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Cutaneous Cholesterol Emboli: Differential Diagnoses & Workup

Author: Robert A Schwartz, MD, MPH, Professor and Head, Dermatology, Professor of Pathology, Pediatrics, Medicine, and 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: Nov 15, 2009

Differential Diagnoses

Other Problems to Be Considered

Polymyositis
Mononeuritis multiplex
Giant cell arteritis
Heparin necrosis
Wegener granulomatosis or an allergic vasculitis
Buerger disease
Subacute bacterial endocarditis
Symmetric peripheral gangrene from sepsis
Diabetic vasculitis or neuropathy
Other collagen vascular diseases
Cryoglobulinemia
Immune complex disease
Macroglobulinemia
Dysproteinemias
Raynaud phenomenon
Obliterative arteriosclerosis
Thrombophlebitis
Polycythemia vera

CE may be classified as a cyanotic-infarctive pseudovasculitis due vaso-occlusion by emboli, thrombi, or fibrointimal hyperplasia (endarteritis obliterans).20 Thus, the differential diagnosis of CE includes purpura fulminans, warfarin (Coumadin) necrosis, antiphospholipid antibody syndrome, cardiac myxoma, calciphylaxis, and radiation arteritis.

CE has been called the great masquerader because of the variety of clinical manifestations. One of the more common clinical pictures simulates a vasculitis. In a study of 73 cases of CCE, 12 (16%) were mistaken for vasculitis, 9 (12%) specifically for polyarteritis nodosa (PAN). Patients with CCE have also been mistakenly diagnosed with polymyositis, mononeuritis multiplex, giant cell arteritis, and heparin necrosis.

In cases simulating PAN, patients often report an abrupt onset of lower extremity pain followed by the appearance of tender nodules and LR in the presence of normal pulses. Systemic symptoms may involve the gastrointestinal and nervous systems. Laboratory findings include hypertension, neutrophilic leukocytosis, eosinophilia, elevation of the sedimentation rate, melena, hematuria, albuminuria, and azotemia.

Helpful in distinguishing between the two is a history of hypersensitivity in patients with PAN or a history of intra-arterial manipulation in patients with CCE. Clinically, PAN has a more generalized distribution than CE, which favors the lower half of the body because of the severity of abdominal aortic disease. Ischemic neuropathy and joint involvement are also common in patients with PAN but are rare in persons with CE.

Histologically, PAN may involve larger arteries or veins, while in CE, adventitial fibrosis is insignificant, vascular lumina and fibrinoid necrosis are eccentric, and necrosis usually involves only a portion of the wall. The principal cellular reaction is endothelial and mononuclear with few acute inflammatory cells. Most importantly, close inspection should reveal cholesterol clefts. Finally, a response to steroids may also help differentiate PAN from CE.

Two patients with presentations similar to polymyositis have been described who experienced the sudden onset of leg pain, cool legs with normal peripheral pulses, petechiae, LR, and elevated tender nodules that represented muscle necrosis (after biopsy). Laboratory abnormalities included elevation of the sedimentation rate, serum aspartate aminotransferase level, lactate dehydrogenase level, and creatine kinase and aldolase values and a myopathic pattern on electromyography.

Workup

Laboratory Studies

  • The most common findings in one group of patients with CCE were an elevated erythrocyte sedimentation rate, blood eosinophilia, and rising serum urea nitrogen and creatinine values.
  • Others have reported positive findings for antinuclear antibodies, rheumatoid factor, perinuclear antineutrophil cytoplasmic antibodies with antimyeloperoxidase specificity, and hypocomplementemia.

Imaging Studies

  • Angiography is useful for identifying arterial lesions that may represent the source of emboli. Studies should include the entire abdominal aorta with iliac, femoral, popliteal, and tibial arteries.
  • Some also recommend digital arteriography, which may demonstrate a sharp cutoff pattern representing embolization to digital arteries.
  • Biplanar arteriography, including lateral projection, is recommended to detect anterior and posterior lesions that may be missed with the standard frontal projection.
  • Ultrasonography is a useful noninvasive method to assess for aortic aneurysms.
  • Transesophageal echocardiography can be especially useful in identifying thoracic aortic sources of CE but is limited in its ability to visualize the abdominal portion.

Other Tests

  • Ophthalmoscopy may reveal bright orange or yellow plaques in the retinal arterioles, representing CE.
  • Careful palpation of the abdomen and auscultation for pulsations, thrills, and bruits should be performed to assess for aneurysms.

Procedures

  • A skin or muscle biopsy is the most effective method used to diagnose CCE. Its efficacy has been proven in an autopsy study of 20 patients with confirmed CE.
    • Random biopsy specimens from the gastrocnemius and quadriceps muscle groups were positive for emboli in 19 cases.
    • Seven of 7 patients with clinical symptoms suggestive of CCE had a positive diagnosis antemortem after muscle biopsy.
    • In a review of CCE, diagnosis was possible in 22 (92%) of 24 cases in which a skin biopsy was performed.
    • Many have emphasized the need for deep biopsies (eg, incisional), in order to obtain vessels of sufficient size that are likely to be occluded with emboli, and the need for subserial sectioning of specimens.
  • Percutaneous renal biopsy and endoscopic gastrointestinal biopsy are more invasive methods of diagnosing CE and are used in cases of systemic embolization.
  • Amputated limbs or toes can be scrutinized for emboli in the vessels.
  • Embolectomy specimens can also be examined for cholesterol crystals.
  • Although rare, cholesterol clefts have been found in bone marrow biopsy samples and remnants from prostatic curettage.

Histologic Findings

When examined with polarized light, cholesterol crystals in frozen section appear as birefringent rhomboids. They can also be identified by the Schultz modification of the Lieberman-Burchard reaction for cholesterol. Crystals are green within a few minutes and then brown at 30 minutes. Paraffin embedding used in routine histologic processing dissolves cholesterol crystals, replacing them with characteristic biconvex or lenticular clefts or spaces.

Emboli have been observed in the lumina of arteries ranging from 55-900 mm in external diameter but favor vessels in the 150- to 200-µm range. Initially, cholesterol clefts with or without hyaline material and rarely an aggregate of lipid-filled histiocytes are observed. Thrombosis superimposed on the embolus is variable. Shortly thereafter, reactive hyperplasia of the intima occurs with dense infiltration of the media and adventitia or surrounding tissue with neutrophils and, occasionally, eosinophils. Fibrinoid necrosis of the vessel walls and interruption of the internal elastic membrane are also variable findings.

In older lesions, the infiltrate is replaced by mononuclear and foreign body giant cells and prominent fibrosis. The crystals may persist, disappear, or extrude through vessel walls. In heavily infarcted areas, coagulative and early liquefactive necrosis of the epidermis, dermis, and panniculus may be observed.

While generally considered pathognomonic for CCE, the presence of intravascular cholesterol crystals has recently been described in biopsy and excision specimens of nonmelanotic skin cancers from patients with no evidence of CCE. The authors of one paper suggest that in such cases, this finding may be artifactual and perhaps related to wound healing.

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

cutaneous cholesterol embolism, 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, Dermatology, Professor of Pathology, Pediatrics, Medicine, and 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, 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.

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 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, 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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