Overview

• Blood vessel inflammation caused by endothelial injury or extension of adjacent inflammation or infection.
• Endothelial damage by infectious agent, parasite infestation, endotoxin, or immune complex deposition initiates local inflammation, neutrophil accumulation, and complement activation. Neutrophils release lysosomal enzymes, leading to necrosis of vessel wall, thrombosis, and hemorrhage. In humans and dogs with polyarteritis nodosa, intimal proliferation and vessel wall degeneration and necrosis predominate and lead to hemorrhage, thrombosis, and necrosis of involved vessels and adjacent tissues in most patients.
• Non-dermal vasculitis (e.g., renal, hepatic, and serosal surfaces of body cavities) may be the mechanism leading to development of clinically apparent signs of systemic disease (e.g., polyarthritis and proteinuria) without causing obvious external lesions.

Signalment

Dog and cat

Signs

Causes & Risk Factors

Differential Diagnosis

• Cutaneous signs developing after administration of medication implicate drug reaction (usually not immediate, may develop after days or weeks).
• Vasculitis associated with polyarthropathy and pyrexia implicates immune or infectious cause.
• Cold hemagglutinin disease suggested by distribution of cyanotic or necrotic lesions (nose, ears, toes, tail tip, prepuce) and history of exposure to cold.

CBC/Biochemistry/Urinalysis

Results depend on underlying disease.

Other Laboratory Tests

• Serologic tests may aid diagnosis of infectious (i.e., rickettsial, Leishmania) disease.
• ANA titer positive in patients with SLE, may also be positive in patients with other systemic illnesses.
• Occult heartworm test positive in patient with dirofilariasis.
• Angiostrongylus infestation diagnosed by fecal examination and cytologic examination of tracheal wash.

Imaging

Radiographs help diagnose dirofilariasis and Angiostrongylus infection.

Diagnostic Procedures

• Skin biopsy specimen from edge of developing lesion may be diagnostic for vasculitis but may not reveal cause.
• Immunofluorescence test of skin biopsy specimen may rule-out pemphigus and pemphigoid diseases.
• If allergic response is suspected, resolution of signs upon discontinuation of suspect medication or food supports diagnosis.

Drug(s)

• Infectious or immune-related-treat underlying disease (see specific condition); supportive care.
• Lupus-like drug reactions-discontinue drug; supportive care.
• Type III hypersensitivity-discontinue drug; supportive care.
• Polyarteritis nodosa-glucocorticoids and cyclophosphamide (unknown value).
• “Idiopathic” vasculitis-if other causes have been ruled-out, administer dapsone (1 mg/kg PO q8h for 14 days, then 1 mg/kg PO q12h for 14 days, then 1 mg/kg PO q24h; may eventually be decreased to q48h to maintain remission); alternative-sulfasalazine (45 mg/kg PO q8h). Neither drug's effectiveness is well documented. Pentoxifylline has been used in limited numbers of cases at doses of 25–35 mg/kg PO q12h. Immunosuppressive doses of corticosteroids may be helpful in idiopathic cases.

Contraindications/Possible Interactions

• Do not administer sulfasalazine to patients sensitive to sulfonamides.
• Pentoxifylline is a methylxanthine derivative and may reduce blood pressure.

See Also

• Lupus Erythematosus, Systemic
• Vasculitis, Cutaneous

Abbreviations

• ANA = antinuclear antibody
• CNS = central nervous system
• SLE = systemic lupus erythematosus