目的:探讨颅脑损伤患者术中急性脑膨出的病因、诊断及治疗。方法:对127例术中发生急性脑膨出的颅脑损伤患者的临床资料进行回顾性分析。结果:急性脑膨出的原因为同侧脑肿胀者74例,为对侧迟发性血肿者51例,而为同侧迟发性血肿者2例。共死亡48例(37.8%),其中31例因脑疝死亡。结论:通过钻孔探查或积极的CT扫描,及时发现颅脑损伤患者术中急性脑膨出的原因,并尽早正确处理极其重要,是抢救此类患者成功的关键。
目的:总结分析1387例重型颅脑损伤的救治情况，以利在今后的工作中进一步改善和提高对重型颅脑损伤的救治水平。方法:回顾性分析1983年1月～2008年1月间1387例重型颅脑损伤患者的救治情况。结果:1387例重型颅脑损伤患者，其中手术治疗857例，非手术治疗530例。按GOS评分，出院时恢复良好475例（34.2%），中残206例（14.8%），重残202例（14.5%），植物生存89例（6.4%），死亡415例（29.9%）。结论:重型颅脑损伤仍然具有较高的病死率和致残率，早期及时手术清除颅内血肿，解除脑疝以及采取积极恰当的综合治疗措施是抢救治疗成功的关键。
摘要:目的:探讨重型颅脑损伤后早期精神障碍临床特征及治疗方法,以提高患者的生活质量。方法:对我院48例重型颅脑损伤后早期精神障碍患者进行回顾性分析,观察精神障碍出现的时间、精神障碍的类型及预后及颅脑损伤的部位与精神障碍的关系。结果:重型颅脑损伤后精神障碍主要出现在伤后3周内,多继发于颞叶损伤,其次为额叶。临床上主要有躁狂型、抑郁型、痴呆型、精神分裂性等四型,其中以躁狂型为多见。通过治疗后,lt;1个月精神症状痊愈25例、lt;2个月痊愈13例、治疗gt;2个月仍有精神症状10例。结论:颅脑损伤后精神障碍在原发脑损伤的有效治疗前提下,辅以抗精神障碍药物治疗、心理治疗及高压氧治疗等可取得较好疗效。
目的:探讨颅脑损伤合并视神经损伤的发病机制及治疗.方法:对23例颅脑损伤合并视神经损伤患者的临床资料做回顾性分析。结果:经过积极治疗部分患者视力有不同程度改善。结论:治疗颅脑损伤合并视神经损伤,强调神经外科和眼科协同处理,掌握治疗时机。
目的:探讨行气管切开术抢救成功的重型颅脑损伤及高血压脑出血患者直接除管的安全性和可行性。方法:在507监护仪行SPO2监测和严密观察下,不经过试阻管而直接将气管套管拔除。结果:本组除1例患者因带管时间长,切口周围气管内炎性肉芽生长而重新插管外,其余患者呼吸平稳,呼吸道通畅,无呼吸急促、呛咳、紫绀及SPO2降低。结论:此法避免了传统除管前试阻管的繁锁和由阻管而引起的多种不良反应,有临床实用价值。
ObjectiveTo investigate the mechanism of Semaphorin 3A (Sema3A) in fracture healing after nerve injury by observing the expression of Sema3A in the tibia fracture healing after traumatic brain injury (TBI). MethodsA total of 192 Wistar female rats, 8-10 weeks old and weighing 220-250 g, were randomly divided into tibia fracture group (group A, n=48), TBI group (group B, n=48), TBI with tibia fracture group (group C, n=48), and control group (group D, n=48). The tibia fracture model was established at the right side of group A; TBI model was made in group B by the improved Feeney method; the TBI and tibia fracture model was made in group C; no treatment was given in group D. The tissue samples were respectively collected at 3, 5, 7, 14, 21, and 28 days after operation; HE staining, immunohistochemistry staining, and Western blot method were used for the location and quantitative detection of Sema3A in callus tissue. ResultsHE staining showed that no obvious changes were observed at each time point in groups B and D. At 3 and 5 days, there was no obvious callus growth at fracture site with inflammatory cells and fibrous tissue filling in groups A and C. At 7 and 14 days, fibrous tissue grew from periosteum to fracture site in groups A and C; the proliferation of chondrocytes in exterior periosteum gradually formed osteoid callus at fracture site in groups A and C. The chondrocyte had bigger size, looser arrangement, and more osteoid in group C than group A. Group B had disorder periosteum, slight subperiosteal bone hyperplasia, and no obvious change of bone trabecula in group B when compared with group D. At 21 and 28 days, cartilage callus was gradually replaced by new bone trabecula in groups A and C. Group C had loose arrange, disorder structure, and low density of bone trabecula, big callus area and few chondrocyte and osteoid when compared with group A; group B was similar to Group D. Immunohistochemistry staining showed that Sema3A expression in chondrocytes in group C was higher than that in group A, particularly at 7, 14, and 21 day. Sema3A was significantly higher in osteoblasts of new bone trabecula in group A than group C, especially at 14 and 21 days (P<0.05). Western blot results showed that the Sema3A had the same expression trend during fracture healing in groups A and C. However, the expression of Sema3A protein was significantly higher in group C than group A (P<0.05) and in group B than group D (P<0.05) at 7, 14, 21, and 28 days. ConclusionAbnormal expression of Sema3A may play a role in fracture healing after nerve injury by promoting the chondrocytes proliferation and reducing the distribution of sensory nerve fibers and osteoblast differentiation.
目的:探讨颅脑损伤后脑耗盐综合征患者的诊断与治疗策略。方法:对我科2006~2007年收治的37例CSWS患者临床资料进行回顾性分析和总结。结果:经治疗,37例CSWS患者31例血钠恢复正常,4例死亡,无1例发生桥脑髓鞘溶解症。结论:脑耗盐综合征是颅脑损伤后患者低钠血症的最主要原因。早期明确诊断,积极稳妥补液补钠是有效治疗CSWS患者的关键。