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An Urban Experience
C. Pucheu-Haston1
1Louisiana State University School of Veterinary Medicine, Veterinary Clinical Sciences, Baton Rouge, USA
CM Pucheu-Haston, DVM, PhD, DACVD
Department of Veterinary Clinical Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA
Vascular inflammation and / or insufficiency (vasculitis, vasculopathy) is a common cause of dermatologic disease in humans and animals. Disruption of the cutaneous vasculature may be associated with a
number of local or systemic disorders, including drug
or vaccine administration, infection, inflammation, neoplasia, hypersensitivity, photodermatitis and immune mediated phenomena, or may be idiopathic (Table 1). Regardless of the underlying cause, the resulting vascular compromise impedes tissue oxygenation, causing cutaneous atrophy and potentially overt necrosis. Proper management of these phenomena requires a thorough understanding of potential etiologies and appropriate diagnostic measures.
Immunopathogenesis: Numerous immunologic phenomena may result in the development of vasculitis. IgE-mediated mast cell degranulation may be seen
in early urticarial vasculitis. The development of anti- neutrophil cytoplasmic antibodies can trigger mediator release and secondary endothelial damage. These antibodies have been reported to play a role in some forms of vasculitis in humans, although this association with vasculitis has not yet been reported in animals.
Perhaps the most relevant pathophysiologic mechanism in the development of vasculitis is immune complex formation / deposition (Type III hypersensitivity). Large antigen-antibody complexes deposit in blood vessels, resulting in the activation of complement and endothelial damage. This in turn results in the recruitment of neutrophils and further cell damage.
Clinical appearance, general: Mildly affected animals may present with only alopecia (secondary to ischemic follicular atrophy), recurrent urticaria or edema. More severe cases may be associated with crusting, erosion,
ulceration or frank necrosis, especially on areas with poor collateral circulation (such as the pinnae and tail
tip) or which are prone to trauma (face and over bony prominences). Lesions often heal with scarring. Footpads (especially digital pads) may develop circular “punched- out” areas of erosion or ulceration. Another common syndrome is palpable purpura, in which raised indurated areas of erythema or violaceous change are seen.
Patients with vasculitis may or may not demonstrate systemic signs at the time of presentation.
Concurrent organ involvement may include kidneys (glomerulonephritis), mesothelium (pleuritis, pericarditis, peritonitis), the gastrointestinal tract, muscle (myositis), joints (polyarthropathy), heart, lungs and CNS. Depending upon the degree of associated endothelial damage, patients may be in a hypercoagulable state secondary to widespread platelet and clotting factor activation.
Specific clinical vasculitis syndromes:
Vaccine induced vasculitis: Any vaccine may be associated with this phenomenon, especially rabies vaccines. Lesions may occur at the site of vaccination and/or at locations distant from it. Injection site lesions often appear initially as dermal induration, which may
be followed by focal alopecia and cutaneous atrophy. Atrophic lesions often feel somewhat “adhered” to underlying tissue. Myositis or muscle atrophy may also be seen. Distant lesions typically affect areas with poor collateral circulation and/or areas prone to trauma. Mild lesions may present with focal or multifocal alopecia, while more severe lesions may demonstrate crusting, erosion and ulceration. “Punched out” lesions on the digital pads are particularly suggestive. Sloughing of one or multiple nails and/or erosion of mucous membranes may be seen. Most patients are systemically well, but severe systemic involvement has been reported.
Fulminant multisystemic vasculitis associated with
human serum albumin (HSA) administration: Several cases have been reported of vasculitis following a single administration of HSA. In one report, several healthy dogs administered HSA developed reactions between
5 and 13 days following administration. These included lameness, edema, “cutaneous lesions indicative of vasculitis”, ecchymoses, vomiting, bloody diarrhea
and facial muscle atrophy. One of these dogs had also experienced an immediate hypersensitivity event. Four of the dogs required hospitalization. In two dogs, symptoms progressed to include oliguric renal failure and pulmonary edema, resulting in death.
Cutaneous and renal vasculopathy: This condition has been reported most commonly in racing greyhounds fed raw or undercooked beef, but can be seen in non-racing

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