一起光气等有毒物质泄漏事故分析

目的 分析一起光气等化合物泄漏事故的原因、危害程度以及抢救危重病人成功经验.方法 通过现场调查,危重病人抢救的全过程病例分析,以及其他接触者的系统观察分析.结果 该次事故共有561人受毒物泄漏污染影响,经按GBZ 29-2002《职业性急性光气中毒诊断标准》诊断,急性光气重度中毒2例（死亡1例）、中度中毒1例、轻度中毒18例、刺激反应10例,另有14例医护人员因受固体光气污染出现刺激反应.结论该次毒气泄漏事故主要毒物是光气和固体光气,由于抢救及时,处理得当,没有造成严重后果.     

光气中毒机制与治疗进展

光气中毒可引起迟发性肺水肿甚至急性呼吸窘迫综合征(ARDS).该文综述了光气中毒的机理及治疗进展,以求为临床救治光气中毒提供依据.     

近30年我国急性光气中毒与接触反应1 132例分析

通过文献检索,对576例光气接触反应者及556例急性光气中毒者的临床特点及治疗情况进行汇总。光气吸入后,呼吸系统刺激症状的发生率由高至低依次为胸闷、咳嗽、气急、恶心、头痛、咳痰等,吸入光气量越大,发生肺水肿的潜伏期越短,病情越严重。急性光气中毒可引起心肌的继发性损害,也可能对肝脏有一定的损伤作用。急性光气中毒者在经过正确的治疗后,尚未发现心脏及肝脏有明显的后遗症,数例临床治愈后对肺脏仍有一定的影响。死亡病例大多发生在急性光气中毒后24 h以内,因此中毒后及时正确的救治非常关键。     

急性光气中毒研究进展

光气常用于染料、塑料、橡胶、农药、制药、合成纤维等工业中，其临床特点是接触当时刺激症状较轻，经一定潜伏期后才出现严重病变，极易发生肺水肿甚至急性呼吸窘迫综合征（ＡＲＤＳ）。现将光气中毒的机制及临床研究进展作一简述。一、光气中毒机制光气（包括双光气）主...     

536例群体性急性光气中毒的临床表现及胸部X线特征

[目的]分析光气中毒的临床表现及胸部X线特征.[方法]对536例中毒者临床资料做回顾性分析.[结果]刺激反应者胸片无明显异常;轻度中毒者胸片显示支气管炎或支气管周围炎;中度中毒者胸片显示急性支气管炎或急性间质性肺水肿;重度中毒者胸片有弥漫性肺泡性肺水肿或急性呼吸窘迫综合征(ARDS).[结论]中毒分级与胸部X线征象有一定相关,根据《职业急性光气中毒的诊断标准》,结合临床症状分级与胸片特征做出诊断,及时摄胸片及复查有重要意义.     

急性光气中毒的救治与护理

光气是一种强烈的窒息性毒气,属剧毒类,经呼吸道吸入中毒,其毒性极似氯气,但比氯气大10倍,作用持久。光气中毒是指人在短期内吸入较大量光气,引起以急性呼吸系统损害为主的全身性疾病,严重者发生肺水肿,并致死亡。我院2003年4月至2006年12月,由综合性医院转入急性光气中毒患者3例,经抢救     

接触固体光气致急性光气中毒12例临床分析

目的分析生产过程中应用固体光气因意外事故而导致中毒的12例患者临床资料,了解其临床特点,总结治疗经验。方法对12例患者的职业接触史、发病过程、临床表现、实验室检查结果、诊断救治以及事故原因进行分析。结果12例患者表现为不同程度的呼吸系统损害,严重者出现弥漫性肺水肿,经积极救治,全部患者康复。结论光气中毒经早期、积极的救治,包括吸氧、辅助通气、糖皮质激素及抗生素的应用,一般预后良好。     

急性光气中毒的临床特点研究

目的：探讨急性光气中毒的临床特点。方法：采用本院近28年120例急性光气中毒的病例资料。重点对发病时间，临床所见，诊治结果进行综合分析。结果：急性光气中毒的潜伏期1．5h-3d，中，重度中毒组中，现场及时处理组的潜伏期较未及时处理组延长（P＜0．05），临床表现以呼吸系统症状体征为主，其中呼吸频速，发疳，泡沫痰主要发生在重度中毒组中的ARDS病例，心肌损害发生率各中毒组间比较，差异有显著性（P＜0．01），在轻度中毒组中，入院时X线胸片异常率显著高于肺部听诊阳性率（P＜0．01），结论：急性光气中毒时，若现场能得到及时处理，可使潜伏期延长，肺是靶器官，心肌损害发生率随着中毒程度的加重而增加，X线胸片改变往往早于临床体征，可作为早期重要检测手段之一。     

光气染毒小鼠急性肺损伤的浓时积与效应关系研究

目的通过比较光气染毒浓时积（Ct）的两个参数（浓度C与时间t）对染毒小鼠急性肺损伤程度的影响，探讨光气导致急性肺损伤的机制。方法以不同浓时积和固定浓时积不同浓度与时间进行光气染毒，测定肺脏湿干比、丙二醛（MDA）含量和髓过氧化物酶活力以及血清中MDA含量。结果随染毒浓时积增加，小鼠中毒死亡率增加（P〈0．001）；浓时积固定为12ml·min时，染毒浓度增加，小鼠中毒死亡率增加（P〈0．01），肺湿干比增加（P〈0．001），肺脏髓过氧化物酶活力和MDA浓度升高（P〈0．05）。结论光气染毒随浓时积增加，动物中毒死亡率升高，但在浓时积相同的条件下，暴露毒剂的浓度与暴露时间对急性中毒的影响不同；暴露毒剂的浓度高低对中毒程度的影响远大于暴露时间的影响，短时间高浓度的光气吸入会比低浓度长时间的光气吸入造成更为严重的肺部损伤。     

