Cholesterol emboli syndrome

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Cholesterol embolism (often cholesterol crystal embolism or atheroembolism, sometimes blue toe or purple toe syndrome or trash foot) occurs when cholesterol is released, usually from an atherosclerotic plaque, and travels along with the bloodsteam (embolism) to other places in the body, where it obstructs blood vessels. Most commonly this causes skin symptoms (usually livedo reticularis), gangrene of the extremities and sometimes renal failure; problems with other organs may arise, depending on the site at which the cholesterol crystals enter the bloodstream.^[1] When the kidneys are involved, the disease is referred to as atheroembolic renal disease (AERD).^[2] The diagnosis usually involves biopsy (removing a tissue sample) from an affected organ. Cholesterol embolism is treated by removing the cause and with supportive therapy; statin drugs have been found to improve the prognosis.^[1] CES is underdiagnosed and may mimic other diseases.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Nasrin Nikravangolsefid, MD-MPH [2]

Cholesterol emboli was first described by a Danish pathophysiologist called Peter Ludvig Panum in 1862. The first case series of Arterial Occlusions due to Emboli were reported from 267 autopsies in the New York Hospital by Curtis M. Flory in 1945. The cholesterol crystals were first identified by polarized light in 1956. atheromatous embolization following vascular surgery was first diagnosed by Thurlbeck and Castleman in 1957. The cholesterol emboli in the retinal arterioles was first described by an ophthalmologist called Dr Robert Hollenhorst in 1961, which is known as Hollenhorst plaques. In 1961, first cases of blue toe syndrome, described as painful toes, following treatment with oral anticoagulation were reported by Feder and Auerbach. But the term of blue toe syndrome was first used in 1976. The association between aortic plaque on TEE and development of emboli was reported in 1990.

• Cholesterol emboli was first described by a Danish pathophysiologist called Peter Ludvig Panum in 1862. ^{[1] [2]}
• In 1945, the first case series of Arterial Occlusions due to Emboli were reported from 267 autopsies in the New York Hospital by Curtis M. Flory. ^{[3] [2]}
• The cholesterol crystals were first identified by polarized light in 1956. ^[2]
• atheromatous embolization following vascular surgery was first diagnosed by Thurlbeck and Castleman in 1957. ^[2]
• The cholesterol emboli in the retinal arterioles was first described by an ophthalmologist called Dr Robert Hollenhorst in 1961, which is known as Hollenhorst plaques. ^[4]
• In 1961, first cases of blue toe syndrome described as painful toes following treatment with oral anticoagulation were reported by Feder and Auerbach. ^[5]But the term of blue toe syndrome was first used in 1976. ^[6]
• In 1990, the association between aortic plaque on TEE and development of emboli was first reported. ^[2]

• Embolism

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Nasrin Nikravangolsefid, MD-MPH [2]

Cholesterol emboli syndrome (CES) is the result of the rupture and release of cholesterol crystals from atherosclerotic plaques, produced either spontaneously or iatrogenic that lead to mechanical obstruction of arterioles and inflammatory response activation that cause multiple organ damage.

• It is thought that cholesterol emboli syndrome (CES) is the result of the rupture and release of cholesterol crystals from atherosclerotic plaques, produced either spontaneously or as a result of iatrogenesis.^[1][2]
• Cholesterol emboli syndrome (CES) is defined as the occlusion of 100-200 µm arterioles by cholesterol crystals after their dislodgment from atheromatous plaques, which arise from proximal large arteries such as aorta.^[1]
• Embolization of cholesterol crystals lead to several damages including^[1]
  • Endothelial injury
  • Activation of complement system
  • Oxidative stress injury
  • Activation of the renin–angiotensin–aldosterone system (RAAS) due to renal arteries obstruction and hypoperfusion
  • Leukocyte infiltration and release of its enzymes which cause inflammation
• Cholesterol emboli can involve many organs including brain, kidneys, eyes, skin, muscles, and gastrointestinal tract. ^[3]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Nasrin Nikravangolsefid, MD-MPH [2]

Common causes of Cholesterol emboli syndrome (CES) include spontaneously due to atherosclerosis of the large arteries and iatrogenic secondary to medical interventions such as vascular surgery or angiography. Less common causes of CES include intake of anticoagulants such as warfarin or thrombolytic medications.

• Common causes of Cholesterol emboli syndrome (CES) include:
  • spontaneously (25%): It usually occurs in patients with severe atherosclerosis of the large arteries such as aorta.
  • Iatrogenic (75%): a complication of medical procedures involving the blood vessels, such as vascular surgery or angiography.
    • The incidence of CES after coronary catheterization is 1.4%. ^[1]
    • But the overall prevalence of CES after coronary catheterization is 25% to 30%. ^[2]
• less Common causes of Cholesterol emboli syndrome (CES) include:
  • intake of anticoagulants such as warfarin or thrombolytic medications such as tissue plasminogen activatorthat decrease blood clotting or dissolve blood clots, respectively. They probably lead to cholesterol emboli by removing blood clots that cover up a damaged atherosclerotic plaque; cholesterol-rich debris can then enter the bloodsteam. ^{[3] [4]}

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

• CES may resemble a systemic vasculitis like PAN, with multiple scattered areas of ischemic damage, with skin, renal, extremity, intestinal, and neurologic manifestations.
• Signs of peripheral ischemia without large vessel disease

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

• Cholesterol emboli syndrome is more common in male patients (~75%) with severe atherosclerotic disease, and often occurs days to weeks after an invasive procedure.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Nasrin Nikravangolsefid, MD-MPH [2]

The most potent risk factor in the development of cholesterol emboli syndrome is atherosclerosis. Other risk factors include cardiovascular interventions such as angiography and cardiovascular surgery, aortic aneurysm, diabetes mellitus, hypertension, dyslipidemia, smoking, aging, male sex, anticoagulants such as warfarin, thrombolytic therapy and higher serum CRP levels.

• The most potent risk factor in the development of cholesterol emboli syndrome is atherosclerosis. ^[1]
• Other risk factors include^{[1][2][3][4][5][6]}:
  • cardiovascular interventions such as angiography, cardiovascular surgery
  • aortic aneurysm
  • diabetes mellitus
  • hypertension
  • dyslipidemia
  • smoking
  • aging
  • male sex
  • anticoagulants such as warfarin
  • thrombolytic therapy
  • higher serum CRP levels

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Nasrin Nikravangolsefid, MD-MPH [2]

There is insufficient evidence to recommend routine screening for cholesterol emboli syndrome.

There is insufficient evidence to recommend routine screening for cholesterol emboli syndrome.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Nasrin Nikravangolsefid, MD-MPH [2]

Common complications of Cholesterol emboli syndrome include atheroembolic renal disease, acute kidney injury, chronic kidney disease, myocardial infarction, cerebrovascular accident bowel ischemia, liver failure, end organ damage and death. Prognosis is generally poor, and the incidence of mortality among patients with Cholesterol emboli syndrome is approximately 63-80 %.

• Common complications of Cholesterol emboli syndrome include atheroembolic renal disease, acute kidney injury, chronic kidney disease, myocardial infarction, cerebrovascular accident bowel ischemia, liver failure, end organ damage and death. ^[1][2]

• Prognosis is generally poor, and the incidence of mortality among patients with Cholesterol emboli syndrome is approximately 63-80 %.^[1][3]

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