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1.
目的探讨颅脑损伤开颅术中急性脑膨出的原因和防治措施。方法对近年来手术中出现脑膨出的72例重型颅脑损伤病人进行回顾性分析。总结其形成原因及易发因素,比较各种防治措施的疗效。结果术中迟发性颅内血肿形成急性弥漫性脑肿胀、脑组织缺氧和休克、脑疝时间过长、严重脑挫裂伤等是颅脑损伤术中急性脑膨出的主要原因,彻底清除颅内血肿、缓慢降低颅内压、术中过度换气、应用脱水剂、控制血压等是防治术中脑膨出的有效措施。结论针对不同病因采取相应的措施,可防治重型颅脑损伤术中急性脑膨出,取得较好疗效,降低病死率。  相似文献   

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目的探讨颅脑损伤开颅术中急性脑膨出的原因和防治措施。方法对近年来手术中出现脑膨出的72例重型颅脑损伤病人进行回顾性分析。总结其形成原因及易发因素,比较各种防治措施的疗效。结果术中迟发性颅内血肿形成急性弥漫性脑肿胀、脑组织缺氧和休克、脑疝时间过长、严重脑挫裂伤等是颅脑损伤术中急性脑膨出的主要原因,彻底清除颅内血肿、缓慢降低颅内压、术中过度换气、应用脱水剂、控制血压等是防治术中脑膨出的有效措施。结论针对不同病因采取相应的措施,可防治重型颅脑损伤术中急性脑膨出,取得较好疗效,降低病死率。  相似文献   

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目的探讨重型颅脑损伤手术中急性脑膨出的机理与处理措施。方法回顾性分析58例在颅脑手术过程中发生脑膨出的重型颅脑损伤患者临床资料,影像学资料及应对措施,采用标准大骨瓣减压、过度通气、咬除颅底骨质、阶梯性减压、及时复查颅脑CT等综合措施。结果术后随访三月按GOS评定预后恢复良好19例、轻残11例、重残11例、植物生存5例、死亡12例。迟发性血肿(63.8%),弥漫性脑肿胀(27.6%)及脑梗死(8.6%)是重型颅脑损伤手术中急性脑膨出的主要原因。结论对重型颅脑损伤手术中急性脑膨出的患者要正确判断,区别原因采取相应的措施。  相似文献   

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重型颅脑损伤术中急性脑膨出23例的治疗分析   总被引:3,自引:1,他引:2  
目的探讨重型颅脑损伤手术中急性脑膨出的原因及防治措施。方法对23例重型颅脑损伤患者术中出现脑膨出进行回顾性分析、分析其形成原因、疗效及防治措施。结果23例患者中,死亡13例,其中迟发性颅内血肿引起脑膨出8例,死亡3例;弥漫性脑肿胀5例,死亡4例;其他原因10例、死亡6例;迟发性颅内血肿术后GOS评分良好率为25%。结论术中出现急性脑膨出对于不同病因应积极采取相应治疗,可提高患者生存率。  相似文献   

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目的探讨重型颅脑损伤开颅血肿清除术中急性脑膨出的原因及综合治疗措施。方法回顾分析42例术中出现脑膨出的重型颅脑损伤病人受伤机制、临床表现、CT扫描结果,总结脑膨出的原因。结果按GOS标准,治疗后6个月评定治疗结果,恢复良好6例,中残8例,重残9例,植物生存2例,死亡17例。急性弥漫性脑肿胀、迟发性颅内血肿形成、脑组织缺血、缺氧和低血压、长时间脑疝、严重脑挫裂伤是颅脑损伤术中急性脑膨出的主要原因,采取综合治疗是防治术中脑膨出的有效措施。结论结合临床和CT扫描可判定术中脑膨出发生的可能性,对各种原因所致术中急性脑膨出及时采取相应综合措施可获良效。  相似文献   

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目的 探讨重型颅脑损伤术中发生急性脑膨出的防治措施.方法 对36例重型颅脑损伤术中急性脑膨出的形成原因等资料进行回顾性分析.结果 术中迟发性颅内血肿、弥漫性脑肿胀、严重广泛脑挫裂伤等是重型颅脑损伤术中急性脑膨出的主要原因.结论 针对不同病因采取相应的防治措施,尽快彻底清除迟发性血肿,使用过度换气、脱水剂等降低颅内压,充分减压、控制血压等措施,可提高患者的存活率.  相似文献   

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重型颅脑损伤术中急性脑膨出的治疗体会   总被引:1,自引:0,他引:1  
目的 探讨重型颅脑损伤术中急性脑膨出的原因及有效防治措施.方法 对68例重型颅脑损伤术中急性脑膨出的病例作回顾性分析,总结急性脑膨出的原因、相应特点及采取治疗措施.结果 术中颅内迟发出血、急性弥漫性脑肿胀、重度脑挫裂伤、术前、术中缺氧、低血压等原因引起急性脑膨出,迅速清除颅内迟发血肿、大骨窗开颅、控制血压、纠正缺氧是防...  相似文献   

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目的分析重型颅脑损伤术中急性脑膨出的临床特点。方法将重型颅脑损伤术中出现急性脑膨出的38例病人进行回顾性分析,总结其形成原因及易发条件,比较各种防治措施的效果。结果迟发性血肿、手术处理不当、急性脑肿胀等是颅脑损伤术中急性脑膨出形成的主要原因,正确的手术处理、缓慢的降低颅内压、控制性低血压、过度换气等是防治术中急性脑膨出的有效措施。结论应根据形成原因的不同而采取相应的措施防治颅脑损伤术中急性脑膨出。  相似文献   

