Inhalación masiva de amoniaco: reporte de dos casos / Massive ammonia inhalation: report of two cases

Ammonia (NH3) is an irritant and corrosive gas whose inhalation at high concentrations mainly occurs during agricultural and industrial activities, as occupational accidents. The extent and severity of the damage depends on the concentration and time of exposure to the toxic, which can cause skin, eye, respiratory and life-threatening injuries. We present two cases of patients acutely exposed to high concentrations of NH3. Both patients survived to the acute phase of the respiratory injury, but developed chronic lung derangements.

El amoniaco (NH3) es un gas irritante y corrosivo cuya inhalación aguda en altas concentraciones se produce principalmente durante accidentes laborales en el sector agrícola e industrial. La extensión y severidad del daño depende de la concentración y tiempo de exposición al tóxico, el cual puede causar lesiones a nivel cutáneo, ocular, respiratorio y riesgo vital. Presentamos dos casos de pacientes expuestos en forma aguda a NH3 en altas concentraciones. Ambos pacientes sobrevivieron a la fase aguda y evolucionaron con lesiones respiratorias crónicas.

Clinical Outcome of Paraquat Poisoning

No abstract available.

Marked Recovery From Paraquat-Induced Lung Injury During Long-Term Follow-up

BACKGROUND/AIMS: Paraquat-induced lung injury has been considered a progressive and irreversible disease. The purpose of this study was to report the long-term evolution of lung lesions in eight survivors with significant paraquat-induced lung injuries who could be followed-up for longer than 6 months. METHODS: We retrospectively examined high-resolution computed tomography and pulmonary function test of eight survivors with significant paraquat-induced lung injurys. RESULTS: High-resolution computed tomography revealed a predominant pattern of irregularly shaped consolidation with traction bronchiectasis at 1-2 months after paraquat poisoning, a mixed pattern of irregularly shaped consolidation and ground-glass opacity at 3-12 months, and a mixed pattern of consolidation, groundglass opacity, and honeycombing at 1-2 years. At 3-12 months after paraquat ingestion, the areas of consolidation had markedly decreased and the decreased lung volume had returned to normal. At 1-2 years after paraquat poisoning, the cystic changes had disappeared. At 2-3 years after paraquat poisoning, the decrease in forced vital capacity had greatly improved to the normal range. CONCLUSIONS: Recovery of nearly normal pulmonary structure and function may occur over several years following paraquat poisoning. Pulmonary function (both forced vital capacity and forced expiratory volume in 1 sec) evolved toward normal in the long-term survivors of paraquat poisoning with initial prominent lung injuries.

Development of bronchiectasis; a late sequela of mustard gas exposure

Bronchiectasis following inhalation of chemical gases, mainly ammonia, has been occasionally reported in literature. The widespread use of sulfur mustard gas, as a warfare agent by Iraqi forces, during the Iran-Iraq war, has resulted in chronic lung diseases including bronchiectasis, among Iranian veterans exposed to this agent. In this cross-sectional clinical study, we present 16 proven cases of bronchiectasis following a single episode of inhalation of sulfur mustard gas. Both diffuse and focal forms of bronchiectasis were encountered in this group of patients. In the majority of patients, pulmonary function tests showed either obstructive or mixed obstructive and restrictive patterns. The lesions were more frequently in the lower lung lobes. Bronchiectasis is a relatively common chronic pulmonary sequela of sulfur mustard gas injury. The observation that only a subset of victims exposed to mustard gas have developed bronchiectasis underlines the hypothesis that individual susceptibility is important for development of bronchiectasis