A 70-year-old male was treated with conservative management for a minor case of hemoptysis. However, massive hemoptysis (about 500 mL/24 hours) and hypoxemia occurred and the patient deteriorated. The patient had a history of pulmonary tuberculosis about 30 years prior, had suffered from congestive heart failure with arrhythmia for ten years, and had been treated for upper thoracic tuberculous spondylitis with posterior spinal fusion for the last 15 days.

A chest radiograph revealed severe destructive changes of both upper lobes, secondary emphysematous changes of both lower lobes and recent development of bilateral consolidations due to aspirated blood.

Embolization treatment was performed with a 5-Fr catheter and a coaxial 2.5-Fr microcatheter (Renegade; Boston Scientific, Watertown, MA) for both bronchial and other possible systemic arteries with polyvinyl alcohol (PVA) particles, 350-500 µm in diameter (Contour; Boston Scientific, Watertown, MA) and microcoils (Tornado embolization microcoil: Cook, Bloomington, IN). Two days later, the patient suffered massive hemoptysis. No evidence of recanalization of previously embolized arteries on angiography was found and additional embolization of both upper lobar pulmonary arteries was performed, because radiologically undetectable pulmonary artery bleeding was suspected. However, the patient continued to suffer from hemoptysis.

On the third trial of angiography, five hours after the second embolization, coronary angiography showed a CBF (proximal left circumflex arterial branch) from the left circumflex coronary artery to the left bronchial artery combined with a severe pulmonary artery shunt at the left upper lung. The CBF was embolized after superselection across the CBF to prevent embolization of the coronary artery (Fig. 1).

Hemoptysis was stopped immediately after the third embolization but the patient died 12 hours later due to further deterioration of hypoxemia despite intensive ventilator care.

A 57-year-old male arrived at the emergency room due to cardiac arrest. He had a history of diabetes and pneumonia six and two years prior, respectively, and underwent embolization treatment for hemoptysis five days prior and was discharged one day earlier. He was diagnosed with pulmonary and endobronchial tuberculosis and was prescribed medications for tuberculosis.

About one hour before arriving at the emergency room, about 700 mL of hemoptysis occurred. For the first angiography performed five days prior, the right interocostobronchial artery to the left lower lung, aberrant bronchial arteries from the left internal mammary artery supplying the left upper lung, and several left posterior intercostal arteries supplying the left lower lung were successfully embolized with PVA particles.

Computed tomography (CT) showed no enlarged bronchial arteries, and angiography of the descending thoracic aorta and left subclavian artery showed no systemic hypervascularization in either lung. Both coronary angiographies showed a CBF (sinoatrial nodal artery) from the right coronary artery coursing along the left main bronchus (Fig. 2). However, cannulation and embolization of CBF failed due to spastic changes of CBF and tachycardia. Bleeding through the endotracheal tube and hypoxemia persisted despite intensive care resulting in death two days after embolization.

A 68-year-old female experienced four episodes of hemoptysis (more than 400 mL/48 hours). She had a history of pulmonary tuberculosis that was diagnosed about 50 years prior and had underwent embolization of both bronchial arteries and multiple systemic collaterals due to recurrent hemoptysis (seven times) over the five years prior to presentation. Serial chest radiographs and CT showed severe destructive changes with bronchiectasis and cavitary lesions at the left lung.

Because bronchial or systemic arteries causing hemoptysis were not found, right and left coronary angiographies were performed. The coronary angiography revealed two CBFs from both coronary arteries (sinoatrial nodal artery from right coronary artery and distal left circumflex arterial branch) to the left upper and lower lung as well as a massive pulmonary artery shunt (Fig. 3). After careful selection of CBFs as far from the coronary arterial branches as possible with a microcatheter, an embolization was performed with PVA particles and small amounts of Gelfoam particles, resulting in no visible residual hypervascularization or pulmonary artery shunt. The patient was asymptomatic without hemoptysis, but abnormal electrocardiography (EKG) (unusual P axis and short PR, probably junctional tachycardia) and increased cardiac enzyme (serum creatine kinase 375 IU/L, normal range 22-269; creatine kinase-MB 33.0 ng/mL, normal range 0.0-3.4; troponin-I 11.04 ng/mL, normal range 0.0-0.3) were noted the next day. Echocardiography showed normal left ventricular systolic function and EKG was normalized on the sixth day post-embolization. The patient was discharged without any symptoms.