A 59-year-old male presented to our hospital with progressive dyspnea, productive cough, and hemoptysis of 2 weeks duration. Three days prior to admission his history was significant for massive hemoptysis, averaging 200-500 mL of gross blood daily. However, there was no evidence of chest pain, fever, night sweats, weight loss, recent travel, or contact with the sick, nor was there any other bleeding noted. His past medical history was significant for asthma and 30 years of smoking. He was also treated for active pulmonary tuberculosis 7 years ago. He had one similar episode of hemoptysis 1 year prior to this admission, but declined full work-up and failed to follow up after discharge.
Upon presentation, his vital signs were within normal limits, with a respiratory rate of 20 cycles/minute and oxygen saturation of 96% on room air. The lungs were clear to both percussion and auscultation, except for a decreased breath sound at the left upper lobe apex. Other findings on physical examination were within normal limits. Laboratory results were as follows: hemoglobin, 11.2 g/dL; hematocrit, 33.1 g/dL; white blood cell count, 5.7 x 109/L; and a normal differential count. Basic metabolic profile, liver chemistry, and coagulation parameters were all within normal limits. A chest radiograph revealed hyperinflation, bilateral nodularity, pleural thickening with fibrocystic changes in the left apex and a possible cavitary lesion. Further work-up with a chest computed tomogram (Figure 1) revealed irregular speculated density, representing a cavitary lesion filled with mycetoma (fungal ball), numerous nodules scattered throughout both lungs and extensive bullous disease, especially at the left upper lobe. Sputum staining for acid-fast organisms was negative, but Haemophilus parainfluenzae was grown on culture media. Left upper lung biopsy revealed CPAM type 1 with aspergilloma (Figures 2 and 3). The Periodic acid-Schiff and Grocott's methenamine silver stains showed tightly packed septate hyphae. He was started on itraconazole and ceftriaxone. Due to persistent massive hemoptysis, he was referred for bronchial artery angiography and embolization. The bronchial arteriogram showed neovascularity supplying the inflammatory changes within both apices of the lungs, which were successfully embolized. Subsequently, he had some improvement of the cough and hemoptysis; however, 2 days after the embolization, massive hemoptysis recurred, which necessitated emergency surgical intervention. He had a left upper lobectomy. Intraoperatively, he developed diffuse oozing from the dissected surfaces, leading to hemodynamic instability and disseminated intravascular coagulopathy. Every effort to resuscitate him including massive transfusion of blood products was futile. He died from hemorrhagic shock secondary to left lobectomy.