创伤性休克病人的早期急救护理体会

目的:讨论在院前和急诊科对创伤性休克病人施行早期急救护理,对挽救病人的生命及伤情预后有重要的意义.方法:对我科1997年2月至2001年4月27例创伤性休克病人进行早期,快速,积极的补液,输血增加有效循环量,监测生命体征等综合性抢救治疗与护理措施.结果:经早期积极急救护理,26例病人收缩压维持在60mmHg以上,意识清醒,脉搏有力,转入手术室或专科治疗,1例病人伤势严重抢救无效死亡.结论:创伤性休克病人,伤势复杂,死亡率高,伤后早期院前与急诊科的有效救护,是提高抢救成功率的关键.     

间接免疫荧光法检测特异性IgG抗体对流行性出血热诊断意义

本文报告用间接免疫荧光法检测特异性IgG抗体对流行性出血热的诊断意义。53例不同病期的出血热患者的血清,其间接荧光抗体的阳性率为49/53(占92.45％)。有77.36％的患者血清,检出IgG抗体的时间是在发病后的1～2周。血清中IgG的滴度与疾病的严重性无密切相关。另25例非EHF患者,其血清特异性IgG抗体均为阴性。可见检测特异性IgG抗体对EHF的诊断颇为有用。     

Functioning and disability 6–15 years after traumatic brain injuries in northern Sweden

Objectives –  To assess long‐term functioning and disability after traumatic brain injury (TBI). Material and methods –  Individuals (n = 88) in Norrbotten, northern Sweden, who had been transferred for neurosurgical care were assessed with internationally established TBI outcome measures 6–15 years post‐injury. Results –  There was an improvement in overall outcome from discharge from inpatient rehabilitation to follow‐up. Many individuals had a high degree of motor and cognitive functioning, which enabled them to live independently in their own home without assistance, but there remained a disability related to community reintegration and social participation. This affected their productivity and to some degree their marital stability. The remaining disability and reduced productivity were related to the age at injury and the injury severity. Conclusions –  Our data showed that individuals with a TBI can achieve and maintain a high degree of functioning many years after the injury. Increasing age and a greater injury severity contributed to their long‐term disability.     

热休克蛋白90对大鼠缺氧心肌细胞丝氨酸苏氨酸蛋白激酶表达的影响

目的探讨内源性热休克蛋白90（HSP90）在缺氧心肌细胞丝氨酸苏氨酸蛋白激酶（AKT）相关信号通路中的作用。方法建立新生Wistar大鼠心肌细胞缺氧模型，将细胞分为正常组、缺氧组、加入HSP90特异性阻断剂格尔德霉素后再缺氧组（格尔德霉素＋缺氧组）。于缺氧后1、3、6、12、24、48h用噻唑蓝法检测心肌细胞的活力；缺氧24h，原位缺口末端标记法检测心肌细胞凋亡指数（AI）；缺氧1、3、6、12、24h，蛋白质印迹法检测大鼠心肌细胞中内源性HSP90及AKT表达水平。结果（1）缺氧24、48h，缺氧组、格尔德霉素＋缺氧组细胞活力均较正常组明显下降（P〈0．05）；格尔德霉素＋缺氧组细胞活力缺氧12h即开始明显下降，缺氧48h时明显低于缺氧组（P〈0．05）。（2）缺氧24h，缺氧组细胞AI为（10．7±1．2）％，明显高于正常组[（1．9±0．3）％．P〈0．05]；格尔德霉素＋缺氧组细胞AI为（26、3±5．3）％，明显高于缺氧组（P〈0．01）。（3）缺氧12h，缺氧组心肌细胞内源性HSP90及AKT表达水平高于正常组与格尔德霉素＋缺氧组；缺氧24h，缺氧组有所下降．格尔德霉素＋缺氧组则下降更明显。结论内源性HSP90对维持心肌细胞的活力有重要作用．缺氧心肌细胞AKT表达水平可受内源性HSP90表达水平的影响。     

