluation indicators: Continuous intracranial pressure monitoring was performed on 14 days after admission, and the mean intracranial pressure was calculated on 1, 3, 5, 7, 10 and 14 days after injury; GCS was assessed on the first, 3, 5, 7, 10, 14 and 21 days after injury respectively; middle cerebral artery TCD was performed on 1, 3, 5, 7, 14 and 21 days after injury to monitor the blood flow velocity of middle cerebral artery. CVS was indicated at 120cm/s, followed up at 3 months after injury, and prognosis was assessed by GOS. The prognosis was divided into five grades: good, moderate, severe, vegetative survival and death. And mental disorders, life can not be self-care; moderate disability, that is, life can be self-care, but because of neurological dysfunction or mental disorders loss of normal working ability; good, that is, to return to normal work, can be accompanied by mild neurological dysfunction or mental dysfunction; and good, moderate disability is classified as a good prognosis, the rest of the prognosis is not good After the experiment, GCS, middle cerebral artery blood flow velocity, intracranial pressure and prognosis were statistically analyzed.
5. Statistical analysis: The data of measurement were expressed by X + s, and all were analyzed by SPSS13.0 statistical software. The comparison of measurement data was made by repeated measurement analysis of variance (LSD method was used for all variances, Games-Howell method for all variances). Criterion of sex.
Result:
1. Comparison of GCS scores between the two groups: The GCS values of the treatment group and the control group at admission were 9.03 (+ 1.89), 8.97 (+ 1.91) respectively. After treatment, the GCS values of the two groups increased gradually. The GCS values of the treatment group on the 3rd, 5th, 7th, 10th, 14th and 21st days after treatment were 9.23 (+ 2.17), 9.68 (+ 1.94), 10.65 (+ 1.6211.87) + 1.78, 12.55 (+ 1.52), 14.52 (+ 0.89), respectively. The GCS values of 14 and 21 days were 9.10 (+ 1.97), 9.35 (+ 1.89), 9.42 (+ 1.95), 10.35 (+ 1.94), 11.58 (+ 1.82) and 13.58 (+ 1.46), respectively. There were significant differences in GCS scores between the two groups (F group = 5.612, P 0.05). There were significant differences in GCS scores between the two groups (F time = 73.383, P 0.05), and the interaction between groups and time (F interaction = 2.246, P 0.05), 7. Days later, the treatment group was significantly higher than that of the control group (P0.05).
2. Comparison of intracranial pressure between the two groups: In this experiment, the intracranial pressure of the control group before treatment was 21.65 + 3.73 mmHg, then gradually increased, and reached 25.77 + 3.68 mmHg three days later, peaked at about 5 days after treatment (27.19 + 3.80 mmHg), then began to gradually decrease, and returned to 15.74 + 1.71 mmHg at 2 weeks, but still slightly higher than the normal value. The intracranial pressure of the two groups increased to a certain extent at first and then decreased to a certain extent at the end of two weeks, but the intracranial pressure of the treatment group was significantly earlier than that of the control group. There was statistical significance (F group = 60.597, P 0.05), the difference of intracranial pressure at different time was statistically significant (F time = 157.320, P 0.05), and the interaction between group and time was statistically significant (F interaction = 28.854, P 0.05).
3. Comparison of MCA blood flow velocity between the two groups: 38 patients (61.3%) experienced at least one CVS in the trial, and most of them occurred within 5 days after injury, lasting no more than 14 days; the incidence of CVS in the treatment group (35.5%, 11/31) was significantly lower than that in the control group (61.3%, 19/31), the difference was statistically significant (2 = 4.473, P 0.05). In the design test, the MCA blood flow velocity of the control group was 128.45 (+ 20.07 cm/s) before and after treatment, which was significantly higher than that of the normal control group. The MCA blood flow velocity peaked at 132.97 (+ 21.28 cm/s) after 3 days, and decreased slightly at the 5th day after treatment (129.16 (+ 17.42 cm/s), but remained at a higher level. On the 7th day of treatment, the MCA blood flow velocity continued to decrease (118.35 (+ 14.54 cm/s) and returned to normal level two weeks later. The blood flow velocity of MCA in the treatment group did not increase significantly from the beginning of treatment, but decreased gradually, and returned to normal range after one week (106.90 (+ 11.34 cm / s). The blood flow velocity of MCA on the injured side in the treatment group was significantly lower than that in the control group after three days of treatment. Significance (F group = 9.762, P 0.05), different time Vp difference was statistically significant (F time = 76.580, 0.05), grouping and time interaction was statistically significant (F interaction = 3.257, P 0.05).