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重型颅脑损伤术中急性脑膨出   总被引:10,自引:0,他引:10  
目的 分析重型颅脑损伤手术中急性脑膨出的原因及防治措施。方法 对术中出现脑膨出的18例脑损伤病人进行回顾性分析、分析形成原因及防治措施。结果 急性弥漫性脑肿胀、迟发颅内出血、低氧血症、天幕裂孔疝所致脑干受压、广泛脑挫伤是颅脑损伤术中急性膨出的主要原因。降低颅压、清除迟发血肿、过度通气、使用脱水剂、提高胶体渗透压、控制血压是防治术中脑膨出的有效措施。结论 对于不同病因采取相应措施,可提高生存率。  相似文献   

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目的探讨重型颅脑损伤术中急性脑膨出的原因及防治对策。方法分析1例典型的重型颅脑损伤术中急性脑膨出患者的临床资料,并复习关于术中急性脑膨出形成原因及防治的文献。结果本例患者开颅术中发生急性脑膨出,在术中死亡。结论迟发性颅内血肿、弥漫性脑肿胀及大面积脑梗死是术中形成急性脑膨出的主要原因,术前正确评估及术中采取相应的对策可有效防治急性脑膨出,提高患者的生存率。  相似文献   

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Fine structural characteristics of synapses in the spiral organ of Corti were examined, with reference to differences between inner and outer haircell systems, and to location of neurons of origin of efferent axons. Surgical interruption of crossed olivocochlear bundle, of vestibular nerve, of facial nerve, and excision of superior cervical ganglia were used to determine the pathways of efferent axons. Interruption of the vestibular nerve near the brainstem results in degeneration of all efferent terminals on outer hair cells. Mid-line lesions at, and caudal to, the facial colliculus result in degeneration of about half of these efferent terminals. Efferent synaptic bulbs to the inner hair-cell system are small, of the order of one micron, and form type 2 junctions with afferent dendrites. They tend to have more large dense-core vesicles (about 80 nm) than the large efferent terminals of the outer hair-cell system, and appear to be the terminals of axons in the habenula perforata, which exhibit varicosities laden with large dense core vesicles. The varicosities are unaffected by excision of the superior cervical ganglia. So far as our material can reveal, it appears that the varicosities in the habenula perforata do not survive vestibular root interruption, nor do the efferent processes in the internal spiral bundle or at the base of inner hair cells. Most interestingly, the afferent processes of the inner hair-cell system, as identified for example by their relation to pre-synaptic bodies in the inner hair cells, are subject to a trans-synaptic reaction after severance of the vestibular root. They undergo a dramatic cytological transformation, characterized by increase of volume, engorgement with microtubules, microfilaments, microvesicles of various sizes, and clusters of lysosomes. Thus, both the efferent and afferent terminals of the inner hair-cell system show marked cytological differences from the corresponding terminals of the outer hair cell system.  相似文献   

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Tubocurarine (Tc) effect on membrane currents elicited by acetylcholine (ACh) was studied in isolated superior cervical ganglion neurons of rat using patch-clamp method in the whole-cell recording mode. The "use-dependent" block of ACh current by Tc was revealed in the experiments with ACh applications, indicating that Tc blocked the channels opened by ACh. Mean lifetime of Tc-open channel complex, tau, was found to be 9.8 +/- 0.5 s (n = 7) at -50 mV and 20-24 degrees C. tau exponentially increased with membrane hyperpolarization (e-fold change in tau corresponded to the membrane potential shift by 61 mV). Inhibition of the ACh-induced current by Tc (3-30 microM/1) was completely abolished by membrane depolarization to the level of 80-100 mV. Inhibition of ACh-induced current was augmented at increased ACh doses. It is concluded that the open channel block produced by Tc is likely to be the only mechanism for Tc action on nicotinic acetylcholine receptors in superior cervical ganglion neurons of rat.  相似文献   

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Background Dementia occurs in the majority of patients with Parkinson’s disease (PD). Late onset of PD has been reported to be associated with a higher risk for dementia. However, age at onset (AAO) and age at baseline assessment are often correlated. The aim of this study was to explore whether AAO of PD symptoms is a risk factor for dementia independent of the general effect of age. Methods Two community-based studies of PD in New York (n = 281) and Rogaland county, Norway (n = 227) and two population-based groups of healthy elderly from New York (n = 180) and Odense, Denmark (n = 2414) were followed prospectively for 3–4 years and assessed for dementia according to DSM-IIIR. All PD and control cases underwent neurological examination and were followed with neurological and neuropsychological assessments. We used Cox proportional hazards regression based on three different time scales to explore the effect of AAO of PD on risk of dementia, adjusting for age at baseline and other demographic and clinical variables. Findings In both PD groups and in the pooled analyses, there was a significant effect of age at baseline assessment on the time to develop dementia, but there was no effect of AAO independent of age itself. Consistent with these results, there was no increased relative effect of age on the time to develop dementia in PD cases compared with controls. Interpretation This study shows that it is the general effect of age, rather than AAO that is associated with incident dementia in subjects with PD. Received in revised form: 22 December 2005  相似文献   

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After a hopeful beginning, the social process of the reintegration of those with severe mental illness has come to a standstill. I am led to wonder whether "the community" really wants to live together with people suffering from severe mental illness, and if so, how closely? As long as the medical treatment of mental illness provided by the general practitioners is fundamentally deficient, as they are not able to prescribe the necessary interventions--such as out-patient psychiatric nursing, and service providers in the out-patient sector are content with offering increasingly intensive forms of care for the less seriously ill at the cost of the Social Welfare System--the reintegration of those with serious mental illness remains an illusion--which is mainly to the benefit of providers of residential care in homes and hostels.  相似文献   

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