Chest Film Clinic: What caused progressive dyspneain this patient with chronic asthma?

Chest Film Clinic: What caused progressive dyspneain this patient with chronic asthma?

A 51-year-old man with a 20-year history of asthma and seasonal allergies presented with low-grade fever, progressive dyspnea on exertion, and wheezing that had persisted for 2 weeks. Four days earlier, he had been seen by his primary care physician and had started levofloxacin therapy. However, his respiratory symptoms had worsened, warranting hospitalization. He also reported pain in the abdomen and left flank and pain and swelling in the right metacarpophalangeal and right shoulder joints.

The patient's daily medications included salmeterol and budesonide. He reported intermittent use of albuterol, particularly before exercise. Within the previous year, he had required multiple brief courses of prednisone for asthma exacerbations, which represented worsening of his asthma control compared with previous years.

Two months before presentation, he was treated with antibiotics for left lower lobe pneumonia. Within the 6 months before presentation, he had multiple, recurrent episodes of sinus congestion and purulent discharge, which were treated with 3 courses of antibiotics and nasal irrigation with a mucolytic agent.

He had a family history of asthma. He was a chiropractor, and he denied significant occupational exposures; contact with birds or other animals, except for a pet dog; recent travel; and exposure to tuberculosis. He also denied smoking.

The patient was in no acute distress, with normal pulse, respiration rate, and blood pressure. His temperature was 37.7ºC (99.8ºF). Oxygen saturation was 99% on room air. Auscultation of the lungs revealed bilateral diffuse expiratory wheezing. The remaining examination findings were remarkable for erythematous patches on the scalp and mild erythema and tenderness in the metacarpophalangeal joints of the right hand.

Peak expiratory flow rates in the setting of acute symptoms were 300 L/min, compared with his baseline of 500 L/min. Laboratory tests revealed a white blood cell (WBC) count of 17,400/µL, with 48% neutrophils, 3% bands, 11% lymphocytes, 4% monocytes, and 34% eosinophils. Other findings: a hematocrit value of 40.3%, with mean corpuscular volume of 97 fL; platelet count of 569 3 103/µL; erythrocyte sedimentation rate (ESR) of 67 mm/h; and an IgE level of 935 IU/mL. Rheumatoid factor and antinuclear antibody test results were negative.

The patient's chest radiograph obtained on admission is shown below (Figure 1).

Making the diagnosis

The patient's chest radiograph revealed nonsegmental areas of consolidation with a predominantly peripheral and upper lobe distribution. An additional focus of consolidation was seen in the lingula.

Axial CT scanning of the chest with coronal reformations demonstrated peripheral, nonsegmental foci of airspace consolidation and ground-glass opacities (defined as hazy areas of increased opacity that do not obscure normal vascular structures) in both upper lobes (Figure 2). Less prominent ground-glass opacities were present in the right middle lobe, lingula, and the lower lobes.

These findings were new compared with those from a CT scan obtained 4 months earlier for follow-up of small noncalcified lung nodules. The number and size of mediastinal lymph nodes were increased. Prominent bilateral hilar lymph nodes appeared unchanged from the previous CT scan. A concurrent CT scan of the sinuses revealed sinonasal polyposis.

Based on the imaging findings of peripheral lung opacities, along with the history of asthma and eosinophilia, the patient was thought to have eosinophilic pneumonia. Levofloxacin was discontinued, and oral prednisone therapy was initiated. The patient remained afebrile, and his respiratory status improved. He was discharged. A chest radiograph at 1-week follow-up demonstrated marked improvement in pulmonary opacities. He was maintained with oral prednisone, 40 mg daily.

Three months later, the patient presented with a 10-day history of intermittent, periumbilical abdominal pain, which was sharp and burning, worse after eating, and worse when lying flat or with movement. The patient denied fever and shortness of breath. His WBC count was 21,500/µL, with 8% eosinophils.

Abdominal CT findings were compatible with gastroparesis. Results from an upper endoscopy demonstrated mild gastritis and duodenitis. Results of antral and duodenal biopsies, performed while the patient was taking prednisone, did not reveal any evidence of eosinophilic gastroenteritis. The patient's symptoms were relieved by metoclopramide.

On admission, the patient reported a 2-month history of transient, migratory distal muscle weakness and paresthesias. The symptoms began after a low-speed motor vehicle accident and were initially associated with neck stiffness. Findings from MRI of the head and cervical spine performed at another institution were reportedly normal.

A left exophthalmus and right-sided ophthalmoplegia localized to the inferior oblique muscle developed 2 to 4 months after admission. Polyneuropathy secondary to Churg-Strauss syndrome was suspected. Results of a left sural nerve biopsy, performed while the patient was taking prednisone, showed no significant inflammation. However, based on the constellation of imaging, clinical, and laboratory findings, a diagnosis of Churg-Strauss syndrome was made.


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