4. Comparison of prognosis between the two groups: All patients were followed up with GOS score at 3 months after injury, 19 cases (61.3%), 7 cases (22.6%) with moderate disability and 5 cases (16.1%) with severe disability in the treatment group; 16 cases (51.6%) with good recovery in the control group, 2 cases (6.5%) with moderate disability and 13 cases (41.9%) with severe disability in the control group; and 83.9% with good prognosis in the treatment group (26/31) was obvious. Higher than the control group (58.1%, 18/31). The difference was statistically significant (x 2=5.010, P0.05).
conclusion
The results showed that the incidence of early cerebral vasospasm in patients with traumatic subarachnoid hemorrhage was higher than that in the nimodipine treatment group, and the good prognosis rate in the nimodipine treatment group was higher than that in the control group. The occurrence of tSAH significantly improved the prognosis of patients.
【学位授予单位】：南方医科大学
【学位级别】：硕士
【学位授予年份】：2014
【分类号】：R651.15
本文编号：2227031
[Abstract]:No matter in peacetime or wartime, craniocerebral trauma ranks second in the incidence of all kinds of trauma, second only to limb trauma, and its mortality rate ranks first. In the United States, the incidence of craniocerebral trauma is 200 people per 100,000 population, about 500,000 new cases of craniocerebral trauma every year, of which about 20,000 people die and 30,000 people become disabled. About 600,000 patients suffer from craniocerebral trauma each year, of which 100,000 are dead, resulting in direct and indirect economic losses of more than 10 billion yuan. In clinical cases, 39% - 65% of the patients suffer from craniocerebral trauma combined with SAH. Therefore, after craniocerebral trauma, brain tissue contusion and laceration, small blood vessel injury and hemorrhage in the cerebral basal or surface cortex are directly influxed into the brain. This clinical syndrome of subarachnoid space is defined as traumatic subarachnoid hemorrhage. According to its blood distribution, it can be divided into three types: subarachnoid hemorrhage on brain surface, subarachnoid cistern on skull base and mixed type of arachnoid cistern on brain surface and skull base. Graham et al found that about 90% of the patients died of traumatic brain injury had ischemic changes in brain tissue, while the incidence of CVS was as high as 67% in patients with tSAH. Hanlon et al. confirmed that traumatic subarachnoid hemorrhage was one of the most common symptoms in patients with severe brain injury. Nimodipine is a 1,4-dihydropyridine calcium channel antagonist with high liposolubility, which can smoothly cross the blood-brain barrier, selectively block the opening of calcium channel on the cell membrane, reduce the influx of extracellular calcium ions, and inhibit cerebrovascular diseases. Smooth muscle contraction, while enhancing the activity of Ca2+-ATPase, increasing intracellular calcium excretion, reducing intracellular calcium overload, protecting nerve cells, and nimodipine is highly selective to cerebrovascular, improve cerebral artery blood flow is far greater than the effect of peripheral blood vessels, the brain injury area perfusion of insufficient parts of the increase is usually high. Previous studies have confirmed that nimodipine is the only effective drug with evidence-based medical support that has preventive and therapeutic effects on CVS after aSAH. However, there is no definite evidence that nimodipine has the same effect on CVS caused by tSAH. The conclusion is made.
objective
Continuous intracranial pressure monitoring, TCD, GCS, GOS were used to analyze the clinical effect of nimodipine in preventing CVS after tSAH and improving the prognosis of tSAH, so as to provide theoretical basis for its clinical application.
1. Inclusion and exclusion criteria: (1) Inclusion criteria: acute craniocerebral injury, admission within 6 hours after injury; head CT showed subarachnoid hemorrhage; 320 row head CT angiography excluded aneurysm rupture and hemorrhage; supratentorial hematoma volume 30 ml, subtentorial hematoma 10 ml, midline shift 5 mm; age 18-65 years; admission GCS score 6-12 points. (2) Exclusion criteria Gunshot injury and open craniocerebral injury; severe diffuse axonal injury with severe hepatorenal insufficiency; systolic blood pressure below 100 mmHg for more than 1 hour; pregnant women; patients with a history of nicardipine or other calcium antagonists used in clinical trials two weeks prior to onset of the disease; and patients whose condition changes halfway require craniotomy or discontinuation of the trial A person.
