Key result
Enoxaparin stabilizes recurrent pulmonary embolism in a patient with underrecognized obstructive sleep apnea.
Why the study?
While established risk factors for pulmonary embolism are well known, many cases are unprovoked and carry a high risk of recurrence.
Case Report (n=1)
This case highlights the limitations of point-of-care ultrasound and biomarkers in diagnosing recurrent pulmonary embolism, emphasizing the importance of multimodal imaging and addressing underrecognized risk factors like sleep apnea and occupational strain.
Introduction Pulmonary embolism (PE) is a life-threatening condition with diverse presentations. While established risk factors such as surgery, malignancy, immobility, and thrombophilia are well known, many cases are unprovoked and carry a high risk of recurrence. Case Report A 37-year-old man presented with pleuritic chest pain similar to prior PE episodes (2017, 2018, 2020). Despite being advised to continue lifelong anticoagulation, he admitted to non-adherence. His history included obstructive sleep apnea (on continuous positive airway pressure), glucose-6-phosphate dehydrogenase deficiency, patent foramen ovale (PFO), and a 15-year history of tobacco use. On examination, he was tachycardic, tachypneic, and hypoxic (oxygen saturation 94% on 2L nasal cannula). Electrocardiogram revealed an S wave in lead I and inverted T wave in lead III. Computed tomography pulmonary angiography confirmed acute segmental emboli in the right upper/lower lobes and left lower lobe, with chronic filling defects and right ventricular strain. Echocardiography showed hyperdynamic left ventricular function (ejection fraction >70%), with a dilated left atrium, and interatrial septal aneurysm. Right ventricular size and function were normal. Point-of-care ultrasound showed no right ventricular strain or septal bowing. Laboratory studies, including cardiac biomarkers, were unremarkable. He was started on enoxaparin and stabilized. Discussion This case highlights underrecognized venous thromboembolism (VTE) risk factors, such as obstructive sleep apnea (OSA) and effort-related thoracic outlet thrombosis (Paget-Schroetter syndrome, PSS), where occupational upper limb strain may cause vascular compression, implicated in PSS and potentially contributing to systemic VTE. Structural anomalies like a patent foramen ovale (PFO) and left atrial dilation may facilitate embolic transit. The notable discrepancy between point-of-care ultrasound (POCUS) and CT findings underscores the limitations of bedside tools and emphasizes the need for a multimodal approach in diagnosing pulmonary embolism (PE). This case serves as a critical reminder that the absence of overt deep vein thrombosis (DVT), negative biomarkers, or reassuring POCUS results does not exclude significant PE, particularly in patients with prior PE, known anatomic vulnerabilities (e.g., PFO), or underrecognized risk factors such as OSA and occupational strain. Furthermore, it highlights the ongoing challenge of ensuring adherence to anticoagulant therapy, especially in young adults less inclined to accept lifelong treatment, particularly when asymptomatic. Structured patient education, follow-up, and joint decision-making are essential to improving long-term outcomes. The integration of various diagnostic modalities, including risk stratification, biomarkers, imaging, and clinical assessment, remains central to providing high-quality care for PE. This abstract is funded by: None
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Tayyab et al. (2026) conducted a case report in Pulmonary embolism (n=1). Enoxaparin was evaluated. A 37-year-old man with recurrent pulmonary embolism and underrecognized risk factors, including obstructive sleep apnea, was successfully stabilized with enoxaparin.
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