Hematoma enlargement-related factors in hypertensive cerebral hemorrhage☆

BACKGROUND：Continuous hemorrhage or hematoma enlargement often occurs following cerebral hemorrhage attacks. OBJECTIVE： To retrospectively analyze the influential factors for hematoma enlargement in patients with hypertensive cerebral hemorrhage prior to minimally invasive surgery. DESIGN, TIME AND SETTING： A comparative analysis of 90 patients with cerebral hemorrhage undergoing minimally invasive surgery at the Department of Neurology, Tongji Hospital of Tongji Medical College, Huazhong University of Science and Technology between April 2005 and February 2007. PARTICIPANTS： Fifty-eight males and thirty-one females aged （52.7 ± 5.23） years （range, 28-73 years）. METHODS： Cranial CT was performed twice to objectively identify hematoma enlargement. Patients with hematoma enlargement prior to surgery were selected as the observation group （n = 30）, and those with no obvious hematoma changes served as the control group （n = 60）. Following cranial CT localization, the two groups underwent minimally invasive hematoma aspiration and drainage, according to Standardized Treatment Guidelines for Micro-invasive Aspiration and Drainage of Intracranial Hematoma. MAIN OUTCOME MEASURES： Hemorrhage site, coagulation function, diabetes history, and clinical symptoms. RESULTS： There were no significant differences in hemorrhage sites between the two groups （χ2 = 2.262, P 〉 0.05）. The percent of intemperance patients in the observation group was significantly larger than the control group （χ2 = 6.923, P 〈 0.01）. No significant differences in terms of percent of coagulation dysfunction or diabetes were determined between the two groups （χ2 = 0.03, 0.08, P 〉 0.05）. The percent of patients with clinical deterioration was significantly higher in the observation group, compared to the control group （χ2 = 25.57, P 〈 0.01）. CONCLUSION： Intemperance and preoperative clinical deterioration may increase incidence of hematoma enlargement prior to minimally invasive surgery in patien     

Hematoma enlargement-related factors in hypertensive cerebral hemorrhage

BACKGROUND:Continuous hemorrhage or hematoma enlargement often occurs following cerebral hemorrhage attacks. OBJECTIVE: To retrospectively analyze the influential factors for hematoma enlargement in patients with hypertensive cerebral hemorrhage prior to minimally invasive surgery. DESIGN, TIME AND SETTING: A comparative analysis of 90 patients with cerebral hemorrhage undergoing minimally invasive surgery at the Department of Neurology, Tongji Hospital of Tongji Medical College, Huazhong University of Scie...     

Real-time analysis of inflammatory cytokines and regulatory gene expression in tissues surrounding the hematoma after intracerebral hemorrhage**○

BACKGROUND： Secondary lesions can occur in tissues surrounding the hematoma following intracerebral hemorrhage, with the presence of inflammatory reactions, cytokine expression and apoptosis These have been confirmed in animal studies. Our study sought to determine whether these could be detected in human tissues surrounding the hematoma following intracerebral hemorrhage. OBJECTIVE： To investigate expression of inflammatory cytokines, Bax and Bcl-x, and identify neural cell apoptosis in tissues surrounding the hematoma, and to analyze the correlation between them and pathological damage in intracerebral hemorrhage patients. DESIGN, TIME AND SETTING： This histopathology, controlled study was performed at the Department of Neurosurgery, Sichuan People＇s Hospital, China, from January 2003 to January 2005. PARTICIPANTS： Brain tissues 1 cm from the hematoma in 30 intracerebral hemorrhage patients served as the experimental group. Brain tissues located away from the hematoma in 7 patients served as the control group. METHODS： TUNEL was used to detect neural cell apoptosis. Immunohistochemistry （labeled dextran polymer） and RT-PCR were used to measure tumor necrosis factor- α, interleukin-1 β, interleukin-6, Bax and Bcl-x protein and mRNA expression. Pathological changes in brain tissues surrounding the hematoma were observed following HE staining. MAIN OUTCOME MEASURES： Neural cell apoptosis, inflammatory cytokines, Bax and Bcl-x protein and mRNA expression, pathological changes in brain tissues surrounding the hematoma. RESULTS： Brain tissues surrounding the hematoma were mildly damaged within 6 hours, severely damaged at 24-72 hours, and significantly improved 1 week following intracerebral hemorrhage. Expression of tumor necrosis factor- α protein and mRNA, interleukin-1β and interleukin-6 mRNA was not significant in tissues surrounding the hematoma, which was identical to the control group within 6 hours after intracerebral hemorrhage. This expression was significantly higher compared with     

