Makindo Medical Notes

Related Subjects: |Acute Stroke Assessment (ROSIER&NIHSS) |Atrial Fibrillation |Atrial Myxoma |Causes of Stroke |Ischaemic Stroke |Cancer and Stroke |Cardioembolic stroke |CT Basics for Stroke |Endocarditis and Stroke |Haemorrhagic Stroke |Stroke Thrombolysis |Hyperacute Stroke Care

Introduction

Paradoxical embolism refers to the passage of embolic material, typically a thrombus (blood clot), from the venous circulation into the arterial system, bypassing the filtering mechanism of the pulmonary capillary bed. This occurs through a right-to-left cardiac or pulmonary shunt, allowing emboli from the systemic veins to enter the arterial circulation and potentially cause ischemic events such as stroke or systemic embolism.

Etiology

The pulmonary circulation normally filters out small thrombi from the venous system, preventing them from entering the systemic arterial circulation. Paradoxical embolism occurs when a right-to-left shunt permits emboli to bypass the lungs. Common anatomical defects that facilitate this include intracardiac communications such as patent foramen ovale (PFO), atrial septal defect (ASD), ventricular septal defect (VSD), or pulmonary arteriovenous malformations (AVMs). Conditions that increase right atrial pressure, such as pulmonary hypertension or Valsalva maneuvers, can promote right-to-left shunting.

Pathophysiology

For a paradoxical embolus to occur, three key factors are typically present:

• Source of Emboli: Usually deep vein thrombosis (DVT) in the lower extremities or pelvis.
• Right-to-Left Shunt: An anatomical defect allowing emboli to bypass the pulmonary circulation.
• Pressure Gradient Favoring Shunt: Increased right atrial pressure compared to left atrial pressure, which can occur transiently during activities like coughing, sneezing, or straining.

Common Causes of Right-to-Left Shunt

Clinical Presentation

• Ischemic Stroke: Sudden neurological deficits due to cerebral arterial occlusion.
• Transient Ischemic Attack (TIA): Temporary neurological symptoms resolving within 24 hours.
• Peripheral Arterial Embolism: Acute limb ischaemia with pain, pallor, and pulselessness.
• Myocardial Infarction: Rarely, emboli can occlude coronary arteries.
• Multisystem Emboli: Simultaneous embolic events in different organs.

Symptoms may be precipitated by activities that increase right atrial pressure, such as Valsalva maneuvers, coughing, or heavy lifting.

Investigations

• Blood Tests: Complete blood count (FBC), electrolytes (U&E), erythrocyte sedimentation rate (ESR), liver function tests (LFTs), coagulation profile.
• Electrocardiogram (ECG): To assess for arrhythmias like atrial fibrillation (AF); right bundle branch block (RBBB) and right-axis deviation may suggest ASD.
• Chest X-Ray (CXR): May reveal signs of pulmonary AVMs or cardiomegaly.
• Neuroimaging:
  • Computed Tomography (CT) Scan: Identifies areas of cerebral infarction.
  • Magnetic Resonance Imaging (MRI): More sensitive for detecting acute infarcts; multiple territory infarcts raise suspicion for embolic source.
• Computed Tomography Pulmonary Angiography (CTPA): Useful in detecting pulmonary AVMs or pulmonary embolism.
• Echocardiography:
  • Transthoracic Echocardiogram (TTE): Initial assessment of cardiac structure; may detect large defects.
  • Transesophageal Echocardiogram (TEE): Provides better visualization of interatrial septum and small shunts.
  • Bubble Study: Injection of agitated saline during echocardiography to detect right-to-left shunt; appearance of microbubbles in the left atrium indicates a shunt.
• Doppler Ultrasound of Lower Extremities: To identify DVT as a source of emboli.
• Transcranial Doppler Ultrasound with Bubble Study: Non-invasive method to detect intracardiac shunts by monitoring cerebral vessels for microbubbles.
• Coagulation Studies: To assess for hypercoagulable states (e.g., antiphospholipid syndrome, factor V Leiden mutation).

Evidence For and Against Paradoxical Embolism

Certain clinical and radiological findings may support or argue against the diagnosis of paradoxical embolism.

Evidence For Paradoxical Embolism

• Multiple territory infarcts on neuroimaging.
• Concurrent DVT or pulmonary embolism (PE).
• Positive findings on echocardiography indicating a right-to-left shunt.
• Sudden onset of neurological deficits, especially after Valsalva maneuver.
• Presence of prothrombotic conditions.

Evidence Against Paradoxical Embolism

• Identifiable alternative causes of stroke (e.g., atrial fibrillation).
• Stereotypical or recurrent stroke symptoms in the same vascular territory.
• Lack of right-to-left shunt on echocardiography.
• No evidence of DVT or hypercoagulable state.
• Single territory infarcts consistent with large artery atherosclerosis.

Management

Treatment focuses on preventing further embolic events by addressing both the source of emboli and the shunt:

• Antithrombotic Therapy:
  • Anticoagulation: Use of heparin followed by warfarin or direct oral anticoagulants (DOACs) to prevent thrombus formation, especially in the presence of DVT.
  • Antiplatelet Agents: May be used in certain cases but less effective than anticoagulation for venous thromboembolism.
• Interventional Procedures:
  • PFO/ASD Closure: Percutaneous device closure can reduce the risk of recurrent stroke in selected patients.
  • Surgical Repair: Indicated for certain congenital heart defects not amenable to percutaneous intervention.
  • Pulmonary AVM Embolization: Transcatheter occlusion of AVMs to eliminate shunt.
• Management of DVT/PE:
  • Early mobilization, compression stockings, and pharmacological prophylaxis in at-risk patients.
  • Thrombolytic therapy may be considered in massive PE.
• Risk Factor Modification:
  • Smoking cessation, weight management, and control of hypertension and diabetes.
• Patient Education:
  • Avoidance of activities that increase intrathoracic pressure unless medically supervised.
  • Awareness of symptoms of DVT and stroke for prompt medical attention.

Prognosis

The risk of recurrent paradoxical embolism is significant, especially if the underlying shunt and source of emboli are not addressed. Appropriate intervention can substantially reduce the risk of recurrence and improve outcomes.

References

• Alsheikh-Ali AA, Thaler DE, Kent DM. Patent foramen ovale in cryptogenic stroke: incidental or pathogenic? Stroke. 2009;40(7):2349-2355.
• Overell JR, Bone I, Lees KR. Interatrial septal abnormalities and stroke: a meta-analysis of case-control studies. Neurology. 2000;55(8):1172-1179.
• Mojadidi MK, Zaman MO, Elgendy IY, et al. Cryptogenic Stroke and Patent Foramen Ovale. J Am Coll Cardiol. 2018;71(9):1035-1043.
• Rodés-Cabau J, Masson JB, Bernier M, et al. Device closure of patent foramen ovale in patients with paradoxical embolism: immediate and long-term results. J Am Coll Cardiol. 2009;53(21):201-208.
• Thompson RD, Hilpert PL, Warshauer DM. Pulmonary arteriovenous malformations: diagnosis with contrast-enhanced thoracic CT. Radiology. 1999;210(1):18-23.
• Kasner SE, Swaminathan B, Lavados P, et al. Rivaroxaban or Aspirin for Patent Foramen Ovale and Embolic Stroke of Undetermined Source. Stroke. 2021;52(1):561-568.