Abstract

We present a case of a 36-year old male who was a long-term smoker and was found to have giant bullous emphysema on chest imaging as an accidental finding. At the time, when his first chest CT was obtained, he was asymptomatic and was recommended to consult a pulmonologist but was lost to follow-up for a year until he presented to the emergency department with fever, dyspnea, and chest pain. He was admitted to a pulmonology department. Chest CT was performed and it revealed infected bullae containing air-fluid levels as a complication of community-acquired pneumonia. After successful antibacterial treatment, the patient was discharged and recommended to consult with a thoracic surgeon. A few months later, he had video-assisted thoracoscopic surgery and left upper lobectomy as part of definitive treatment.

Highlights

  • Giant bullous emphysema (GBE), known as vanishing lung disease or type I bullous disease, is defined by giant bullae in one or both upper lobes occupying at least one-third of the hemithorax and compressing the normal surrounding parenchyma [1]

  • Giant bullous emphysema (GBE), referred to as vanishing lung syndrome, is a rare condition that typically presents in young male smokers or α1-antitrypsin deficient (AATD) patients

  • The exact prevalence of vanishing lung syndrome remains unknown as only a small number of case reports and series have been reported

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Summary

Introduction

Giant bullous emphysema (GBE), known as vanishing lung disease or type I bullous disease, is defined by giant bullae in one or both upper lobes occupying at least one-third of the hemithorax and compressing the normal surrounding parenchyma [1]. It is a progressive disease in which the affected regions of the lung do not participate in gas exchange often leading to dyspnea, hypoxia, chest tightness, and spontaneous pneumothorax. Vanishing lung disease can often be asymptomatic, especially in younger patients, and manifests only when complications occur – most commonly infection of bullae or pneumothorax. The development of GBE is associated with smoking, inhaled drug abuse, alpha-1 antitrypsin deficiency, and connective tissue disorders

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