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Angiodermatitis
In general, the lower extremities are subjected to greater hydrostatic pressures than other anatomic sites; in keeping with this
physiologic distinction, the vessels of the skin of the lower extremities, particularly those of the legs, are likely to respond to minor inflammatory processes, or to neoplasms, with a proliferative hyperplasia.
These responses are manifested by lobular collections of tortuous, thick-walled vessels; the vascular changes are most prominent in the papillary dermis and the upper portion of the reticular dermis. In association
with abnormal increases in venous pressures, such as those that occur in stasis dermatitis, these vascular changes are a variable, but sometimes prominent feature (S8C28P14-1).
In stasis dermatitis, lobular collections of abnormal, tortuous, thick-walled vessels are prominent in the upper portion of the
dermis (S8C27P13-1-7) and may even be found at deeper levels. The
degree of the angioplasia is proportional to the degree of stasis. The vessels are supported by a watery or myxoid matrix. In uncomplicated cases, the perivascular spaces are relatively free of inflammatory cells.
In symptomatic angiodermatitis, in which the vascular changes accompany an inflammatory disorder such as nummular eczema, or arise in association with an neoplasm, there may be prominent infiltrates of inflammatory
cells (S8C28P14-3). In severe examples, thick-walled veins may be a
prominent feature in the lower portion of the dermis. In a stasis ulcer, the lobular aggregates are found in the dermis adjacent to the ulcer and may also be represented in the dermis beneath an ulcer (S8C27P13-3, & S8C28P14-4-6). In severe stasis dermatitis, plasma cells are a common
feature of the infiltrates.
Samlaska CP, James WD: Superficial thrombophlebitis II. Secondary hypercoagulable states. J Am Acad Dermatol 1990;23: 1-18.
Perivascular spaces beneath a stasis ulcer often contain prominent infiltrates of inflammatory cells, including plasma cells.
Hemosiderin deposits may be a prominent feature (S8C28P14-2). In
angiodermatitis, it fairly common for some of the vessels in the lobules to show focal areas of fibrinoid necrosis and thrombosis (livedo vasculitis-like changes) (S8C27P13-5). Livedo vasculitis is a generic designation for thrombotic
disorders affecting small vessels of the skin of the extremities (S8C29P15-3-5).
Such lesions heal with the formation of a poorly vascularized scar (atrophie blanche). The pattern of a thrombotic angiitis, especially in the absence of significant angiodermatitis, carries with it the implication
that there may be a generalized coagulopathy.
The lobules of newly formed vessels in a lesions of angiodermatitis generally are most prominent in the
papillary dermis. In contrast, in non-polypoid lesions of Kaposi disease (fibrotic variant), the vascular changes tend to spare the papillary dermis.
Generally, granulation tissue in the bed of an ulcer is distinguished by regularly spaced, parallel vessels in a delicate myxoid
matrix. Inflammation is a variable feature (S8C29P15-1& 2).
Valencia IC, et al: Chronic venous insufficiency and venous leg ulceration. J Am Acad Dermatol 2001;44: 401-21.
Arbiser JL: Angiogenesis and the skin; a primer. J Am Acad Dermatol 1996;34: 486-97.
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