2. Case collection and grouping: From February 2012 to November 2013 in Wuhan General Hospital of Guangzhou Military Region, 62 patients with tSAH were enrolled, including 50 males and 12 females; the youngest was 18 years old, the oldest was 65 years old, with an average age of (38 + 12.6); the GCS score at admission was 6-8 in 23 cases, and 9-12 in 39 cases. The treatment group consisted of 26 males and 5 females, aged 18-62 with an average age of 36. The control group consisted of 24 males and 7 females, aged 20-65 with an average age of 40.
3. Treatment: The control group was given routine treatment such as wake-up stimulation, nerve nutrition, hemostasis, prevention of gastrointestinal ulcer, dehydration, prevention of infection, sedation, etc. The treatment group was given Nimodipine Injection by micro-pump after continuous intracranial pressure monitoring on the basis of routine treatment in the control group (German Bayer Company, specifications 50ml:10mg). Body dose depends on body weight (for those with body weight less than 70 kg, the initial dose is 0.5 ml/h, if no adverse reactions such as rapid increase of intracranial pressure, hypotension, etc., and then changed to lmg/h after 2 hours; for those with body weight of 70 kg, the initial dose is 1 mg/h, if tolerated well, changed to 2 mg/h after 2 hours), the daily intravenous dose is 24-48 mg, and nimodipine tablets are orally taken after 14 days (60 mg, daily). The 4 time; Bayer company in Germany, specifications for 30mg/ tablets), a course of treatment for 7 days, sharing drugs 3 courses.
4. Evaluation indicators: Continuous intracranial pressure monitoring was performed on 14 days after admission, and the mean intracranial pressure was calculated on 1, 3, 5, 7, 10 and 14 days after injury; GCS was assessed on the first, 3, 5, 7, 10, 14 and 21 days after injury respectively; middle cerebral artery TCD was performed on 1, 3, 5, 7, 14 and 21 days after injury to monitor the blood flow velocity of middle cerebral artery. CVS was indicated at 120cm/s, followed up at 3 months after injury, and prognosis was assessed by GOS. The prognosis was divided into five grades: good, moderate, severe, vegetative survival and death. And mental disorders, life can not be self-care; moderate disability, that is, life can be self-care, but because of neurological dysfunction or mental disorders loss of normal working ability; good, that is, to return to normal work, can be accompanied by mild neurological dysfunction or mental dysfunction; and good, moderate disability is classified as a good prognosis, the rest of the prognosis is not good After the experiment, GCS, middle cerebral artery blood flow velocity, intracranial pressure and prognosis were statistically analyzed.
5. Statistical analysis: The data of measurement were expressed by X + s, and all were analyzed by SPSS13.0 statistical software. The comparison of measurement data was made by repeated measurement analysis of variance (LSD method was used for all variances, Games-Howell method for all variances). Criterion of sex.
Result:
1. Comparison of GCS scores between the two groups: The GCS values of the treatment group and the control group at admission were 9.03 (+ 1.89), 8.97 (+ 1.91) respectively. After treatment, the GCS values of the two groups increased gradually. The GCS values of the treatment group on the 3rd, 5th, 7th, 10th, 14th and 21st days after treatment were 9.23 (+ 2.17), 9.68 (+ 1.94), 10.65 (+ 1.6211.87) + 1.78, 12.55 (+ 1.52), 14.52 (+ 0.89), respectively. The GCS values of 14 and 21 days were 9.10 (+ 1.97), 9.35 (+ 1.89), 9.42 (+ 1.95), 10.35 (+ 1.94), 11.58 (+ 1.82) and 13.58 (+ 1.46), respectively. There were significant differences in GCS scores between the two groups (F group = 5.612, P 0.05). There were significant differences in GCS scores between the two groups (F time = 73.383, P 0.05), and the interaction between groups and time (F interaction = 2.246, P 0.05), 7. Days later, the treatment group was significantly higher than that of the control group (P0.05).
2. Comparison of intracranial pressure between the two groups: In this experiment, the intracranial pressure of the control group before treatment was 21.65 + 3.73 mmHg, then gradually increased, and reached 25.77 + 3.68 mmHg three days later, peaked at about 5 days after treatment (27.19 + 3.80 mmHg), then began to gradually decrease, and returned to 15.74 + 1.71 mmHg at 2 weeks, but still slightly higher than the normal value. The intracranial pressure of the two groups increased to a certain extent at first and then decreased to a certain extent at the end of two weeks, but the intracranial pressure of the treatment group was significantly earlier than that of the control group. There was statistical significance (F group = 60.597, P 0.05), the difference of intracranial pressure at different time was statistically significant (F time = 157.320, P 0.05), and the interaction between group and time was statistically significant (F interaction = 28.854, P 0.05).
