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Drug induced acute myopia with supraciliary choroidal effusion in a patient with Wegener's granulomatosis
  1. J C Ramos-Esteban,
  2. S Goldberg,
  3. J Danias
  1. Department of Ophthalmology, Mount Sinai School of Medicine, One Gustave L Levy Place, Box 1183, New York, NY 10029-6574, USA
  1. Correspondence to: John Danias, MD, PhD; john.danias{at}mssm.edu

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Acute transient myopia with shallowing of the anterior chamber is a rare idiosyncratic response to systemic and topical use of many medications1 including sulphonamides.2 Although many such cases have been reported in the past, they have been relatively rare in recent years. A-scan ultrasonography has been used to measure anterior chamber depth and lens thickness during the myopic phase.3 Ultrasound biomicroscopic (UBM) imaging during the acute phase has only been reported twice.4,5 We present a case of drug induced bilateral transient myopia with shallow anterior chambers, where UBM aided in the diagnosis and provided clues to the mechanism responsible for this reaction.

Case report

A 39 year old white woman complained of acute onset of blurry vision and decreased visual acuity at distance starting on the morning of the day she presented to her primary ophthalmologist. On examination by the primary ophthalmologist the patient was found to have a myopic shift of 7.00 dioptres in both eyes and was noted to have narrow angles. She was referred the same day to JD for treatment of bilateral angle closure.

Her medical history was significant for Wegener's granulomatosis diagnosed 1 year earlier and confirmed with a renal biopsy. She had been treated with Cytoxan and prednisone, despite which renal failure ensued. Approximately 4 months before presentation the patient had begun haemodialysis and 1 month before presentation she was started on peritoneal dialysis. The patient was maintained on a regimen of immunosuppressives, which included Cytoxan and prednisone. Twelve hours before presentation, she had received the first dose of Bactrim (160 mg trimethoprim and 800 mg sulphamethoxazole) as prophylaxis for Pneumocystis carinii.

Her examination was significant for mild dehydration. The patient had recently noted a negative fluid balance on peritoneal dialysis. The patient had a negative family history for glaucoma and her social history was not contributory. On examination (at approximately 4.30 pm on the day of presentation), visual acuity with her current correction of −6.00 −1.75 × 173° right eye and −4.00 −2.25 × 180° left eye was 20/200 both eyes. Manifest refraction improved visual acuity to 20/20 both eyes with −9.25 −2.00 × 180° right eye and −8.00 −2.25 × 180° left eye. Confrontational visual fields were intact. External examination revealed normal lids in both eyes. Conjunctival chemosis was present in both eyes. Pupils were 4 mm reactive in both eyes with no afferent pupillary defect. Slit lamp examination revealed normal corneas.

Anterior chambers were shallow in both eyes. Goldmann applanation tonometry revealed intraocular pressure (IOP) of 25 mm Hg right eye and 26 mm Hg left eye. Zeiss four mirror gonioscopy was performed and revealed slit angles in both eyes. Indentation gonioscopy opened the angle to + 1 right eye. No PAS could be observed. Indentation gonioscopy of the left eye opened the angles slightly more, however only the top of the trabecular meshwork could be visualised. Undilated funduscopic examination with a 90 D lens revealed an intact posterior pole. The optic nerves appeared to have small central cups in both eyes.

UBM was subsequently performed (Fig 1), and confirmed the presence of shallow anterior chambers with narrow angles in both eyes. The angle opening distance (AOD) (distance between the posterior corneal surface and anterior iris surface measured 500 μm from the scleral spur) was measured on the UBM images according to Pavlin.6 AOD was less than 10 μm in both eyes. In addition, anterior chamber depth (ACD) was measured in one available image right eye and was found to be 1.7 mm. A ciliochoroidal effusion extending in all quadrants was present in both eyes. The ciliary body appeared slightly engorged and rotated anteriorly.

Figure 1

Ultrasound biomicroscopic images ((A) right eye, (B) left eye) of the angle and ciliary body during the acute phase. Anterior chamber angle (thin arrow) almost completely closed. Choroidal effusion (thick arrow) is present. The ciliary body (open arrow) is rotated anteriorly

The patient was advised to discontinue Bactrim and was treated with fluorometholone and topical aqueous suppressants. On the following day, the anterior chambers were slightly deeper and the myopic shift was now only 2.25D. This further decreased over the following days with progressive deepening of the anterior chamber. One week after discontinuation of Bactrim, the patient's visual acuity was 20/20 in both eyes with her old prescription. Zeiss four mirror gonioscopy revealed grade IV open angles with some very fine PAS in the inferior angle in both eyes. Goldmann applanation tonometry revealed IOP of 10 mm Hg in both eyes off aqueous suppressants. UBM was repeated (Fig 2), confirming complete resolution of the choroidal effusion and significant reduction in the size of the ciliary body. AOD was 203 μm right eye and 240 μm left eye. Dilated fundus examination revealed normal periphery, normal discs with a cup to disc ratio approximately of 0.2 both eyes, and normal maculas in both eyes.

