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* From the Department of Medicine (Dr. Chandra), Division of Pulmonary and Critical Care Medicine (Dr. Soubra), and Division of Infectious Diseases (Dr. Musher), Baylor College of Medicine, Houston, TX.
Correspondence to: Divay Chandra, MD, Department of Medicine, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030; e-mail: divayc{at}bcm.edu
A 57-year-old man with very severe bullous emphysema presented with fever and a history of right-sided pleuritic chest pain for 5 days. He denied an increase in cough, sputum production, or weight loss. He had a 75-pack-year smoking history and had undergone resection of the right upper lobe for non-small cell lung cancer in 1994. He had gradually worsening shortness of breath for 4 months before hospital admission; therapy with oral prednisone, 20 mg/d, had been started 2 months prior to presentation, with intermittent increases to 60 mg/d, without clinical improvement. His medications included inhaled albuterol, tiotropium, and fluticasone. There was no history of diabetes, seizures, aspiration, alcohol abuse, or recent travel outside Houston.
Physical Examination
Vital sign measurements were as follows: respiratory rate, 24 breaths/min; BP, 116/68 mm Hg; temperature, 102.1°F; heart rate, 116 beats/min; and oxygen saturation, 96% (while breathing room air). Heart sounds were distant but normal. The thorax was hyperresonant to percussion; bilateral air entry was very impaired, and no adventitious sounds were present on auscultation. The findings of the remainder of the examination were unremarkable.
Laboratory Findings
Laboratory findings were as follows: hematocrit, 30%; hemoglobin concentration, 10 g/dL; and WBC count, 34,700 cells/µL with 90% neutrophils. The patient’s blood glucose level was 107 mg/dL. Blood culture findings were negative, and he was unable to provide a sputum sample. A chest radiograph obtained at presentation is shown in Figure 1 , and a CT scan obtained at presentation is shown in Figure 2 . The FEV1 level measured 1 year prior to presentation was 21% predicted.
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Diagnosis: Infection of an emphysematous bulla with methicillin-resistant Staphylococcus aureus
Discussion
Infected emphysematous bullae are a common but underreported complication of COPD. The diagnosis is best made when a fluid level appears in a preexisting bulla of a patient with bullous emphysema. Unfortunately, the term infected emphysematous bulla has some times been incorrectly used in the literature to describe other fluid-containing lung cavities such as lung abscesses or tuberculous cavities. The findings from three published case series of patients with infected bullae are summarized in Table 1 and are discussed below.
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In evaluating patients with suspected infected emphysematous bullae, clinicians should note that signs of a deep-seated lung infection are often lacking. The low WBC counts previously reported corroborate the benign clinical presentations of most patients (Table 1). Sputum cultures have rarely been positive, and, because the percutaneous aspiration of infected bullae has been traditionally discouraged, data to confirm that the isolated organisms were actually responsible for the infection has not been available. Blood culture findings have been reported as uniformly negative in prior reports. Bronchoscopy has not been shown to provide any useful diagnostic or therapeutic information.
Radiologic evidence of the existence of a bulla prior to the accumulation of fluid is a sine qua non for the diagnosis. In our case, comparison with a CT scan performed 3 months prior to presentation proved that the patient’s fluid-containing lung cavity was, in fact, an infected bulla (Fig 3 ). When prior radiology is not available, certain features can support the diagnosis. These include the presence of other bullae in a patient with established obstructive airway disease, a thin-walled cavity, disproportionately lesser symptoms than the chest radiograph would suggest, and rapid changes in the amount of fluid that were not accompanied by changes in clinical status. CT scans provide detailed information on the exact size and location of the fluid collection, and should be obtained if percutaneous drainage is planned.
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In managing the present patient, we decided in favor of emergent percutaneous drainage in addition to therapy with IV antibiotics because our patient was more acutely ill at presentation and had more advanced lung disease than the majority of patients with this condition. Also, there was a previous report of a very similar patient with a large infected bulla who did not improve after 10 days of treatment with different empiric IV antibiotics. That patient then underwent uncomplicated percutaneous drainage with the removal of 500 mL of culture-negative fluid with marked improvement over the next 24 h. In our patient, percutaneous drainage via a 10F pigtail catheter removed 500 mL of pus. Gram stain revealed Gram-positive cocci in pairs and clusters. A culture yielded the presence of methicillin-resistant Staphylococcus aureus (MRSA) that was sensitive to vancomycin, clindamycin, and trimethoprim/sulfamethoxazole, which is suggestive of the community-acquired strain (there had been no recent hospitalization prior to presentation).
To the best of our knowledge, this is the first reported case of percutaneous aspiration at presentation and of MRSA causing such an infection. The clinical response to drainage was excellent with the resolution of fevers within 48 h and a steady decline in the WBC count. Following the aspiration, there was no air leak and minimal drainage of fluid through the catheter, which was removed 5 weeks after insertion. The patient was initially treated with vancomycin and then was switched to oral clindamycin for a total of 6 weeks of antibiotic treatment. We chose not to perform a bronchoscopy because there is no evidence to show that it is of any utility in these patients.
Over 12 weeks of outpatient follow-up, and in the absence of any change in the medication regimen, the patient reported an unexpected increase in exercise tolerance, from walking half a block prior to the onset of symptoms to more than two blocks. A repeat CT scan showed that the bulla had remained collapsed (Fig 4 ), and repeat pulmonary function test results showed a significant improvement in lung volumes as well as in expiratory flow rate (Table 2 ). The physiologic improvement is conceptually similar to what might be seen after the Brompton technique, which is a well-described surgical method for treating large noninfected lung bullae. In this procedure, the bulla is opened and the cavity insufflated with talc, after which a Foley catheter is left in place to produce negative pressure. The resulting inflammatory response in the collapsed bulla stimulates fibrosis, which leads to permanent deflation of the bulla.
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Footnotes
The authors have reported to the ACCP that no significant conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.
Received for publication January 14, 2006. Accepted for publication March 2, 2006.
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