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Corneal Endothelial Decompansation and Ocular Hypotony in a Case With Temporal Arteritis

Bayar, Sezin A. MD; Gokmen, Onur MD; Pinarci, Eylem Y. MD; Altinors, Dilek D. MD; Gedik, Şansal MD

Journal of Neuro-Ophthalmology: December 2012 - Volume 32 - Issue 4 - p 385
doi: 10.1097/WNO.0b013e31827285cf
Letter to the Editor

Department of Ophthalmology, Baskent University Hospital Ankara,

Department of Ophthalmology, Baskent University Hospital Ankara, Turkey

Department of Ophthalmology, Baskent University Hospital Istanbul, Turkey

Department of Ophthalmology, Baskent University Hospital Ankara, Turkey

Department of Ophthalmology, Selçuk University Hospital Konya, Turkey

In patients with giant cell arteritis (GCA), anterior segment ischemia can cause anterior uveitis, corneal edema, corneal ulceration, and ocular hypotony (1–3). We present a patient who developed severe anterior segment ischemia because of GCA, despite the use of high-dose intravenous corticosteroid therapy.

A 71-year-old man, with a 15-day history of right-sided headaches, experienced sudden complete loss of vision in his right eye. He had a history of hypertension, which had been well controlled with medication. Visual acuity was no light perception, right eye, and 20/70, left eye. The right pupil was amaurotic. Anterior segment examination of the right eye revealed folds in Descemet membrane and marked corneal edema (Fig. 1A) with a dense cataract. Intraocular pressures were 4 mm Hg, right eye and 12 mm Hg, left eye. The right fundus could not be visualized. There was a cataract present on examination of the left anterior segment while the left fundus was normal including fluorescein angiography. Confocal microscopy of the right cornea showed irregularities in endothelial cell size and morphology with loss and shift in cell nuclei (Fig. 1B). The patient was hospitalized and treated immediately with intravenous pulse methylprednisolone at a dose of 1,000 mg/day for 3 days.

FIG. 1

FIG. 1

Erythrocyte sedimentation rate was 97 mm per hour, and temporal artery biopsy showed chronic inflammation with giant cells. Carotid doppler revealed moderate stenosis of the right internal carotid artery and mild stenosis of the left internal carotid artery with normal flow. The patient was given a 6-week course of systemic corticosteroids, but at 3-month follow up, there was no recovery of vision in the right eye.

There are several reports of corneal involvement in GCA (3–5). However, hypotony occurs infrequently, and it is thought to be caused by a reduction in aqueous production as a result of inflammation of the ciliary body (2–4,6–8). Hypotony was detected in one third of patients without other signs of anterior segment ischemia in a study by Huna-Baron et al (2). They suggested that low intraocular pressure may help distinguish arteritic from nonarteritic anterior ischemic optic neuropathy.

Mild corneal edema and Descemet folds have been reported in GCA (3–5) in several cases, but severe corneal edema and corneal decompensation is unusual. Our patient had a 15-day history of visual loss prior to beginning corticosteroids, and this delay possibly contributed to the poor visual outcome. Our report is similar to that of Hwang et al (6) documenting that severe corneal edema and hypotony in patients with GCA may be refractory to even high-dose corticosteroid therapy.

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