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Cutaneous Manifestations of Cholesterol Embolism Medication

  • Author: Laura F McGevna, MD; Chief Editor: William D James, MD  more...
 
Updated: Jun 27, 2016
 

Medication Summary

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

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Blood viscosity reducing agents

Class Summary

These agents increase the fluid characteristics of blood.

Pentoxifylline (Trental)

 

Pentoxifylline is a methylxanthine derivative that reduces blood viscosity and improves erythrocyte flexibility.

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HMG-CoA reductase inhibitors

Class Summary

These agents usually lower LDL cholesterol levels and sometimes lower triglyceride levels, and they may modestly elevate high-density lipoprotein cholesterol levels. These agents may be of value to patients with hypercholesterolemia.

Simvastatin (Zocor)

 

Simvastatin inhibits HMG-CoA reductase, which, in turn, inhibits cholesterol synthesis and increases cholesterol metabolism.

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Prostaglandin analogs

Class Summary

These agents inhibit the cyclooxygenase system, decreasing the level of thromboxane A2, which is a potent platelet activator.

Iloprost (Ilomedin)

 

Iloprost is a chemically stable analog of prostacyclin (epoprostenol) and effective inhibitor of platelet aggregation by increasing intracellular levels of cyclic adenosine monophosphate. Clinical benefit has been observed in occlusive peripheral vascular disease and Raynaud phenomenon, although further clinical trials are needed to assess its place in therapy in these conditions.

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Contributor Information and Disclosures
Author

Laura F McGevna, MD Assistant Professor of Medicine, Dermatology Division, University of Vermont College of Medicine

Laura F McGevna, MD is a member of the following medical societies: American Academy of Dermatology, Dermatology Foundation

Disclosure: Nothing to disclose.

Coauthor(s)

Gregory J Raugi, MD, PhD Professor, Department of Internal Medicine, Division of Dermatology, University of Washington at Seattle School of Medicine; Chief, Dermatology Section, Primary and Specialty Care Service, Veterans Administration Medical Center of Seattle

Gregory J Raugi, MD, PhD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Samreen R Raza, MD Resident Physician, Department of Internal Medicine, University of Vermont College of Medicine

Samreen R Raza, MD is a member of the following medical societies: American College of Physicians, Royal Society of Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Richard P Vinson, MD Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA

Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Texas Medical Association, Association of Military Dermatologists, Texas Dermatological Society

Disclosure: Nothing to disclose.

Warren R Heymann, MD Head, Division of Dermatology, Professor, Department of Internal Medicine, Rutgers New Jersey Medical School

Warren R Heymann, MD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Chief Editor

William D James, MD Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine

William D James, MD is a member of the following medical societies: American Academy of Dermatology, Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

Catharine Lisa Kauffman, MD, FACP Georgetown Dermatology and Georgetown Dermpath

Catharine Lisa Kauffman, MD, FACP is a member of the following medical societies: American Academy of Dermatology, Royal Society of Medicine, Women's Dermatologic Society, American Medical Association, Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Acknowledgements

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors, Edwin Rhim, MD, and Heather D. Rogers, MD, to the development and writing of this article.

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A 76-year-old man with a history of aortobifemoral bypass graft developed this eruption after an angiographic procedure. This image shows the plantar surface of the right foot with some of the discoloration resulting from petechiae arranged in a reticulated pattern. This is not livedo reticularis. Petechiae do not blanch on diascopy, but the lesions of livedo reticularis do blanch.
Aorta with an ulcerated plaque (black arrowhead) on the luminal side photographed under water to enhance reflection of cholesterol crystals (white arrowhead).
Low-power view of a skin biopsy specimen demonstrating an arteriole within the subcutaneous fat occluded with thrombus material that contains (black arrowhead) needle-shaped cholesterol clefts (hematoxylin and eosin stain, original magnification X40).
High-power view of occluded vessel (hematoxylin and eosin stain, original magnification X100).
Symmetric involvement of the feet with livedo reticularis on the plantar surface of the forefoot and cyanosis of the left fifth toe. The painful cyanotic toe is typical of blue toe syndrome.
Dorsal surface of the toes of the right foot of a patient with discoloration resulting from petechiae. This image shows cyanosis of the fourth toe. The dominant eruption is petechial. Note the pallor of the tip of the great toe and the second toe. This finding indicates acute loss of perfusion.
Plantar surface of the right foot. The distal half of the great toe is gangrenous, with a sharp demarcation between the necrotic tissue and the normal proximal skin. Livedo reticularis is present on the distal plantar forefoot, and petechiae are present on the distal pad of the second and fourth toes.
The lower extremities show well-developed livedo reticularis and focal areas of erosion and ulceration.
Photomicrographs of histologic sections of an aorta with van Gieson stain. (Left) An atherosclerotic plaque with the fibrous cap (black arrowhead) overlying a necrotic core of cellular debris, extracellular lipids, and cholesterol clefts (white arrowhead). Underneath the plaque is the elastic media (arrow). (Right) A ruptured atherosclerotic plaque exposing the atheromatous debris containing cholesterol crystals to the bloodstream on the luminal side of the aorta.
CT scan of an infrarenal abdominal aortic aneurysm showing the mural thrombosis (white arrowhead) and the bright atherosclerotic calcifications (black arrowhead).
 
 
 
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