Real-time analysis of inflammatory cytokines and regulatory gene expression in tissues surrounding the hematoma after intracerebral hemorrhage

BACKGROUND: Secondary lesions can occur in tissues surrounding the hematoma following intracerebral hemorrhage, with the presence of inflammatory reactions, cytokine expression and apoptosis. These have been confirmed in animal studies. Our study sought to determine whether these could be detected in human tissues surrounding the hematoma following intracerebral hemorrhage. OBJECTIVE: To investigate expression of inflammatory cytokines, Bax and Bcl-x, and identify neural cell apoptosis in tissues surrounding the hematoma, and to analyze the correlation between them and pathological damage in intracerebral hemorrhage patients. DESIGN, TIME AND SETTING: This histopathology, controlled study was performed at the Department of Neurosurgery, Sichuan People's Hospital, China, from January 2003 to January 2005. PARTICIPANTS: Brain tissues I cm from the hematoma in 30 intracerebral hemorrhage patients sewed as the experimental group. Brain tissues located away from the hematoma in 7 patients served as the control group. METHODS: TUNEL was used to detect neural cell apoptosis, lmmunohistochemistry (labeled dextran polymer) and RT-PCR were used to measure tumor necrosis factor-α , interleukin-1β, interleukin-6, Bax and Bcl-x protein and mRNA expression. Pathological changes in brain tissues surrounding the hematoma were observed following HE staining. MAIN OUTCOME MEASURES: Neural cell apoptosis, inflammatory cytokines, Bax and Bcl-x protein and mRNA expression, pathological changes in brain tissues surrounding the hematoma. RESULTS: Brain tissues surrounding the hematoma were mildly damaged within 6 hours, severely damaged at 24-72 hours, and significantly improved 1 week following intracerebral hemorrhage. Expression of tumor necrosis factor-α protein and mRNA, interleukin-1 β and interleukin-6 mRNA was not significant in tissues surrounding the hematoma, which was identical to the control group within 6 hours after intracerebral hemorrhage. This expression was significantly higher compared with the control group from 12-72 hours, and gradually decreased after 72 hours. The number of apoptotic neural ceils reached a peak between 12-72 hours. Tumor necrosis factor-α protein and mRNA, interleukin-1β and interleuldn-6 mRNA levels were positively correlated with apoptosis, Bax protein and mRNA levels (P < 0.01). CONCLUSION: Tumor necrosis factor-α, interleukin-1β, and interleukin-6 levels are highly correlated with apoptosis. With the decrease in tumor necrosis factor-α, interleukin-1β and interleukin-6 levels, the number of apoptotic cells gradually reduced.     

Mild hypothermia effects on matrix metalloproteinase-9 expression in the perihematomal region of rats following experimental intracerebral hemorrhage**☆

BACKGROUND： Matrix metalloproteinase-9 （MMP-9） expression increases with intracerebral hemorrhage, and participates in the pathophysiological processes of secondary brain injury after intracerebral hemorrhage.
OBJECTIVE： To investigate the effects of mild hypothermia on MMP-9 expression and brain edema in the perihematomal region of experimental intracerebral hemorrhage rats.
DESIGN, TIME AND SETTING： The randomized, controlled experiment was performed at the Central Laboratory of Shandong Provincial Hospital between May and September 2007.
MATERIALS： Seventy-two, Wistar, male rats, 12-weeks old, were used for this study. Rabbit anti-MMP-9 primary antibody was purchased from Boster, China.
METHODS： Wistar rats were equally and randomly divided into normothermia and mild hypothermia groups. The two groups each comprised control, 6-hour intracerebral hemorrhage, 24-hour intracerebral hemorrhage, 48-hour intracerebral hemorrhage, 72-hour intracerebral hemorrhage, and l-week intracerebral hemorrhage subgroups, with six rats in each subgroup. Rat models of intracerebral hemorrhage were established by injecting 100 μL of autologous blood into the rat caudate nucleus. Rats in the mild hypothermia group received four hours of local mild hypothermia immediately following the injection. lntracerebral temperature was maintained at （33 ± 0.5） ℃. Subsequently, intracerebral temperature was spontaneously recovered at 25 ℃. Rats in the control subgroup were not injected with autologous blood and received only with intracerebral hemorrhage.
MAIN OUTCOME MEASURES： Brain water content and MMP-9 expression surrounding the hematoma region. RESULTS： MMP-9 expression increased at 6 hours, and brain edema reached a peak at 48 hours after intracerebral hemorrhage. MMP-9 expression was significantly decreased in the mild hypothermia group compared with the normothermia group at each time point （P 〈 0.05）.
CONCLUSION： Mild hypothermia can significantly inhibit MMP-9 overexpression and reliev     

