胸部爆震伤致兔急性呼吸窘迫综合征模型的建立及相关因素分析

目的 构建室内胸部爆震伤致兔急性呼吸窘迫综合征(ARDS)模型并分析其发生机制及早期死亡原因,为研究肺爆震伤早期预警体系和治疗方法提供依据.方法 按照不同炸药量和致伤距离所产生的压强,将60只新西兰大白兔按随机数字表法分为5个致伤组和1个无致伤对照组.伤后观察存活率和组织病理学,并监测病理生理学指标、肺含水量.结果 冲击波压强低于1 210.5 mm Hg(1 mm Hg=0.133 kPa,A、B组)时,肺损伤较轻,表现为点状肺挫伤,肺简明损伤评定分级法(ALS)均在2级内,动物伤后24 h内全部恢复,长期存活无并发症.冲击波压强高于2 036.1 mm Hg(D、E组)时,肺损伤过重,表现为广泛的肺挫伤、肺门撕裂伤和肺内大血肿,AIS均大于5级,动物于伤后1 h内全部死亡.冲击波压强为1 917.3 mm Hg(C组)时,肺表现为广泛而恒定的挫伤,累及4个肺叶以上,AIS 4～5级,伤后6 h内出现动脉氧分压下降;肺组织可见肺泡壁水肿,部分肺泡壁断裂,肺泡融合;肺泡内充满大量炎性细胞,偶见透明膜形成.与对照组比较,C组兔致伤6 h肺湿/干重比值即显著升高(6.46±0.24比3.98±0.19,P＜0.01),血浆及支气管肺泡灌洗液(BALF)中肿瘤坏死因子-α(TNF-α)和白细胞介素-6(IL-6)即明显升高[血浆TNF-α(ng/L):328.89±6.26比62.12±2.98,BALF TNF-α(ng/L):164.87±4.59比29.51±1.12;血浆IL-6(ng/L):128.51±4.13比19.32±1.53,BALF IL-6(ng/L):94.97±1.14比22.72±0.19,均P＜0.05].结论 在1 917.3 mm Hg爆炸压强的密闭环境下,冲击伤可诱导兔发生ARDS;TNF-α及IL-6参与爆震伤致ARDS的形成与发展;特定环境下,肺脏破裂致气胸为早期死亡原因,而冲击波致循环系统功能紊乱也是引起早期死亡的重要原因.

Abstract：

Objective To reproduce acute respiratory distress syndrome (ARDS) model in rabbit induced by chest blast injury and to analyze the pathogenesis and causes of early death in order to provide the basis for the early diagnosis of lung blast injury and its early-warning system to facilitate an early treatment.Methods Sixty healthy New Zealand white rabbits were divided into six groups according to the different explosion distance with the random number table method. The survival rate and its resulting pathological changes were observed and patho-physiological indexes and lung fluid content were determined at sequential time points post-explosion. Results Shock wave pressure less than 1 210. 5 mm Hg (1 mm Hg=0. 133 kPa,group A, B) resulted in limited injury to the lung within grade-2 as assessed with the abbreviated injury scale (AIS). The rabbits in these groups recovered soon and survived without any complication. Shock pressure higher than 2 036. 1 mm Hg (group D, E) caused severe injuries to the lung, including deep laceration, disruption of lung hilus and large hematoma in the lung, and the injury severity of lungs was assessed above grade-5 as assessed with AIS. All rabbits died within 1 hour post-explosion. The groups described above failed to meet the demand of an ARDS model for the present study. Shock wave pressure at 1 917. 3 mm Hg (group C) produced extensive contusion from grade-4 to grade-5 as assessed with AIS. The rabbits survived in poor general condition, and arterial partial pressure of oxygen (PaO2) lowered within 6 hours. Pathological examination showed extensive and constant multi-focal bleeding involving more than four lobes. The alveolar wall was edematous, with partial rupture and alveolar fusion in lung tissues was observed in the group C. Alveoli were filled with inflammatory cells, and hyaline membrane was formed occasionally. Compared with control group, the wet to dry weight ratio (W/D) in lungs increased obviously (6.46±0. 24 vs. 3. 98±0. 19, P＜ 0. 01) in group C within 6 hours postinjury. The contents of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in plasma and bronchoalveolar lavage fluid (BALF) were also increased distinctly compared with the control group [TNF-α (ng/L) in plasma: 328. 89± 6.26 vs.62.12±2. 98, TNF-α (ng/L) in BALF: 164.87±4.59 vs. 29. 51±1.12; IL-6 (ng/L) in plasma: 128. 51±4.13 vs. 19.32±1.53: IL-6 (ng/L) in BALF: 94.97±1.14 vs. 22.72±0. 19, all P＜0. 05]. Conclusion In an airtight environment, rabbit ARDS model can be reproduced successfully by blast injury with 1 917.3 mm Hg explosion pressure; TNF-α and IL-6 are involved in the pathogenesis and development of ARDS in blast injury. Pneumothorax as a result of lung rupture is the chief reason for early death and dysfunction of circulatory system is also an important reason in producing early death.     

