eMedicine Specialties > Dermatology > Internal Medicine

Cutaneous Cholesterol Emboli

Author: Robert A Schwartz, MD, MPH, Professor and Head of Dermatology, Professor of Medicine, Professor of Pediatrics, Professor of Pathology, Professor of Preventive Medicine and Community Health, UMDNJ-New Jersey Medical School
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
Contributor Information and Disclosures

Updated: Dec 26, 2008

Introduction

Background

The general term atheromatous emboli describes the embolization of any atheromatous material. Atheroemboli refers to the dislodgment of relatively large portions of atheromatous plaques containing RBCs and fibrin aggregates, which includes cholesterol crystals of sufficient size to occlude a major systemic artery and potentially result in major organ dysfunction. Cholesterol emboli (CE), on the other hand, result from ulceration of plaques and the subsequent release of cholesterol crystals. These emboli are smaller and usually more numerous, often producing multisystem disease.

The term cutaneous CE (CCE) is used when CE result in disease of the skin. The terms peripheral emboli, lower extremity atheromatous emboli syndrome, blue toe syndrome, purple toe syndrome, and trash foot refer to special cases of CE to the lower extremities in which cutaneous manifestations are usually present, the latter 3 occurring in association with anticoagulation or vascular surgery.

In 1945, Flory was the first to suggest that CE may produce skin disease.1 His hypothesis was later validated by Hoye and associates in 1959, who observed arteries occluded with cholesterol crystals in areas of gangrene on the feet and toes.2

CCE is a disease primarily of elderly white men with ulcerous atherosclerosis. Atherosclerotic foci release cholesterol crystals spontaneously or after anticoagulation or endovascular manipulation, inducing the obstruction of small arteries. Cholesterol embolization syndrome is a systemic disease due to distal showering of cholesterol crystals after angiography, major vessel surgery, or thrombolysis. Obstruction of cutaneous vasculature most often results in a clinical picture of livedo reticularis (LR). It is more common in patients with atherosclerotic disease, hypertension, a history of smoking, and elevated baseline plasma C-reactive protein levels. Gangrene, cyanosis, ulcers, nodules, and purpura can also be observed. In cases of multisystem involvement, CCE may masquerade as many different diseases, but the clinical picture most often mimics a vasculitis. Skin or muscle specimens demonstrate the cholesterol crystals characteristic of this disease.

Treatment is based on the identification of the source of emboli through angiography and on the exclusion of that source from the circulation. Medical therapy has largely been unsuccessful. Gangrene necessitating amputation is the major complication of CCE, but complications may occur in practically any organ system. Without surgery, CCE is a recurrent process with a high mortality rate.

Pathophysiology

The most likely explanation for the cutaneous manifestation of CCE is trapping of cholesterol crystals in blood vessels leading to occlusion and tissue ischemia. Other contributing factors include underlying lowered arterial pressure from proximal atherosclerosis and the ability of emboli to activate the complement system.

The pattern of LR may be the first clinical sign of CCE and is thought to result from incomplete disturbance of circulation and desaturation of blood that initially occurs with subtotal occlusion of vessels.3,4,5,6,7 As spasm and complete occlusion occur, the other signs of CCE become evident. In addition to the blockage of small vascular channels, lower arterial pressure from narrowing of larger proximal arteries may be necessary for the cutaneous manifestations of CCE because intact collateral supply should normally avert it. In one study, injections of a cholesterol suspension in the femoral arteries of dogs produced gangrene, but only in cases with associated thrombosis of the femoral artery. This indicates that embolism is a contributing factor in necrosis with a vascular supply already compromised by atherosclerosis or other occlusive disease. Neither thrombosis alone nor CE alone would produce necrosis.

Other evidence suggests that in addition to a purely mechanical effect, crystalline cholesterol may amplify infarctive tissue damage through the activation of plasma complement, which is capable of potently aggregating polymorphonuclear (PMN) leukocytes and provoking them to damage endothelial cells via toxic oxygen radical release. In both experimental and clinical infarction, evidence of plasma complement activation, often with depletion of complement components, is observed. Animals depleted of complement prior to experimental infarction experience smaller infarcts than controls. In one report, a man suspected of having CE with cutaneous lesions, including LR and digital infarcts, reportedly had plasma with PMN leukocyte–aggregating activity that contained a component of molecular weight and antigenicity consistent with C5a.

