1215

Abstract

Introduction: Chlorine is an irritant gas that is commonly used for water treatment and as part of household bleach. We present a case of ARDS in a homemaker secondary to household use of chlorine-based bleach. Case Presentation: A 46-year-old African-American woman presented to the emergency room with 1-day history of rapidly progressive dyspnea after using a relatively higher than usual amount of bleach with poor ventilation at home. In the past, she used to have some fatigue after use of this bleach which resolved over few hours. On examination, she was in obvious respiratory distress with tachycardia, tachypnea and oxygen saturation at 79% on ambient air. She had diffuse coarse crackles bilaterally on lung auscultation, but no wheezing. Arterial blood gas analysis showed a pH of 7.41, pCO2 of 37 and pO2 of 66 on FiO2 of 40% (PaO2/FiO2 ratio of 165). CT scan of the chest showed bilateral diffuse interstitial infiltrates and multifocal patchy areas of solid consolidation, both worse in upper lung zones. She was admitted to the intensive care unit and was started on intravenous steroids for presumed acute inhalation lung injury. Her hypoxia and dyspnea improved over the next 2 days and she was discharged on day 4 of hospitalization with a slow prednisone taper starting at 40 mg daily over 1 month and supplemental oxygen at rest and activity. At 1-month follow up, her oxygen saturation was normal at 100% on ambient air. Repeat CT chest at 2-month follow up showed complete resolution of previously seen infiltrates. Discussion: The usual description of accidental chlorine injury is reactive airway dysfunction syndrome, while non-cardiogenic pulmonary edema and ARDS have been reported in association with high levels of exposures such as transportation accidents, industrial or swimming pool spills. Our case is rare as the patient had a near-fatal presentation from household exposure to bleach which she has otherwise been using in the past. Both acute and chronic exposures to chlorine have been associated with airflow obstruction and bronchial airway hyperreactivity (AHR). Our patient did not show any evidence airflow obstruction on spirometry performed 4 weeks after the acute event. A methacholine challenge test was performed and it did not demonstrate any AHR as well. Animal models of high-dose chlorine exposure have shown that much of chlorine damage is oxidative in nature. There is histologic evidence of airway and alveolar epithelial damage and alveolar edema that usually resolves in 10 days. It is likely that genetic susceptibility to oxidative injury determines which patients would present with AHR versus alveolar damage. Conclusion: Household exposure to chlorine-based bleach may present with ARDS in susceptible individuals. Apart from a rare presentation of household chlorine exposure, this case also highlights the importance of detailed exposure history in the context of clinical presentation. Our patient had no recurrence of symptoms after switching to non-chlorine based bleach.