Article Text

Acute retinal necrosis presenting with scleritis and raised intraocular pressure
  1. ANDREW RAMSAY
  1. Moorfields Eye Hospital, City Road
  2. London EC1V 2PD, UK
  3. Proctor Foundation, 95 Kirkham Street
  4. San Francisco, CA 94122, USA
  5. Moorfields Eye Hospital, City Road
  6. London EC1V 2PD, UK
  1. EMMETT CUNNINGHAM
  1. Moorfields Eye Hospital, City Road
  2. London EC1V 2PD, UK
  3. Proctor Foundation, 95 Kirkham Street
  4. San Francisco, CA 94122, USA
  5. Moorfields Eye Hospital, City Road
  6. London EC1V 2PD, UK
  1. CARLOS PAVESIO
  1. Moorfields Eye Hospital, City Road
  2. London EC1V 2PD, UK
  3. Proctor Foundation, 95 Kirkham Street
  4. San Francisco, CA 94122, USA
  5. Moorfields Eye Hospital, City Road
  6. London EC1V 2PD, UK
  1. Mr Andrew Ramsay

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Editor,—Acute retinal necrosis (ARN) is a necrotising herpetic retinopathy (NHR), which commonly presents as a painless, rapidly advancing retinitis. We report a patient with ARN who was initially diagnosed with anterior scleritis.

CASE REPORT

A 50 year old woman presented to the casualty department with a 3 day history of intense pain and tenderness in her right eye. She was fit and well with no notable past ocular or medical history. The right eye had 6/12+2 Snellen visual acuity and normal Ishihara colour vision with no relative afferent pupillary defect. The intense hyperaemia did not blanch with 10% phenylephrine and demonstrated scleral oedema with red-free light. The intraocular pressure on the right was raised at 30 mm Hg. The left eye was normal, seeing 6/5.

The patient was treated with flurbiprofen 50 mg three times per day and an appointment was made for her in the scleritis clinic 3 days later when the pain had eased. However, she now noted a positive scotoma and funduscopy through moderate vitreous condensations revealed an inferior, pale area of retinitis and occlusive retinal vasculitis (Figs1 and 2).

Figure 1

Acute retinal necrosis showing retinitis and vasculitis.

Figure 2

Acute retinal necrosis showing retinitis and vasculitis.

The clinical diagnosis of ARN was supported by a rapid increase in the area of retinal whitening over the next 2 days and confirmed by stabilisation in response to intravenous aciclovir treatment. Flurbiprofen 100 mg three times per day did not control her pain, and in view of optic disc swelling prednisolone 80 mg per day was prescribed together with dexamethasone 0.1% four times per day and cyclopentolate 1% twice per day. Betagan 0.5% twice per day was successful in controlling the intraocular pressure.

Three days after starting intravenous aciclovir the area of affected retina stabilised at about 5 disc diameters and argon laser was applied to wall off the area of necrotic retina from the posterior pole. The disc became gradually less swollen and increased vitreous activity dropped vision to 6/24. The dose of prednisolone was reduced slowly as the vitritis cleared. Final vision was 6/12 being limited by an epiretinal membrane.

COMMENT

Pain, redness and, sometimes, even scleritis may accompany ARN early in its course which should always be considered when these signs are present.1 2 The diagnosis of ARN is clinically defined as one or more areas of retinal necrosis with discrete borders primarily located in peripheral retina, rapid circumferential progression, occlusive vasculopathy with arteriolar involvement, and inflammatory reaction in vitreous and anterior chamber.3

The one other disease that can have scleritis, high IOP, and retinitis is toxoplasmosis.4 5 Although polymerase chain reaction (PCR) for herpes and toxoplasma can distinguish the two, ARN was diagnosed clinically in view of the rapidity of advancement, rendering PCR unnecessary.6

Although herpes viruses may become active simultaneously in more than one site, the anterior scleritis was probably a local response to ARN.7

ARN should be considered in patients with raised intraocular pressure and scleritis because useful vision can be maintained with prompt treatment.

Acknowledgments

The authors have no proprietary interests in any product named in this report.

References

Contributors please note:

Communications fromall countries except the UK and Republic of Ireland should be sent to Professor C Hoyt, Editor, British Journal of Ophthalmology, University of California, Department of Ophthalmology, 10 Kirkham Street, K 301, San Francisco, CA 94143-0730, USA (tel: 001 415 502-6871; fax: 001 415 514-1521).

Manuscripts from theUK and the Republic of Ireland should be sent to Professor Andrew Dick, UK Editor, British Journal of Ophthalmology, Division of Ophthalmology, Unversity of Bristol, Lower Maudlin Street, Bristol BS1 2LX (tel: +44 (0) 0117 929-4496; fax: +44 (0)117 929-4607).

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