儿童急性光气中毒8例临床分析

某厂生产甲苯二异氰酸酯的高温光化锅的视镜突然爆破,光气等混合物料急剧喷出,迅速扩散厂外下风侧的居民区,引起数十人急性光气中毒,其中儿童8例。为探讨儿童光气中毒的特点及总结诊断治疗的经验教训,现报告如下。     

Pathogenesis of phosgene poisoning

Phosgene inhalation in concentrations greater than 1 ppm may produce a transient bioprotective vagus reflex with rapid shallow breathing in some individuals. Phosgene concentrations greater than 3 ppm are moderately irritating to eyes and upper airways. Toxic phosgene doses (greater than or equal to 30 ppm X min) inhaled into the terminal respiratory passages render the blood-air-barrier more permeable to blood plasma, which gradually collects in the lung. Some time passes, however, until the collection of fluid provokes signs and symptoms. This period in which the patient experiences relative well-being is known as the clinical latent phase. The clinical symptoms which follow and the pathological changes underlying them are discussed in detail; dose-effect relationships are demonstrated. The regression phase after poisoning has been overcome is briefly sketched.     

Early diagnosis of phosgene overexposure

At the present time, the following parameters can be recommended for "early diagnosis" of phosgene overexposure: Phosgene indicator paper badges, to be worn by all persons involved in handling phosgene (these badges permit immediate estimation of the exposure dose in each individual case); Observation of the initial irritative symptoms of the eye and the upper respiratory tract after phosgene inhalation can provide a rough indication of the inhalation concentration and dose; X-ray photographs of the lungs make it possible to detect incipient toxic pulmonary edema at an early stage, during the clinical latent period. A number of additional parameters require further critical investigation.     

Therapeutic strategy in phosgene poisoning

For the treatment of phosgene poisoning, glucocorticoids and positive pressure ventilation can be recommended as well as supporting measures such as physical rest, antitussives, buffers, sedatives, antibiotics, antispasmodics and possibly diuretics. Roentgenological evaluation of the lungs is advisable. A therapeutic strategy is presented which is based on the phosgene exposure intensity.     

急性光气中毒三例

我院于2005年8月5日收治3例急性光气中毒病例,现报告如下. 1.一般资料：2005年8月4日上午10时许,天津某有机化工厂氯代脂车问因管道突然破裂,使含有光气和辛醇等气体、液体喷出,造成3人中毒.中毒患者均为男性,年龄46、53、54岁.     

Response of pulmonary energy metabolism to phosgene

Rats were exposed to phosgene at a concentration of 1.0 ppm for 4 hours in a Rochester-type chamber. At intervals thereafter over a 4 day period, lungs were obtained for histological and biochemical assessments. Edema was estimated by histological examination and by measurement of lung wet and dry weights. In parallel studies, pulmonary mitochondrial respiratory activity was measured using Clark oxygen electrodes. The significant reduction in respiratory control index (State 3 respiration/State 4 respiration) found immediately following phosgene exposure coincided with the highest level of % lung water. There was a concomitant decrease of ATP concentration that persisted on the third day after exposure. Na-K-ATPase activity was reduced 1 day after exposure, thus a lowered ATP level preceded a reduction in Na-K-ATPase or sodium pump activity. The reduction in ATP level and Na-K-ATPase activity may play a major role in damage to lung tissue following exposure to phosgene.     

47例急性光气刺激反应及其救治

目的 总结急性光气刺激反应的临床表现及综合性救治的临床疗效.方法 回顾分析本医疗中心2007年11月至2009年7月救治的47例急性光气刺激反应患者的临床症状、体征、血氧饱和度和X射线胸片等临床资料.结果 采用糖皮质激素(必可酮喷雾剂)+吸氧等常规治疗后,患者临床症状、体征等均获得明显好转.结论 急性光气刺激反应引起的急性呼吸道及眼部刺激症状,通过糖皮质激素喷雾、小剂量低流量持续吸氧为主的综合治疗,可以在短时间内得到缓解、痊愈.     

Response of the pulmonary surfactant system to phosgene

Rats were exposed to 240 ppm X min phosgene (1.0 ppm for 4 hrs) in a Rochester-type chamber. At intervals thereafter over a 4 day period, lungs were removed for determination of wet weight; total, microsomal and surfactant protein concentrations; surfactant phospholipid concentrations; and 1-acyl-2-lyso-phosphatidylcholine: palmitoyl-CoA acyl transferase activity. Immediately upon termination of the phosgene exposure, microsomal protein and acyl transferase activity were reduced below, and lung wet weight was elevated above, control levels. From Day 1 through Day 3 after the exposure, all measured parameters, except for the phosphatidylinositol constituent of the surfactant fraction, were increased above the control values. In general, maximum levels were observed on Day 2; however, the acyl transferase activity and surfactant concentration continued to increase on Day 3. The results suggest components of the pulmonary surfactant system may be involved in maintenance of pulmonary fluid balance and the presence of excess water in the lungs as a result of phosgene exposure may represent a signal for increased synthesis of anti-edematogenic materials in order to promote removal of the inappropriate fluid.     

A literature review: therapy for phosgene poisoning

A literature search designed to collect information on therapy for phosgene poisoning has been conducted for the period 1920-1982. To achieve this goal, literature services were consulted, cross references were carefully followed and, whenever possible, unpublished reports (e.g., from Edgewood Arsenal and Porton Research Station) were evaluated. The various therapeutic agents and measures described in the literature are presented in alphabetical order. When available, detailed data are given for the phosgene dose, interval of time between exposure and institution of therapy, therapeutic effect and parameters used to assess efficacy. A final summary presents general recommendations for therapy and for further research.