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ALL / Cardiology
Cholesterol embolisation
Cholesterol embolisation
Cholesterol embolisation syndrome occurs when cholesterol crystals from ulcerated atherosclerotic plaques shower into small arteries, causing ischaemia and an inflammatory reaction. It classically presents after an invasive arterial procedure in a patient with diffuse atherosclerosis.Pathophysiology
- cholesterol crystals usually arise from unstable aortic or large-artery atheroma
- most cases follow vascular surgery, angiography or anticoagulation/thrombolysis, which disrupt plaque
- emboli lodge in small arteries (commonly renal, skin, gastrointestinal and retinal vessels)
- this causes partial occlusion and a marked inflammatory/foreign-body response
- explains the eosinophilia and the often subacute course
Features
- acute or subacute kidney injury
- often develops days to weeks after angiography, unlike contrast-induced nephropathy which occurs within 24-72 hours
- skin signs
- livedo reticularis
- purpura
- painful blue toes with preserved peripheral pulses
- constitutional features
- fever, weight loss, myalgia
- bloods
- eosinophilia
- raised inflammatory markers
- low complement may be seen
- other organ involvement
- retinal Hollenhorst plaques
- abdominal pain or gastrointestinal bleeding
Diagnosis
- clinical suspicion in an at-risk patient with AKI and peripheral ischaemic skin changes after an arterial procedure
- urine findings are non-specific
- biopsy of affected skin or kidney may confirm cholesterol clefts, but is not always required
Management
- supportive management of end-organ injury, especially renal impairment
- stop precipitating factors where possible
- aggressive cardiovascular risk reduction
- high-intensity statin, smoking cessation, blood pressure and diabetes control
- avoid further unnecessary arterial instrumentation
- dialysis may be required if severe renal failure develops
+PassMedicine Notes
Cholesterol embolisation syndrome occurs when cholesterol crystals from ulcerated atherosclerotic plaques shower into small arteries, causing ischaemia and an inflammatory reaction. It classically presents after an invasive arterial procedure in a patient with diffuse atherosclerosis.
Pathophysiology- cholesterol crystals usually arise from unstable aortic or large-artery atheroma
- most cases follow vascular surgery, angiography or anticoagulation/thrombolysis, which disrupt plaque
- emboli lodge in small arteries (commonly renal, skin, gastrointestinal and retinal vessels)
- this causes partial occlusion and a marked inflammatory/foreign-body response
- explains the eosinophilia and the often subacute course
- acute or subacute kidney injury
- often develops days to weeks after angiography, unlike contrast-induced nephropathy which occurs within 24-72 hours
- skin signs
- livedo reticularis
- purpura
- painful blue toes with preserved peripheral pulses
- constitutional features
- fever, weight loss, myalgia
- bloods
- eosinophilia
- raised inflammatory markers
- low complement may be seen
- other organ involvement
- retinal Hollenhorst plaques
- abdominal pain or gastrointestinal bleeding
- clinical suspicion in an at-risk patient with AKI and peripheral ischaemic skin changes after an arterial procedure
- urine findings are non-specific
- biopsy of affected skin or kidney may confirm cholesterol clefts, but is not always required
- supportive management of end-organ injury, especially renal impairment
- stop precipitating factors where possible
- aggressive cardiovascular risk reduction
- high-intensity statin, smoking cessation, blood pressure and diabetes control
- avoid further unnecessary arterial instrumentation
- dialysis may be required if severe renal failure develops