A 58-year-old man was admitted because of acute onset of non-productive cough, fever, myalgia and progressive dyspnea over a one-week period. This was associated with bilateral pulmonary infiltrates on chest PA. Prior to his illness, the patient had been completely well, without past history of either cardiac or respiratory disease. Of particular note, he was an ex-smoker who was unemployed and did not have hobbies which might have exposed him to possible harmful antigens. Neither the patient nor any of his close associates suffered from tuberculosis, and he denied taking drugs or exposing himself to noxious gases prior to his illness.
On admission to hospital, he was distressed, tachypneic, and pyrexial with a respiratory rate of 35 per minute and a body temperature of 38 C. He was normotensive and his pulse rate was 90 beats per minute. The patient was not jaundiced. The head and neck were entirely normal.
Examination of the chest revealed intercostal recession, but the respiratory excursion was equal bilaterally. The chest was resonant to percussion. The most striking feature on auscultation was the presence of extensive, bilateral, late inspiratory crepitations predominantly over the middle and lower lung zones. Vocal resonance was normal. Cardiac and abdominal examination were within normal limits. The chest radiographs showed multifocal and patchy distribution of opacities in the periphery of both lung zones (Fig. 1). Serial radiographs showed migratory natures of consolidations. High resolutional computed tomographic scan (HRCT) revealed nonsegmental and peribronchial distribution of alveolar consolidation and ground glass attenuation in the subpleural area, predominantly (Fig. 2). But, the consolidation had vertical zonal or anterior-posterior predominance. Several poorly defined centrilobular nodules and bronchial wall thickening with dilatation in the area of consolidation were seen. There was no evidence of pleural effusion or lymphadenopathy. Also, noted irregular lines were seen in both upper lung zones, suggestive due to previous centrilobular emphysema. Pulmonary function studies revealed an FVC of 3.28 L (88 percent predicted) and an FEV1 of 2.62 L (86 percent predicted) with an FEV1/FVC ratio of 98 percent. The patient's arterial blood gas levels (at room air) were as follows: pH; 7.48, PaCO2; 27.8mmHg, PaO2; 43.8mmHg and HCO3-; 21.1mmol/L. The ECG was normal. Laboratory findings disclosed the following values: erythrocyte sedimentation rate (ESR), 60mm/h; hemoglobin level 13.8g/dl; leukocyte count 22,100/mm3, with a normal differential cell count; platelet count, 473,000/mm3; BUN, 6mg/dl; creatinine, 0.8mg/dl; sodium 140mEq/L; potassium 3.8mEq/L; lactate dehydrogenase, 263.6 IU/L; alkaline phosphatase, 84.4 IU/L; GOT 16.2 IU/L; GPT 9.7 IU/dl. Levels of antinuclear antibody, rheumatoid factor and anticardiolipin antibody were all normal and complement levels were normal. Mycoplasma serology was negative. Cultures of blood and sputum were negative. Results of the urinalysis were normal. He underwent bronchoalveolar lavage that revealed 61x104/ml with 63 percent macrophages, 6 percent lymphocytes and 31 percent neutrophils. An open lung biopsy was performed on the fifth hospital day which showed BOOP. The section showed well demarcated areas of fibrosis involving air spaces in patchy distribution (Fig. 3). Fibrosis consisted of young fibroblasts and inflammatory cells in myxoid-matrix-forming fibroblast polyps. These fibroblast polyps occluded distal bronchioles, alveolar ducts and adjacent alveolar spaces and they were sometimes covered by a lining of bronchiolar or alveolar epithelial cells. Most bronchiolar lumens or air spaces were filled with fibrinous exudate containing granular eosinophilic necrotic cellular debris (Fig. 4). On the second hospital day, viral culture was performed from his throat swab in the National Institute of Health, Korea and adenovirus was isolated. He received supportive treatments including oxygen inhalation with partial rebreathing mask, without application of mechanical ventilation and PEEP. One day later, dyspnea subsided gradually. There was improvement in gas exchange and clearing of roentgenographic infiltrates without corticosteroid and antibiotics therapy. At discharge, arterial blood gas levels (at room air) were as follows: pH 7.46, PaCO2 37.8mmHg, PaO2 83.4mmHg; HCO3-, 23.8mmol/L. He has continued to do well two months following discharge and the follow-up HRCT scan after 2 months showed almost disappeared subpleural air-space consolidation with poorly defined nodule and nearly normalized bronchial wall thickening with dilatation.
High resolution computer tomography (HRCT) shows bilateral patchy involvement of alveolar consolidation in mainly both lower lobe and focal ground-glass lesion is also noted.