早期脑室置管行颅内压监护对中型颅脑损伤患者的预后影响

目的　探讨早期脑室置管行颅内压 (ICP)和脑灌注压 (CPP)监护在中型颅脑损伤中的临床应用价值。方法　将 12 5例伤后 2 4h入院无手术指征的中型颅脑损伤 (GCS 9～ 12分 )患者 ,随机分为ICP监护组 :入院后即经恻脑室内穿刺置管行ICP与CPP连续监测 ,根据颅内压变化调整治疗方案 ;对照组 :入院后不做ICP监测 ,依据临床观察的意识及生命体征变化 ,进行治疗。结果　颅内压监护组脱水剂剂量、应用时间均低于对照组 ,疗效优于对照组 ,两组差异有显著意义 (P <0 0 5 )。结论　中型颅脑损伤病情极不稳定 ,早期行ICP监护能及早发现病情变化 ,对及时采取有效治疗措施 ,降低死残率 ,改善预后有重要意义。     

Acute encephalopathy associated with influenza and other viral infections

Acute encephalopathy is the most serious complication of pediatric viral infections, such as influenza and exanthem subitum. It occurs worldwide, but is most prevalent in East Asia, and every year several hundreds of Japanese children are affected by influenza-associated encephalopathy. Mortality has recently declined, but is still high. Many survivors are left with motor and intellectual disabilities, and some with epilepsy. This article reviews various syndromes of acute encephalopathy by classifying them into three major categories. The first group caused by metabolic derangement consists of various inherited metabolic disorders and the classical Reye syndrome. Salicylate is a risk factor of the latter condition. The second group, characterized by a systemic cytokine storm and vasogenic brain edema, includes Reye-like syndrome, hemorrhagic shock and encephalopathy syndrome, and acute necrotizing encephalopathy. Non-steroidal anti-inflammatory drugs, such as diclofenac sodium and mephenamic acid, may aggravate these syndromes. Severe cases are complicated by multiple organ failure and disseminated intravascular coagulation. Mortality is high, although methylprednisolone pulse therapy may be beneficial in some cases. The third group, characterized by localized edema of the cerebral cortex, has recently been termed acute encephalopathy with febrile convulsive status epilepticus, and includes hemiconvulsion-hemiplegia syndrome and acute infantile encephalopathy predominantly affecting the frontal lobes. Theophylline is a risk factor of these syndromes. The pathogenesis is yet to be clarified, but an increasing body of evidence points to excitotoxicity and delayed neuronal death.     

Extacorporeal shock wave therapy unsuccessful for chronic medial epicondylitis

Medial epicondylitis is a chronic noninflammatory condition resulting from mechanical injury. Despite many treatment options, including rest, medications, physiotherapy and operative interventions, the results are too often poor; thus new treatment options are sought. We treated 4 men with chronic epicondylitis (5 affected joints) with extracorporeal shock wave therapy after failed attempts of other treatments. The patients’ complaints were graded with the Nirschl scoring system prior to and six months after therapy. The treatment consisted of three sessions, at 20-day intervals, of 3000 pulses of ultrasonic shock waves from a Piezolith 3000 unit (energy dosage was gradually increased to reach step 10 equaling 0.9 mJ/mm²). At the 6-month follow-up, no patient was pain free. Three cases had slightly lower Nirschl scores than prior to the procedure but the patients rated this difference as insignificant; two cases were unchanged. No complications were observed but all patients rated the procedure as very unpleasant. The well recognized biologic effects of ultrasonographic waves (heat generation, oscillations, cavitation, etc.) that result in functional and structural changes of cellular membranes with sonochemical reactions (acceleration of normal metabolism, oxygenation and reduction in water solutions, polymer degradation, etc.), even if present in our cases, did not result in a noticeable decrease of symptoms, even though we used high energy and more impulses per session. Significant variations in methodology make inconclusive the results of numerous reports on the use of extracorporeal shock waves in epicondylar degenerative problems, although ineffectiveness of such therapy is the conclusion of a review by Haake and colleagues.     

盲肠结扎穿刺致豚鼠急性肺损伤动物模型建立

目的 研究败血性急性肺损伤的动物模型，并探讨其在急性肺损伤研究中的意义。方法 用盲肠结扎穿刺(CLP)法的豚鼠急性肺损伤模型，结合动脉血气分析、外周血白细胞计数、肺湿重／干重比值(W／D)及肺组织病理观察。结果 CLP模型中动物的症状和表现缓慢出现，逐渐恶化．最后导致败血性休克，于2d左右出现大量死亡。结论 用盲肠结扎穿刺的方法制作豚鼠急性肺损伤动物模型较大鼠内毒素性休克，表现更类似于人类的肠源性肺损伤，且症状缓慢发生，逐渐恶化，有利于观察和进行各种干预。