Acute retinal necrosis after neonatal herpes encephalitis
- Ralph Levinson, MD, Eye Associates of New Mexico and Southwest Colorado, 806 Martin Luther King Jr Avenue NE, Albuquerque, NM 87102, USA.
- Accepted 22 September 1998
Editor,—We read with interest the letter of Pavesioet al reporting acute retinal necrosis (ARN) in a 17 year old who had had neonatal herpes simplex virus (HSV) encephalitis.1 We would like to report a patient who also had neonatal HSV encephalitis who had been treated with parenteral aciclovir and developed ARN 16 years later.
CASE REPORT
A 16 year old white woman with a history of mental retardation and seizures as a result of neonatal HSV encephalitis presented with a 5 day history of her left eye being red and apparently uncomfortable. On presentation she was found to have moderate anterior chamber and vitreous inflammation and peripheral retinal necrosis in her left eye for 8 clock hours. There were no chorioretinal scars or optic atrophy indicating earlier infection. The right eye was normal. The diagnosis of ARN was made and she was treated with intravenous aciclovir. There was no history of any recurrent HSV and she was otherwise in good health. Her seizure disorder remained well controlled on her usual dose of carbamazepine.
After 6 days of treatment her retinitis was responding to parenteral aciclovir but she was found to have a small peripheral retinal detachment and a vitrectomy was performed. Polymerase chain reaction (PCR) was performed at the National Eye Institute on the vitreous biopsy and revealed the presence of HSV DNA.
COMMENT
Both our patient and the patient reported by Pavesio et al 1 developed ARN at about the same age, but it will take a larger series to know whether this is significant. Thompson et al reported two patients with neonatal and infantile central nervous system (CNS) HSV infections who developed ARN at ages 10 and 4, respectively.2 A 30 year old woman with ARN who first had intraocular inflammation in her mid-twenties and who may have had neonatal HSV encephalitis has also been reported.3
The role of long term prophylaxis with aciclovir in children who had herpetic encephalitis as suggested by Pavesio et al,1 is an important issue. Prophylaxis could be considered after HSV encephalitis to prevent ARN or after ARN to prevent second eye involvement. Aciclovir used as prophylaxis for recurrent genital HSV infection in adults for 5 or more years has been associated with minimal toxicity and the selection of resistant strains has not been demonstrated,4 5 but there is little experience with the duration of prophylaxis that would have been necessary to prevent ARN in our patients. The presence or absence of earlier ocular involvement may not be a good indication of the need for long term prophylaxis to prevent ARN after HSV encephalitis as has been suggested.1 One child reported by Thompsonet al had recurrent presumed cutaneous herpes and the other had chorioretinal scars,2 and the patient reported by Pavesio et al had optic atrophy before the diagnosis of ARN.1 Our patient had no apparent previous ocular findings nor has she had any other recurrent HSV disease, although small lesions in the periphery may have been obscured by the active retinitis. Whether such findings are indicative of an increased risk of the development of ARN cannot be determined from isolated case reports.
Second eye involvement in ARN is not uncommon.6 Although Palay et al reported that treatment of ARN with aciclovir does decrease second eye involvement in the short term in an adult population with most cases likely to be from varicella zoster virus, they did not recommend long term prophylaxis.6 Like Pavesio et al 1 we have chosen to continue oral aciclovir as long term prophylaxis against second eye involvement, but more data are needed to guide us in the appropriate management of these patients.