CD163 promotes hematoma absorption and improves neurological functions in patients with intracerebral hemorrhage

Clinical outcomes are positively associated with hematoma absorption.The monocyte-macrophage scavenger receptor,CD163,plays an important role in the metabolism of hemoglobin,and a soluble form of CD163 is present in plasma and other tissue fluids;therefore,we speculated that serum CD163 affects hematoma absorption after intracerebral hemorrhage.Patients with intracerebral hemorrhage were divided into high-and low-level groups according to the average CD163 level(1,977.79 ± 832.91 ng/m L).Compared with the high-level group,the low-level group had a significantly slower hematoma absorption rate,and significantly increased National Institutes of Health Stroke Scale scores and modified Rankin Scale scores.These results suggest that CD163 promotes hematoma absorption and the recovery of neurological function in patients with intracerebral hemorrhage.     

Effects of basic fibroblast growth factor on superoxide dismutase activity and malondialdehyde content in the rat brain following intracerebral hemorrhage*☆

BACKGROUND： Studies have confirmed that basic fibroblast growth factor （bFGF） promotes neuronal survival and neurite outgrowth. OBJECTIVE： To compare and verify the effects of bFGF on superoxide dismutase activity and malondialdehyde content in rat brain tissues surrounding a hemorrhagic lesion, as well as the hippocampus at the hemorrhagic side. DESIGN, TIME AND SETTING： The randomized, controlled, neurobiological study was performed at the Science Experimental Center and Research Laboratory, Guangxi Medical University, China, from September to December 2006. MATERIALS： Ninety-two adult, healthy, Wistar rats of equal gender were used to establish intracerebral hemorrhage by infusing type VII collagenase into the left internal capsule. Type Ⅶ collagenase （Sigma, USA）, superoxide dismutase and malondialdehyde kits （Jiancheng, China）, and bFGF （Institute of Bioengineering, Ji＇nan University, China） were used for this study. METHODS： Ninety successfully lesioned rats were equally and randomly divided into three groups. Rats in the bFGF group were intramuscularly injected daily with bFGF （8 ug/kg）. Rats in the saline control group received an equal volume of saline. The rats in the model group did not receive other interventions. Superoxide dismutase activity was measured using the xanthine oxidase method. Malondialdehyde contents were detected using the thiobarbituric acid method. MAIN OUTCOME MEASURES： At 1, 3, and 7 days following intracerebral hemorrhage, superoxide dismutase and malondialdehyde were determined in the brain tissue surrounding the hematoma and in the hippocampus in the affected hemisphere. RESULTS： In brain tissue surrounding the hematoma, superoxide dismutase activity was significantly increased in the bFGF group at 3 and 7 days after intracerebral hemorrhage compared with the saline control group, whereas malondialdehyde content was significantly decreased （P 〈 0.05）. In the hippocampus, superoxide dismutase activity was significantly increased in the     

Neurovascular compression and decompression of the intracranial vagus for blood pressure

