Abstract Introduction Acute pulmonary embolism (PE) is a life-threatening condition caused by obstruction of the pulmonary arteries by thromboemboli. Major complications include right heart failure, pulmonary hypertension, and pulmonary infarction. Parenchymal injury results from distal arterial occlusion, leading to increased bronchial circulatory pressure, erythrocyte extravasation, and subsequent hemorrhagic infarction and necrosis. Although rare, cavitation may occur secondary to infection of infarcted tissue or sterile necrosis. We present a case of acute pulmonary embolism complicated by pulmonary infarction and infectious cavitation. Case Report A 64-year-old female with a history of coronary artery disease, peripheral artery disease, and type 2 diabetes mellitus presented to the emergency department with pleuritic chest pain radiating to the left flank. She was hypoxic with oxygen saturation of 80% on room air. Computed tomography (CT) revealed left lower lobe segmental and subsegmental pulmonary emboli with evidence of right heart strain and evolving pulmonary infarction. Cardiac biomarkers, including troponin and brain natriuretic peptide, were elevated. The patient was started on systemic anticoagulation and improved clinically. However, on hospital day five, she developed worsening hypoxia and hypercapnia, requiring intubation. Repeat CT imaging demonstrated new cavitation within the left lower lobe. A gram stain from a thoracostomy yielded fluid positive for Klebsiella species. Surgical intervention via VATS was deferred due to her comorbidities and poor operative candidacy. Following hemodynamic stabilization, she was extubated and completed a four-week course of intravenous ceftriaxone for Klebsiella pneumoniae pneumonia and empyema. Follow-up imaging showed decreased cavitation volume, and the patient was discharged to short-term rehabilitation with outpatient pulmonary follow-up. Discussion This case demonstrates a rare but serious complication of pulmonary embolism, an infected cavitation secondary to pulmonary infarction. The absence of cavitation on initial imaging supports the hypothesis that tissue infarction from embolic occlusion created a nidus for subsequent Klebsiella infection and necrosis. This case underscores the importance of repeat imaging and clinical suspicion of different etiologies of hypoxia in patients with pulmonary embolism who experience clinical deterioration despite standard therapy. This abstract is funded by: None
Haley et al. (Fri,) studied this question.