48-Year-Old Woman With Dyspnea, Cough, and Weight Loss

Abstract

A 48-year-old woman presented to our emergency department with progressive dyspnea, cough with clear sputum, and a 9-kg weight loss. Evaluation at an outside emergency department 6 months previously had revealed a right middle lobe infiltrate on chest radiography (CXR), and she was treated with a 10-day course of levofloxacin for presumed community-acquired pneumonia. Her symptoms continued, and 1 month later, she went to an outside pulmonologist who found bilateral alveolar infiltrates on chest computed tomography (CT).On presentation to our emergency department, the patient reported no orthopnea, fevers, chills, or night sweats. Her medical history was notable for nonischemic dilated cardiomyopathy that was treated with cardiac resynchronization therapy and an automatic implantable cardioverter-defibrillator (AICD), atrial fibrillation, and myelodysplastic syndrome. She had a 10-pack-year smoking history but had quit smoking 1 year previously. Her medications included furosemide, losartan, digoxin, coumadin, amiodarone, and spironolactone. No new medications had been added to her treatment regimen during the past 10 years.On admission, the patient's vital signs were as follows: temperature, 37.0 o C; blood pressure, 101/64 mm Hg; respiratory rate, 18 breaths/min; and oxygen saturation, 94% while the patient breathed room air. She was in no acute distress. Her sclera had a blue-grey discoloration. Cardiac examination revealed a regular rhythm, grade 1/6 systolic murmur heard at the left upper sternal border, no gallops, no jugular venous distention, and no peripheral edema. Pulmonary examination revealed crackles over the right middle lobe but otherwise normal results. Abdominal, musculoskeletal, and neurologic examination findings were unremarkable.Chest radiography showed bilateral dense consolidations that were greater on the right with clear costophrenic angles, an AICD, and cardiomegaly. Chest CT revealed asymmetric bilateral, multilobar alveolar consolidations without pleural effusions or engorgement of the intralobar space, 4-chamber cardiomegaly, and an AICD.Laboratory studies yielded the following results (reference ranges shown parenthetically): hemoglobin, 10.1 g/dL (12.0-15.5 g/dL; previous level, 10.0 g/dL); white blood cell count, 1.6 ϫ 10 9 /L (3.5-10.5 ϫ 10 9 /L); 10% segmented neutrophils; 59% lymphocytes with an absolute neutrophil count of 2.0 ϫ 10 9 /L (0.9-2.9 ϫ 10 9 /L); platelet count, 125 ϫ 10 9 /L (150-450 ϫ 10 9 /L); erythrocyte sedimentation rate, 64 mm/h (Ͻ29 mm/h); international normalized ratio, 1.7 (0.8-1.2); brain naturietic peptide (BNP), 1260 pg/mL (Ͻ71 pg/mL); digoxin, 1.59 ng/mL (0.5-2.0 ng/mL); thyroid stimulating hormone, 0.52 mIU/L (0.3-5.0 mIU/L); and human immunodeficiency virus antibody, negative. The patient was admitted to the hospital for evaluation of new neutropenia, progressive dyspnea, and undiagnosed pulmonary infiltrate.

Amiodarone-induced Hemoptysis: A Rare Presentation of Amiodarone-induced Pulmonary Toxicity Occurs at a Low Dose

“…Diagnosis of APT should include three or more of the following: new or worsening dyspnea or new findings on lung exam, abnormalities on imaging, abnormalities in total lung capacity or diffusion lung capacity (DLCO), CD8+ lymphocytes in BAL fluid, lung biopsy showing DAH, interstitial pneumonitis, pulmonary fibrosis or organizing pneumonia [10]. The presented case met diagnostic criteria as the patient had new dyspnea, bilateral patchy opacifications on chest CT, and diffuse crackles appreciated throughout all lung fields on physical exam.…”

“…It is left to clinical judgement to decide the risk-benefit analysis of using steroids with respiratory status being a key consideration. Duello et al elected to avoid steroids entirely as their patient only required a mild oxygen supplement [10]. There were reservations in maintaining such an extensive dose of steroids in a metabolic syndrome patient with questionable A1c.…”

ECMO for pulmonary rescue in an adult with amiodarone-induced toxicity

“…Toxicity can occur within days, months or years and can present either acutely in the form of fever, pleuritic chest pain, and cough or subacutely with chronic dyspnea, dry cough, and hypoxia [4]. Higher daily doses are associated with a greater incidence of pulmonary toxicity but may occur in patients taking lower doses (200 mg/day) [5]. Symptoms are non-specific and differentiating subacute amiodarone pulmonary toxicity from chronic heart failure is especially difficult, since most patients receiving amiodarone have underlying cardiomyopathy.…”

“…Patients generally improve with discontinuation of amiodarone with or without corticosteroids over a period of 1-6 months. Radiographic follow-up shows complete clearing of opacities in about 85 % of patients [5,10,12]. Interestingly, there have been several reports of APT with complete resolution of ground-glass opacities after treatment with discontinuation of amiodarone and corticosteroids administration, but none reporting such refractoriness needing treatment with extracorporeal membrane oxygenation.…”