Skip to main content
Open Access Publications from the University of California

Dermatology Online Journal

Dermatology Online Journal bannerUC Davis

Lividoid Vasculitis

Main Content

Lividoid Vasculitis
Joshua P. Fogelman,MD
Dermatology Online Journal 7(1): 19

Department of Dermatology, New York University

PATIENT: 53-year-old man

DURATION: Three weeks



The patient presented to the New York Harbor Health Care System Dermatology Clinic with a three-week history of an enlarging, painful ulcer on his left ankle. This ulcer was complicated by bacterial infection, which resolved with dicloxacillin therapy. He denied trauma, pruritus, or diabetes mellitus.

His daily dose of aspirin for cardiac prophylaxis was increased to 325 mg. orally twice daily. Control of analgesia was obtained with oxycodone. Initial wound care included Bacitracin ointment covered by gauze; however, the ulcer enlarged and developed rolled borders. The patient was treated with a ten-day, tapered course of systemic prednisone without improvement. After resolution of the infection, weekly applications of Duoderm to the ulcer underneath an Unna boot resulted in improvement of the ulcer with decreased pain.

Past medical history includes hepatitis 30 years ago, renal calculus, and surgery of the left ankle after a fracture in 1991. His mother has sickle-cell trait while his sister has sickle-cell disease. He is not taking any medications and has no known drug allergies.

Physical examination

A tender, irregular, 3.0-x 2.5-cm ulcer in a stellate configuration was noted on the medial aspect of the left ankle with a trace of pedal edema. There was no livedo reticularis.

Figure 1Figure 2

Laboratory data

A complete blood count demonstrated a decreased hematocrit of 36.0% with a normal differential analysis. Liver function tests were normal except for elevated direct and total bilirubin levels of9


Many small blood vessels within the superficial and mid-dermis have thickened walls and fibrin thrombi within their lumens. There was a very sparse, superficial, perivascular lymphocytic inflammatory infiltrate.


Livedoid vasculitis


Livedoid vasculitis, also known as livedo reticularis with summer/winter ulcerations, segmental hyalinizing vasculitis, and atrophie blanche, is a rare, chronic vasculopathic disorder. In most clinical series, there is a female preponderance with age of onset greater than 40 years. Symptoms include pain and swelling of the affected extremity. It is usually not associated with systemic disease, but patients may have associated livedo reticularis, venous insufficiency, arteriosclerosis, or systemic lupus erythematosus. This condition may have a seasonal course, with increased incidence during the winter and summer. The course is chronic with spontaneous remissions and exacerbations. One series reports disease duration ranging from 2.5 months to 21 years.

Livedoid vasculitis presents as purpuric macules and papules that progress to small, tender, irregular ulcers of the lower legs, ankles, and/or dorsal aspects of the feet. These ulcers, which may recur, heal with stellate or polyangular, ivory-white atrophic plaques, sometimes with surrounding hyperpigmentation and telangiectases. Atrophie blanche describes the end stage clinical lesions, which are characterized by irregular, white or ivory, depressed scars on the lower extremities.

Histopathologic examination demonstrates a vasculopathy with fibrin deposition in the vessel wall and/or lumen in early lesions. A predominantly lymphocytic infiltrate and infarction with hemorrhage may be present at this stage. Leukocytoclasis is not observed. Epidermal atrophy with sclerosis of the dermis and a minimal cellular infiltrate characterize late lesions. Vessel walls may have segmental thickening and hyalinization of the intima. Recanalized thrombotic vessels may be noted. The involved vessels may be superficial or deep.

The etiology of this disorder is not known, although the deposition of fibrinoid material in dermal vessels with secondary ischemic change of the overlying epidermis suggests a thrombotic/occlusive mechanism. Hypothesized causes include defective endothelial cell synthesis of tissue plasminogen activator and/or prostacyclin, dysregulation of coagulation and fibrinolysis, dysfunction of platelets or erythrocytes, vasospasm, and changes in hydrostatic pressure.

Therapeutic modalities include antiplatelet agents (aspirin, dipyridamole), fibrinolytic agents (danazol, tissue plasminogen activator), anticoagulant agents (subcutaneous heparin or coumadin), vasodilating agents (nifedipine, nicotinic acid), anti-inflammatory agents (prednisone), and pentoxifylline, which may alter blood viscosity and erythrocyte flexibility. Local debridement and treatment of infection may be indicated. Leg elevation, compression therapy, bed rest, and topical wound care may aid healing.


1. Bard JW, Winkelmann RK. Livedo vasculitis. Segmental hyalinizing vasculitis of the dermis. Arch Dermatol 1967;96(5):489-99. PubMed

2. Drucker CR, Duncan WC. Antiplatelet therapy in atrophie blanche and livedo vasculitis. J Am Acad Dermatol 1982;7(3):359-63. PubMed

3. Shornick JK, Nicholes BK, Bergstresser PR, Gilliam JN. Idiopathic atrophie blanche. J Am Acad Dermatol 1983;8(6):792-8. PubMed

4. Hsiao GH, Chiu HC. Livedoid vasculitis: response to low-dose danazol. Arch Dermatol 1996;132(7):749-51. PubMed

5. Maessen-Visch MB, Koedam MI, Hamulyak K, Neumann HA. Atrophie blanche. Int J Dermatol 38(3):161-72. PubMed

© 2001 Dermatology Online Journal