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108 Clinical Pathways in Neuro-Ophthalmology, second edition potential side effects in patients with GCA (Mizen, 1991). Hunder emphasized that the goal of therapy is to use the lowest dose of steroid over the shortest period of time to adequately control the symptoms of GCA (Hunder, 1990a). Unfortunately, the dosage and duration of therapy are variable among patients and must be determined on an individual and empirical basis (Hunder, 1990a). Gradual tapering of the steroid dose by 10% per week as long as symptoms and ESR remain stable is a reasonable approach. Most patients can be tapered off steroids within 1 year, but some patients (especially those with neurologic or other systemic symptoms) may require prolonged (years) or indefinite therapy. Recurrences may also occur years later. Turner et al reported a normalization of the ESR in 87% of 47 patients within 4 weeks of treatment (Turner, 1974). Huston et al reported a duration of steroid treatment of 1 to 77 months (median 7 months) (Huston, 1978). Cullen and Coleiro felt that an ESR of less than 20 mm=hour was a desirable goal (Cullen, 1976). Delecoeullerie et al reported a mean duration of therapy of 30.9 months in 210 patients (Delecoeullerie, 1988), but Anderson et al reported an average duration of 5 years (Anderson, 1986). Tapering of steroids is equally important as starting therapy in GCA because the risk of fracture is increased sixfold and that of cataract formation fourfold after 5 years of steroid therapy (Robb- Nicholson, 1988). Recurrent symptoms and=or ESR elevation may prompt increasing the steroid dosage, but clinical symptoms may be a better indicator than the ESR alone (Brittain, 1991). As corticosteroid doses are lowered, the ESR may rise and, if it increases to above normal rates, the tapering schedule may be interrupted for 2 to 4 weeks to allow stabilization of the ESR. Although a rise in the ESR is often associated with clinical recurrence of GCA, ischemic complications may occur on steroid therapy despite a stable ESR. Every-other-day steroid therapy does not seem to sufficiently control disease activity but may eventually be used once active GCA is under control. If Major Steroid Complications Occur, Therapy Is Prolonged, or the Disease Is Still Active, What Should Be Done? A repeat TAB could be considered, but it subjects the patient to a second surgical procedure. In addition, as already stated, a negative TAB (first or second), especially after prolonged steroid therapy, does not exclude GCA. Nevertheless, Cohen reported 13 patients with known GCA and a rising ESR with any attempt at tapering steroid therapy (Cohen, 1973). Nine of these patients underwent a second TAB and one of those had a third TAB to determine if active GCA was present histologically or whether the ESR was elevated due to alternative etiologies. Steroid-related complications (e.g., cushingoid appearance, melena, hematuria, osteoporosis) had developed in nine patients. Five of the 10 second TABs (50%) continued to show active inflammation, and patients were continued on steroid therapy, whereas the five (50%) patients with inactive TAB were tapered off steroids. If a second TAB is not performed or the clinical suspicion for active disease remains high, then patients with significant contraindications to steroid therapy, those who fail steroid therapy (Wilke, 1995), and those who develop steroid complications may benefit from other immunosuppressive agents. Steroid derivatives such as deflazacort (Cimmino, 1994) and other immunosuppressive regimens such as cyclophosphamide
Figure 5–1. Evaluation of giant cell arteritis. Arteritic Anterior Ischemic Optic Neuropathy and Giant Cell Arteritis 109
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To our wives, Hilary and Liz and to
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x Preface We would again like to th
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Table 1-12. Clinical Features of Ra
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13 r Sixth Nerve Palsies What is th
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