BACKGROUND: Previous researches demonstrated that neurovascular decompression could cure hypertension; however, whether it could effectively control refractory hypertension after hypertensive cerebral hemorrhage should be further studied. OBJECTIVE: To observe the effect of neruovascular compression on intracranial vagus for blood pressure of dogs and investigate the effect of neurovascular decompression on blood pressure of patients with hypertensive cerebral hemorrhage. DESIGN: Randomized controlled animal study, clinical effects and retrospective analysis. SETTING: Department of Neurosurgery, Changzheng Hospital Affiliated to the Second Military Medical University of Chinese PLA. MATERIALS: The experiment was carried out in the Department of Neurosurgery, Changzheng Hospital Affiliated to the Second Military Medical University of Chinese PLA from May to October 2006. A total of 15 healthy adult dogs of both genders were randomly divided into experimental group (n =10) and control group (n =5). Clinical observation: A total of 41 patients with hypertensive cerebral hemorrhage were selected from the Department of Neurosurgery, General Hospital of Nanjing Military Area Command of Chinese PLA and the Department of Neurosurgery, Changzheng Hospital Affiliated to the Second Military Medical University of Chinese PLA from October 1999 to October 2006. Among them, one patient had brain stem hemorrhage. There were 27 males and 14 females aged from 41 to 66 years. Inclusion criteria: All patients were diagnosed with CT examination once or several times. Volume of hematoma ranged from 50 to 120 mL and had obviously operative indication. All patients provided consents. In addition, another 281 patients with hypertensive cerebral hemorrhage who received traditionally internal and surgical therapies in our departments of neurosurgery, neurology and emergency room were selected in the control group. METHODS: ① Animal experiments: 20 cm autochthonous great saphenous vein was taken from dogs in the experimental group and coincided with tip of facial artery to form arterial loop so as to oppress left vagus and lateral bulb abdomen. In addition, 20 cm autochthonous great saphenous vein was taken from dogs in the control group and coincided with tip of facial artery to establish arterial loop so as to oppress left cerebellum to observe changes of blood pressure before and at 1, 2, 3 and 4 weeks after operation. ② Clinical observation: Among 41 patients with hypertensive cerebral hemorrhage including one with brain stem hemorrhage, they received microvascular decompression of vagus immediately after getting rid of intracerebral hematoma and stopping bleeding to observe its effect of depressurization. All patients and their relatives provided consents. ③ A total of 281 patients with hypertensive cerebral hemorrhage who discharged after the treatment of traditionally internal and surgical therapies were studied retrospectively to observe changes of blood pressure after routine treatment and compare the results with neurovascular decompression. MAIN OUTCOME MEASURES: ① Changes of blood pressure of experimental dogs; ② effect of vascular decompression of vagus for blood pressure of patients with hypertensive cerebral hemorrhage after clearing intracerebral hematoma; ③ different effects of neurovascular decompression and routinely internal and surgical therapies on hypertension. RESULTS: ① Results of animal experiments: Nine dogs in the experimental group survived. At 1, 2, 3 and 4 weeks after operation, blood pressure of dogs in the experimental group was (139.77±4.06), (149.11±4.90), (148.10±4.16), (147.76±4.15) mm Hg (1 mm Hg=0.133 kPa), which was higher than that of dogs in the control group [(117.20±2.74), (116.65±3.74), (116.26±1.8), (115.81±3.76) mm Hg, P < 0.01]. ② Results of clinical observation: Among 41 patients, 8 (20%) cases died during the operation. In addition, among other 33 (80%) survival patients, 11 (33%) cases had normal blood pressure; blood pressure of 14 (43%) cases was improved or closed to normal value; blood pressure of 8 (24%) cases was not changed obviously as compared with that before operation. ③ The results demonstrated that, by using traditionally internal and surgical therapies, among 281 patients with hypertensive cerebral hemorrhage, blood pressure of about 15% cases was recovered or closed to normal value. Those mentioned above did not have history of hypertension before hemorrhage. However, patients who had history of hypertension before hemorrhage received the traditionally internal or surgical therapies, and the blood pressure was not improved to the normal value after the treatment. CONCLUSION: ① Neurovascular compression in left intracranial vagus can cause obvious increase of blood pressure of dogs, and the increasing volume was 30 mm Hg. ② Vascular decompression of vagus has a great effect on refractory hypertension, and the improvement of blood pressure is superior to traditionally internal and surgical therapies in clinic.     

