A 58-year-old male was transferred from an outlying facility for evaluation of suspected large left bullae on the left chest at risk for rupture (Figure 1). Four days prior to admission, he
noted a sudden-onset cough accompanied by hemoptysis and pleuritic chest pain. The patient also experienced progressive dyspnea with and without exertion and pillow orthopnea. His pain was epigastric with radiation to the infrascapular region. He denied any previous episodes or other medical care in the past 10 years. The patient had smoked 15 cigarettes daily for 15 years but had quit 20 years ago. His history included remote use of marijuana and freebase crack cocaine, and he consumed 12 to 18 beers each weekend. By trade, he was a general construction worker.
At the time of his evaluation, he was resting on 4 L of oxygen by nasal cannula without signs of respiratory distress. On physical examination, the patient's vital signs were as follows: temperature, 97.1˚F; heart rate, 82 beats per minute; BP, 152/10 mm Hg; respiratory rate, 24 breaths per minute; oxygen saturation, 99% (with oxygen therapy). Pulmonary examination demonstrated decreased breath sounds in the bilateral bases with coarse breath sounds anteriorly and end-expiratory wheezes. The remainder of the examination was unremarkable. The patient was being treated empirically for a suspected concomitant pneumonia. Arterial blood gas (ABG) test results were as follows: pH, 7.33; PaCO2, 56 mm Hg; PaO2, 96 mm Hg; HCO3, 30 mmol/L; and base excess, 2 mmol/L. CT of the chest was ordered.
DISCUSSION
Chest CT confirmed large left bullous emphysema that occupied more than two-thirds of the left chest wall. Mass effect with mediastinal shifting was seen. Less prominent multiseptated bullae of the right lung were also noted (Figure 2). For this reason, pulmonary function tests (PFTs), a ventilation perfusion (V/Q) scan, and cardiac evaluation were ordered. PFTs revealed severe airway obstruction, suggesting a restrictive process. Forced expiratory volume in 1 second (FEV1) was diminished at 40% of the predicted value. Forced vital capacity (FVC) was 43% of the predicted value, and the FEV1/FVC ratio was 73% with a predicted value of 80%. The V/Q scan was negative for a pulmonary embolism. Two-dimensional (2D) echocardiography revealed an ejection fraction of 55% to 60%.
Pulmonary/emphysematous blebs are accumulations of air in the subpleural space that occur when air escapes from the parenchyma. Their apical predominance remains elusive. As a rule, blebs measure less than 1 cm in diameter and increase the risk of spontaneous pneumothorax. Conversely, bullous emphysema produces air spaces greater than 1 cm in diameter with complete destruction of lung tissue. The outer surface of bullae is made of visceral pleura while the inner layer consists of fibrous tissue formed by the destroyed adjacent lung.1 Bullous disease may be associated with irreversible respiratory failure.2
Chronic obstructive pulmonary disease (COPD), often the cause of bullae, is the fourth leading cause of death in the United States, afflicting approximately 10 to 20 million Americans. There are two main forms of COPD: chronic bronchitis and emphysema. Most patients have a combination of both conditions. Of late, the notion of asthma as a tertiary pathophysiology has been considered. Primary treatment of COPD consists of medical management along with mainstay pharmacotherapy, including bronchodilators, anticholinergics, oxygen therapy, and corticosteroids either with or without antibiotics in patients with acute exacerbations. Surgical options are reserved for patients with advanced disease and include lung transplantation and lung volume reduction surgery (LVRS). The goal of LVRS is to reduce the area of hyperinflation and to improve overall lung function and quality of life.
Emphysema, which affects 2 million Americans, results when pulmonary parenchyma deteriorate and impair gas exchange. Alveoli lose elasticity, fill with air during inspiration, and are unable to empty during exhalation. This progressive, irregular hyperexpansion encroaches upon the healthy parenchyma, leading to inefficient breathing mechanics.3