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Dilemmas in dealing with the blue toe syndrome: aortic versus peripheral source
Insights
Peripheral atherosclerotic lesions are the primary source of blue toe syndrome emboli. Exploring these distal lesions first in patients with aortoiliac disease leads to effective treatment with minimal complications.
Area of Science:
- Vascular Surgery
- Cardiovascular Medicine
- Interventional Cardiology
Background:
- Blue toe syndrome presents a diagnostic challenge in identifying the source of emboli.
- Distinguishing between central aortic and peripheral embolization is crucial for effective treatment.
Observation:
- Six patients with unilateral blue toe syndrome were evaluated.
- Two patients had moderate aortoiliac atherosclerosis with superficial femoral artery stenoses.
- Four patients had mild aortoiliac disease with localized plaques in the superficial femoral or popliteal arteries.
Findings:
- Peripheral lesions were explored first in all patients.
- Ulcerated plaques with adherent white thrombi were identified as the source of embolization.
- Localized thromboendarterectomy or reversed saphenous vein grafting were performed with no morbidity or mortality.
Implications:
- Distal atherosclerotic lesions should be prioritized as the source of embolization in blue toe syndrome.
- Direct exploration of peripheral lesions is essential, even with concomitant aortoiliac disease.
- This approach offers a curative solution with minimal patient risk.
Abstract:
Six patients with unilateral blue toe syndrome presented a diagnostic dilemma with regard to the source of embolization: central aortic versus peripheral. Two patients had moderately severe aortoiliac atherosclerosis associated with focal stenoses in the superficial femoral arteries, and four patients had mild aortoiliac disease associated with localized plaques confined to either the superficial femoral or popliteal arteries. In all patients, it was elected to explore the peripheral lesions first. At operation, ulcerated plaques or focal stenoses were found, and all lesions had adherent white thrombi on their surfaces. All patients were treated either by localized thromboendarterectomy or short reversed saphenous vein grafting. There was no morbidity or mortality. Recurrent embolization did not occur during a follow-up of 8 to 24 months. Distal atherosclerotic lesions should be sought to explain distal embolization before more complex aortoiliac disease is incriminated. In the presence of concomitant aortoiliac disease, it is mandatory to directly explore the peripheral lesion, open the artery, and carefully examine the lesion in situ. Thrombus adherent to the surface of an ulcerated plaque is evidence of an embolizing source. This approach is associated with minimal morbidity and may be curative. If these findings are not present, it would be appropriate to proceed with staged correction of aortoiliac disease.