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Editor,—Schwartz–Matsuo syndrome describes a condition characterised by rhegmatogenous retinal detachment, with ‘cells’ in the anterior chamber and elevated intraocular pressure, often in the evening.1 The detachment is typically caused by a dialysis at the ora serrata or a break in the non-pigmented epithelium of the pars plana or pars plicata of the ciliary body.23 The elevated intraocular pressure is usually discovered incidentally at the time of diagnosis of the retinal detachment, and resolves without specific treatment when the retina is reattached. We present a case in which the reverse was found. The patient presented with acute open angle glaucoma and the retinal detachment was found incidentally.
A 24-year-old man presented with a 1 day history of pain in the right eye and blurred vision, following 6 months of intermittent episodes of blurring of vision in that eye. He reported being kicked in this eye by his 2-year-old son 6 months previously. Corrected visual acuity was 6/12 right eye and 6/5 left eye. The right eye showed mild conjunctival injection, with moderate epithelial oedema of the cornea, cells in the anterior chamber, and intraocular pressures of 56 mm Hg right eye and 18 mm Hg left eye (applanation). Neither the drainage angle nor the peripheral retina of the right eye could be seen at this time because of the corneal oedema, but the posterior pole showed no abnormality. The left eye was normal with open angle on gonioscopy.
An initial diagnosis of Posner–Schlossman syndrome was made4 and treatment started with acetazolamide 500 mg intravenously, followed by oral acetazolamide and betamethasone eyedrops. The following morning the pain had settled and intraocular pressure was 20 mm Hg in the right eye. The cornea was clear and gonioscopy revealed an open angle. Anterior chamber cells were less frequent.
Following this initial response the anterior chamber cellular activity continued to fluctuate despite the use of topical corticosteroids. In addition, the intraocular pressure varied between 10 and 46 mm Hg the higher reading always occurring in the evening, despite the use of topical β blockers and oral acetazolamide to a maximum dose of 250 mg four times a day. Two weeks after initial presentation ‘tobacco dust’ pigmentation was identified in the anterior vitreous, together with a shallow inferonasal detachment of the retina extending from the 2 o’clock to the 8 o’clock meridian, sparing the macula. The longstanding nature of the detachment was suggested by the presence of wrinkling of the retinal surface and a ‘high water mark’ line in the mid periphery. No retinal break was identified but the detachment was treated by cryotherapy and circumferential external plombage of the nasal hemisphere in the area of the expected break.
Following surgery the intraocular pressure returned to normal within 48 hours, with gradual clearing of cells from the anterior chamber. All topical and systemic medications were discontinued within 2 weeks with no further increase in intraocular pressure or recurrence of aqueous cells. The retina remained flat and the corrected visual acuity was 6/9 3 months later.
Schwartz first described the association of raised intraocular pressure and aqueous cells with rhegmatogenous retinal detachment in 1973.1 The ages of these 11 patients ranged from 6 to 53 years, and 10 were male. Five of the 11 patients had a history of blunt trauma to the eye or face, and in nine patients the duration of the retinal detachment was 3 months or more. In all 11 patients the intraocular pressure returned to normal after the retina was reattached.
In 1986 Matsuo et al investigated seven similar patients whose ages ranged from 11 to 31 years. In these cases the ‘uveitis’ was resistant to topical corticosteroids, but resolved completely after successful retinal detachment surgery. They performed paracentesis on these patients, and, using transmission electron microscopy, established that the ‘cells’ in the aqueous were photoreceptor outer segments rather than inflammatory cells. The lamellar structure of these fragments led to the conclusion that they might have been derived from rods. They speculated that the peripheral retinal break (caused by blunt trauma in 50% of Schwartz’s cases), allows free communication between the subretinal space and aqueous humour. Outer segments then flow into the aqueous and obstruct the trabecular meshwork. This increases the coefficient of outflow resulting in reduced aqueous drainage and increased intraocular pressure.2Understandably, this has been difficult to demonstrate histologically because of the difficult in obtaining tissue for examination.
Our case has enough features to allow the diagnosis of Schwartz–Matsuo syndrome: young male with a history of blunt trauma to the eye, presenting with symptoms of acutely raised intraocular pressure, ‘cells’ in the anterior chamber, and a retinal detachment found subsequently. This appears to be the first reported case where raised intraocular pressure rather than retinal detachment led to presentation.
We believe, therefore, that the Schwartz–Matsuo syndrome should be considered in the differential diagnosis of acute open angle glaucoma, especially if occurring in a young male with a history of blunt trauma.
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