A 68 year old White female with atrial fibrillation presented with worsening dyspnea and cough. She was previously followed for similar symptoms and a computed tomography (CT) scan of the chest done in November 2012 demonstrated minimal basilar airspace disease. At that time an extensive workup including autoimmune serology was unrevealing and her symptoms were attributed to gastro-esophageal reflux disease. Over the next several years her dyspnea worsened and she developed progressive hypoxia requiring home oxygen therapy. During this time she also demonstrated radiographic worsening and a repeat CT scan done in August 2016 demonstrated progression of DPLD with bronchiectasis suggestive of Usual Interstitial Pneumonia (UIP). Given the clinical and radiographic worsening, the patient was admitted to the hospital and a repeat CT of the chest showed bilateral diffuse ground glass opacities on the background of DPLD. An echocardiogram was normal and minimal diuresis was provided.
She was treated with broad spectrum antibiotics; however she decompensated and required intubation. She subsequently underwent a bronchoscopy which demonstrated sequentially progressive hemorrhagic bronchoalveolar lavage return. Among all her medications the only plausible agent was deemed to be sotalol, which was discontinued. The patient was then treated with pulse dose methylprednisolone 1g/d and she rapidly demonstrated both clinical and radiologic improvement.
Discussion:
Respiratory complications from use of beta-blockers usually include exacerbations of obstructive lung disease, hypersensitivity pneumonitis and drug induced lupus. However, there are limited case reports of DPLD associated with beta blockade. Sotalol is a Class II/III antidysrhythmic agent commonly used in the maintenance of sinus rhythm for patients with atrial fibrillation and there are several cases reported in the literature, to our knowledge that associated sotalol with DPLD. However DAH has never been seen with the use of this therapy and this novel case highlights this association. Our patient showed a progressive and insidious process of respiratory deterioration that closely mirrored her sotalol exposure. The striking response to immunosuppression following discontinuation of sotalol emphasizes the need for close medication examination in these patients.
Conclusions:
Sotalol is generally thought to have few significant pulmonary side effects; however, several case reports have demonstrated associations between sotalol and various diffuse parenchymal lung diseases (DPLD). Diffuse alveolar hemorrhage (DAH) as an adverse effect of sotalol therapy has not been reported and here we aim to present an interesting case that delineates this association.