The patient appeared to be recovering well, but a few months later, his symptoms would recur.
John, 29 years old, was seen in May with a history of intermittent left-sided chest pain. He first noticed the pain after coughing while brushing his teeth one Sunday morning. When his symptoms failed to resolve over the course of a week, John came to see me, his primary-care clinician.
John described his continuing discomfort as a dull, intermittent, 3-4/10 pain that was exacerbated by inspiration. On questioning, he reported an eight-day history of wheezing, nonproductive cough, exertional dyspnea, and migratory anteroposterior chest pain. He denied any earlier similar episodes or trauma. John had no significant past medical history. He did not smoke and was not taking any medications. A review of systems did not indicate a history of cardiopulmonary disease. A family history was unremarkable. Both parents and two sisters were alive and well; one sister had a history of asthma.
On physical examination, John was in some distress, with mild tachycardia (pulse 105 beats per minute). The remainder of his vital signs were normal. Auscultation revealed absence of breath sounds and hyperresonance to percussion on the left side. After chest x-rays showed some abnormalities (Figure 1), John was sent to a local emergency department (ED).
John was tachypneic (respirations 24/minute) and mildly hypertensive (BP 142/91). Moreover, his tachycardia had worsened (pulse 120), and his oxygen saturation had dropped to 95% on 2 L of oxygen by nasal cannula. A complete blood count and basic metabolic panel were normal. Following tube thoracostomy in the ED, John was admitted for ongoing care.
After discharge, John came in for follow-up. He appeared well but was referred to pulmonology for evaluation. The pulmonologist found that John had returned to his baseline level of functioning and was able to exercise without difficulty or shortness of breath. Since he had no previous significant history, no further pulmonary evaluation was recommended.
In October, John was doing pull-ups when he again felt a sharp left-sided chest pain. He went to the ED with the same symptoms he had in May. His vital signs were also consistent with his previous episode (temperature 97.8°F, BP 115/85, pulse 112, respirations 20, pulse oximetry 98% on room air). Lab results were unremarkable. Two days after another abnormal chest x-ray and a second admission, John underwent left-sided chemical pleurodesis with doxycycline (Vibramycin).
John went back to see the pulmonologist the following month. A chest CT indicated bilateral lower-lobe atelectasis. Some residual scarring on the left was attributed to his recent pleurodesis. Since this procedure was considered curative and expected to prevent any future episodes, John was cleared to resume normal activity.
In January, John’s follow-up CT was without evidence of scarring. The previously present atelectasis and inflammatory changes had resolved. No further episodes were anticipated, but less than a week after this evaluation, John suffered yet another recurrence of left-sided chest pain.
While running, John felt some cramping on his left side. When the cramping began to escalate in intensity, he was hospitalized for the third time at the end of January. A CT indicated small-bleb disease in the apex of his left lung. Three days later, he underwent elective left video-assisted thoracoscopic surgery (VATS) with small-bleb resection and mechanical pleurodesis. The pathology report from his left upper-lobe wedge resection was consistent with bleb disease.
At his most recent pulmonary evaluation in August, John was doing well. He can now run two to three miles without much difficulty. A recent CT revealed some scarring in his left lower lung but was otherwise unremarkable. There was no indication of further blebs or underlying parenchymal disease.
Following thoracoscopy and wedge resection indicating small-bleb disease in the apex of his left lung, John was diagnosed with recurrent primary spontaneous pneumothorax. As opposed to traumatic pneumothoraces, primary spontaneous pneumothoraces are thought to be caused by the rupture of these apical blebs.
Patients typically present with a history of acute chest pain and dyspnea at rest. On physical examination, breath sounds are absent and hyperresonance to percussion is detected on the affected side. John’s initial symptoms and physical examination were consistent with this clinical presentation.
Although smoking and small-airway inflammation are potential causal factors for the formation of apical blebs, John had no history of tobacco use. A personal history of underlying lung disease or medical condition placing John at risk for secondary spontaneous pneumothorax, or a family history of spontaneous pneumothorax, would have placed John at increased risk; neither of these historical factors pertained in this case. And although John’s primary episode of pneumothorax put him at increased risk of recurrence on the same side during his first year, no further management was initially planned.
Therapy for John’s first pneumothorax consisted of tube thoracostomy in the ED. After suffering a second episode five months later, he again underwent tube thoracostomy, followed by chemical pleurodesis with doxycycline. Finally, after John’s third pneumothorax, more definitive treatment was achieved through VATS and mechanical or abrasive pleurodesis.
John’s mechanical pleurodesis appears to have been successful in achieving adequate pleural symphysis. He continues to do well and remains symptom-free at this time.