Cutaneous Cholesterol Emboli Treatment & Management

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

Medical Care

Medical treatment of CCE has largely been unsuccessful, with the exception of a few anecdotal reports. The early goals of treatment are to augment the circulation and to try to prevent occlusion. Some believe this can be achieved with drugs that inhibit coagulation, platelet aggregation, and RBC sludging. Vasodilators and corticosteroids have also been used. Variable results have been reported with the use of heparin, streptokinase, urokinase, tissue plasminogen activator, warfarin, bishydroxycoumarin, aspirin, pentoxifylline, dipyridamole, prostaglandins, prostacyclin, intra-arterial papaverine, sulfinpyrazone, low–molecular-weight dextran, nifedipine, prednisone, and methylprednisolone. Some have also recently reported success with hemostatic and lipid-lowering agents (eg, vitamin K, carbazochrome, tranexamic acid, reptilase, lovastatin, cholestyramine, probucol).

Although anticoagulants have been observed to cause CCE and many reports indicate the cessation of symptoms upon discontinuation, in 2 patients, heparin resulted in resolution of their myalgias, tenderness, and pregangrene. Furthermore, they did not have any recurrence of symptoms or signs. Another group reported clinical and radiographic improvement following therapy with intra-arterial streptokinase, heparin, and prostacyclin. Iloprost, a prostacyclin analog, has also been reported to improve renal function and peripheral symptoms in patients with CE. Subcutaneous heparin, which is intermittently administered through the tissue to provide trough periods, may allow more effective healing of plaques than the intravenous form.

Some recommend a trial of corticosteroids for their anti-inflammatory effect to limit arteritis and the subsequent fibrotic occlusion of vessels; however, in 9 patients with CCE thought to have vasculitis who were treated with corticosteroids, 7 died.

Lovastatin may effect healing by inducing the regression of atherosclerosis and by decreasing plaque cholesterol content, which is linked to an increased incidence of emboli.

One group used the combination of hemostatic (ie, vitamin K, carbazochrome, tranexamic acid, reptilase) and antihyperlipidemic (ie, cholestyramine, probucol) drugs and had positive results.

The clinical effect of circulator boot therapy in patients with cholesterol embolization syndrome of the lower extremities in patients following cardiac or vascular procedures may be an effective noninvasive therapeutic option.[24]

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Surgical Care

Removal of the source of the emboli using thromboendarterectomy or excision and replacement of the prosthesis has resulted in resolution of CCE. Because gangrene is more likely to occur in persons whose circulation is already compromised, reconstruction of the stenotic proximal artery, which may or may not be the source of emboli, is also advised. Other forms of surgical treatment include embolectomy, sympathectomy, and primary excision of necrotic tissue, possibly involving amputation.

Thoracoabdominal repair is the criterion standard of treatment. Bypass without vessel ligation is contraindicated because it does not remove the source of emboli. Improvement and healing of cutaneous lesions was observed in 2 of 3 patients after resection of abdominal aortic aneurysms. Another group reported that 4 of 5 patients with ischemic lesions from toe gangrene or necrosis benefited from arterial reconstruction. For multilevel occlusive disease, proximal reconstructions are performed prior to distal ones, but the reverse may be appropriate for blue toe syndrome.

If the entire aorta is diffusely ulcerative, the source of emboli is inaccessible, or the patient is a poor surgical candidate, then thoracoabdominal repair may not be possible. Palliative treatment for such patients is axillobifemoral bypass with external iliac ligation. Four patients with peripheral emboli who underwent this procedure had cessation of new lesions, healing, and pain relief. Embolization to the pelvic circulation may be controlled by iliac ligation at the aortic bifurcation or by individual interruption of the internal iliac arteries. Another group had similar success with this technique and was able to salvage 12 limbs in 6 patients, apart from the loss of a fifth toe.

Embolectomy may be effective in cases of the larger atheroemboli.

Peripheral nerve blockade or lumbar sympathectomy has been used to deter cutaneous breakdown and promote healing. They are advocated for patients with persistent areas of pain, cyanosis, or cutaneous gangrene in the involved limb. Sympathetic blockade influences the microcirculation of the skin through a direct effect on arteriovenous communications that are almost entirely made of smooth muscle.

If peripheral circulation is intact, hard eschars from infarcted skin and/or muscle on the legs should be excised primarily.

If circulation is inadequate, amputation may be the only way to stop the advance of ascending gangrene.

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Consultations

CE can cause severe dysfunction of practically any organ, but renal emboli resulting in hypertension and renal insufficiency or failure is the most common complication. Management by a nephrologist, with possible referral to a dialysis service, may be necessary.

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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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