A Novel Cause of Diffuse Alveolar Hemorrhage

Abstract

INTRODUCTION: Diffuse alveolar hemorrhage (DAH) is a potentially life-threatening syndrome resulting from widespread bleeding of alveolar capillaries into the alveoli. Here we describe a patient who developed DAH after smoke inhalation from a house fire. CASE PRESENTATION: An 84 year-old female sustained burns to her face and hands during a house fire caused by a faulty electric blanket. She was intubated and transferred to our regional burn center. Upon arrival she was afebrile and hemodynamically stable. On exam she had partial thickness burns of her face and hands, blackened nares, and clear breath sounds. Carboxyhemoglobin was undetectable and no anion gap was present. Chest x-ray was consistent with bilateral perihilar interstitial changes. Bronchoscopy to assess for thermal airway injury revealed significant upper airway edema and marked erythema throughout the bronchial tree. The airway edema was slow to resolve, and a tracheostomy was performed on day 11 to facilitate vent weaning. On hospital day 20 significant bleeding was noted on tracheostomy suctioning. Repeat bronchoscopy revealed traces of bleeding throughout the bronchial tree (Figure 1) and serial bronchoalveolar lavages were progressively bloodier, consistent with DAH. Chest CT demonstrated diffuse, bilateral ground glass and interstitial densities throughout both lung fields (Figure 2). High dose methylprednisolone and aminocaproic acid were administered. Workup for infectious and vasculitic etiologies was negative. She continued to have bloody tracheal aspirates confirmed by bronchoscopy on day 23 and endobronchial factor VII was administered. Soon thereafter the bleeding resolved. With supportive care she slowly improved and was discharged to a long-term care facility on minimal ventilator support. DISCUSSION: DAH is a syndrome with three distinct histopathologic patterns: pulmonary capillaritis, bland pulmonary hemorrhage, and diffuse alveolar damage. We believe our patient initially suffered a chemical pneumonitis from smoke inhalation, which led to the development of diffuse alveolar damage and subsequently DAH. House fires lead to chemical injury of the tracheobronchial tree and lower airway injury due to direct toxin damage. Physicians need to be conscious of carbon monoxide and cyanide toxicity in addition to the sequelae of thermal and chemical injury. We posit DAH as novel and dangerous consequence of smoke inhalation that may have a delayed presentation. CONCLUSION(S): This is the first reported case of DAH caused by smoke inhalation. Clinicians involved in the care of these patients should be aware of the possibility of this potentially life-threatening condition.