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University of Saskatoon Saskatoon, SK, Canada
Correspondence to: John Reid, MD, University of Saskatchewan, Fifth Floor, Ellis Hall, 103 Hospital Dr, Saskatoon, SK, Canada S7N 0Z1; e-mail: reidj1970{at}hotmail.com
To the Editor:
Emphysema is a pathologic diagnosis that often accompanies the clinical finding of chronic airflow limitation. Although these two components often coexist, they may not necessarily progress in synchrony. We report a patient with severe smoking-related centrilobular emphysema and hypoxemic respiratory failure, whose pulmonary function was normal except for a low diffusing capacity of the lung for carbon monoxide (DLCO).
An 81-year-old white woman, a 30-pack-year ex-smoker, had progressive and marked exertional dyspnea, and resting hypoxemia requiring supplemental oxygen. She was slightly overweight with no chest wall deformity and no clubbing. Breath sounds were normal with no wheezes and only few inspiratory crackles in both bases. There was an accentuated pulmonic component of the second heart sound but no evidence of left- or right-heart failure.
Expiratory flow rates were normal (FEV1, 1.3 L [108%]; FVC, 2.0 L [107%]). Lung volumes via dilution were all slightly elevated. DLCO was severely reduced, at 4 mL/mm Hg/min (23%). The expiratory flow-volume loop is shown in Figure 1 . Chest radiographic findings were normal. Radionucleotide ventilation-perfusion lung scan findings were low probability for thromboembolism, and ultrasound revealed patent leg veins. Resting room air blood gases showed the following findings: PaO2, 52 mm Hg; PaCO2, 37 mm Hg; arterial oxygen saturation, 88%, which decreased to 78% following a brief walk. Hemoglobin level was 16.6 g/dL. High-resolution CT scan (HRCT) showed diffuse centrilobular emphysema, with no bullae or interstitial disease (Fig 2 ). Home oxygen therapy was continued, and treatment with inhaled bronchodilation was initiated in attempt to improve her dyspnea. She remained in clinically stable condition and was oxygen dependent.
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The classic teaching holds that emphysema causes loss of elastic recoil and thereby "functional" airways obstruction. Although emphysematous airspace destruction commonly occurs with airflow obstruction, the two are not interdependent processes.1 2 3 Results of the HRCT of the chest correlate well with histologic emphysema4 5 and have helped to identify patients with emphysema but not airflow obstruction. To our knowledge, other reported patients have had mild clinical disease, without resting hypoxemia. This patient is unusual because of the severity of her symptoms and hypoxemia, despite normal expiratory airflow. This patient demonstrates that although emphysema and airflow limitation commonly occur together, they are actually separate disease processes.
References
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