Bilateral spontaneous pneumothorax secondary to aspiration pneumonia induced by a wristwatch lodged at the pharyngoesophageal junction

Abstract

Bilateral spontaneous pneumothorax secondary to disease is rare and seldom encountered in forensic autopsies; however, traumatic bilateral pneumothorax occurs often. Herein, we present a forensic case involving a 50-year-old woman who died 4 days after ingesting a wristwatch. Postmortem computed tomography and autopsy findings demonstrated that the wristwatch was lodged at the pharyngoesophageal junction, that she had a bilateral pneumothorax unaccompanied by any thoracic wound, and that macular hemorrhagic lesions on the lung surfaces were responsible for the pneumothorax. A histological examination of the macular lesions revealed that they were aspiration pneumonia foci with many birefringent foreign materials. Furthermore, a necrotic process secondary to aspiration pneumonia with a one way check-valve hyperinflation caused by foreign materials in the bronchioles was the most probable pathogenesis of her pneumothorax. To our knowledge, this is the first reported case of a bilateral secondary spontaneous pneumothorax caused by a large foreign body at the pharyngoesophageal junction leading to death.

Pneumothorax and Pneumomediastinum Complicating Organophosphate Poisoning: A Case Series of Complications Less Understood

“…Associated with OP poisoning, the Macklin-like phenomenon involves the destruction of type II pneumocytes that results in secondary atelectasis, rupture, and emphysematous changes, which consequently cause an increase in surface tension and the subsequent formation of peripheral or subpleural bullae that rupture, which then causes pneumothorax and escape of the gas to dissect along vascular sheaths and connective tissue planes in the mediastinum, ultimately resulting in pneumomediastinum [ 13 ]. Other explanations may be ARDS or aspiration pneumonitis, both of which can independently produce spontaneous pneumothorax or pneumomediastinum during the acute phase [ 14 , 15 ]. Laniee et al, in their animal experiment, found that OP poisoning causes exudative infiltration by breaking down the alveolar epithelial-endothelial barrier and that this effect was the beginning of ARDS [ 16 ].…”