重型颅脑损伤合并多发伤救治策略

目的探讨重型颅脑损伤合并多发伤的救治策略。方法回顾性分析桂林市灵川县人民医院收治的73例重型颅脑损伤合并多发伤患者的临床资料,统计治疗6个月后格拉斯哥预后分级(GOS)情况,对救治情况进行总结分析。结果随访6个月,73例患者中GOS分级良好26例(35.6%),中残17例(23.3%),重残14例(19.2%),植物生存7例(9.6%),死亡9例(12.3%)。结论重型颅脑损伤合并多发伤严重危害患者生命健康,在诊治过程中,应遵循先救命后治伤,多学科协作,加强监护,优化气道、血压管理,优先处置危及生命的严重损伤,提高救治的成功率,提升患者生存质量。     

重型颅脑损伤的治疗体会

目的总结重型颅脑损伤患者(GCS评分≤8分)的治疗经验,不断提高救治水平。方法对我院2005年1月至2008年6月收治的172例重型颅脑损伤患者进行回顾性分析。结果随访3个月～1年,存活120例(69.77%),按GOS预后分级:良好73例(42.44%),中残24例(13.95%),重残19例(11.05%),植物生存4例(2.33%),死亡52例(30.23%)。结论早期诊断,及时手术,综合治疗,可改善重型颅脑损伤患者的预后,提高救治成功率。     

重型颅脑伤的诊治体会

我院于1996-01～12,收治车祸所致的颅脑伤172例,其中重型颅脑伤58例(33.7％),现就其救治体会报告如下:1 临床资料1.1 一般资料 本组中男43例,女15例。年龄3～78y。伤后0.5～46h入院。1.2 临床表现 (1)入院时呈昏迷者51例,嗜睡者7例。昏迷程度评分:13～15分者5例,9～12分者10例,6～8分者34例,3～5分者9例。     

100例重型颅脑外伤合并多发伤急诊患者临床救治分析

目的分析100例重型颅脑外伤合并多发伤急诊患者的临床救治方法。方法本次研究选取2015年1月~2016年1月期间我院救治的重型颅脑外伤合并多发伤急诊患者50例作为对照组(常规急诊救治),将2016年2月~2017年2月收治的重型颅脑外伤合并多发伤急诊患者50例作为观察组(急诊一体化救治)。对比两组重型颅脑外伤合并多发伤急诊患者的送诊时间、到手术时间、合并器官损伤数以及GCS评分、临床效果。结果观察组重型颅脑外伤合并多发伤急诊患者上述各项指标均优于对照组患者,差异有统计学意义(P<0.05)。结论对重型颅脑外伤合并多发伤急诊患者采用急诊一体化救治方法的效果确切,临床推广价值高。     

煤矿和交通事故致多发伤伴重型颅脑损伤的临床特点与救治

目的 探讨矿井和交通事故所致多发伤伴重型颅脑损伤的临床特点和救治策略.方法 本组72例,GCS评分均＜8分,均伴身体其他部位多处损伤,均需外科处理.行开颅手术清除血肿52例,去骨瓣减压46例,其他损伤均经外科治疗.在治疗中贯彻损伤控制外科(damage control surgery,DCS)原则.即快速控制伤情、复苏和确定性手术.结果 存活50例(69.4﹪),死亡22 例(33.6﹪),38例出院后6个月行GCS评分,显示恢复良好9例(23.7﹪),中度残废16例(42.1﹪),重度残废13例(34.2﹪),植物生存2例(5.3﹪).结论 应用DCS原则处理多发伤伴重型颅脑损伤有助于提高其生存率,对颅脑损伤的积极治疗是提高病人生存质量的重要环节.     

