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Cholesterol embolisation syndromeT88.8

Author:Prof. Dr. med. Peter Altmeyer

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Last updated on: 02.09.2022

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Synonym(s)

Arteriosclerotic ulcer; Cholesterol crystal embolization; Cholesterol Embolism; Cholesterol Embolization Syndrome; Cholesterol embolization syndromes

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HistoryThis section has been translated automatically.

Panum, 1862

DefinitionThis section has been translated automatically.

Embolisation of skin vessels by cholesterol crystals probably from activated, vulnerable arteriosclerotic plaques, which empty spontaneously, after mechanical irritation by angiography, aortic surgery or after therapy with anticoagulants, streptokinase and plasminogen activator.

EtiopathogenesisThis section has been translated automatically.

Spontaneously occurring or as a result of vascular surgery, oral anticoagulation, thrombolytic therapy, angiography or trauma

It is caused by the rupture of atherosclerotic plaques in an arterial vessel with release of a conglomerate of cholesterol crystals into the vascular lumen. Such ruptures from unstable, vulnerable plaques with release of cholesterol-containing content also play a pathogenetic role in myocardial infarction.

The sharp crystal structure of the accumulated cholesterol crystals plays an essential role in the rupture. On the one hand, these cause local inflammation, thereby maintaining the inflammatory process in the plaques (unstable plaque). This mechanism can be compared in a broader sense with the inflammation in uric acid deposits of gout (Ghanem F et al.(2017).

ManifestationThis section has been translated automatically.

Especially in men > 60 years of age; in the past history often hypertension and nicotine abuse.

Clinical featuresThis section has been translated automatically.

The main symptom is the acute, localized, sharp pain of the skin.

In previously unaltered skin suddenly appearing, differently sized, bizarrely configured, red-livid spots or plaques (image of livedo racemosa in about 35% of cases).

In the further course of the disease, very painful, chronic and poorly healing, bizarrely limited, often poorly documented, flat ulcers develop. The ulcers prove to be very resistant to therapy.

They are permanently highly painful (permanent, local oxygen deficiency).

LaboratoryThis section has been translated automatically.

BSG and leukocyte elevation. Transient eosinophilia in 80% of cases.

HistologyThis section has been translated automatically.

Cholesterol crystals in the vascular lumen (only detectable in serial sections!), which appear as intravascular spindle-shaped clefts. Perivascular mixed cell, often eosinophilic infiltrate.

DiagnosisThis section has been translated automatically.

Clinic with livedo racemosa without other signs of vasculitis. Pain in the extremities, kidney failure possible. High age and arteriosclerosis as well as previous vascular surgery speak for the diagnosis.

Differential diagnosisThis section has been translated automatically.

Deep vein thrombosis; diabetic ulcer; live symptoms of other genesis; interstitial nephritis; myocardial infarction; acute gastritis; acute pancreatitis.

TherapyThis section has been translated automatically.

Symptomatic: pain therapy.

Furthermore aspirin/clopidogrel; possibly high-dose statins gfls. combined with short-term use of glucocorticosteroids.

Notice! Important is the treatment of the underlying internal disease.

External therapyThis section has been translated automatically.

In the initial stage of erythematous inflammatory changes, short-term external glucocorticoids, e.g. 0.05% betamethasone cream R028 or 0.25% prednicarbate cream/ointment (e.g. Dermatop) and moist compresses In case of extensive ulceration, removal of necroses, enzymatic wound cleansing (e.g. Iruxol N ointment) or hydrocolloid dressings (e.g. Varihesive extra thin). S.a.u. Wound treatment.

Operative therapieThis section has been translated automatically.

Smaller ulcerations can also be completely excised and primarily closed.

Note(s)This section has been translated automatically.

The skin infarcts of the cholesterol-embolism syndrome are only a (possibly monitoric) partial manifestation of a systemic arteriosclerotic"embolic disease". Target organs are besides skin, kidneys and brain.

LiteratureThis section has been translated automatically.

  1. Ghanem F et al(2017) Cholesterol crystal embolization following plaque rupture: a systemic disease with unusual features.J Biomed Res 31:82-94.
  2. Gibbs MB et al (2005) Livedo reticularis: an update. J Am Acad Dermatol 52: 1009-1019
  3. Lukacs A et al (1992) Cutaneous, ulcerated cholesterol embolism under the image of a livedo racemosa after cardiac catheterization. Nude Dermatol 18: 14-16
  4. Panum PL (1862) Experimental contributions to the theory of embolism. Virchows Arch 25: 308-310
  5. Pennington M, et al (2002) Cholesterol embolization syndrome: cutaneous histopathological features and the variable onset of symptoms in patients with different risk factors. Br J Dermatol 146: 511-517
  6. Resnik KS (2003) Intravscular cholesterol clefts as an incidental finding. At J Dermatopathol 25: 497-499
  7. Scolari F et al (2000) Cholesterol crystal embolism: A recognizable cause of renal disease. On J Kidney Dis 36: 1089-1109

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Last updated on: 02.09.2022

Author: Prof. Dr. med. Peter Altmeyer