Intravitreal triamcinolone in two patients with refractory macular oedema in sarcoid uveitis

Editor, Cystoid macular oedema (CME) is probably the most common cause of visual loss in posterior uveitis caused by sarcoidosis. The most common treatments to control the inflammation are corticosteroids given periocularly or systemically, cyclosporin, and vitrectomy (McCluskey et al. 2000; Kiryu et al. 2001). Recently, it has been suggested that intravitreal triamcinolone injections may be effective in controlling CME in patients with posterior uveitis (Antcliff et al. 2001; Young et al. 2001; Karacorlu et al. 2004). We herein report two cases of refractory macular oedema in sarcoid uveitis, which improved after intravitreal injections of triamcinolone A 67-year-old woman presented in November 1999 with floaters and blurring of vision in both eyes. Visual acuity (VA) was 20/50 RE and 20/200 LE. Cystoid macular oedema was present in both eyes. The patient was treated with high doses of corticosteroids and cyclosporin. As the vision continued to deteriorate, peribulbar injections of 40 mg triamcinolone were given in both eyes, with only slight improvement. In 2002 the patient developed cataract and cataract extraction and vitrectomy were performed in both eyes, with almost no visual improvement. In August 2003, VA was 20/50 RE and 20/200 LE. Optical coherence tomography (OCT) showed retinal thickening in the macula of 550 µm RE and 700 µm LE (Fig. 1). Both eyes were treated with an intravitreal injection of 4 mg triamcinolone. Two weeks after the injections, VA improved to 20/40 RE and 20/80 LE. Examination by OCT showed normal maculae without CME (Fig. 2). In May 2004, the subject's vision deteriorated again and another intravitreal injection was given with the same good result. By October 2004 the subject was no longer receiving any systemic treatment and VA was 20/30 RE and 20/60 LE. Examination by OCT showed the absence of CME. The OCT picture shows the RE of case 1 before intravitreal injection. A prominent cystoid macular oedema is present. The same eye as in Fig. 1, 4 weeks after the injection. The macula oedema has disappeared and the normal foveal shape is visible. A 60-year-old woman presented in October 2000 with floaters and blurring of vision in both eyes. Visual acuity was 20/30 RE and 20/50 LE. Cystoid macular oedema was present in both eyes. The patient was managed as case 1, with high doses of corticosteroids and cyclosporin. Peribulbar injections of metylprednisolone, cataract extraction and vitrectomy were performed in both eyes. Although the LE responded favourably to the vitrectomy, the RE still had CME. In September 2003, VA was 20/50 RE and 20/30 LE. Examination by OCT showed retinal thickening of 450 µm RE and 297 µm LE. An intravitreal triamcinolone injection was given to the RE. One month later, VA had improved to 20/30 and the OCT measurement was 420 µm. Both patients were given all conventional treatments including vitrectomy. However, only in one eye did the uveitis and CME settle on this. The other three eyes improved only when intravitreal injections of triamcinolone were given and it was possible to discontinue systemic treatment in both patients. It seems reasonable to suggest that intravitreal injections of triamcinolone may represent a viable treatment alternative in persistent CME caused by ocular sarcoidosis, thus reducing, and possibly even eliminating, the need for systemic treatment.