Recurrent intracerebral hemorrhage

Objective: In order to study the clinical manifestation and risk factor of recurrent intracerebral hemorrhage(ICH).Methods:The 256 patients were analysed who admitted to our hospital for intracerebral hemorrhage between 1995 and 1997.The 15(5 .86%)patients had a recurrent ICH.There were 9 men and 6 women and the mean age of the patients was 63.5 ± 6.4years at the first bleeding episode and 67.8± 8. 5 years at the second. The mean interval between the two bleeding episodes was 44.6 ± 12.5 months. The 73.3%patients were hypertensive .′The site of the first hemorrhage was ganglionic in 8 patients , ]ohar in six paients and brainstem in one .The recurrent hemorrhage occurred at a different location from the previous ICH.The most common pattern of recurrence was “ganglionic -ganglionic” (7 patients), lobar - ganglionic (3 patients), lobar-lobar(three patients), which was always observed in hypertensive patients. The outcome after the recurrent hemorrhage was usually poor. By comparison with 24 patients followed up to average 47.5± 18.7 months with isolated ICH without recurrence .Only lobar hematoma and a younger age were risk factors for recurrences whereas sex and previous hypertension were not. The mechanism of recurrence of ICH were multiple(hypertension, cerebral amyloid angiopathy).Contral of blood pressure and good living habit after the first hemorrhage may prevent ICH recurrences.     

Correlation between serum fructosamine and hyperglycemia in patients with acute cerebrovascular disease

BACKGROUND: Diabetes mellitus is one of the risk factors in patients with acute cerebral disease, and always leads to stroke or get it worse. There is often a high level of blood glucose in those patients with diabetes mellitus and cerebral disease, but it is hard to distinguish from both kinds of hyperglycemia. Serum fructosamine is said to be correlated with blood glucose. OBJECTIVE: To explore the relationship between serum fructosamine and blood glucose in patients with acute cerebrovascular disease. DESIGN: A case-controlled study. SETTINGS: Department of Clinical Laboratory, Health Department for Cadres and Department of Neurology of Affiliated Hospital, Qingdao University Medical College. PARTICIPANTS: Forty-eight inpatients and outpatients with cerebrovascular diseases were selected from the Department of Neurology, Affiliated Hospital of Qingdao University Medical College from December 2004 to April 2005. All the patients were confirmed with CT and MRI. There were 25 patients with diabetes mellitus secondary cerebrovascular diseases, who met the diagnostic standards of diabetes mellitus set by WHO, including 12 males and 13 females with an average of (60±8) years old, the course of diabetes mellitus ranged from 1 to 21 years.. The other 23 patients had no diabetes mellitus (without diabetes mellitus group), including 14 males and 9 females with an average of (62±6) years old. Meanwhile, another 50 healthy physical examinees in the hospital were selected as control group, including 26 males and 24 females with the average age of (62±5) years old. Informed content was obtained from all the participants. METHODS: Venous blood was drawn from all the participants, and content of blood glucose was assayed by means of glucose oxidase, and the concentration of serum fructosamine was determined by nitroblue tetrazolium colorimetric method. Comparison between groups was performed by the analysis of variance and q test, and the correlation was tested by linear regression analysis. MAIN OUTCOME MEASURES: ① Comparison of blood glucose and serum fructosamine among the groups; ② Correlation between serum fructosamine and blood glucose in patients with diabetes mellitus secondary cerebrovascular diseases and those without diabetes mellitus. RESULTS: All the 48 patients with cerebrovascular disease and 50 healthy subjects were involved in the analysis of results. ① Contents of blood glucose and serum fructosamine: There were obvious differences in the contents of blood glucose and serum fructosamine among the diabetes mellitus group, without diabetes mellitus group and control group (F =577.7, 115.1, P < 0. 01). The content of serum fructosamine in the diabetes mellitus group [(4.25±1.35) mmol/ L] was obviously higher than those in the control group and without diabetes mellitus group [(1.65±0.27), (1.96±0.25) mmol/ L, q =1.47, 1.30, P < 0.01], whereas there was no significant difference between the without diabetes mellitus group and control group (P > 0.05). The content of blood glucose was obviously higher in the patients with and without diabetes mellitus groups [(15.80±2.13), (9.50 ±1.78) mmol/L] than in the control group [(4.56 ±0.77) mmol/L, q =1.86, 2.46, P < 0.01], also markedly higher in the with diabetes mellitus group than in the without diabetes mellitus group (q =1.42, P < 0.01). ② Results of correlation analysis: The content of serum fructosamine was positively correlated with the level of fasting blood glucose in the patients with diabetes mellitus secondary cerebrovascular diseases (r = 0.603, P < 0.01). But there was no relationship between serum fructosamine and fasting blood glucose in the patients without diabetes mellitus (r =0.357, P > 0.05). CONCLUSION: The contents of blood glucose and serum fructosamine were obviously different among the diabetes mellitus group, without diabetes mellitus group and control group. There are closer relations between serum fructosamine and blood glucose in patients with diabetes mellitus secondary cerebral disorders, which are not observed in the patients without diabetes mellitus. Fructosamine is significant in differentiating the reasons for the increased blood glucose in patients with acute cerebrovascular disease.     