Cholesterol crystals and lipids from atheromata incubated with plasma or serum activate complement, as evidenced by immunoelectrophoresis that showed conversion of C3 to C5. On the other hand, serum or plasma depleted of complement or from a patient with congenital C5 deficiency resists activation. PMN leukocytes incubated with endothelial cells to which C5a or cholesterol-incubated plasma was added show evidence of endothelial damage via increased superoxide production, while the addition of plasma alone or cholesterol-incubated plasma without PMN leukocytes does not cause any damage beyond that which spontaneously occurs. This damage is partially inhibited by the addition of superoxide dismutase and catalase.

A related eMedicine article is Cutaneous Manifestations of Cholesterol Embolism.

Frequency

United States

The frequency of CCE is difficult to estimate because routine necropsy is often limited and does not include evaluation of the skin; however, because the abdominal aorta is usually the site of the most advanced intimal disease, one would anticipate that the lower extremities and associated skin and musculature would be one of the most frequently involved sites. In one study, skin and muscle biopsy specimens were obtained from the lower extremities of 100 consecutive autopsies and a 4% rate of CCE was observed. In a large review of 223 patients with all types of CE, 78 (35%) had skin involvement.

International

In the Netherlands, cutaneous involvement is observed in approximately 24% of cases of CE.8

Mortality/Morbidity

In the most extensive review of CCE cases, the mortality rate was very high. Forty-nine (78%) of 68 patients died.

Race

Of 31 cases of CCE in which race was mentioned, all patients were white.

Sex

In the same study, 64 (82%) of 78 cases of CCE were in men.

Age

Ages of those affected with CCE in the same study ranged from 26-90 years (mean, 63 y).

Clinical

History

  • In addition to describing the typical cutaneous signs of CCE, patients also often report the following:
    • Repetitive bouts of sudden spontaneous severe pain: The character of the pain has been described as tightness, burning, stinging, or soreness.
    • Myalgias
    • Claudication in the lower half of the body that may be exacerbated by cold or dependency
  • Numbness, coolness, and paresthesias of the extremities have also been reported.
  • According to Fukumoto in 2003, the diagnosis of CCE can be made when patients who undergo left-sided heart catheterization have peripheral cutaneous involvement (LR, blue toe syndrome, and digital gangrene) or renal dysfunction.9 Elevated preprocedure plasma levels of C-reactive protein are linked with subsequent CCE in patients who undergo vascular procedures.

Physical

  • The most comprehensive review of CCE is by Falanga and associates from 1986.10 The cutaneous findings in 78 patients with CE were LR in 38 (49%), gangrene in 27 (35%), cyanosis in 22 (28%), ulceration in 13 (17%), purple toes in 11 (14%), nodules in 8 (10%), and purpura in 7 (9%). Many of these signs are exacerbated with limb dependency.
    • LR was usually bilateral and almost always involved the feet and legs, extending to the thighs, trunk, and even upper extremities in some. In one review, it was observed as late as 5-16 weeks after an inciting event.
    • Gangrene was neither consistently unilateral nor bilateral and primarily occurred in the toes.
    • Cyanosis was usually bilateral and located on the toes but also involved the feet and, rarely, the upper extremities.
    • Ulceration was more often unilateral and occurred mostly on the toes and feet but was also observed on the legs.
    • Nodules occurred exclusively on the lower extremities, mostly from the ankles to the waist.
    • Purpura was always below the knee, mostly on the legs and feet.
  • Several reports have emphasized involvement of the genitals. Findings have included scrotal ischemia and necrosis and penile necrosis with ulceration of the glans. Balanitis may progress to preputial necrosis.
  • Other associated cutaneous findings include splinter and subungual hemorrhages.
  • Distal pulses are often reported to be normal in persons with CCE, especially early in the disease. However, in a review of 51 cases of CCE in which pulses were mentioned, 29 (57%) were normal, 20 (39%) were bilaterally decreased, and 2 (4%) were absent.
  • The most common noncutaneous findings in patients with CCE are fever, myalgia, weight loss, altered mental status, and the sudden onset of arterial hypertension.

Causes

Ulcerated atherosclerosis is the primary risk factor for CCE and is especially prevalent in persons with aortic aneurysms; however, the size of the aneurysm does not correlate with the risk of emboli. Single cases of fibromuscular dysplasia of the external iliac arteries and aortic dissection leading to emboli have also been reported. In the latter 2 cases, abnormal turbulence near the diseased artery and disruption of an atheromatous plaque in the area of dissection were thought to be the cause of embolization. In all these patients, CCE can be spontaneous or precipitated by anticoagulant therapy, vascular procedures or surgery, or, rarely, trauma.

