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Updated: Sep 30, 2025

A Porcine Model of Acute Autologous Pulmonary Embolism
Published on: September 6, 2024
Acute neurological deficit with submassive pulmonary emboli
Adam Calthrop1, Asad Shabbir2, Michael Raffles2
1Royal Berkshire NHS Foundation Trust, Reading, UK adam.calthrop@nhs.net.
A high-risk pulmonary embolism (PE) case presented with collapse and unresponsiveness despite normal hemodynamics. This was due to a paradoxical embolism through a patent foramen ovale, causing cerebral infarction.
Area of Science:
- Cardiology
- Neurology
- Emergency Medicine
Background:
- Pulmonary embolism (PE) is a common emergency department diagnosis.
- Syncope in PE can indicate impending hemodynamic collapse and increased mortality.
- Neurological deficits in thromboembolic disease can arise from causes beyond cerebral hypoperfusion.
Observation:
- A woman in her 60s presented with high-risk PE features.
- She collapsed and became unresponsive (Glasgow Coma Scale 4/15) despite stable hemodynamics.
- Neurological signs and CT confirmed a large cerebral infarction.
Findings:
- The patient had a large territory cerebral infarction.
- Cardiovascular investigations revealed a grade 4 patent foramen ovale.
- The clinical presentation was attributed to a paradoxical embolism complicating venous thromboembolism.
Implications:
- This case highlights the importance of considering paradoxical embolism in PE patients with neurological deficits.
- Thorough clinical examination and investigation are crucial for diagnosing complex presentations.
- Effective management strategies for venous thromboembolism with paradoxical embolism require further evidence-based discussion.
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