Electrocardiogram changes during hematoma enlargement in intracerebral hemorrhage patients

BACKGROUND: It has been reported that cerebrovascular disease causes changes in electrocardiogram results. OBJECTIVE: To investigate changes in electrocardiogram results in patients with intracerebral hematoma enlargement. DESIGN, TIME AND SETTING: The present case-retrospective analysis study was performed at the Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology from January 2005 to October 2006. PARTICIPANTS: A total of 225 intracerebral hemorrhage patients (142 males and 83 females) that were hospitalized at the Department of Neurology were enrolled the present study. The patient selection was in accordance with diagnostic criteria from the Fourth National Cerebrovascular Disease Congress of China in 1995, and diagnosis was confLrrned using computed tomography. All patients underwent computed tomography twice within 24 hours following intracerebral hemorrhage, and were subjected to electrocardiogram examination after admission. METHODS: According to hematoma enlargement following intracerebral hemorrhage, all patients were divided into hematoma enlargement (n = 20) and non-hematoma enlargement (n = 205) groups. Because of the large patient number difference between the two groups, the hematoma enlargement group was matched with the non-hematoma enlargement group. Patients meeting these conditions were included in the non-hematoma enlargement group. Finally, 75 patients were included in the final analysis, 19 in the hematoma enlargement group and 56 in the non-hematoma enlargement group. Clinical data from the two groups were statistically analyzed. MAIN OUTCOME MEASURES: The incidence of electrocardiographic abnormalities between the hematoma enlargement and non-hematoma enlargement groups. RESULTS: In the hematoma enlargement group, 15 patients (79%) developed electrocardiographic abnormalities. In the non-hematoma enlargement group, 24 patients (43%) presented with electrocardiographic abnormalities. There were significant differences in electrocardiographic abnormalities between the groups (P < 0.01 ). CONCLUSION: Patients with electrocardiographic abnormalities suffered from hematoma enlargement following admission.     

高血压脑出血血肿扩大相关因素分析

目的通过对比分析明确幕上高血压脑出血血肿扩大的危险因素。方法将幕上高血压脑出血患者313例,根据是否存在血肿扩大,分为血肿扩大组和非血肿扩大组,明确血压、早期使用甘露醇、血肿特点、发病时搬动与血肿扩大的关系。结果 (1)血肿扩大组入院时收缩压200mmHg者占40.34%,非血肿扩大组占12.37%;血肿扩大组入院时舒张压110mmHg者占57.14%,非血肿扩大组占26.80%,两组比较,血肿扩大组血压明显高于非血肿扩大组,差异显著(P0.01)。(2)血肿扩大组早期(发病6h内)使用甘露醇者占85.71%,非血肿扩大组占54.12%,差异显著(P0.01)。(3)血肿扩大组丘脑出血占38.66%,显著多于非血肿扩大组的26.28%(P0.05);血肿扩大组出血量20ml者58.82%,显著高于非血肿扩大组的16.50%(P0.01);血肿扩大组血肿形态不规则者93.28%,显著高于非血肿扩大组的61.34%(P0.01)。(4)血肿扩大组存在搬动史者57.98%,非血肿扩大组41.75%,差异显著(P0.01)。结论血压升高(收缩压200mmHg和/或舒张压110mmHg)、发病早期(6h内)使用甘露醇、丘脑出血、出血量大于20ml、血肿形态不规则、发病早期存在搬动是脑出血血肿扩大的危险因素。     