列车后送危重伤员的相关护理问题探讨

运用列车进行后送在战争或自然灾害条件下,造成成批大量伤员进行紧急救治和运送的一种方式。我院自2007—05组建列车卫生医疗队,经过模拟实战进行反复演练和不断改进,特别是通过2008年“5．12”汶川大地震中实地伤员的护送以及“卫勤使命-2009”全军军事联合演习中的实践,对于运用列车后送危重伤员的救治与护理初步积累了一些经验,总结如下。     

复张性肺水肿的相关临床护理对策

复张性肺水肿(Reexpansion pulmonary ede- ma,RPE)是指继发于各种原因所致的肺萎陷在肺迅速复张后所发生的急性肺水肿,多见于气、液胸患者,经大量排气排液之后,摘除胸腔巨大肿瘤,解除支气管阻塞之后以及开胸术中、术后肺复张过快等, 是临床上较为少见的非心源性肺水肿,其特点是急性间质性肺水肿。临床经过较为凶险,死亡率高达     

开胸术后单侧喉返神经损伤致肺炎的预防及护理

单侧喉返神经损伤是开胸术后主要并发症之一,由于左侧喉返神经的特殊解剖位置,其损伤在临床中多见[1],其主要原因是主动脉弓下淋巴结清扫损伤喉返神经结果,它的损伤会引起单侧声带完全性麻痹:患侧声带外展及内收功能均消失而出现声嘶,影响咳嗽排痰,出现进流食呛咳症状,增加了发生肺炎的危险[2],而术后并发肺炎是胸部手术后最危险的并发症之一[3]。因此,喉返神经损伤后肺炎的预防及护理十分重要,现报道如下。     

食管癌贲门癌伴糖尿病的围手术期处理

1　糖尿病的病理生理糖尿病 (ｄｉａｂｅｔｅｓｍｅｌｉｔｕｓ,ＤＭ)主要分为 2型 ,1型ＤＭ和2型ＤＭ ,1型ＤＭ一般发生在儿童、青少年和年轻人 ,2型糖尿病是老年人的常见病 ,6 0岁以上发病较为普遍。手术时 ,创伤引起的应激反应使机体内分泌代谢发生明显改变。ＤＭ患者本身就存在内分泌代谢障碍 ,其与没有ＤＭ的患者相比 ,围手术期并发症发生的危险性及死亡率大大增加。具体的并发症主要包括 :高血糖导致的高渗性利尿 ;高渗状态下可出现血液黏滞性增高 ,血栓形成和脑水肿 ;酮症和ＤＭ酮症酸中毒 ;蛋白质分解和氨基酸转运减少至伤口愈合延迟…     

反流致大鼠Barrett's食管及其腺癌过程中诱导型一氧化氮合酶的表达及意义

目的: 探讨反流致大鼠Barrett's食管(Barrett's esophagus,BE)及食管腺癌(esophageal adenocarcinoma,EAC)发生过程中局部诱导型一氧化氮合酶(iNOS)的表达及意义.方法: 将8 wk龄雄性SD大鼠65只,通过手术建立十二指肠胃食管反流模型组,分别于术后1,4,8,12,16,20 wk随机取若干动物食管全长,制成纵切面石蜡切片,分别进行苏木精-伊红(HE)染色及iNOS免疫组化染色,在光镜下观察食管黏膜病变及iNOS染色结果.另设无反流对照组(10只).结果: ①对照组未见病变;模型组术后引发反流性食管炎,食管下段黏膜炎症和增生的程度随观察时间的延长逐渐加重,并有部分发展为BE和起源于BE的EAC.BE、EAC最早分别出现于术后第8周和第12 周,在以后的各时间点两者发生率呈上升趋势,到术后20 wk达86.6%和53.3%.②对照组iNOS阴性.模型组术后1,4,8,12,16,20 wk食管下段黏膜iNOS表达率分别为: 0,0,50%,80%,100%,100%,阳性染色位于上皮下的巨噬细胞.BE,EAC均见于iNOS阳性者.结论: 反流致BE及EAC过程中局部iNOS产生的过量一氧化氮具有重要的病理作用,可能参与致癌过程.     

老年食管癌患者术后的护理

0 引言老年食管癌患者一般状况多较差,合并疾病和术后并发症多,术后护理显得尤为重要. 我院1998-05/2003-05手术治疗老年食管癌183例,通过严格术后各项护理措施,取得满意临床效果.……     

开胸术后气管切开患者ICU肺部感染原因分析及护理对策

目的探讨开胸手术气管切开患者ICU肺部感染与茵群的关系及其护理对策。方法对58例ICU肺部感染患者做痰液培养和药敏试验。结果细菌种类多是其特点；其原因主要有该组患者开胸术后免疫防御功能严重受损，抵抗力差．易受感染；气管切开插管后各种治疗护理增加感染机率；大量使用抗生素和多重用药使呼吸道正常茵群破坏，导致防御屏障受损；无菌观念不强．护理操作不当。结论造成开胸术后气管切开肺部感染的原因很多，其中做好气管切开术后护理显得十分重要。