Abstract Introduction Nitrofurantoin is an antibiotic often used to treat uncomplicated urinary tract infections UTI and prevent recurrent cystitis. It is generally well tolerated, but nitrofurantoin has been linked to pulmonary toxicity. The reported incidence of pulmonary reaction is approximately 1%, with 90% of nitrofurantoin pulmonary toxicities reported as acute – occurring within one month of the first dose. Several mechanisms have been proposed to explain toxicity including lymphocyte activation and cytokine release causing lymphocytic alveolitis, drug-induced production of oxidants causing injury, and immune-complex-mediated reactions. Diagnosis depends on clinical evaluation and a high degree of suspicion. Case Presentation A 78-year-old female with a medical history of coronary artery disease, hypertension, and hyperlipidemia presented to the emergency department with dyspnea and a productive cough that had persisted for one week. She had been treated for a urinary tract infection caused by E. coli resistant to cephalosporins two weeks prior., with nitrofurantoin. On admission, the patient was hypoxic and tachypneic. Labs demonstrated elevated inflammatory markers, including C-reactive protein 200 mg/L, erythrocyte sedimentation rate 70 mm/hr, and pro-BNP 5,452 pg/mL. A viral panel and sputum culture returned negative results. Chest X-ray showed new bilateral diffuse interstitial opacities. A computed tomography CT of the chest revealed diffuse, heterogeneous, and irregular ground-glass opacities throughout both lungs, more prominent in the upper lobes with relative sparing of the lung bases. Bi-level positive airway pressure was initiated with empiric treatment that included intravenous IV azithromycin, ceftriaxone, methylprednisolone, and furosemide, along with bronchodilator therapy. The patient’s respiratory status improved and was successfully discharged home on a prednisone taper and supplemental oxygen. At her four-week follow-up appointment, the patient had successfully weaned off supplemental oxygen. Repeat CT imaging demonstrated improvement in bilateral ground-glass opacities, which now appeared as ill-defined curvilinear and polygonal patterns with continued sparing of the lung bases. Discussion Upon admission, the differential diagnosis included hospital-acquired pneumonia, viral pneumonitis, drug-induced pneumonitis, pulmonary edema, and cryptogenic organizing pneumonia. However, the timing of nitrofurantoin use, symptoms, and radiologic findings suggested drug-induced pneumonitis as the most likely etiology for respiratory failure. Our treatment focused on immune suppression with steroids, preventing further lung injury and fibrosis. Resolution of symptoms and improved imaging following treatment support diagnosis of nitrofurantoin-induced pneumonitis. Recognizing nitrofurantoin as a potential cause of acute lung injury is important for clinicians and requires a high index of suspicion when evaluating a patient’s medications and prescription history. This abstract is funded by: None
Mitchell et al. (Fri,) studied this question.