Figure 2

Ultrasound biomicroscopic images ((A) right eye, (B) left eye) of the angle and ciliary body during the convalescent phase. Anterior chamber angle (thin arrow) is now open. No choroidal effusion is present (thick arrow).

Comment

We report a case of acute transient myopia in a patient with renal failure secondary to Wegener's granulomatosis, treated with sulphonamides. The development of acute myopia in patients with renal failure from nephropathia epidemica (NE) cause by the Puumala virus has been documented.7 NE is the most common systemic condition associated with acute transient myopia. The Puumala virus multiplies in capillary endothelial cells, causing endothelial wall damage and increased capillary permeability to plasma and red blood cells. Leaky capillaries lead to ciliary body oedema and subsequent forward displacement of the iris-lens diaphragm, which is responsible for acute myopia, shallowing of the anterior chamber, and acute angle closure.

To our knowledge acute myopia and ciliary body oedema due to renal failure has not been described as an ocular manifestation of Wegener's granulomatosis, or as a direct consequence of acute renal failure in the presence of Wegener's granulomatosis. The onset of increased myopia immediately after the initiation of sulphonamide therapy and the resolution of symptoms after discontinuation of Bactrim points to a causative relation between these agents and the acute myopic shift seen in our patient. Although a relation between Wegener's granulomatosis and the development of acute myopia cannot be completely ruled out, such a relation is unlikely. Nevertheless, one cannot rule out a possible interaction between the use of sulphonamides and any effects of Wegener's granulomatosis in the eye.

Transient myopia is a rare idiosyncratic reaction to systemic administration of sulphonamides. The myopic shift is usually bilateral and is completely reversible after discontinuation of the sulphonamide therapy. Various degrees of anterior chamber shallowing and angle narrowing have been reported. The proposed mechanisms responsible for this myopic shift are: (1) spasm of accommodation, (2) lens oedema, (3) ciliary body oedema with associated choroidal effusion.8

Of these proposed mechanisms, spasm of accommodation is the most unlikely, as cycloplegic instillation almost never abolishes the refractive error change in medication induced acute transient myopia.

Lens oedema can be partially responsible for the drug induced acute myopic shift. Such oedema can theoretically occur from osmotic changes or metabolic alterations produced by sulphonamides.9 However, lens oedema is not present in all cases of sulpha drug and other drug induced acute myopia.10. Even when lens oedema is present, it cannot always fully explain the change in refraction, which is sometimes up to 7 dioptres,8 and the degree of anterior chamber shallowing in some patients.3

Although we cannot completely rule out lens oedema as a possible mechanism, as we did not perform A-scan measurements, we believe that the anterior rotation and oedema of the ciliary body causing an anterior movement of the lens can fully explain the myopic shift seen in our patient.

The UBM images support this proposed mechanism for the pathogenesis of acute drug induced myopia. The oedematous ciliary body became anteriorly rotated secondary to a choroidal effusion. This caused anterior movement of the lens-iris diaphragm with subsequent narrowing of the angle. Oedema of the ciliary processes might have also caused relaxation of the zonules leading to an increase in lens thickness and forward displacement of the anterior lens surface further into the anterior chamber. AOD (a measure of angle dimensions) decreased almost to zero during the acute attack for our patient. In addition, ACD in the right eye was significantly decreased to only 1.7 mm. Upon resolution of the symptoms, AOD returned to what is considered to be a normal range (normal range 185–665 μm).11

This is the third reported case of acute myopia where ultrasound biomicroscopy has aided in the diagnosis of this extremely rare drug reaction. Although, this condition generally has a benign course if recognised early, it can potentially have devastating consequences if left untreated or misdiagnosed as primary angle closure glaucoma. Physicians should be aware of this side effect of sulphonamides and their derivates and warn patients to report changes in their vision when initiating therapy with such agents.

Acknowledgments

Support: Eye Bank for Sight Restoration Glaucoma Research and Training Fund, unrestricted fund from Research to Prevent Blindness, May and Samuel Rudin Foundation, Inc.

References

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