Hemoptysis is the expectoration of blood from the lower respiratory tract (airways or lungs).^1–6 The expectoration of blood-tinged sputum and mild to moderate hemoptysis should be distinguished from life-threatening, massive hemoptysis.⁴ More than 90% of hemoptysis cases are mild, self-limiting, and have a good prognosis with conservative management.^5,7 However, massive hemoptysis has a mortality rate of greater than 50%.^3,5,6,8

Causes

The differential diagnosis of hemoptysis is broad, with the incidence of various etiologies depending on geographic location and care setting (Table 1^1,3–6,9 and Table 2^10–13). Worldwide, tuberculosis is the most common cause of hemoptysis.² In ambulatory settings of countries without limited resources, hemoptysis is often caused by acute respiratory infections, chronic obstructive pulmonary disease, cancer, and bronchiectasis.^2,10,11 However, 20% to 50% of cases are cryptogenic, with no cause found on computed tomography (CT) or bronchoscopy.^3–5

The etiology of hemoptysis often determines the source of bleeding. In 90% of cases of severe hemoptysis requiring treatment, bleeding is from the bronchial arteries.^4–6 Bleeding from the pulmonary arteries (5%) and nonbronchial systemic arteries (5%) is less common.^4,6 Bronchial arteries supply the intrapulmonary airways and are connected to pulmonary arteries by anastomoses.^4–6 When pulmonary arterial perfusion is impaired (e.g., pulmonary embolism, vasculitis, hypoxic pulmonary vasoconstriction), increases in bronchial arterial flow result in greater flow through the anastomoses, which can hypertrophy, become thin-walled, and break into alveoli and bronchi, causing hemoptysis.^5,6 Bleeding from pulmonary arteries usually results from pseudoaneurysms that are created by erosion of the artery caused by the destruction of nearby pulmonary parenchyma from chronic inflammation (e.g., cancer, tuberculosis, aspergillosis/mycetoma, lung abscess, trauma [e.g., Swan-Ganz catheter placement]).^4,5,8 In inflammatory states, angiogenic growth factors cause neovascularization and recruitment of collateral vessels from nearby nonbronchial systemic arteries, which form anastomoses with the pulmonary arterial circulation that are fragile and can rupture into airways, causing hemoptysis.^5,6,8,14

Initial Evaluation

Massive hemoptysis, previously defined as a specific volume of expectorated blood within a particular amount of time, has transitioned to a more functional definition focused on the effects of the bleeding.^3–6 The definition has shifted because of the difficulty in quantifying the volume of hemoptysis.^1,4 Clinical factors such as the rate of bleeding, the patient's ability to maintain a patent airway (dependent on the rate of blood clearance, internalized bleeding, airway obstruction, and respiratory status), and the patient's physiologic reserve (a function of hemodynamic stability, cardiopulmonary reserve, and risk of recurrent bleeding) are more important than volume.^4,5 The mortality rate from untreated massive hemoptysis is greater than 50%.⁸ The most immediate life-threatening risk is usually asphyxia due to airway obstruction, rather than exsanguination; therefore, any degree of hemoptysis causing cardiovascular collapse should be considered life-threatening.^5,6