重型颅脑伤气管切开术后常见并发症的原因与护理对策

我科自1997年2月～2001年6月,在重型颅脑伤救治中行气管切开者146例,本文对146例重型颅脑伤患者行气管切开术后常见并发症分析报告如下:1 临床资料1.1 一般资料 本组146例中男102例,女44例,最大年龄73岁、最小年龄3岁,特重型颅脑损伤(GCS3～5分)53例,重型颅脑伤(GCS5～8分)93例。气管切开维持时间1～130天。     

颅脑损伤合并多发伤的临床分析

目的探讨颅脑损伤合并多发伤的临床救治原则和处理。方法采集本科2006年4月至2009年2月人院的169例重症颅脑损伤合并多发伤患者进行临床资料研究,并对其救治过程进行回顾性分析。结果患者术后依照格拉斯哥结局量表GOS评分恢复良好65例（38．5％）,轻残48例（28．4％）,重残21例（12．4％）,植物生存5例（3．0％）,死亡30例（17．8％）。结论合理救治程序至关重要,重视院前急救和术后综合治疗,强调先重后轻,先开放后闭合的救治原则。早诊断早治疗能提高重型颅脑损伤合并多发伤的治疗效果,同时是减少致残率及降低死亡率的最佳选择。重型颅脑损伤合并多发伤应早期诊断,及时抢救,避免漏诊和误诊,首先处理危及生命的损伤以及专科治疗配合ICU监护是重型颅脑损伤合并多发伤救治成功的关键。     

对重型颅脑伤伤员施行气管切开术

6年(1990-05～1996-05)来我们在救治重型颅脑伤伤员中对62例施行了气管切开术。此期间我们共收治重型颅脑伤370例,施行气管切开术者占16.7％(62/370)。本组伤员均经头颅CT扫描检查,其昏迷程度均按格拉斯哥昏迷评分法(GCS)评分。凡≤8分者为重型颅脑伤。现就气管切开术在重型颅脑伤救治中的作用分析报告如下:     

重型颅脑损伤合并多发伤120例的急救及护理

目的 总结重型颅脑损伤(severe head injury,SHI)合并多发伤的临床急救及护理措施,提高救治成功率.方法 术前院前急救与护理,术中严密监测患者病情,采取先急后缓的治疗策略,配合精心护理,预后以格拉斯分级标准(glasgow coma scale,GCS)评价患者恢复情况.结果 结局良好32例(26.7%),中残29例(24.2%),重残21例(17.5%),植物生存12例(10.0%),死亡26例(21.7%),且死亡病例以中老年患者(＞65岁)居多,占52%(78/150).结论 早诊断、早治疗、合理正确的救治次序是增强SHI合并多发伤治疗效果、降低致残病死率的关键.     

重型颅脑损伤合并多发伤早期救治护理现状

随着社会的发展,车祸、工伤、群体伤日益增多,多发伤的发生率以及严重程度呈上升趋势,其中重型颅脑损伤（severe head injury,SHI）合并多发伤占10％-21％,死亡率高达77％。按国际颅脑损伤分类,Glasgow（GCS）评分〈8分者为SHI,SHI合并多发伤在处理上要比单纯颅脑损伤复杂,     

Thalidomide-induced severe hepatotoxicity

Thalidomide is a relatively safe and efficacious form of therapy in the treatment of advanced, refractory multiple myeloma. Hepatotoxicity is listed as an extremely rare adverse effect associated with its use. We describe a 76-year-old woman with multiple myeloma who was treated with dexamethasone and thalidomide. By week 6 of therapy, she had developed acute increases in her aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels to more than 50 times the upper limit of normal. Her liver function test results had been within the normal ranges before and immediately after the start of therapy, and the patient had no known history of underlying liver disease. A liver biopsy specimen demonstrated evidence of acute injury with chronic changes of underlying steatosis and bridging fibrosis due to previously undiagnosed nonalcoholic steatohepatitis. Immediately after discontinuing thalidomide, her liver function test results began trending downward. Seven days later, her AST and ALT levels had improved to 86 and 165 U/L, respectively. This case and a limited number of other reports demonstrate severe hepatotoxicity as a rare but potentially serious adverse effect of thalidomide therapy. With the expanding use of thalidomide as a therapeutic agent, clinicians must recognize severe hepatotoxicity as a potential complication. Whether patients with preexisting liver disease are at increased risk when receiving thalidomide remains to be seen.     

