Cholesterol embolism

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Cholesterol embolism
Other namesCholesterol crystal embolism, atheroembolism, blue toe, purple toe syndrome, trash foot, warfarin blue toe syndrome
Kidney biopsy. H&E stain.
SpecialtyCardiology Edit this on Wikidata

Cholesterol embolism occurs when cholesterol is released, usually from an atherosclerotic plaque, and travels as an embolus in the bloodstream to lodge (as an embolism) causing an obstruction in blood vessels further away. Most commonly this causes skin symptoms (usually livedo reticularis), gangrene of the extremities and sometimes kidney failure; problems with other organs may arise, depending on the site at which the cholesterol crystals enter the bloodstream.[2] When the kidneys are involved, the disease is referred to as atheroembolic renal disease.[3] The diagnosis usually involves biopsy (removing a tissue sample) from an affected organ. Cholesterol embolism is treated by removing the cause and giving supportive therapy; statin drugs have been found to improve the prognosis.[2]

Signs and symptoms

The symptoms experienced in cholesterol embolism depend largely on the organ involved.

livedo reticularis.[3] The pain is usually severe and requires opiates. If the ulcerated plaque is below the renal arteries the manifestations appear in both lower extremities. Very rarely the ulcerated plaque is below the aortic bifurcation and those cases the changes occur only in one lower extremity.[citation needed
]

Kidney involvement leads to the symptoms of

irregular heartbeat. Some patients report hematuria (bloody urine) but this may only be detectable on microscopic examination of the urine. Increased amounts of protein in the urine may cause edema (swelling) of the skin (a combination of symptoms known as nephrotic syndrome).[3]

If emboli have spread to the

gastrointestinal hemorrhage (vomiting blood, or admixture of blood in the stool), and occasionally acute pancreatitis (inflammation of the pancreas).[3]

Both the

mononeuropathy.[3]

Causes

It is relatively unusual (25% of the total number of cases) for cholesterol emboli to occur spontaneously; this usually happens in people with severe atherosclerosis of the large arteries such as the aorta. In the other 75% it is a complication of medical procedures involving the blood vessels, such as vascular surgery or angiography. In coronary catheterization, for instance, the incidence is 1.4%.[5] Furthermore, cholesterol embolism may develop after the commencement of anticoagulants or thrombolytic medication that 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 bloodstream.[3]

Diagnosis

Kidney biopsy. H&E stain
.

Differential diagnosis

Findings on general investigations (such as

contrast nephropathy). Other causes that may lead to similar symptoms include ischemic kidney failure (kidney dysfunction due to an interrupted blood supply), a group of diseases known as thrombotic microangiopathies and endocarditis (infection of the heart valves with small clumps of infected tissue embolizing through the body).[3]

Blood and urine

Tests for

casts as seen under the microscope) and increased levels of protein; in a third of the cases with kidney involvement, eosinophils can also be detected in the urine.[3] If vasculitis is suspected, complement levels may be determined as reduced levels are often encountered in vasculitis; complement is a group of proteins that forms part of the innate immune system. Complement levels are frequently reduced in cholesterol embolism, limiting the use of this test in the distinction between vasculitis and cholesterol embolism.[6]

Tissue diagnosis

The microscopic examination of tissue (histology) gives the definitive diagnosis. The diagnostic histopathologic finding is intravascular cholesterol crystals, which are seen as cholesterol clefts in routinely processed tissue (embedded in paraffin wax).[7] The cholesterol crystals may be associated with macrophages, including giant cells, and eosinophils.[citation needed]

The

atherosclerotic plaques (that are cholesterol-laden and have a thin fibrous cap). While biopsy findings may not be diagnostic, they have significant value, as they help exclude alternate diagnoses, e.g. vasculitis, that often cannot be made confidently based on clinical criteria.[citation needed
]

Treatment

Treatment of an episode of cholesterol emboli is generally symptomatic, i.e. it deals with the symptoms and complications but cannot reverse the phenomenon itself.[5] In kidney failure resulting from cholesterol crystal emboli, statins (medication that reduces cholesterol levels) have been shown to halve the risk of requiring hemodialysis.[2]

History

The phenomenon of embolisation of cholesterol was first recognized by the

pathologist Dr. Peter Ludvig Panum and published in 1862.[8] Further evidence that eroded atheroma was the source of emboli came from American pathologist Dr. Curtis M. Flory, who in 1945 reported the phenomenon in 3.4% of a large autopsy series of older individuals with severe atherosclerosis of the aorta.[3][9]

References

  1. ISBN 978-1-4160-2999-1
    .
  2. ^
    PMID 17606842
    .
  3. ^
    PMID 11461954
    .
  4. PMID 2335833
    .
  5. ^
    PMID 12875753
    .
  6. S2CID 30580788
    .
  7. ISBN 978-0-7817-7942-5
    .
  8. S2CID 29504624
    .
  9. PMID 19970827
    .

External links
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