Infections

Prior to antituberculous medical therapy, TB and its sequelae were the most common cause of massive hemoptysis through various mechanisms: (1) active cavitary disease eroding into adjacent vessels, (2) Rasmussen’s (pulmonary artery) aneurysm eroding into an adjacent cavity, (3) residual bronchiectasis from a prior infection, (4) erosion of a broncholith through a vessel into an airway, and (5) mycetoma formation in a prior cavity.

Bronchiectasis is characterized by abnormal bronchial wall thickening with luminal dilatation that manifests clinically as daily cough with sputum production and airflow obstruction (see Box 79.1 for list of causes). Repeated bacterial infections, particularly with Staphylococcus aureus and Pseudomonas aeruginosa, and chronic airway inflammation are bronchiectasis hallmarks that can lead to enlarged and tortuous bronchial arteries, systemic-pulmonary vascular anastomoses, or parasitized intercostal arteries. Rupture of these vessels can cause rapidly fatal massive hemoptysis.

Fungal infections have become an increasingly common source of massive hemoptysis, particularly in two patient populations: those with preexisting cavitary lung disease and profoundly immunocompromised patients (e.g., hematopoietic stem cell transplantation). Patients with cavitary lung disease can develop intracavitary fungal colonization and mycetoma formation (e.g., aspergilloma). The bronchial and intercostal artery dilation and hypertrophy surrounding these cavities can be dramatic. From 50% to 90% of these patients can have hemoptysis at some course during their disease. Interestingly, massive hemoptysis tends to be uncommon in cases of immunocompromised invasive fungal infections until neutrophil count recovery begins after a prolonged neutropenic period.

Other pulmonary infections can cause massive hemoptysis. Lung abscesses caused by polymicrobial and anaerobic bacteria or necrotizing pneumonias caused by Staphylococcus species, Klebsiella pneumoniae, or Legionella pneumoniae can cause massive hemoptysis. Community-acquired methicillin-resistant S. aureus has been a source of massive hemoptysis resulting from its tendency to cause both parenchymal cavitation and necrosis.

Neoplasms

Any type of bronchogenic carcinoma can cause hemoptysis, which can occur either at presentation (7% to 10 % of cases) or subsequently during the malignancy course (20% of cases). In a large retrospective analysis of more than 800 cases of lung cancer, squamous cell histology was the most frequent cell type associated with massive hemoptysis, followed by adenocarcinoma, small cell carcinoma, and large cell carcinoma. Endobronchial location or cavitation was associated with a higher hemoptysis incidence. New targeted, chemotherapeutic agents (e.g., bevacizumab) with dramatic cavitary responses can predispose to massive hemoptysis.

Any endobronchial or intraparenchymal metastatic tumor to the lung can cause massive hemoptysis. Melanoma, lung, colon, breast, or prostate cancer tends to form endobronchial metastases, whereas renal cell carcinoma, thyroid cancer, and sarcomas tend to form parenchymal metastases that are prone to cause massive hemoptysis.

Cardiovascular Disease

Among the primary cardiac hemoptysis sources (see Box 79.1), elevated pulmonary venous pressure leads to venous dilation and varix formation, which may rupture and bleed during sudden pulmonary venous pressure increases (e.g., systolic or diastolic failure, cough, Valsalva). Such hemoptysis is generally self-limited but can be severe and life threatening on occasion.