重型颅脑损伤后应激性溃疡出血防治分析

本院自1999年1月至2001年12月,共收治重型颅脑损伤115例,分别应用洛赛克、西咪替丁防治应激性溃疡出血.现结合文献分析如下.     

重型颅脑损伤病人早期鼻饲预防应激性溃疡的护理

将120例重型颅脑损伤的昏迷病人随机分为观察组和对照组各60例,观察组入院48 h内留置胃管鼻饲营养液.并进行观察和护理;对照组采取传统方法。入院6 d后留置胃管进行鼻饲。结果两组应激性溃疡发生率、腹胀腹泻、压疮、窒息、病死率等方面比较,盖异有显著性意义(P<0.01或P<0.05)。提示早期留置胃管.配合细致的观察护理.可预防应激性溃疡,改善营养.促进病人康复.     

不同鼻饲模式防治重型颅脑损伤后应激性溃疡的临床研究

目的探讨防治重型颅脑损伤后应激性溃疡发生的最佳鼻饲模式。方法将重型颅脑损伤患者随机分为对照组(37例)、观察1组(52例)和观察2组(45例)。对照组按传统间断方法间隔2h经鼻饲管注入营养液,观察1组用微量输液泵将营养液24h持续恒速注入胃内,观察2组则采用间隔1h推注营养液的模式。三组采用同样的营养液。记录应激性溃疡的发生率及治疗效果,并监测胃液pH值。结果应激性溃疡发生率观察1组显著低于对照组和观察2组(P<0.01和P<0.05);pH值观察1组显著高于对照组和观察2组(均P<0.05)。治疗效果三组差异无显著性意义(P>0.05)。结论重型颅脑损伤患者采用24h持续恒速注入的鼻饲模式能显著降低应激性溃疡发生率。     

早期置胃管预防重型颅脑损伤应激性溃疡

目的 探讨早期胃内营养支持对预防重型颅脑损伤患者应激性溃疡的作用。方法 将118例患者按随机原则分成观察组（56例）和对照组（62例），观察组在伤后36-72h内置胃管行要素饮食胃肠内营养；对照组置胃管时间在72h后。结果 观察组胃液潜血试验阳性率及病死率均显著低于对照组（均P〈0．01）。结论 重型颅脑损伤早期置胃管肠内营养可减少应激性溃疡的发生。     

早期置胃管预防重型颅脑损伤应激性溃疡

目的探讨早期胃内营养支持对预防重型颅脑损伤患者应激性溃疡的作用.方法将118例患者按随机原则分成观察组(56例)和对照组(62例),观察组在伤后36～72 h内置胃管行要素饮食胃肠内营养;对照组置胃管时间在72 h后.结果观察组胃液潜血试验阳性率及病死率均显著低于对照组(均P＜0.01).结论重型颅脑损伤早期置胃管肠内营养可减少应激性溃疡的发生.     

重型颅脑损伤并应激性溃疡的护理干预中体会

目的观察分析重型颅脑损伤并应激性溃疡的护理干预效果。方法对36例重型颅脑损伤并应激性溃疡患者,施行预防出血、留置胃管、出血期合理干预、饮食护理等精心护理措施。结果本组36例患者出血持续3~17 d,12例行输血治疗,输血量400~1000 m L,3例因止血困难而行胃大部切除术。34例患者经上述治疗,消化道出血被有效控制,2例高龄患者因并发肺部严重感染引发多脏器功能衰竭死亡。结论精心护理干预对重型颅脑损伤并发应激性溃疡具有较好效果。     

重型颅脑损伤并发应激性溃疡的相关因素分析

严重颅脑损伤并发应激性溃疡出血者,死亡率达３０％～５０％［１］。为预防应激性溃疡出血,提高抢救成功率,分析我院１９９６年１月至１９９９年２月５２例重型颅脑损伤患者中并发应激性溃疡２５例的发病相关因素,报告如下。１　临床资料２５例中,男２１例,女４例,年龄５～７２岁,平均４０－１岁。车祸伤１２例,坠落伤或撞伤１２例,殴打伤１例。２５例经头颅ＣＴ示硬膜下血肿１０例,脑内血肿５例,硬膜外血肿４例,单纯性脑挫伤３例,混合血肿３例。应激性溃疡出血发生在伤后≤５ｄ１２例,６～１０ｄ１２例,≥１１ｄ１例。呕血…     

重型颅脑损伤致应激性溃疡48例的临床分析

应激性溃疡是重型颅脑损伤的常见并发症之一。本院2003年1月至2006年12月共收治重型颅脑损伤210例．其中并发应激性溃疡48例，现报告分析如下。     

重型颅脑损伤患者并发应激性溃疡的研究进展

应激性溃疡是重型颅脑外伤患者的常见并发症,可引起消化道出血、穿孔,使原有病情恶化并明显提高病死率。预防应激性溃疡是抢救重型颅脑外伤患者的关键,本文就颅脑外伤患者应激性溃疡的机制、预防性治疗、早期肠内营养、医院获得性肺炎等相关并发症的最新研究进展予以综述。     

Xanthotoxol alleviates secondary brain injury after intracerebral hemorrhage by inhibiting microglia-mediated neuroinflammation and oxidative stress

BackgroundOxidative damage and inflammation are two critical mechanisms underlying secondary brain injury (SBI) following intracerebral hemorrhage (ICH). Xanthotoxol is reported to alleviate brain edema and inhibit inflammatory responses. Herein, we investigated the effects of xanthotoxol and its related mechanisms in SBI post-ICH.MethodsTo explore the clinical effects of xanthotoxol an animal model of ICH was established. Neurological scores, survival rates and brain water content were measured. Inflammatory responses and oxidative damage in the peri-hemorrhagic areas were determined by measuring pro-inflammatory cytokines and oxidative related factors. The activation of the M1/M2 phenotype was detected by western blotting and immunofluorescence.ResultsXanthotoxol improved the neurological functions and reduced cerebral edema in ICH mice. Additionally, xanthotoxol inhibited microglia activation and promotes microglial phagocytosis. Simultaneously, xanthotoxol promoted the transformation of BV2 cells from M1 phenotype to M2 phenotype, and protected BV2 cells against hemin-induced inflammation and oxidative stress. Mechanistically, xanthotoxol inactivated the NF-κB p65 signaling pathway in the hemin-challenged BV2 cells.ConclusionXanthotoxol ameliorates SBI post-ICH by suppressing microglia-mediated neuroinflammation and oxidative stress and enhancing microglial phagocytosis through inhibition of NF-κB signaling.     

