Citation

Homma S, Jones R, Qvist J, Zapol WM, Reid LW. Hum. Pathol. 1992; 23(1): 45-50.

Affiliation

Department of Pathology, Harvard Medical School and Children's Hospital, Boston, MA 02115.

Copyright

(Copyright © 1992, Elsevier Publishing)

DOI

unavailable

PMID

1544669

Abstract

Two soldiers were fatally injured by accidental inhalation of zinc chloride (ZnCl2) from a smoke bomb. Although exposed to a relatively short but high smoke concentration, acute injury was minor and for 10 days the patients were clinically satisfactory. Unexpectedly, both then rapidly developed features typical of severe adult respiratory distress syndrome with pulmonary hypertension. Intubation and mechanical ventilation were instigated on day 15 (patient no. 1) and day 12 (patient no. 2) after the inhalation, but death followed at days 25 and 32, respectively. Lung vascular injury was assessed by angiography and morphometric techniques. The lungs showed extensive interstitial and intra-alveolar space fibrosis. Vessels showed a significant lumen reduction by contracture (that is, reduction in vessel external diameter) affecting preacinar and intraacinar arterial and venous segments, the extent of injury suggesting that hexite causes more severe venous injury than seen in other types of adult respiratory distress syndrome. In microvessels there was obliteration and widespread occlusion by endothelial cell proliferation and clot. No evidence of infection was identified during life or at autopsy. It is unclear whether the long lag time was due to the fact that the infection was not a complicating event or because steroids, administered prophylactically, had sufficed to delay, but not to prevent, the amplification of injury that seems responsible for the adult respiratory distress syndrome.

Language: en