自发性脑出血血肿扩大的影响因素与预后分析

目的探讨自发性脑出血血肿扩大的影响因素，并分析其与预后的关系。 方法选取自2013年12月至2018年12月陕西中医药大学附属医院脑外科收治的670例自发性脑出血患者，根据72 h内复查CT的情况分为血肿扩大组（77例）和血肿稳定组（593例），记录2组患者的临床资料，分析血肿扩大的影响因素，出院后随访3个月，比较2组患者的预后。 结果670例患者中发生血肿扩大77例，发生率11.49%（77/670），其中预后不良45例，预后良好32例，血肿稳定组593例，其中预后不良261例，预后良好332例，2组患者预后不良率比较差异有统计学意义（P<0.05）。单因素分析显示，血肿扩大组的活化部分凝血活酶时间、首次CT血肿体积、血肿形态、高血压病、卒中病史与血肿稳定组相比差异有统计学意义（P<0.05）。多因素分析显示，高血压病、卒中病史、血肿形态是自发性脑出血血肿扩大的独立危险因素（OR>1，P<0.05）。 结论自发性脑出血患者出现血肿扩大的独立危险因素包括高血压病、卒中病史、不规则血肿形态，血肿扩大可增加不良预后。     

高血压性脑出血血肿扩大相关因素分析

目的探讨高血压性脑出血后血肿继续扩大的相关因素。方法回顾性分析187例高血压性脑出血病例的临床资料,其中56例出现血肿持续扩大,将其与未出现血肿扩大者进行对比分析。结果①单因素logistic回归分析显示高血压病程、长期饮酒、糖尿病史、长期服用阿司匹林、体重指数高、发病至第一次CT时间短(<2h)、丘脑出血、血肿形态不规则、入院时血压值高、高血糖和早期大量使用甘露醇是高血压性脑出血后血肿扩大的危险因素;②多因素logistic回归分析显示长期饮酒、长期服用阿司匹林、发病至第一次CT时间短(<2h)、丘脑出血、血肿形态不规则、入院时血压值高和早期大量使用甘露醇是高血压性脑出血血肿扩大的独立危险因素。结论对长期饮酒、长期服用阿司匹林、丘脑出血、血肿形态不规则、入院时血压值高以及出血后大量使用甘露醇的高血压性脑出血患者要严密观察病情变化,高度警惕血肿继续扩大以免延误治疗。     

用凝血功能综合评分法分析高血压脑出血急性期血肿扩大的相关因素

目的旨在用凝血功能综合评分法(CFCS)分析高血压脑出血急性期血肿扩大的相关因素。方法收集2010年3月至2012年3月收治的高血压脑出血患者152例,其中男90例、女62例;年龄平均(54.7±11.3)岁。应用头颅CT观察患者急性期血肿扩大的情况。参照国际血栓和止血协会制定的凝血功能检测指标设计CFCS进行评分;对包括CFCS在内的多个血肿扩大危险因素进行单因素χ2检验及多因素Logistic回归分析。结果共入组152例患者,血肿体积平均(26.2±12.1)mL;入院时GCS评分平均(9.8±3.7)分。入选病例在急性期出现血肿扩大57例(37.5%)。χ2检验发现起病时血肿部位、入院时血压情况、CFCS评分等是血肿扩大的候选危险因素(P0.05)。将上述因素引入Logistic回归方程,逐步前进法分析得出入院时收缩压、CFCS评分、早期使用甘露醇是高血压脑出血急性期血肿扩大的独立危险因素。结论CFCS评分与高血压脑出血急性期血肿扩大以及预后密切相关,可以作为临床判断血肿扩大因素的参考指标,有利于早期发现血肿扩大并及时进行干预。     

自发性脑出血早期血肿扩大首诊CT分析

探讨首诊头部CT影像对自发性脑出血早期血肿扩大的预测价值。300例发病后6h内入院的自发性脑出血患者,经CT检查显示其中61例(20.33%)发生早期血肿扩大,经单因素和多因素Logistic回归分析显示,早期血肿扩大与首诊CT距发病时间短、血肿密度不均匀、中至重度脑萎缩及血     

