Paradoxical embolism is a clinical scenario in which an embolism arising in the venous system crosses into the arterial circulation where it causes tissue infarction. The most common clinically important site of embolization is the cerebral circulation.
The prevalence of paradoxical embolism is likely under reported due to its difficulty to diagnose. It likely makes up a significant portion of cryptogenic strokes, that is strokes that has no identifiable cause. Cryptogenic strokes represent up to 45% of ischemic strokes. The presence of paradoxical embolism should be considered in these patients.
The presentation of a paradoxical embolism depends on the area of resulting infarction. It is usually indistinguishable from other forms of embolization as the responsible shunts are generally asymptomatic and not diagnosed. Less commonly patient’s may have coexistent hypercoagulable state, deep vein thrombosis or pulmonary embolism.
The common underlying pathology in paradoxical embolism in any right-to-left shunt. The emboli itself is usually a venous thromboembolus, however, emboli consisting of fat, air, amniotic fluid and tumor tissue have been reported.
The main routes of paradoxical emboli include:
- patent foramen ovale: most common
- iatrogenic communication (battle defect, Fontan conduit, Rashkind device)
- other congenital anomalies: atrial spetal defect, ventricular septal defect, unroofed coronary sinus
- pulmonary arteriovenous malformation
- systemic to pulmonary venous shunts
- arterioarterial shunts (patent ductus arteriosus) or venovenous communications
Usually only the resulting arterial occlusion is detected via imaging, which may include:
Radiographic diagnosis of the responsible defect is dependent on the type.
Treatment and prognosis
Treatment can be medical with a combination of anticoagulant and/or antiplatelet therapy. In addition to this percutaneous (e.g. atrial septal occlusion device) or surgical correction of the underling routes of paradoxical embolism can be performed.