替罗非班致重度血小板减少

1例56岁男性急性心肌梗死患者规律口服阿司匹林和氯吡格雷2个月后接受冠状动脉造影及经皮冠状动脉介入治疗.术前血小板计数为185×109/L.术中给予普通肝素,支架植入后用微量注射泵以0.1 μg/（kg·min）的速度持续静脉输注替罗非班36 h.输注替罗非班约12h,患者双上肢出现散在瘀斑,血小板计数下降至5×109/L.立即停用替罗非班、阿司匹林和氯吡格雷,并给予地塞米松.术后第4天,恢复使用氯吡格雷.术后第5天,恢复阿司匹林.术后第6天,患者瘀斑消失,血小板计数恢复至正常水平.考虑患者出现重度血小板减少是替罗非班所致.     

克林霉素致重度血小板减少

1例3岁男性患儿因溃疡性口炎给予克林霉素0.15 g,1次/d静脉滴注,治疗前血小板计数150×109/L。第1天,患儿左膝关节出现红色瘀斑。第3天,患儿出现齿龈出血及皮肤散在出血点,血小板计数为0,活化部分凝血活酶时间31 s。停用克林霉素,静脉滴注甲泼尼龙（30 mg,1次/d）及人免疫球蛋白（6 g,1次/d）,口服氨肽素（0.1 g,3次/d）。第4天,患儿血小板计数64×109/L,活化部分凝血活酶时间16 s,凝血酶原时间11 s。1周后,患儿血小板计数升至135×109/L,瘀斑消退。     

284例重及特重型颅脑创伤的手术疗效分析

目的 探讨重及特重型颅脑创伤不同时间的手术疗效.方法 本组284例患者全部行开颅血肿清除和/或去骨瓣减压术.其中超早期(3～6 h)手术201例,占70.8%;早期(7～12 h)手术63例,占22.2%;晚期(13～24 h)手术加例,占7.0%.结果 本组病例中3～6 h手术201例,死亡58例(28.2%);7～12 h手术63例,死亡20例(31.7%);13～24 h手术20例,死亡8例(40.0%).按出院时格拉斯哥预后评分(GOS)评估疗效:良好130例占65.7%,中残36例占18.2%,重残23例占11.6%,植物生存9例占4.5%,死亡86例占30.3%.结论 重及特重型颅脑创伤,伤势重,伤情复杂,病情变化快,病死率高;强调现场与院前抢救技术的熟练和救治系统的质量保证是成功的关键;同时要加强多器官继发性损害的治疗,预防并及时准确处理各种并发症.     

顺铂引起剧烈头痛

患者女,56岁。因便血半年,经直肠镜检查诊断为直肠癌,于2002年9月7日入院,行直肠癌根治术。术后病理为溃疡型,中分化腺癌,浸达浆膜,无淋巴结转移。术后恢复良好。术后半月进行首次全身化疗。方案为第一组5%葡萄糖注射液500mL 氟尿嘧啶0.75g;第二组5%葡萄糖注射液500mL 亚叶酸钙0.1g静滴。2003年12月10日患者再次入院,经临床医师检查后调整化疗方案如下:第一组,5%葡萄糖注射液500mL 氟尿嘧啶0.5g;第二组,5%葡萄糖注射液500mL 顺铂20mg;静脉滴注。当患者输入第二组液体约20min后,患者出现头痛、恶心、呕吐、头部不能转动,疼痛剧烈难忍,而呈…     

伯氨喹啉致严重皮疹

患者男,23岁。因畏寒、寒战、发热3d,于2005年6月9日住院。3d前患者无明显诱因出现畏寒、寒战、发热、全身不适,体温持续不退(高峰不详),伴乏力,纳差、头痛,无恶心呕吐。既往无药物过敏史,无6-磷酸葡萄糖脱氢酶缺乏症家族史。体检:T39.5℃,P65次/min,R22次/min,BP100/60mmHg(1mmHg=0.133kPa),神志清楚,精神差,急性热病容,皮肤黏膜无黄染及皮疹。浅表淋巴结无肿大,心、肺、腹无异常。辅助检查:外周血WBC7.63×109/L,HB171g/L,PLT86×109/L,末梢血涂片查到恶性疟原虫,肝、肾功能、电解质及大、小便常规均正常,初步诊断为恶性疟疾。给…     

Management of severe osteoporosis

Introduction: Severe osteoporosis represents a disease of high mortality and morbidity. Recognition of what constitutes and causes severe osteoporosis and aggressive intervention with pharmacological agents with evidence to reduce fracture risk are outlined in this review.

