The contents are under continuing development and improvements and may contain errors of omission or fact. This is not to be used for the assessment, diagnosis or management of patients. It should not be regarded as medical advice by healthcare workers or laypeople. It is for educational purposes only. Please adhere to your local protocols. If you are unwell please seek urgent healthcare advice. If you do not accept this then please do not use the website.


Cholesterol Embolisation Syndrome

Learning objectives

  • Incidence and prevalence of Cholesterol Embolization Syndrome
  • Clinical presentation with thunderclap headaches
  • Diagnostics and Management


  • Embolisation of the contents of an atherosclerotic plaque (primarily cholesterol crystals) from a proximal large artery
  • Causes distal small to medium arteries causing mechanical plugging and an inflammatory response.
  • Embolisation distal to head/neck vessel scan cause acute limb, renal, gut is ischaemia but is not covered here


  • Causes stroke and neurological damage if lesions are proximal to head and neck vessels
  • Generally characterized by a multitude of small emboli/microemboli occurring over time.
  • Usually would involve ascending aorta
  • Usually causes diffuse and small infarcts
  • Non-specific acute inflammatory response
  • Plaque damage during procedures e.g. coronary angiography but this seems rare

Pathological criteria

The following 6 key elements are required for the development of cholesterol embolisation syndrome:
  • Presence of a plaque in a proximal, large-caliber artery (such as the internal carotid artery, the iliac arteries, or the aorta)
  • Plaque rupture (spontaneous, traumatic, or iatrogenic)
  • Embolization of plaque debris (containing cholesterol crystals, platelets, fibrin, and calcified detritus)
  • Lodging of the emboli in small to medium arteries with a diameter of 100 to 200 micrometres, leading to mechanical occlusion
  • Foreign-body inflammatory response to cholesterol emboli
  • End-organ damage due to a combined effect of mechanical plugging and inflammation


  • Acute ischaemic stroke may be caused often diffuse and small
  • Constitutional symptoms such as fever and malaise
  • These episodes may be recurrent
  • Visual symptoms : cholesterol emboli may be seen by fundoscopy
  • Livedo reticularis, blue toe syndrome, skin ulcers, digital gangrene
  • Acute renal failure and hypertension


  • Artery to arterial thromboembolism in which thrombus that forms over an atheromatous plaque in large artery which embolises. This is much commoner.
  • Cardioembolic stroke


  • Raised WCC (hypereosinophilia) and elevated ESR and CRP due perhaps to IL-5 release
  • U&E : may show an AKI
  • Transoesophageal echocardiography (TEE) is the most commonly used imaging technique for the detection and measurement of the aortic atherosclerotic plaque
  • CT/MRI Aorta can also detect aortic plaque
  • CT Brain - may show infarction(s) but MRI more sensitive showing distribution
  • Carotid duplex : may show plaque
  • ECG and 24 hr tape and Echo: exclude AF and cardioembolic causes
  • Skin or Muscle biopsy: may be done to confirm diagnosis


  • No specific treatment beyond acute stroke care. Uncertainty over the use of thrombolysis.
  • It is a manifestation of atherosclerosis so management of smoking, hypertension, and serum cholesterol strongly advised
  • Statin therapy may decrease the risk of cholesterol embolisation syndrome

References and further reading

Note: The plan is to keep the website free through donations and advertisers that do not present any conflicts of interest. I am keen to advertise courses and conferences. If you have found the site useful or have any constructive comments please write to me at drokane (at) I keep a list of patrons to whom I am indebted who have contributed. If you would like to advertise a course or conference then please contact me directly for costs and to discuss a sponsored link from this site.

free web counter Hits