Nicaeus T, Wilhelm H
Abteilungen I (Allgemeine Augenheilkunde mit Poliklinik), Augenklinik der Eberhard-Karls-Universität Tübingen.
Klin Monbl Augenheilkd. 1999 Mar;214(3):175-7. doi: 10.1055/s-2008-1034771.
Infections with varicella zoster virus may involve the optic nerve and the retina. Different pathomechanisms have been discussed. We present a case with an autoimmune inflammatory reaction according to the clinical course.
A 69-year-old female was referred to our clinic because of suspected bilateral anterior ischemic optic neuropathy. She complained of severe visual loss the day before admission. Her ophthalmological and general history was unremarkable apart from treatment with 5 to 7.5 mg prednisolone alternately because of rheumatoid arthritis. Best corrected visual acuity was 1/15 OD and 0.1 OS. A relative afferent pupillary defect on the right eye was present. Optic disc oedema with multiple hemorrhages of the retina extending into the peripheral funds, slightly attenuated retinal arteries and macular oedema were seen fundoscopically in both eyes. THERAPY AND CLINICAL OUTCOME: After immediate treatment with steroids (initial dose 250 mg prednisolone per day) visual acuity improved. Because of a clinically suspected and serologically proven active varicella-zoster infection an additional virostatic therapy with valaciclovir was started and steroids were lowered gradually. Within 2 months, visual acuity increased to 0.8 OD and 1.0 OS. Oedema of optic discs and macula resolved and retinal hemorrhages disappeared.
A severe hemorrhagic neuro-retinitis involving the optic discs was seen in the course of a varicella-zoster infection, possibly reactivated by chronic steroid therapy of a rheumatoid arthritis. Because of the normalization of visual function an ischemic pathogenesis is unlikely. An autoimmune inflammatory reaction seems to be the predominant mechanism, supported by the good effect of steroid and valaciclovir therapy.
