Cutaneous Cholesterol Emboli Medication

Updated: Apr 12, 2021
  • Author: Robert A Schwartz, MD, MPH; Chief Editor: Dirk M Elston, MD  more...
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Medication Summary

Little success has been achieved with medical treatment of CCE. General strategies involve the use of anticoagulants, antiplatelet and antisludging drugs, vasodilators, corticosteroids, and lipid-lowering agents to prevent or reduce vascular occlusion, augment circulation, decrease inflammation, and help induce the regression of atherosclerotic plaques. None of these therapies has been proven effective in controlled trials, and, in most cases, the rationale for using them is based on anecdotal reports, such low-density lipoprotein apheresis (LDL-A) followed by steroids, which has been suggested as beneficial, especially in patients with cutaneous involvement. [38]


Anticoagulant/antithrombolytic agents

Class Summary

Anticoagulant/antithrombolytic agents prevent, limit, or degrade thrombosis to reestablish blood flow.

Heparin (Hep-Lock)

Heparin augments the activity of antithrombin III and heparin cofactor to inhibit thrombin and factor Xa. It prevents conversion of fibrinogen to fibrin. It does not actively lyse but is able to inhibit further thrombogenesis. Heparin prevents reaccumulation of clot after spontaneous fibrinolysis, and it prolongs the aPTT.

Warfarin (Coumadin)

Warfarin interferes with hepatic synthesis of vitamin K–dependent coagulation factors (eg, II, VII, IX, X, proteins C and S). It is used for prophylaxis and treatment of venous thrombosis, pulmonary embolism, and thromboembolic disorders. Tailor the dose to maintain an INR of 2-3.


Antiplatelet/antisludging agents

Class Summary

Antiplatelet/antisludging agents prevent vascular occlusion.

Aspirin (Anacin, Bayer, Empirin)

Aspirin inhibits prostaglandin synthesis, preventing the formation of platelet-aggregating thromboxane A2. It may be used in a low dose to inhibit platelet aggregation and improve complications of venous stases and thrombosis.

Pentoxifylline (Trental)

Pentoxifylline may alter the rheology of RBCs, which, in turn, reduces blood viscosity.

Dipyridamole (Persantine)

Dipyridamole is used to complement usual warfarin therapy. It is a platelet adhesion inhibitor that possibly inhibits RBC uptake of adenosine, itself an inhibitor of platelet reactivity. In addition, it may inhibit phosphodiesterase activity, leading to increased cyclic-3',5'-adenosine monophosphate within platelets and formation of the potent platelet activator thromboxane A2.



Class Summary

Vasodilators relax blood vessels to help reestablish blood flow.

Papaverine (Pavabid, Pavatine)

Papaverine is a benzylisoquinoline derivative with direct nonspecific relaxant effect on vascular, cardiac, and other smooth muscle.


Nifedipine inhibits calcium influx into vascular smooth muscle and myocardium. It relaxes coronary smooth muscle and produces coronary vasodilation, which, in turn, improves myocardial oxygen delivery and increases blood flow.



Class Summary

Corticosteroids have anti-inflammatory properties and cause profound and varied metabolic effects. They modify body's immune response to diverse stimuli and reduce vascular inflammation.

Prednisone (Deltasone, Orasone, Meticorten)

Prednisone is an anti-inflammatory agent that suppresses the function of inflammatory cells and stabilizes lysosomal membranes.

Methylprednisolone (Medrol, Solu-Medrol)

Methylprednisolone is an anti-inflammatory agent that suppresses the function of inflammatory cells and stabilizes lysosomal membranes.


Cholesterol-lowering agents

Class Summary

Cholesterol-lowering agents induce regression of atherosclerotic plaques.

Lovastatin (Mevacor)

Lovastatin competitively inhibits 3-hydroxyl-3-methylglutaryl-coenzyme A reductase, which catalyzes the rate-limiting step in cholesterol synthesis.

Cholestyramine (Questran)

Cholestyramine forms a nonabsorbable complex with bile acids in the intestine, which, in turn, inhibits enterohepatic reuptake of intestinal bile salts.