What is the pathogenesis of hemoptysis in pulmonary tuberculosis?

Pathogenesis of Hemoptysis in Pulmonary Tuberculosis

Hemoptysis in pulmonary tuberculosis results primarily from erosion of hypertrophied bronchial arteries and, less commonly, from pulmonary artery pseudoaneurysms (Rasmussen aneurysms), with the fundamental mechanism being inflammatory destruction of vessel walls within or adjacent to tuberculous cavities. 1, 2

Primary Vascular Mechanisms

Bronchial Artery Hypertrophy and Erosion

• Over 90% of TB-related hemoptysis originates from the systemic bronchial arterial circulation, not the pulmonary arteries, due to marked proliferation and hypertrophy of bronchial vessels in response to chronic inflammation 3, 4
• The inflammatory process causes direct erosion of bronchial artery walls as tuberculous granulomas and cavities expand, leading to vessel rupture into airways 5, 6
• Chronic inflammation triggers neovascularization with formation of fragile, tortuous bronchial arteries that are prone to bleeding 3, 1

Pulmonary Artery Involvement (Rasmussen Aneurysm)

• Rasmussen aneurysms are pulmonary artery pseudoaneurysms that develop when tuberculous cavities directly erode into adjacent pulmonary artery branches, creating a false aneurysm within the cavity wall 2, 7
• These pseudoaneurysms occur in approximately 5% of cavitary TB cases but carry extremely high mortality when they rupture, causing massive hemoptysis 2, 7
• The pulmonary arterial source accounts for 8-10% of massive hemoptysis cases in TB patients 3

Structural Lung Damage Mechanisms

Active Disease

• Cavitary infiltration creates direct communication between eroded vessels and airways, with the cavity serving as both the site of vessel destruction and the conduit for blood expectoration 5
• Necrotizing granulomatous inflammation weakens vessel walls through direct mycobacterial invasion and immune-mediated arteritis 6

Post-TB Sequelae (Chronic Mechanisms)

• Bronchiectasis from chronic inflammation persists decades after microbiologic cure, with permanently dilated airways containing hypertrophied bronchial arteries that remain prone to bleeding 1, 8
• Aspergilloma formation in residual TB cavities causes recurrent hemoptysis through mechanical friction and local vascular erosion, with a 55% recurrence rate after initial embolization 3, 8
• Broncholithiasis (calcified lymph nodes eroding into airways) creates focal bronchiectasis and vascular injury 1
• Destroyed lung architecture with extensive fibrosis distorts normal vascular anatomy, creating arteriovenous malformations 1

Geographic and Epidemiologic Context

• In endemic regions (Asia, Africa, Middle East), TB accounts for 55-74% of all massive hemoptysis cases, making it the dominant etiology 1, 8
• Studies from China show 55-100% of hemoptysis cases related to active or sequelae TB, while Indian series report 74% 8

Critical Pathophysiologic Distinction

• The primary cause of death is asphyxiation from airway obstruction by blood clots, not exsanguination, as patients "drown" in their own blood when rapid bleeding overwhelms airway clearance mechanisms 1, 4
• The rate of bleeding is more critical than total volume—rapid hemorrhage prevents effective coughing and airway clearance even with modest blood loss 4

Common Pitfalls

• Do not assume hemoptysis only occurs during active TB—post-TB structural changes cause bleeding decades after microbiologic cure through bronchiectasis, aspergillomas, and destroyed lung 8
• Always consider Rasmussen aneurysm in cavitary TB with massive hemoptysis, as this requires pulmonary artery embolization rather than bronchial artery embolization alone 2, 7
• Contrast-enhanced chest CT is essential to differentiate bronchial from pulmonary arterial sources and to exclude aorto-bronchial fistula in patients with thoracic aortic disease 1