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a Fluminense Federal University, Rua Marquês do Paraná, 303 Centro, Niterói, CEP 24110.000, Rio de Janeiro, Brazil
b The Cardiothoracic Centre-Liverpool NHS Trust, and The Royal Liverpool, University Hospital, Thomas Drive, L14 3PE, Liverpool, Merseyside, UK
(Email: edmarchiori{at}gmail.com).
We read with great interest the case reported by Caceres and colleagues [1], which described a drug user who presented with spontaneous pneumothorax and diffuse cavitary pulmonary nodules.
The report described the patient with productive cough, dyspnea, fever and chills, and a past medical history of tibial osteomyelitis. A computed tomographic scan (CT) of the chest revealed multiple cavitary nodules. The patient was treated with intravenous antibiotics for a presumed community-acquired pneumonia, and 4 days later tension pneumothorax developed. A second CT scan performed 1 month later revealed pleural effusion and persistent cavitary pulmonary lesions. Biopsy showed multiple noncaseating granulomas and bi-refringent particles in the lung parenchyma, consistent with talc. Cultures of the pleural fluid were negative. The patient then admitted to intravenous use of methadone. A subsequent CT scan of the chest at 2 months postoperatively revealed only residual pleural scarring and re-expansion of the left lung.
The authors attributed the cavitary nodules to talcosis and assumed it was an unusual case of talc-induced pulmonary granulomatosis presenting with unique radiographic findings, consisting of multiple subpleural pulmonary cavitary lesions associated with pneumothorax.
However, this case shows some peculiarities that we would like to discuss. The involution of the nodular lesions, according to the CT performed 2 months later that showed only residual pleural scarring, seems strange to us. The biopsy findings were described as granulomas with talc, which would not explain the development of reversible cavitary nodules. Actually, intravenous talc granulomatous disease of the lung causes an irreversible pulmonary disease with the development of fibrosis, which is sometimes fatal, even when drug use is discontinued [1–3].
For this reason, septic pulmonary embolization, which is a complication described in intravenous drug users, should also be considered in the differential diagnosis. A CT characteristically shows multiple ill-defined, peripherally distributed lung nodules in various phases of cavitation [3, 4], which is very similar to the aspect observed in this case.
Nonsterile injection techniques may cause bacteremia, which predisposes to tricuspid valve endocarditis. Infective endocarditis has been the major cause of morbidity and mortality among intravenous drug users with infections, mostly involving the tricuspid valve. The responsible pathogen, in most cases, is Staphylococcus aureus. Pulmonary complications of septic pulmonary embolism include pulmonary infarction, pulmonary abscess, pleural effusion, empyema, and spontaneous pneumothorax. The last is believed to be due to rupture of the subpleural lesions [3–5].
As previously described, the patient had clinical signs of infection with fever and chills, and also had a past medical history of tibial osteomyelitis. He was treated with intravenous antibiotics (which types were not cited by the authors). Likewise, results of laboratory tests (complete blood count, erythrocyte sedimentation rate, C-reactive protein, and blood cultures) and echocardiography (for the detection of valvular vegetations) were not described. Although cultures were negative, the absence of growth of microorganisms in pleural fluid cultures was described in half of the cases [4]. For this reason, the diagnosis of septic embolism must be convincingly discarded before attributing such particular aspect (ie, reversible cavitary nodules) to pulmonary talcosis.
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  M. Caceres and H. Garrett Jr Reply Ann. Thorac. Surg., July 1, 2010; 90(1): 363 - 363. [Full Text] [PDF]
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