Necrotising herpetic retinopathy in patients with advance HIV disease.

OBJECTIVES: To describe the presenting features, clinical and laboratory diagnosis, response to treatment, and outcome of necrotising herpetic retinopathy (NHR) in HIV infected patients. METHODS: Retrospective case records/laboratory data review of five HIV infected patients presenting to the specialist HIV/AIDS unit at UCL Hospitals, London from April 1994 to August 1996 with a clinical diagnosis of NHR. RESULTS: All patients had advanced HIV disease with a median CD4 count of 20.10(6)/1. Three patients had cutaneous varicella zoster virus (VZV) infection within the preceding 8 weeks. All had uniocular loss of visual acuity; one also had headache and another ocular pain. All had typical retinal appearances. VZV DNA was detected in cerebrospinal fluid of four patients (and in vitreous fluid of one of the four) and in vitreous fluid of one other. One patient refused therapy and rapidly became blind. Four patients received intravenous foscarnet with intravenous aciclovir for 6 weeks: three subsequently received oral famciclovir and one oral valaciclovir; two patients also had intravitreal injections of foscarnet. In none of the four did treatment bring about improvement in visual acuity, but in all four visual loss from retinitis was halted. CONCLUSIONS: NHR occurs in HIV infected patients with advanced HIV disease and is strongly associated with evidence of VZV infection. With aggressive use of antiviral drugs the outcome is not uniformly poor.

Herpes zoster ophthalmicus followed by contralateral hemiparesis: report of two cases and review of literature.

Two patients with herpes zoster ophthalmicus and contralateral hemiparesis are described, and their findings compared with 49 patients previously reported. These patients presented with delayed contralateral hemiparesis approximately seven weeks after the onset of herpes zoster ophthalmicus. Most patients had evidence of infarction of the ipsilateral middle cerebral artery by angiography or by CT scan. Cerebrospinal fluid pleocytosis and elevated protein commonly were found. Twenty per cent of the reported patients died, but they were older than the patients who survived and predisposed to have diffuse CNS lesions. The pathogenesis of this syndrome is thought to be due to direct viral invasion of the blood vessel wall with resulting angiitis. Further studies need to be performed to clarify the role of specific antiviral therapy or anti-inflammatory agents in treating this complication of herpes zoster.