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Effects of Time of Contact and Concentration of Caustic Agent on Generation of Injuries
Author(s) -
Mattos Gustavo M.,
Lopes Daniel Dias,
Mamede Rui Celso Martins,
Ricz Hilton,
MelloFilho Francisco V.,
Neto José Barbieri
Publication year - 2006
Publication title -
the laryngoscope
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.181
H-Index - 148
eISSN - 1531-4995
pISSN - 0023-852X
DOI - 10.1097/01.mlg.0000199935.74009.60
Subject(s) - necrosis , submucosa , esophagus , perforation , coagulative necrosis , adventitia , lesion , medicine , muscular layer , caustic (mathematics) , pathology , surgery , chemistry , materials science , composite material , punching , physics , mathematical physics
Abstract Objectives: Solid caustic soda (CS) ingestion levels continue high in Brazil. The aggressiveness of a caustic agent depends, among other factors, on its concentration and time of contact with mucosa. However, the interdependence of these factors in the production of caustic lesion in the esophageal mucosa is not known, especially regarding CS as the strongest corrosive agent. We analyze the effects of concentration and time of contact on the aggressiveness of CS to the esophagus of live animals. Study Design/Methods: One milliliter of CS at concentrations between 1.83% and 73.33% was applied to rats. The solution was kept in contact with the mucosa for 10 to 120 minutes. Internal and external organ aspects were analyzed and the epithelium, submucosa, muscle layer, and adventitia were analyzed microscopically Results: Epithelial necrosis was observed at all concentrations. Among the necrotic layers, the submucosa was observed starting at the 7.33% concentration, and the muscular layer and adventitia were observed at 14.66% concentration. Damage to the pulmonary parenchyma and trachea occurred at 33.66% after 10 minutes, and perforation of the esophagus was observed only after 120 minutes. After 10 minutes, important corrosive lesions installed in the esophageal layers, expanding in depth and superficial extension. The use of heparin had no effect on the production of lesions. Conclusions: Ten minutes were sufficient to provoke necrosis, and longer contact increased the area of necrosis. Solution concentration levels were more important in damage production: 1.83% was sufficient for epithelial necrosis, 7.33% caused submucosal necrosis, and 14.66% muscle and adventitia necrosis; 33.66% solutions caused lung and trachea damage after 10 minutes and esophageal perforation after 120 minutes.