By contrast, atheroemboli (commonly known as cholesterol emboli or cholesterol crystal embolization) originate from atherosclerotic plaques in the aorta or another large artery,5 which are prone to embolize if the underlying plaque experiences stress. As the plaque erodes, cholesterol crystals break off and embolize distally. These smaller crystals flood into the circulation, allowing a shower of emboli over time to occlude the arterioles. As occlusion spreads through the arterioles, multiple organ systems are affected. (It was previously thought that procedure-associated cases were common, but a literature review has not borne this out.5)
The shower of emboli often triggers a systemic inflammatory response, causing nondescript abnormalities of laboratory inflammatory markers.6,7 Interestingly, hypereosinophilia is noted in about 80% of patients with CES.8It is not uncommon for atheroemboli of the lower extremity to manifest, as it did in this case, as “blue toe syndrome.”
No disease-specific testing. A confounding factor in validating the diagnosis of CES is the lack of disease-specific testing. However, CES should be considered in a patient with acute kidney injury and hypereosinophilia. Making the diagnosis requires a high degree of clinical suspicion. Any organ can be affected, although the brain, kidneys, gastrointestinal tract, skin, and skeletal muscles of the lower extremities are most frequently involved.9 If left undiagnosed, the results can be devastating: slow and chronic injury to a variety of organ systems over time, which may not be recognized as a harbinger of an insidious underlying process causing end-organ damage.
Technically, definitive diagnosis can be made by biopsy of an affected organ. However, biopsy’s utility is limited due to potential for sampling error, accessibility (as noted, the location of the involved organ[s] may make biopsy nearly impossible without additional surgical risk9), and risk of poor healing to the biopsy site.10
Treatment is two-fold: supportive care for the affected end organ and prevention of subsequent embolic events. The latter entails aggressive risk factor reduction strategies, such as smoking cessation, statin therapy, blood pressure control, and blood sugar control. Warfarin is not recommended for treatment of CES due to the risk of further plaque rupture, hemorrhage, acute and chronic renal failure, and cholesterol microembolization to other organs.11,12
Continue to: Our patient