Abstract Background Massive hemoptysis, defined as expectoration of more than 150 mL of blood within 24 hours, is a life-threatening event requiring rapid, multidisciplinary management. In lung cancer, bleeding often results from tumor invasion or vascular erosion. Inhaled tranexamic acid (TXA) is increasingly used as adjunctive therapy, yet data on its efficacy and safety in massive hemoptysis remain limited. We report a case of EGFR-mutant lung adenocarcinoma on osimertinib presenting with massive hemoptysis complicated by endobronchial clot formation following inhaled TXA administration, successfully managed with therapeutic bronchoscopy, endobronchial blockade, and bronchial artery embolization (BAE) followed by palliative radiation therapy. Case A 71-year-old woman with EGFR-positive lung adenocarcinoma on osimertinib presented with acute onset bright-red hemoptysis (∼500-1000 mL). She had no smoking history, anticoagulant use, or infection. Initially stable, she developed progressive respiratory distress. Nebulized TXA was administered for hemostasis, and she was intubated for airway protection. Hours later, ventilation became difficult with low tidal volumes. Bronchoscopy revealed a large clot obstructing the carina, which was removed with rapid improvement in tidal volumes. A right endobronchial blocker was placed. BAE was performed the next morning. Selective angiography showed a right perihilar tumoral blush with venous pooling (Figure 1); the culprit branch was embolized. Follow-up bronchoscopy demonstrated no active bleeding, allowing blocker removal and extubation. She subsequently underwent palliative radiotherapy directed at the primary tumor and remained stable without recurrent hemoptysis. Discussion In lung cancer, hemoptysis arises from tumor invasion, diffuse alveolar hemorrhage, or rarely from therapy-related effects. EGFR-mutant tumors exhibit enhanced angiogenesis via vascular endothelial growth factor (VEGF) and transforming growth factor-alpha (TGF-α), creating fragile vascular networks prone to bleeding. Although TXA stabilizes fibrin clots and may reduce bleeding duration, it can also promote rapid endobronchial clot formation, risking airway obstruction and ventilatory failure, as seen in this case. TXA should therefore be used cautiously when large-vessel bleeding or heavy clot burden is suspected. Emerging evidence also suggests a possible link between EGFR tyrosine kinase inhibitors (TKIs) and bleeding, though further research is needed to clarify this relationship. Conclusion This case highlights the complex interplay between EGFR-mutant tumor biology, targeted therapy, and airway management in massive hemoptysis. While TXA may assist in hemostasis, it carries a potential risk of airway obstruction. BAE combined with radiotherapy remains an effective, durable hemostatic strategy in malignancy-related hemoptysis. This abstract is funded by: None
Chilamkurthy et al. (Fri,) studied this question.