Medical Care
Medical management is supportive. [14] Hemodynamic monitoring, including pulmonary artery catheterization, may be helpful for fluid and vasopressor adjustments. If acute respiratory distress syndrome (ARDS) occurs, mechanical ventilation may be required for a prolonged period. Dialysis should be started when indicated because patients can recover limited renal function. Aggressive nutritional and metabolic support is essential because these patients often lose considerable lean body mass to ongoing catabolism.
Pharmacologic therapy has not been particularly successful in patients with cholesterol embolism syndrome (CES). Vasodilator therapy with calcium-channel blockers may help relieve the local ischemia resulting from vasospasm, but angiotensin-converting enzyme (ACE) inhibitors should not be used, because of their negative effects on renal afferent arterioles and the glomerular filtration rate (GFR).
Patients presumed to have vasculitis have been treated with high-dose steroids and anti-inflammatory agents, with anecdotal reports of recovery. However, steroids may predispose patients to infectious, metabolic, and nutritional complications and difficulties with wound healing. In a report of four cases of cholesterol embolism after cardiac catheterization that were associated with deteriorating renal function, low-dose (0.3 mg/kg/day) corticosteroid therapy yielded improved renal function in three of the four patients. [15]
The use of anticoagulants is controversial because anticoagulants and thrombolytics have been shown to induce atheroemboli. Anecdotal reports of treatment with apheresis, as well as with iloprost, statins, colchicine, or combinations of these drugs with steroids, reported improvement in some cases. [16, 17, 18, 19, 20]
A study by Ishiyama et al found that low-density-lipoprotein (LDL) apheresis (LDL-A) reduced the incidence of maintenance dialysis and mortality at 24 weeks in 49 patients with cholesterol crystal embolism. [21] In a subsequent study, the same group found that LDL-A plus corticosteroids restored deteriorated renal function better than corticosteroids alone did in patients with cholesterol crystal embolism. [22]
Further invasive vascular procedures and anticoagulant or thrombolytic therapies should be avoided. If such treatments are unavoidable, downstream protection devices to trap atheromatous debris after stenting or angioplasty are suggested. [23]
Surgical Care
Surgical therapy (eg, aortic aneurysm resection) may be necessary to remove the source of atheroembolic material. Stent-grafting may be a less invasive method to reduce risk of embolization. [24]
Damaged tissue should be protected and allowed to demarcate for several months. Surprisingly, a majority of the damaged area may recover. Necrotic tissue should be debrided, and establishing vascular access for dialysis also may be necessary.
In severe cases, lumbar sympathetic block (rarely, surgical sympathectomy) has been used to avoid impending lower-extremity tissue loss resulting from intense vasoconstriction.
Prevention
If an invasive radiologic procedure is necessary, the risk of inducing cholesterol embolism must be considered. If the patient is at high risk, with known or suspected severe aortic atherosclerosis or aortic aneurysm, the Judkins (ie, brachial) approach or a radial artery approach may be used for introducing the catheter into the aorta. However, some investigators found that the approach made no difference, which led them to suspect the ascending aorta as a major source of atheroemboli.
Gentle handling of the severely diseased aorta during cardiac or aortic surgery can reduce the risk of cholesterol embolism. Careful clamping techniques and careful selection of aortotomy sites may minimize disruption of the atherosclerotic plaque.
Consultations
The following consultations should be considered as indicated:
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Nephrologist
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Critical care specialist
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Metabolic and nutritional support specialists
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General surgeon, vascular surgeon, or both
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Cholesterol crystal embolization from upstream coronary artery plaque after percutaneous transluminal coronary angioplasty.
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Necrosis of the abdominal wall in a patient with cholesterol embolism syndrome who received anticoagulation.