In one series of patients with CCE, 26 (36%) of 73 were taking anticoagulants and 31% had undergone vascular procedures. In a series of 15 cases of peripheral emboli, 13 were spontaneous and 2 followed infrarenal aortic operations. In a series of 13 patients with spontaneous CCE, 4 had aortic aneurysms, 2 had femoral aneurysms, and 7 had severe ulcerative atherosclerosis of the aortoiliac segments. In a larger review of 85 cases of peripheral atheroemboli, 38 (45%) were from proximal aneurysms, 37 (43%) were unexplained, 4 were from a nonaneurysmal source, 3 were from other sources, and 3 were iatrogenic.

While the abdominal aorta has traditionally been considered the source of embolization, some have observed embolization from more distal vessels of the arterial tree. In one study, patients with blue toe syndrome were found to have aortoiliac and peripheral (superficial femoral or popliteal artery) atherosclerosis. Surgical exploration of the peripheral lesions revealed ulcerated plaques or focal stenosis, both of which had adherent white thrombi that were interpreted as evidence of these lesions being the source of the emboli. Surgical correction of the peripheral lesions prevented recurrence at 8-24 months of follow-up. In another study on the source of peripheral emboli, 14 were from the aortic or iliac vessels and 28 were below the inguinal ligament. On the other hand, a smaller study showed 8 (57%) aortoiliac lesions versus 6 (43%) femoropopliteal lesions. Thoracic disease, which is more common in conditions such as syphilis or gout, has also been shown to lead to peripheral emboli.

  • Vascular manipulation, either for radiographic or surgical purposes, results in embolization through the mechanical disruption of atherosclerotic plaques by needles, wires, catheters, or clamps and is especially common after prolonged or difficult catheterizations.11,12 Less often, a stream of injected contrast material may dislodge material.
    • Implicated vascular procedures and surgeries include angiography (most often aortography), heart catheterization, coronary artery bypass graft (CABG) surgery, and percutaneous transluminal coronary angioplasty.
    • Procedures near vascular structures that may involve manipulation of such structures can also result in CE; this has been reported after transhiatal esophagectomy.
  • Anticoagulants are frequently reported as a cause of CCE, and such occurrences are often designated blue or purple toe syndrome.
    • Anticoagulants are speculated to cause CE by preventing or removing adequate thrombosis over ulcerated atheromatous lesions.
    • In one study, embolization was observed to occur 3 weeks to several months after initiation of therapy.
    • Agents reported to cause CE include heparin, bishydroxycoumarin, warfarin sodium, streptokinase,13,14,15 and intravenous tissue plasminogen activator.16,17,18
    • In an attempt to define the role of anticoagulation in CE, a prospective study examined 60 patients with acute myocardial infarction who underwent CABG surgery. Twenty-nine received thrombolytic therapy for myocardial infarction, and 31 were treated conservatively. During the CABG surgeries, 2 muscle biopsy specimens and 1 skin biopsy specimen were taken from vein harvest sites. CE was observed in 4 of 29 and 3 of 31 specimens, respectively.
  • Embolization following blunt abdominal trauma from an automobile accident has been reported to precede CE. Vibration of the aortic wall may have dislodged the atheroma.

More on Cutaneous Cholesterol Emboli

Overview: Cutaneous Cholesterol Emboli
Differential Diagnoses & Workup: Cutaneous Cholesterol Emboli
Treatment & Medication: Cutaneous Cholesterol Emboli
Follow-up: Cutaneous Cholesterol Emboli
Multimedia: Cutaneous Cholesterol Emboli
References
[ CLOSE WINDOW ]

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Further Reading

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Keywords

atheroembolism, atheromatous embolism, atheromatous microembolism, cholesterol embolism, cholesterol crystal embolism, multiple cholesterol emboli syndrome, CCE, CE, atherosclerosis, atherosclerotic disease, livedo reticularis, LR, angiography, peripheral emboli, lower extremity atheromatous emboli syndrome, blue toe syndrome, purple toe syndrome, trash foot

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Contributor Information and Disclosures

Author

Robert A Schwartz, MD, MPH, Professor and Head of Dermatology, Professor of Medicine, Professor of Pediatrics, Professor of Pathology, Professor of Preventive Medicine and Community Health, UMDNJ-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.

Medical Editor

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.

Pharmacy Editor

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
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: 3M Pharmaceutical Grant/research funds Other; Graceway Pharmaceuticals Grant/research funds Other

Managing Editor

Jeffrey Meffert, MD, Assistant Clinical Professor of Dermatology, University of Texas Health Science Center-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.

CME Editor

Catherine Quirk, MD, Clinical Assistant Professor, Department of Dermatology, Brown University
Catherine 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, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

 
 
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