CT平扫漩涡征与黑洞征在预测脑出血早期血肿扩大中的价值研究

目的比较CT平扫漩涡征、黑洞征及"漩涡征和黑洞征"在自发性脑出血患者早期血肿扩大中的预测价值。方法选择自2012年1月至2018年12月在苏州大学附属第二医院神经内科首诊并住院治疗的210例自发性脑出血患者进入研究,按照有无出现早期血肿扩大将患者分为血肿扩大组及血肿未扩大组,按照按征象的有无再将患者分为征象阳性组与征象阴性组,分别比较不同组别患者的影像学及临床特征。运用受试者工作特征(ROC)曲线分析漩涡征、黑洞征及"漩涡征和黑洞征"预测早期血肿扩大的准确性,运用多因素Logistic回归分析明确早期血肿扩大的独立危险因素。结果(1)57例早期血肿扩大的患者中,出现漩涡征21例(36.8%),黑洞征17例(29.8%);153例血肿未扩大的患者中,出现漩涡征12例(7.8%),黑洞征22例(14.4%);影像学征象阳性患者比例差异有统计学意义(P<0.05)。与血肿未扩大组患者比较,血肿扩大组患者入院收缩压显著升高,破入脑室者比例显著增多,差异均有统计学意义(P<0.05)。(2)漩涡征阳性(33例)与漩涡征阴性(177例)患者临床及影像学各项指标差异均无统计学意义(P>0.05)。黑洞征阳性患者(39例)的初始血肿量较黑洞征阴性患者(171例)明显增加,差异有统计学意义(P<0.05)。"漩涡征和黑洞征"阳性患者初始血肿量较阴性患者明显增加,差异有统计学意义(P<0.05)。(3)漩涡征、黑洞征及"漩涡征和黑洞征"的ROC曲线下面积分别为0.645、0.577与0.570。(4)多因素Logistic回归分析结果显示,入院收缩压、漩涡征与黑洞征均为早期血肿扩大的独立危险因素(P<0.05)。结论相较于CT平扫黑洞征及"漩涡征和黑洞征",漩涡征在自发性脑出血患者早期血肿扩大中的预测价值更大。     

自发性脑出血发生血肿扩大的影响因素分析

目的探讨自发性脑出血患者发生血肿扩大的影响因素。方法回顾性分析2018年9月至2019年9月苏州大学附属第一医院神经外科收治的224例自发性脑出血患者的临床资料。所有患者入院时行首次头颅CT平扫(发病时间≤8 h),并于24 h后复查头颅CT,将复查时血肿量增加≥33%或增加≥12.5 ml定义为血肿扩大,并分为血肿扩大组(n=70)与血肿未扩大组(n=154)。收集两组年龄、性别、糖尿病史、初始血肿量、入院时收缩压、入院时格拉斯哥昏迷评分(GCS)以及是否有凝血功能异常等临床资料。判读首次头颅CT平扫时是否存在血肿边缘不规则混合密度征、黑洞征、漩涡征、分叶征、混杂征。采用单因素分析和多因素logistic回归分析法判断影响血肿扩大的因素。结果224例患者中,CT显示血肿边缘不规则混合密度征71例,黑洞征56例,漩涡征51例,分叶征53例,混杂征58例。血肿未扩大组与血肿扩大组患者的年龄、性别以及初始血肿量的差异均无统计学意义(均P>0.05)。与血肿未扩大组比较,血肿扩大组有糖尿病史者和凝血功能异常者占比均高,入院时GCS低、收缩压高以及头颅CT显示有血肿边缘不规则混合密度征、黑洞征、漩涡征、分叶征、混杂征者占比均高(均P<0.05)。多因素logistic回归分析结果显示,有糖尿病史、入院时GCS低、入院时收缩压高、凝血功能异常以及头颅CT显示有血肿边缘不规则混合密度征、黑洞征、漩涡征、分叶征、混杂征均为脑出血患者发生血肿扩大的危险因素(均P<0.05)。结论既往有糖尿病史、入院时GCS低、收缩压高、凝血功能异常以及有CT影像学特征性表现的自发性脑出血患者发生血肿扩大的风险高。     

脑出血早期血肿扩大的临床特点及相关因素分析

目的分析脑出血后早期血肿增大的临床特点,探讨其相关危险因素及防治策略。方法 492例脑出血患者,根据病情演变及脑CT变化,分为血肿增大组和血肿稳定组,对两组患者病史、临床特点、生化指标及头颅CT特征进行对比分析。结果 492例患者中,114例出现血肿增大,发生率为23.17%;不规则血肿、肝功能异常、肾功能异常、凝血功能异常、长期饮酒者的患者易发生血肿扩大,两组比较有差异有统计学意义(P<0.05)。结论脑出血后血肿增大多发生在24h内,肝、肾功能受损、凝血功能异常、长期饮酒者可能为血肿增大的主要危险因素。