Acute retinal necrosis secondary to cytomegalovirus

Acute retinal necrosis (ARN) is a clinical syndrome characterized by vitritis, severe occlusive vasculitis which produces a full thickness, necrotizing retinitis. The disease is caused by an acute infection with a member of the herpes virus family,usually VZV or HSV. ARN usually occurs in healthy adults; however immunocompromised patients may also be affected. The prognosis is poor, with significant visual loss. Clinical course most often leads to detachment of the atrophic retina, regardless antiviral treatment. We present an unusual case of ARN caused by cytomegalovirus in an immunocompromised patient. Clinical manifestations, diagnosis, and management are discussed. Case Presentation A 62 year old white female was referred with a history of progressive deterioration of her peripheral vision in both eyes for 2 weeks, getting dramatically worse with loss of central acuity over the last 3 days. Her past ocular history was unremarkable. Her past medical history was significant for Non-Hodgkin’s lymphoma for 3 years. She had active herpes zoster dermatitis at the time of presentation. She was on systemic prednisone 50 mg daily which she had taken for the past year. Ophthalmic examination demonstrated visual acuity of 20/200 in both eyes. There was no afferent pupillary defect. Ocular motility and intraocular pressures were normal. Anterior segment examination revealed 3+ cells and keratic precipitates bilaterally. Dilated funduscopic exam showed moderate vitritis, vasculitis, and extensive perivascular retinitis with areas of retinal hemorrhage and whitening OU (fig.1 A, B, C, D). Our main differential diagnosis included acute retinal necrosis, and CMV retinitis. Other possibilities were lymphomatous retinitis, syphilis, diffuse toxoplasmosis, and acute multifocal hemorrhagic retinal vasculitis. With these possibilities in mind she was started on 500 mg three times a day, and we performed an initial laboratory evaluation including CBC, liver functions, BUN/creatinine, HSV 1 and 2, CMV, and FTA-ABS. The results were significant only for a macrocytic anemia and a positive CMV antibody titer. Because of the rapid progression of her disease and the non diagnostic non invasive evaluation we decided to proceed to diagnostic and therapeutic vitrectomy. Pars plana vitrectomy was performed in the left eye and specimens were obtained for PCR, cytopathology, and microbiology. Because we suspected a member of the herpes virus family based on the clinical picture we injected 400 mg of ganciclovir into the vitreous cavity.