Areas Covered: This review is a blend of evidence obtained from literature searches from PubMed and The National Library of Medicine (USA), clinical experience and the author’s opinions. The review covers the recognition of what constitutes severe osteoporosis, and provides up-to-date references on this sub-set of high risk patients.

Expert Opinion: Severe osteoporosis can be classified by using measurements of bone densitometry, identification of prevalent fractures, and, knowledge of what additional risk factors contribute to high fracture risk. Once recognized, the potential consequences of severe osteoporosis can be mitigated by appropriate selection of pharmacological therapies and modalities to reduce the risk for falling.     

Golimumab for severe asthma

Backgorund: In severe asthma anti-TNF-α therapies might be effective in improving disease control based on preclinical results and on clinical short-term data. However, the long-term efficacy and safety is not known. Objective: To discuss the data on golimumab, an anti-TNF-α monoclonal antibody currently used in various forms of arthritis, evaluated as an add-on anti-inflammatory therapy in severe asthma. Methods/results: Critical appraisal of the efficacy and safety clinical data. Golimumab was not found to be generally efficacious and demonstrated an unfavourable risk–benefit ratio, but in some asthma subsets its better therapeutic effects might support its use provided the long-term safety is acceptable. Conclusions: Although at first sight the safety and efficacy data of long-term use of golimumab in severe asthma might be unsupportive, in some disease subsets it might be really effective.     

Immunopathogenesis of severe asthma

Severe asthma is a complex heterogeneous disease with substantial unmet clinical need. Understanding the immunopathogenesis is likely to provide insights into potential novel therapies. To date researchers have focussed primarily at a single scale for example genome, cell or whole organ physiology. In this review we shall summarise the current knowledge of the immunopathogenesis of severe asthma integrated across multiple scales to provide the insights into the structure function relationships required to begin to unravel the complexity of severe asthma.     

Treating severe metabolic alkalosis

The pathophysiology, symptomatology, and treatment of metabolic alkalosis are reviewed, with emphasis on treatment with intravenous hydrochloric acid. Three buffering systems are used by the body to correct an arterial pH above 7.45--tissue, respiratory, and renal systems. The kidneys have the primary responsibility for correcting a severe metabolic alkalosis, but several conditions (e.g., severe volume contraction) can interfere with the renal mechanisms. No unique symptoms are associated with metabolic alkalosis. Conventional conservative treatment of metabolic alkalosis involves meeting the patient's fluid and electrolyte needs and allowing the body to correct the alkalosis through its own mechanisms. However, when more rapid resolution of the alkalosis is needed or the patient cannot tolerate fluid and electrolyte therapy, mineral acids may be administered. Ammonium chloride and arginine monohydrochloride infusions may both be used; since both require hepatic conversion for full activity, patients with hepatic dysfunction may require alternative therapy. Dilute hydrochloric acid (0.1-0.2 N) may be given intravenously to these patients through a central-venous catheter. Dosage guidelines and formulation procedures are described in the paper, as are other possible therapeutic alternatives (dialysis, acetazolamide, cimetidine). Most cases of metabolic alkalosis can be managed with fluid and electrolyte therapy. When metabolic alkalosis needs to be resolved quickly or when conventional therapy cannot be tolerated, mineral acid administration should be instituted. The primary drug of choice for these patients is intravenous ammonium chloride; patients with hepatic or severe renal dysfunction should receive dilute hydrochloric acid via a central-venous catheter.