[Hydrofluoric acid burn: particulars on multiple pulmonary thrombi].
The production of hydrofluoric acid (HF) and its use have increased remarkably due to the rapid development of the electronic and petrochemical industries. HF has a highly corrosive and penetrating action when it comes in contact with organic material, including body tissue. When burns are caused by a high concentration of HF, fatal cases have been reported, even when the contact with HF is only for a short time or on a small area of the body. The causes of death have been reported to be lung edema, mineral disturbance and systemic injury. But no pathological experiments have been reported. In the present study, experiments of HF burns using mice (d.d.Y., 6w, male) were performed, mainly histopathologically and ultramicroscopically. Histological examination revealed that thrombosis occurred in the lung, and that the group in which mice had more thrombi showed a higher death rate. Thrombosis in the lung may be one of the main causes of death by hydrofluoric acid burns. Other organs showed no significant change. Ultrastructural examination of the lungs, revealed that the thrombi were seen in the capillary of the alveolar septa much more than in the pulmonary arteries and were mainly composed of platelets. The endothelial cells in the lungs were injured and had condensed cytoplasm, intracellular edema, or dilation of the intercellular gap. The basement membrane of the capillary was sometimes bared between the strongly condensed endothelial cells, but no platelets directly touched the membrane. Moreover, that no platelets directly touched the subendothelial tissue and the mechanism of the platelet aggregation is interesting. Platelet aggregation was thought to have resulted from the unbalance between thrombogenic factors and antithrombogenic factors in the blood above the surface of endothelial cells caused by endothelial injury. Endothelial cells in the lungs were assumed to be injured by fluoride, directly or indirectly, because the group which showed higher fluorine contents in the lungs showed more severe injury to the endothelial cells and because the fluorine contents in the lung increased much more than that in the other organs which had no thrombi.
Matsumoto
S
S
Department of Pathology and Surgical Pathology, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan.
D000818:Animals; D002057:Burns, Chemical / Q000378:metabolism / Q000473:pathology*; D002196:Capillaries / Q000187:drug effects / Q000648:ultrastructure; D004730:Endothelium, Vascular / Q000187:drug effects / Q000648:ultrastructure; D005461:Fluorine / Q000032:analysis; D006858:Hydrofluoric Acid / Q000009:adverse effects*; D008168:Lung / Q000032:analysis / Q000098:blood supply / Q000187:drug effects; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D010974:Platelet Aggregation / Q000187:drug effects; D011651:Pulmonary Artery / Q000187:drug effects / Q000648:ultrastructure; D011655:Pulmonary Embolism / Q000139:chemically induced* / Q000378:metabolism / Q000473:pathology
D005461:Fluorine; D006858:Hydrofluoric Acid