Fraire A E, Shahab I, Greenberg S D, Jubran A, Noall M
Department of Pathology, Baylor College of Medicine, Houston.
Chest. 1992 Nov;102(5):1591-4. doi: 10.1378/chest.102.5.1591.
We recently reported the first case of accidental aspiration of polyacrylamide occurring in a 26-year-old man. The patient developed severe airway obstruction and parenchymal lung damage and died. Autopsy revealed numerous polyacrylamide particles in his lungs, as well as extensive bronchiolar and alveolar damage. Gas chromatographic and mass spectrometric assessment of the lung tissue failed to reveal polyacrylamide activity, although assessment of the suspending solvent of the polyacrylamide showed a pattern characteristic of an aliphatic hydrocarbon mixture with a prominent dodecane peak. This experimental study was performed to determine the nature and extent of damage to rat bronchial and alveolar epithelia following endotracheal instillation of polyacrylamide, hydrocarbon mixture (petroleum distillate), dodecane (C12H26), or normal saline. The rat lungs were examined grossly and microscopically 10 min and 24, 72, and 96 h after endotracheal instillation, following inflation and fixation with 10 percent buffered formaldehyde. Gross examination revealed congested, mottled visceral pleural surfaces in the rats treated with polyacrylamide and dodecane. There were no pleural exudates or effusions. Microscopically, vascular engorgement, bronchiolitis, and focal pneumonia were observed. Vascular engorgement was most pronounced at 72 to 96 h in rat lungs treated with polyacrylamide and dodecane and was moderate at 24 h in rats treated with petroleum distillate. Focal organizing pneumonia was marked at 96 h in rats treated with petroleum distillate, at 72 h in those treated with polyacrylamide, and at 24 h in those treated with dodecane. The saline-treated control animals showed no change. Our findings suggest that polyacrylamide, dodecane, and petroleum distillate are strong irritants to the airways. However, a direct obstructive/mechanical effect of the polyacrylamide upon the airway has not been excluded. Airway exposure to polyacrylamide may result in lung injury secondary to the polyacrylamide itself, its suspending agents, or both.
我们最近报道了首例发生在一名26岁男性身上的聚丙烯酰胺意外吸入病例。该患者出现严重气道阻塞和肺实质损伤并死亡。尸检发现其肺部有大量聚丙烯酰胺颗粒,以及广泛的细支气管和肺泡损伤。尽管对聚丙烯酰胺的悬浮溶剂评估显示出具有突出十二烷峰的脂肪烃混合物的特征图谱,但对肺组织进行气相色谱和质谱评估未能揭示聚丙烯酰胺的活性。本实验研究旨在确定经气管内滴注聚丙烯酰胺、烃混合物(石油馏出物)、十二烷(C12H26)或生理盐水后,大鼠支气管和肺泡上皮的损伤性质和程度。在经气管内滴注后10分钟以及24、72和96小时,用10%缓冲甲醛充气并固定后,对大鼠肺部进行大体和显微镜检查。大体检查发现,用聚丙烯酰胺和十二烷处理的大鼠内脏胸膜表面充血、呈斑驳状。没有胸膜渗出物或积液。显微镜下观察到血管充血、细支气管炎和局灶性肺炎。在用聚丙烯酰胺和十二烷处理的大鼠肺中,血管充血在72至96小时最为明显,在用石油馏出物处理的大鼠中,24小时时血管充血程度中等。在用石油馏出物处理的大鼠中,96小时时局灶性机化性肺炎明显,在用聚丙烯酰胺处理的大鼠中,72小时时明显,在用十二烷处理的大鼠中,24小时时明显。用生理盐水处理的对照动物未出现变化。我们的研究结果表明,聚丙烯酰胺、十二烷和石油馏出物对气道有强烈刺激作用。然而,尚未排除聚丙烯酰胺对气道的直接阻塞/机械作用。气道接触聚丙烯酰胺可能导致继发于聚丙烯酰胺本身、其悬浮剂或两者的肺损伤。