B71-19 Necrotic Cavitation Following Pulmonary Infarction: An Uncommon Sequela of Pulmonary Embolism

Abstract Introduction Necrotic Cavitations associated with pulmonary infarction are rare complications of pulmonary embolism. Cavitations occur in 4%-5% of Pulmonary infarctions. These can be aseptic cavitations or superimposed infections following cavitation. Case Presentation 59-year-old male, chronic smoker, presented with a two-week history of productive cough, sputum mixed with blood, fever, shortness of breath and weight loss. Examination revealed decreased air entry to right hemithorax with rhonchi, hypoxia on room air, requiring 15L O2. HIV- negative and Mantoux 0mm. Patient had leucocytosis. Computed Tomography (CT) revealed large wedge-shaped areas of opacification involving the right upper and middle lung lobes with large pleural effusion and lobulated cavitation with septations within the consolidation at the apical aspect; left pulmonary embolism also noted. Pleural fluid and sputum were Polymerase Chain Reaction negative for Mycobacterium Tuberculosis(TB) . No acid-fast Bacilli seen. Culture grew Pseudomonas Aeruginosa and Klebsiella pneumoniae. Culture-directed antibiotics and anticoagulation were commenced. Repeat Imaging showed Bullae, right lung atelectasis and volume loss. Discussion Cavitations usually develop within infarcted lung tissue due to ischemic necrosis, sometimes complicated by secondary infection. Cavities typically are single with upper lobe predilection, often surrounded by consolidation. This involves pulmonary artery vascular occlusion leading to ischemia and coagulative necrosis of lung parenchyma. Over time, necrotic tissue may liquefy and slough, forming a cavity. When bacterial infection supervenes on the infarcted region, the necrotic process accelerates. In this patient, clinical presentation and imaging were consistent with pulmonary infarction. Detection of Pseudomonas aeruginosa and Klebsiella pneumoniae in sputum culture indicates secondary infection of infarcted lung tissue, likely contributing to cavitation. The exudative pleural effusion with negative TB studies further supports non-tuberculous infection. Pulmonary infarction-associated cavitation can lead to complications such as pleural effusion, empyema, pneumothorax, or bronchopleural fistula. In this case, subsequent imaging showed bullous changes, right lung atelectasis and volume loss, findings that may reflect post-infective and post-infarction sequelae. Prompt recognition of this entity is crucial, as the management differs from that of other cavitary lung diseases such as tuberculosis or abscesses of purely infectious origin. Treatment involves addressing both the thromboembolic event with anticoagulation and the secondary infection with appropriate antibiotics. Conclusion Cavitating pulmonary infarction is an uncommon but important complication of pulmonary embolism. Secondary bacterial infection of infarcted lung tissue can exacerbate necrosis, leading to cavitation and further pulmonary compromise. Early identification through imaging, coupled with appropriate anticoagulation and culture-directed antibiotic therapy, is essential for improving outcomes. This abstract is funded by: None