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A6569 - Tension Pneumothorax in a Heart Transplant Recipient
Author Block: M. Kwon1, C. A. Keller2, D. Erasmus2, F. Alvarez2, T. Narula2, J. M. Mallea2; 1Pulmonary and Critical Care Medicine, Mayo Clinic Florida, Jacksonville, FL, United States, 2Transplant Pulmonary Medicine, Mayo Clinic Florida, Jacksonville, FL, United States.
Tension pneumothorax is a true emergency requiring immediate intervention to reverse hemodynamic compromise. We describe a case of due to an unexpected cause.
A 55 year-old male presented to the emergency department (ED) due to acute shortness of breath. He had dilated cardiomyopathy and received an orthotropic heart transplant five months prior to his presentation. He was taking tacrolimus, azathioprine, prednisone, inhaled pentamidine, aspirin and propranolol.
He underwent an uneventful, screening right ventricular endomyocardial biopsy via the right internal jugular vein. Pathology showed no evidence of acute rejection. However, since the procedure, he became progressively dyspneic and eventually presented to the ED after five days. He reported dyspnea, non-productive cough and right-sided chest pain. Blood pressure was 87/64, heart rate was 116, and his oxyhemoglobin saturation was 96%. A chest radiograph revealed a large pneumothorax in the right thorax. Hypotension resolved following chest tube placement.
Upon secondary survey, his laboratory tests were unremarkable and blood cultures were negative. A repeat chest radiograph showed a well-expanded lung with a round opacity in the right lung base. Chest CT revealed multiple bilateral cavitary lesions and an air-fluid level in the right pleural space. Upon bronchoscopic exam, purulent secretions were present in the right lower lobe and Nocardia farcinica grew from the bronchial washing culture. The diagnosis of necrotizing pneumonia due to Nocardia farcinica complicated by tension hydropneumothorax was made. Combination treatment with trimethoprim-sulfamethoxazole and amikacin was initiated. A few days later, chest tube was removed and the patient was discharged in stable condition.
Most tension pneumothoraces are noted in patients receiving mechanical ventilation due to positive pressure. However, as in our case, a spontaneously breathing patient can develop a tension pneumothorax if a one-way-valve mechanism prevents the air from leaving the pleural space during expiration. It may take a few days for air pressure to build up to cause symptoms. Iatrogenic pneumothorax is always a concern following an invasive procedure involving the supraclavicular space. Other causes of pneumothorax should also be sought, including cancer or pneumonia secondary to organisms such as Klebsiella or Pneumocystis in an immunosuppressed host. In this case, the cause of hydropneumothorax was Nocardia pneumonia. At the time of this report there are only two other cases of pulmonary nocardiosis presenting as a hydropneumothorax reported in the literature, neither of them had tension physiology.