Dust in the Wind

A 52-year-old woman presented with a 4-day history of progressive dyspnea, nonproductive cough, pleuritic chest pain, and subjective fevers. She described dyspnea at rest, which worsened with exertion. She reported no chills, night sweats, weight change, wheezing, hemoptysis, orthopnea, lower extremity edema, or nasal congestion. She also denied myalgia, arthralgia, or joint swelling. She reported no rash, itching, or peripheral lymphadenopathy. She had no seasonal allergies. She was treated for presumed bronchitis with azithromycin by her primary care provider 4 days prior to presentation but experienced progressive dyspnea.

The constellation of dry cough, fever, and dyspnea is often infectious in origin, with the nonproductive, dry cough more suggestive of a viral than bacterial syndrome. Atypical organisms such as Mycoplasma pneumoniae, Legionella pneumophila, and Chlamydia pneumoniae may also present with these symptoms. Noninfectious etiologies should also be considered, including pulmonary embolism, systemic lupus erythematosus, asbestosis, hypersensitivity pneumonitis, sarcoidosis, and lung cancer. The dyspnea at rest stands out as a worrisome feature, as it implies hypoxia; therefore, an oxygen saturation is necessary to quickly determine her peripheral oxygen saturation.

Her past medical history was notable for lung adenocarcinoma, for which she had undergone right upper lobectomy, without chemotherapy or radiation, 13 years ago without recurrence. She had no history of chronic obstructive pulmonary disease, asthma, or pneumonia, nor a family history of chronic obstructive pulmonary disease, asthma, pneumonia, or lung cancer. Her only medication was azithromycin. She drank alcohol on occasion and denied illicit drug use. Three weeks prior to admission, she began smoking 4 to 5 cigarettes per day after 13 years of abstinence. Her smoking history prior to abstinence was 1 pack per day for 20 years. She worked as a department store remodeler; she had no exposure to asbestos, mold, or water-damaged wood. She reported no recent travel, sick contacts, or exposure to animals.

A primary lung neoplasm with a pleural effusion could cause her shortness of breath and pleuritic chest pain. Her history of lung cancer at age 39 raises the possibility of recurrence. For cigarette smokers, a second lung cancer may occur many years after the first diagnosis and treatment, even if they have quit smoking. A review of her original cancer records is essential to confirm the diagnosis of pulmonary adenocarcinoma. What is now being described as pulmonary adenocarcinoma may have been a metastatic lesion arising from outside the lung. Although unlikely, a primary adenocarcinoma may remain active.

Infectious etiologies continue to merit consideration. A parapneumonic effusion from a pneumonia or an empyema are consistent with her symptoms. Systemic lupus erythematosus can cause lung disease with pleural effusions. She does exhibit dyspnea and pleurisy, which are consistent with autoimmune disease, but does not exhibit some of the more typical autoimmune symptoms such as arthralgias, joint swelling, and rash. Pneumothorax could also produce her symptoms; however, pneumothorax usually occurs spontaneously in younger patients or after trauma or a procedure. Remote right upper lobectomy would not be a cause of pneumothorax now. Her reported history makes lung disease or pneumoconiosis due to occupational exposure to mold or aspergillosis a possibility. Legionellosis, histoplasmosis, or coccidioidomycosis should be considered if she lives in or has visited a high-risk area. Pulmonary embolism remains a concern for all patients with new-onset shortness of breath. Decision support tools, such as the Wells criteria, are valuable, but the gestalt of the physician does not lag far behind in accuracy.

Cardiac disease is also in the differential. Bibasilar crackles, third heart sound gallop, and jugular vein distension would suggest heart failure. A pericardial friction rub would be highly suggestive of pericarditis. A paradoxical pulse would raise concern for pericardial tamponade. Pleurisy may be associated with a pericardial effusion, making viral pericarditis and myocarditis possibilities.

She was in moderate distress with tachypnea and increased work of breathing. Her temperature was 36.7°C, heart rate 104 beats per minute, respiratory rate 24 breaths per minute, oxygen saturation was 88% on room air, 94% on 3 liters of oxygen, and blood pressure was 147/61 mmHg. Auscultation of the lungs revealed bibasilar crackles and decreased breath sounds at the bases. She was tachycardic, with a regular rhythm and no appreciable murmurs, rubs, or gallops. There was no jugular venous distention or lower extremity edema. Her thyroid was palpable, without appreciation of nodules. Skin and musculoskeletal examinations were normal.

Unless she is immunocompromised, infection has become lower in the differential, as she is afebrile. Decreased breath sounds at the bases and bibasilar crackles may be due to pleural effusions. Congestive heart failure is a possibility, especially given her dyspnea and bibasilar crackles. Volume overload from renal failure is possible, but she does not have other signs of volume overload such as lower extremity edema or jugular venous distension. It is important to note that crackles may be due to other etiologies, including atelectasis, fibrosis, or pneumonia. Pulmonary embolism may cause hypoxia, tachycardia, and pleural effusions. Additional diseases may present similarly, including human immunodeficiency virus with Pneumocystis jirovecii, causing dyspnea, tachypnea, and tachycardia; hematologic malignancy with anemia, causing dyspnea and tachycardia; and thyrotoxic states with thyromegaly, causing dyspnea and tachycardia. Thyroid storm patients appear in distress, are tachycardic, and may have thyromegaly.