Treatment of Vasculitis

By | 2012-11-10

Treatment of purpura hemorrhagica and similar idiopathic vasculitides consists of the following: (1) removing the antigenic stimulus; (2) suppressing the immune response; (3) reducing vessel wall inflammation; and (4) providing supportive care. Any drugs given when the clinical signs occurred should be discontinued, or, if continued medication is necessary, an alternate drug should be chosen from a chemically unrelated class. A thorough examination should be performed to identify a primary disease process. Any bacterial pathogens should be cultured and an in vitro sensitivity performed. Because most cases of purpura hemorrhagica are a sequela of Streptococcus equi infection, penicillin (procaine penicillin G 22,000-44,000 U/kg IM q12h or sodium or potassium penicillin 22,000-44,000 U/kg IV q6h) should be administered for a minimum of 2 weeks unless specifically contraindicated. Any accessible abscess should be drained. If gram-negative bacteria are suspected or isolated, additional appropriate antimicrobial therapy should be used. Antimicrobial therapy is also indicated to limit or prevent secondary septic complications such as cellulitis, tenosynovitis, arthritis, pneumonia, and thrombophlebitis.

Systemic glucocorticoids are warranted because purpura hemorrhagica and other undefined vasculitides are most likely immune-mediated. In addition, systemic glucocorticoids reduce inflammation of the affected vessel walls and subsequent edema formation. Dexamethasone (0.05-0.2 mg/kg IM or IV q24h) or prednisolone (0.5-1.0 mg/kg IM or IV q24h) may be used; however, clinical experience indicates that dexamethasone is more effective during initial therapy. The minimum dose that provides a decrease in clinical signs should be used. After substantial reduction and stabilization of clinical signs, the dose of glucocorticoids may be decreased by 10% per day over 10 to 21 days. When the dose of dexamethasone is 0.01 to 0.04 mg/kg per day, it may be given orally; alternatively, prednisolone may be substituted at ten times the dexamethasone dose. The bioavailability of oral prednisolone is 50%; thus an effective parenteral dose administered orally may result in relapse of clinical signs. Prednisone is poorly absorbed from the gastrointestinal tract and is not detectable in the blood of most horses after oral administration; thus its use is not recommended. Hydrotherapy, application of pressure bandages, and hand-walking should be used to decrease or prevent edema. Furosemide (1 mg/kg IV q12h) may help reduce edema in severe cases. A tracheostomy may be indicated if respiratory stridor is present from edema of the nasal passages, pharynx, and/or larynx. Dysphagic horses should be supported with intravenous or nasogastric administration of fluids. Nutritional support may be necessary in horses with prolonged dysphagia. Nonsteroidal antiinflammatory drugs (flunixin meglumine 1.1 mg/kg IV, IM or PO q12h or phenylbutazone 2.2-4.4 mg/kg IV or PO q12h) are indicated to provide analgesia in horses with lameness, colic, myalgia, or other painful conditions. NSAIDs may also help reduce the inflammation in affected vessel walls.

Horses with equine viral arteritis do not require specific therapy because the majority of cases recover uneventfully. Glucocorticoids are contraindicated because vessel wall damage results from direct viral injury. Occasionally horses with severe clinical signs of lower respiratory disease will need antimicrobial therapy to prevent or treat secondary bacterial pneumonia. Horses with EIA are infected for life. Glucocorticoids are contraindicated because they may result in increased viral replication and occurrence of clinical disease. Horses with equine ehrlichiosis may benefit from glucocorticoid therapy; however, they should be treated with oxytetracycline to eliminate the organism (see: “Equine Monocytic Ehrlichiosis” and: “Hemolytic Anemia”). Horses with photoactivated vasculitis should be stabled during daylight hours to prevent any further exposure to sunlight. The vascular inflammation should be treated with systemic glucocorticoids in a regimen similar to that for purpura hemorrhagica. Topical applications of glucocorticoids with or without antibiotics are not effective. Irritating topical solutions should not be used.