3. Comparison of MCA blood flow velocity between the two groups: 38 patients (61.3%) experienced at least one CVS in the trial, and most of them occurred within 5 days after injury, lasting no more than 14 days; the incidence of CVS in the treatment group (35.5%, 11/31) was significantly lower than that in the control group (61.3%, 19/31), the difference was statistically significant (2 = 4.473, P 0.05). In the design test, the MCA blood flow velocity of the control group was 128.45 (+ 20.07 cm/s) before and after treatment, which was significantly higher than that of the normal control group. The MCA blood flow velocity peaked at 132.97 (+ 21.28 cm/s) after 3 days, and decreased slightly at the 5th day after treatment (129.16 (+ 17.42 cm/s), but remained at a higher level. On the 7th day of treatment, the MCA blood flow velocity continued to decrease (118.35 (+ 14.54 cm/s) and returned to normal level two weeks later. The blood flow velocity of MCA in the treatment group did not increase significantly from the beginning of treatment, but decreased gradually, and returned to normal range after one week (106.90 (+ 11.34 cm / s). The blood flow velocity of MCA on the injured side in the treatment group was significantly lower than that in the control group after three days of treatment. Significance (F group = 9.762, P 0.05), different time Vp difference was statistically significant (F time = 76.580, 0.05), grouping and time interaction was statistically significant (F interaction = 3.257, P 0.05).
4. Comparison of prognosis between the two groups: All patients were followed up with GOS score at 3 months after injury, 19 cases (61.3%), 7 cases (22.6%) with moderate disability and 5 cases (16.1%) with severe disability in the treatment group; 16 cases (51.6%) with good recovery in the control group, 2 cases (6.5%) with moderate disability and 13 cases (41.9%) with severe disability in the control group; and 83.9% with good prognosis in the treatment group (26/31) was obvious. Higher than the control group (58.1%, 18/31). The difference was statistically significant (x 2=5.010, P0.05).
conclusion
The results showed that the incidence of early cerebral vasospasm in patients with traumatic subarachnoid hemorrhage was higher than that in the nimodipine treatment group, and the good prognosis rate in the nimodipine treatment group was higher than that in the control group. The occurrence of tSAH significantly improved the prognosis of patients.
【学位授予单位】：南方医科大学
【学位级别】：硕士
【学位授予年份】：2014
【分类号】：R651.15
【参考文献】
相关期刊论文 前10条
1 苏贺先,马骏,娄飞云,张先闯,张凤银;尼莫通在外伤性蛛网膜下腔出血中的应用[J];蚌埠医学院学报;2000年01期
2 徐如祥,易声禹;Nimodipine对脑外伤后脑水及脑皮质和血清钙含量的影响[J];第一军医大学学报;1992年03期
3 刘剑平;赵树琦;姚太俊;;尼莫地平在颅脑损伤治疗中的脑保护作用[J];广东医学;2006年03期
4 张铭;刘万明;钟宝;周波;全中平;王少波;;经颅多普勒对外伤性蛛网膜下腔出血脑血管监测及临床应用的研究[J];中国实用神经疾病杂志;2007年01期
5 胡晶琼,张苏明;蛛网膜下腔出血后脑血管痉挛的研究进展[J];国外医学脑血管疾病分册;2001年02期
6 吴西;季忠;;利用视觉诱发电位实现无创颅内高压监测[J];生物医学工程学杂志;2007年05期
7 王晓东,薛绛宇;尼莫通对脑挫裂伤合并外伤性蛛网膜下腔出血的近期疗效[J];新乡医学院学报;1999年03期
8 王维治,富羽弘;颅内高压症的监测和治疗进展[J];中风与神经疾病杂志;2000年06期
9 楚胜华,袁先厚,陈卫国,江普查,吴静,郭国炳;经颅多普勒监测和尼膜同对脑外伤后脑血管痉挛的作用[J];中华创伤杂志;2004年06期
10 刘芳龄,刘多三,饶明莉,林世和,张葆樽,田玉旺;蛛网膜下腔出血后迟发性脑血管痉挛并脑梗塞的临床与CT分析[J];中国神经精神疾病杂志;1997年01期
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