Hemoptysis is the expectoration of blood from the lungs or tracheobronchial tree. Severity ranges from mild to severe, and it can be difficult to stop. The challenge is to stabilize the patient while simultaneously determining the source and providing treatment. Most cases of hemoptysis are mild and resolve spontaneously; predicting which individual will develop large-volume bleeding is difficult. Determining the cause, location, and extent of hemoptysis requires a multidisciplinary approach.¹

Assessing the amount of expectorated blood is difficult, because patients may either exaggerate or be unable to quantify the amount. The definition of “massive” or “severe” hemoptysis varies, with reported ranges from 100 mL per 24 hours to >1000 mL per 24 hours,^2,3 with a midpoint value of 600 mL per 24 hours accepted by many.⁴ However, because even small volumes of blood can cause asphyxiation, any hemoptysis requires prompt attention.⁵ Morbidity and mortality depend on the rate of bleeding, the ability of the patient to clear the blood, and the presence of underlying lung disease, which potentiates the effects of blood in the airways. We define “minor” hemoptysis as small-volume expectoration of blood in a patient with no comorbid lung disease, normal/stable oxygenation and ventilation, normal vital signs, and no risk factors for continued bleeding.

Hemoptysis results from disruption of blood vessels within the walls of the airways, from trachea to bronchi, bronchioles, and the lung parenchyma (Table 63-1). The pulmonary arteries account for 99% of the arterial blood flow to the lungs but are a low-pressure system and rarely the source of hemoptysis. The bronchial circulation accounts for only about 1% of the arterial blood flow to the lungs but 90% of the cases of hemoptysis because it is a high-pressure system.⁶ The bronchial arteries typically branch off the thoracic aorta and are responsible for supplying oxygenated blood to the bronchi, pulmonary arteries and veins, and lung parenchyma. They follow the course of bronchi along their tortuous paths. Once the bronchial arteries reach the level of capillaries, three anastomoses occur: the larger bronchial arteries can merge directly with the alveolar microvasculature; the smaller bronchial arteries can merge with the veins of the pleural and pulmonary drainage system; and bronchial capillaries can merge directly with pulmonary capillaries.⁷ These connections produce a physiological right-to-left shunt comprising 5% of the total cardiac output.

Many inflammatory and infectious processes can lead to hemoptysis. Coughing in the setting of transient airway inflammation (e.g., acute bronchitis) can lead to minor bleeding even in otherwise healthy lungs. In chronic inflammatory states like tuberculosis, cystic fibrosis, or chronic obstructive pulmonary disease (COPD), the bronchial arteries can proliferate and enlarge to enhance the delivery of blood to the alveoli. Such neoangiogenesis creates thin-walled, fragile vessels prone to rupture. Chronic disease states can lead to bronchiectasis (chronic bronchial wall inflammation), resulting in dilatation and destruction of the cartilaginous support, predisposing blood vessels to rupture. In the case of Aspergillus infection, there can be necrotic destruction of tissue, but more often there is a colonization of a previous area of pulmonary decay, resulting in cavitary fungal balls. Neoangiogenesis from bronchial artery branches occurs in the cavity walls.⁵ A Rasmussen’s aneurysm is a false aneurysm of dilated, tortuous branches of pulmonary arteries crossing the wall of a tuberculosis cavity. Although tumors can directly invade the bronchial and pulmonary arteries, they also promote neoangiogenesis. In particular, squamous cell carcinoma accounts for a large number of cases of massive hemoptysis.⁵

Traumatic causes of hemoptysis include deceleration injuries and penetrating trauma to the chest. Iatrogenic causes include direct arterial injury by pulmonary artery catheterization or biopsy of lung tissue during bronchoscopy. Biopsy of a carcinoid tumor can be associated with impressive hemoptysis.⁵

Hemoptysis secondary to fistulae between an aortic aneurysm or aortic inflammation and its primary branches can precipitate catastrophic hemoptysis. Tracheo-innominate fistulae result from erosion of a tracheostomy into the innominate artery that courses posterior to the upper sternum.

Arteriovenous fistulas forming between the low-pressure pulmonary arteries and pulmonary veins have thin walls that are easily ruptured. Osler-Weber-Rendu disease is associated with hemorrhagic telangiectasias of pulmonary arteriovenous fistulas as well as telangiectasias of the skin or mucous membranes.

Cardiac disease processes that elevate pulmonary pressure, such as mitral stenosis and congenital heart disease, can trigger hemoptysis. Distal pulmonary embolism can lead to infarction of lung tissue that results in edema and hemorrhage, which can be exacerbated by the use of anticoagulants.

Vasculitis and collagen vascular diseases such as Goodpasture’s syndrome, systemic lupus erythematosus, and granulomatosis with polyangiitis (formerly Wegener’s granulomatosis) damage the lung parenchyma predisposing to alveolar hemorrhage. Anemia can result from chronic diffuse alveolar hemorrhage.⁹