Cutaneous Cholesterol Emboli Medication

  • Author: Robert A Schwartz, MD, MPH; Chief Editor: Dirk M Elston, MD   more...
 
Updated: May 22, 2012
 

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.

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Anticoagulant/antithrombolytic agents

Class Summary

Prevent, limit, or degrade thrombosis to reestablish blood flow.

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Heparin (Hep-Lock)

 

Augments activity of antithrombin III and heparin cofactor to inhibit thrombin and factor Xa. Prevents conversion of fibrinogen to fibrin. Does not actively lyse but is able to inhibit further thrombogenesis. Prevents reaccumulation of clot after spontaneous fibrinolysis.

Prolongs aPTT.

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Streptokinase (Kabikinase, Streptase)

 

Acts with plasminogen to convert plasminogen to plasmin. Plasmin degrades fibrin clots, fibrinogen, and other plasma proteins. Increase in fibrinolytic activity that degrades fibrinogen for 24-36 h occurs with IV infusion.

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Urokinase (Abbokinase)

 

Direct plasminogen activator that acts on endogenous fibrinolytic system and converts plasminogen to the enzyme plasmin, which, in turn, degrades fibrin clots, fibrinogen, and other plasma proteins. Most often used for local fibrinolysis of thrombosed catheters and superficial vessels. Advantage is that agent is nonantigenic. However, more expensive than streptokinase, and thus, cost limits use. When used for local fibrinolysis, urokinase is administered as local infusion directly into area of thrombus and with no bolus given. Adjust dose to achieve clot lysis or patency of affected vessel.

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Warfarin (Coumadin)

 

Interferes with hepatic synthesis of vitamin K–dependent coagulation factors (eg, II, VII, IX, X, proteins C and S). Used for prophylaxis and treatment of venous thrombosis, pulmonary embolism, and thromboembolic disorders.

Tailor dose to maintain INR of 2-3.

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Antiplatelet/antisludging agents

Class Summary

Prevent vascular occlusion.

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Aspirin (Anacin, Bayer, Empirin)

 

Inhibits prostaglandin synthesis, preventing formation of platelet-aggregating thromboxane A2. May be used in low dose to inhibit platelet aggregation and improve complications of venous stases and thrombosis.

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Pentoxifylline (Trental)

 

May alter rheology of RBCs, which, in turn, reduces blood viscosity.

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Dipyridamole (Persantine)

 

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

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Vasodilators

Class Summary

Relax blood vessels to help reestablish blood flow.

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Papaverine (Pavabid, Pavatine)

 

Benzylisoquinoline derivative with direct nonspecific relaxant effect on vascular, cardiac, and other smooth muscle.

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Nifedipine

 

Inhibits calcium influx into vascular smooth muscle and myocardium.

Relaxes coronary smooth muscle and produces coronary vasodilation, which, in turn, improves myocardial oxygen delivery and increases blood flow.

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Corticosteroids

Class Summary

Have anti-inflammatory properties and cause profound and varied metabolic effects. Modify body's immune response to diverse stimuli and reduce vascular inflammation.

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Prednisone (Deltasone, Orasone, Meticorten)

 

Anti-inflammatory agent that suppresses function of inflammatory cells and stabilizes lysosomal membranes.

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Methylprednisolone (Medrol, Solu-Medrol)

 

Anti-inflammatory agent that suppresses function of inflammatory cells and stabilizes lysosomal membranes.

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Cholesterol-lowering agents

Class Summary

Induce regression of atherosclerotic plaques.

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Lovastatin (Mevacor)

 

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

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Cholestyramine (Questran)

 

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

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Contributor Information and Disclosures
Author

Robert A Schwartz, MD, MPH  Professor and Head, Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, University of Medicine and Dentistry of New Jersey-New Jersey Medical School

Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and Sigma Xi

Disclosure: Nothing to disclose.

Coauthor(s)

Jerry Rothenberg, MD  Clinical Associate Professor, Department of Dermatology, University of Medicine and Dentistry of New Jersey, New Jersey Medical School; President, Director, New Jersey Dermatopathology Laboratory, Inc

Disclosure: Nothing to disclose.

Specialty Editor Board

James J Nordlund, MD  Professor Emeritus, Department of Dermatology, University of Cincinnati College of Medicine

James J Nordlund, MD is a member of the following medical societies: American Academy of Dermatology, Sigma Xi, and Society for Investigative Dermatology

Disclosure: Nothing to disclose.

David F Butler, MD  Professor of Dermatology, Texas A&M University College of Medicine; Chair, Department of Dermatology, Director, Dermatology Residency Training Program, Scott and White Clinic, Northside Clinic

David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Association of Military Dermatologists, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Jeffrey Meffert, MD  Assistant Clinical Professor of Dermatology, University of Texas School of Medicine at San Antonio

Jeffrey Meffert, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, Association of Military Dermatologists, and Texas Dermatological Society

Disclosure: Nothing to disclose.

Catherine M Quirk, MD  Clinical Assistant Professor, Department of Dermatology, University of Pennsylvania

Catherine M Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD  Director, Ackerman Academy of Dermatopathology, New York

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous author, Kenneth A. Becker, MD, to the development and writing of this article.

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Chronic leg ulcer due to cutaneous cholesterol emboli on the leg of a 79-year-old woman.
Skin biopsy specimen demonstrating ulceration and an occluded vessel at the right border of the specimen within the fat. Hematoxylin and eosin stain at 22X magnification.
Higher magnification of the same biopsy specimen, demonstrating cholesterol clefts within an occluded arteriole. Hematoxylin and eosin stain at 297X magnification.
 
 
 
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