Choking agents and chlorine gas - History, pathophysiology, clinical effects and treatment.

INTRODUCTION: Choking agent exposure, among them chlorine gas, occurs in household or industrial accidents, chemical warfare and terrorist attacks. AIMS: Review of published animal and human data regarding the history, pathophysiology, clinical effects and management of chlorine exposure. PATHOPHYSIOLOGY: Highly soluble agents cause quick upper respiratory tract symptoms. Chlorine gas has a medium solubility, also causing delayed lower airway symptoms, mainly due to its oxidizing potential by releasing hypochlorous and hydrochloric acid, but also by interacting with Transient Receptor Potential channels. SYMPTOMS: Eyes may show conjunctival injection, abrasions and corrosions. Burns of the oronasal mucosa and trachea can occur. Dyspnea, bronchospasm and possible retrosternal pain occur frequently. Glottis edema or laryngospasm are acute life-threatening emergencies. Chlorine gas can cause toxic pneumonitis, lung edema and acute respiratory distress syndrome (ARDS). MANAGEMENT: General management includes physical examination, pulse oximetry and arterial blood gases. Eyes should be irrigated, humidified oxygen and inhalative bronchodilators administered. An EKG, cardiac enzymes and complete-blood-count should be obtained if there is retrosternal pain. Routine chest x-ray is not recommended - except if pulmonary edema is suspected. Laryngoscopy should be performed if glottis edema is suspected. Sodium bicarbonate inhalation after chlorine gas inhalation is discussed controversially. Mechanical ventilation with continuous-positive-airway-pressure or intubation/tracheotomy with high positive-end-expiratory-pressure may be necessary. Glucocorticoids for prevention of pulmonary edema should be applied restrictively. Prophylactic antibiotics are not recommended. In severe ARDS, extracorporeal membrane oxygenation (ECMO) can be considered. CONCLUSION: Treatment is mainly symptom oriented. New and promising therapies are in development.

The surgical management of esophageal stricture in children. A century of progress.

Early in this century all procedures performed on the esophagus were accomplished through its lumen. Ingestion of caustics was common and resulted in dense strictures for which complicated and ingenious methods of dilation were advised. Because obstructions usually recurred, by-pass operations were devised with conduits of skin or segments of the gastrointestinal tract. Now, in contrast, when burns occur, intensive steroid therapy usually prevents all but localized areas of stricture. These areas, if short, can be treated with hydrostatic balloon dilation under fluoroscopic control. If longer or resistant to dilation, these strictures can be managed by incision and insertion of a colic patch with excellent long-term results. To a previous series of children who have had esophageal patch with a vascularized segment of colon, now added is an experience with a free segment of small intestine with vascular anastomosis to an artery and vein in the neck and another case of a free patch of pericardium to the esophageal stricture.