Risk of Pulmonary Embolism in Thyroid Storm
Thyroid storm carries a significant risk of pulmonary embolism and other thromboembolic complications, even in the absence of atrial fibrillation, and prophylactic anticoagulation should be strongly considered in all patients presenting with thyroid storm.
Understanding the Hypercoagulable State
Thyroid storm creates a hypercoagulable state through an imbalance between coagulation and fibrinolytic factors 1. While the established guidelines for thyroid storm management 2 focus on multimodality treatment including beta-blockade, antithyroid drugs, iodide, and corticosteroids, they do not specifically address thromboembolism risk—a critical gap given emerging evidence.
Clinical Evidence of PE Risk
Multiple case reports demonstrate the real-world occurrence of PE in thyroid storm:
Extensive thromboembolism involving splanchnic, iliac, femoral veins, and pulmonary arteries has been documented in thyroid storm patients who were in sinus rhythm throughout, with no personal history of prothrombotic conditions and normal thrombophilia screens 1
The triad of thyroid storm, rhabdomyolysis, and pulmonary embolism has been reported, with submassive PE occurring concurrently 3
Massive pulmonary embolism complicating thyroid storm has been documented 4, and silent PE with deep vein thrombosis has occurred even after initial stabilization 5
Recent data (2025) shows that higher serum FT3 levels are independently associated with greater pulmonary thromboembolic extent in PE patients 6
Key Clinical Pitfalls
Do not wait for atrial fibrillation to consider thromboembolism risk. While atrial fibrillation occurs in up to 40% of thyroid storm patients 4, thromboembolism can occur in its absence 1. The traditional CHADS2 scoring system underestimates risk in thyroid storm—anticoagulation should be considered regardless of CHADS2 score in severe thyrotoxicosis 4.
Do not anchor prematurely on one diagnosis. PE and thyroid storm can be mutually causative and present simultaneously 7. Both conditions cause tachycardia, dyspnea, and hemodynamic instability, making diagnosis challenging.
Practical Management Approach
Immediate Assessment
- Maintain high clinical suspicion for PE in any thyroid storm patient, particularly those with:
- Persistent or worsening dyspnea despite thyroid storm treatment
- Unexplained hypoxemia
- Lower extremity edema developing during hospitalization 5
- Chest pain or hemodynamic deterioration
Anticoagulation Strategy
- Consider prophylactic anticoagulation routinely in thyroid storm patients 1, 4
- If clinical evidence of thrombosis exists, immediately anticoagulate until hyperthyroidism is controlled 4
- Beta-blockers should still be administered even with concurrent PE, provided there is no evidence of right heart strain 7
Monitoring
- Consider lower limb venous ultrasound or contrast-enhanced CT if DVT is suspected 5
- Be aware that thromboembolism can develop days after initial presentation (reported on day 21 in one case) 5
Special Considerations
In severe cases requiring ECMO support, pulmonary thromboembolism can develop despite heparinization 8. The hypercoagulable state persists until definitive thyroid control is achieved, emphasizing the importance of aggressive antithyroid treatment alongside thromboprophylaxis.
The association between hyperthyroidism and thromboembolism is dose-dependent, with TSH and FT4 levels showing significant associations with DVT and PE risk 9. This supports the concept that the severity of thyrotoxicosis directly correlates with thromboembolic risk.