Morin A M, Zähringer J, Kasper M, von Schmädel E, Suhayda A
Universitätsklinik für Anästhesiologie, Universitätsklinikum Ulm.
Anasthesiol Intensivmed Notfallmed Schmerzther. 1997 Jan;32(1):56-60. doi: 10.1055/s-2007-995011.
Inhalation of inorganic, inert dusts, like concrete dust, has generally not been considered dangerous. Very rarely alterations following chronic exposures can be observed, such as airflow obstruction and increased mucous secretion. Acute reactions in terms of acute respiratory failure have not been described so far.
The present case report introduces a 54-year old male patient who developed acute respiratory failure after sawing a concrete block for several hours without wearing a face mask. Save for a chronic obstructive pulmonary disease he was unremarkable for his past medical history. When the emergency physician arrived, oxyhaemoglobin saturation was only 54%. Severely obstructed breathing sounds and coarse bubbling rales over both lungs were audible. After endotracheal intubation, a great deal of white viscous mucus could be aspirated via the tubus. The chest radiograph after admission demonstrated cloudy, shadowed areas with emphasis on both lower lung fields. As pulmonary function did not improve inspite of drug therapy with prednisolone, theophylline, fenoterol, n-acetylcysteine and respiration therapy with 100% oxygen concentration, the patient was treated daily with bronchoscopic aspiration of the mucus. Only on the fourth day, after an additional ten hours in prone position, the lung function improved. The patient could be extubated on the fifth day. The final chest radiograph indicated no residuum apart from a very small shadowed area on the right angle between heart and diaphragm.
The inhalation of dusts, which have long been considered inert, can cause acute pulmonary reactions. We suggest that the massive, mechanical covering on the alveolar layer with still alkaline concrete dust in conjunction with a history of chronic bronchitis was responsible for the acute inflammation and oedematous swelling of the bronchial mucosa, bronchospasm, secretion of a highly viscid mucus, atelectasis, and thus for the ARDS.
吸入无机惰性粉尘，如混凝土粉尘，一般不被认为具有危险性。慢性接触后很少能观察到改变，如气流阻塞和黏液分泌增加。目前尚未有急性呼吸衰竭方面的急性反应报道。
本病例报告介绍了一名54岁男性患者，他在未戴口罩的情况下锯混凝土块数小时后出现急性呼吸衰竭。除慢性阻塞性肺疾病外，他既往病史无其他异常。急诊医生到达时，氧合血红蛋白饱和度仅为54%。两肺呼吸音严重受阻，可闻及粗大的水泡音。气管插管后，通过导管吸出大量白色黏稠黏液。入院后胸部X线片显示肺部有云雾状阴影区域，以下肺野为主。尽管使用泼尼松龙、茶碱、非诺特罗、N-乙酰半胱氨酸进行药物治疗，并采用100%氧浓度进行呼吸治疗，但肺功能仍未改善，因此每天对患者进行支气管镜下黏液抽吸治疗。仅在第四天，患者在俯卧位额外停留10小时后，肺功能才有所改善。患者于第五天拔管。最终胸部X线片显示除心脏与膈肌夹角右侧有一个非常小的阴影区域外，无残留病变。
长期以来被认为惰性的粉尘吸入可引起急性肺部反应。我们认为，大量碱性混凝土粉尘机械性覆盖肺泡层，再加上慢性支气管炎病史，是导致支气管黏膜急性炎症和水肿性肿胀、支气管痉挛、分泌高度黏稠黏液、肺不张，进而导致急性呼吸窘迫综合征的原因。