肠内营养液温度对重型颅脑损伤患者应激性溃疡的影响

目的探讨不同温度的肠内营养对重型颅脑损伤患者应激性溃疡的影响。方法将90例行肠内营养的重型颅脑损伤患者随机分为A、B、C三组,每组30例。A组肠内营养液温度为22℃恒温,B组为30℃恒温,C组为38℃恒温。观察比较三组行肠内营养后7d内胃液pH值、胃液隐血试验及排便情况。结果三组胃液pH值比较,差异有统计学意义(均P0.01),A组显著高于B、C组(均P0.05);胃液隐血试验阳性率比较,A组低于B、C组,但差异无统计学意义(均P0.05);A组7例发生腹泻,B、C组分别有5例和7例发生,三组腹泻发生率及腹泻开始时间差异无统计学意义(均P0.05)。结论降低肠内营养温度对重型颅脑损伤患者胃黏膜具有保护作用,有利于应激性溃疡的预防,且对腹泻无影响。     

The impact of prophylactic treatment on post-traumatic epilepsy after severe traumatic brain injury

AIM: To assess the incidence of late post-traumatic epilepsy (PTE) in patients with very severe traumatic brain injury (TBI) who either received or did not receive anti-epileptic prophylactic treatment. METHODS: Two populations were studied: 55 patients retrospectively and 82 subjects prospectively. RESULTS: Ten patients (18%) in the first population showed late PTE. Although the incidence was lower in patients who did not receive prophylactic treatment, the difference between the treated and the non-treated group was not statistically significant. Sixty-nine patients in the second group (84%) had prophylactic treatment. Twenty-seven patients (39%) suffered from late PTE during the 2-year follow-up period and 17 of them (63%) showed EEG epileptic abnormalities. No patient who did not receive preventive therapy suffered from late PTE during the observation period. CONCLUSIONS: Due to the negative cognitive effects of anti-epileptic drugs, the preliminary results are of considerable interest for the rehabilitation of patients with very severe TBI.     

Immediate hypertensive response to fluid percussion brain injury may be related to intracerebral hemorrhage and hypothalamic damage.

Fluid percussion brain injury is associated with an immediate rise in mean arterial pressure (MAP). However, the cerebral morphologic basis for this response is still not clear. Thirty-four anesthetized rats were injured using a lateral craniotomy preparation. In 19 rats, impact level was set at 1.73 +/- 0.04 atm, and impact duration was kept at 25 msec to examine the relationship between postinjury hypertensive response and cerebral lesions. MAP was monitored for 1 hour after impact. Fluid percussion produced an increase in MAP from 99 +/- 3 to 134 +/- 4 mm Hg (p less than 0.001), with an increment range of -2 to 87 mm Hg (36 +/- 5 mm Hg) or 0 to 96% increase. The MAP peak occurred at 15 +/- 2 seconds and then rapidly returned to the preimpact level. Histopathological findings, principally hemorrhage, were graded and ranked from 1 to 19 according to relative severity and hypothalamic involvement. There was a significant correlation between MAP rise and the injury ranking (r = 0.52, p = 0.02). No appreciable damage was observed in the brainstem caudal to the diencephalon. Fifteen rats were subjected to higher injury levels. The overall impact magnitude ranged from 1.3 to 3.5 atm. A linear relationship was found between impact magnitude (X, atm) and increment in MAP (Y, mm Hg) (Y = 28.1*X - 14.0, r = 0.62, p less than 0.001). Our study indicates that the immediate postinjury hypertensive response is closely correlated with the impact magnitude and may be related to intracerebral hemorrhage and hypothalamic damage but not necessarily to caudal brainstem damage.     

高血压脑出血的手术治疗

目的:总结67例高血压脑出血的手术治疗经验。方法:根据不同病情需要采用骨瓣成形或颞肌下减压血肿}I{J_除及钻孔抽吸引流术。结果:血肿清除组存活29例,清醒24例,植物生存5例,死亡14例,钻孔引流组,存活19例,消醒17例,2例植物生存,肢体偏瘫恢复15例,死亡5例,结论:高血压脑出血主张超早期手术治疗,重视并发症的及时诊断及处理,提高生存率,降低死亡率。     

重症颅脑损伤并发应激性溃疡的护理分析

目的探讨重症颅脑损伤并发应激性溃疡患者实施优质护理后的临床效果。方法收集2010年1月-2012年11月来我院就诊的重型颅脑损伤并发消化道应激性溃疡患者118例,将患者按照随机数字表法分为研究组和对照组,每组59例,对照组实施常规护理方式。观察组采用优质护理措施。用统计学方法比较两组临床效果。结果研究组显效27例,有效30例,总有效率为96.61%,对照组为81.36%,研究组总有效率高于对照组,两组比较差异有统计学意义（P〈0.05）。结论重症颅脑损伤并发应激性溃疡患者实施优质护理能明显提高患者的有效率,改善患者预后,可以在临床推广应用。