A 36-year-old male patient initially presented to a primary health clinic (PHC) with acute onset of dyspnea and left-sided pleuritic chest pain. The pain was severe enough to wake him from sleep. On initial presentation to the PHC, he was discharged with symptomatic treatment. The patient revisited the PHC after 12 hours with worsening symptoms. Chest x-ray (CXR) was performed at this point which revealed a large pneumothorax with minimal pleural effusion (Figure 1). He was then referred to the ED for further treatment. On arrival at the ED, on initial triage, his vital signs were recorded as a BP of 115/71 mm Hg and an oral temperature of 36.0 C. A regular pulse rate of 153 beats/min, respiratory rate of 28 breaths/min, oxygen saturations of 100% on room air and visual analogue pain score of 30/100 were recorded.
The patient's presenting complaint was progressively worsening breathlessness for a month. He presumed that it was due to his asthma symptoms and kept using bronchodilator inhalers he had previously been prescribed. He didn't seek any medical advice until his symptoms worsened and he no longer responded to the inhaled bronchodilator. He reported 5 kg weight loss in the last two years. He had no history of hemoptysis, cough, fever or night sweats. He reported no history of exposure to pulmonary tuberculosis or any recent trauma. He was a smoker of one pack a day for 20 years and asthmatic for 2 years. He denied any other past medical history.
On physical examination, the patient had diminished air entry on the left side of his chest with hyperresonance to percussion. In the emergency room, while the patient was being managed by an emergency physician, he became distressed and dyspneic. His respiratory rate increased to 50 breaths/min and blood pressure dropped to 88/62 mm Hg. He was sweating profusely. Bedside ultrasound was performed which confirmed features of left-sided pneumothorax with a small amount of fluid in left costophrenic angle. The CXR from the PHC was reviewed, and given the deterioration in the patient's clinical condition, a diagnosis of tension pneumothorax was made. Immediate needle decompression was performed by identifying the landmarks in the second intercostal space in the midclavicular line using a 14G needle which later was connected to a three-way tap with a 50 cc syringe. Following this, the patient improved hemodynamically as well symptomatically. Post-procedure, the observations were recorded as the following: pulse 115 beats/min, BP 110/80 mm Hg, RR 38 breaths/min and an O2 saturation of 100%.
CXR was repeated post-needle decompression (Figure 2), which showed a smaller pneumothorax and an increase in the size of the effusion compared to the first CXR from the PHC (Figure 1). An acute increase in the size of the effusion could be explained by an iatrogenic hemothorax created whilst attempting a needle decompression. At this point, a chest tube was inserted which immediately drained 1.4 liters of blood, suggesting an iatrogenic hemothorax (Figure 3). The patient was admitted to the medical ward as a case of tension pneumothorax and hemothorax for further evaluation and management.
Blood examination showed leukocytosis with a white blood cell (WBC) count of 21.6 x 103 mul (83.5% neutrophils), hematocrit of 29.1%, MCH of 30 picograms/cell, platelets of 202/microliter and anemia (Hb 7.7 g/dl). The patient received antibiotics and blood transfusion respectively. The erythrocyte sedimentation rate was 36 mm/hour and the CRP was 52 mg/L. Pleural fluid analysis showed glucose of 2.6 mmol/L, LDH of 177 U/L, total protein of 55 g/L, a pH of 7.170 and adenosine deaminase in the pleural fluid of 47 IU/L which was high. The pleural fluid appearance was bloody, with a WBC of 7500/microliter, neutrophils 80% and lymphocytes 20% and a RBC of 3570000/microliter. The aspirated pleural fluid was sent for biochemical analysis. The low pH pleural fluid and presence of effusion before needle decompression on initial CXR (Figure 1) indicated a presence of initial empyema. This may have mixed with the iatrogenic hemothorax. Pleural fluid cultures were negative for bacteria, fungi and mycobacteria. Two of three sputum samples showed positive culture for mycobacterium other than tuberculosis, indicating NTM infection. Blood cultures were negative and HIV serology tested negative for the patient.
CT scan was requested post-chest tube insertion, which revealed consolidation in the left lower lung lobe, atelectasis changes in the posterior segment of the left upper lung lobe, a trace of pleural effusion and an air-bronchogram in the left lower lobe (Figure 4). Pleural biopsy revealed skeletal muscle and fibrous tissue with mild chronic inflammation. Zeilh-Neelsen stain for acid-fast bacilli was negative and no definite granuloma was appreciated. Chest tube was removed after one week and the patient improved clinically. The patient was discharged on isoniazid and rifampicin home treatment. Follow up chest x-rays revealed a reduction in pleural effusion, adhesions in the left costophrenic angle as well as a nodular opacity 7 x 6 mm in size above the upper pole of the right hilum.