Angle-Closure Glaucoma Secondary to Acute Myopia
Malik Y. Kahook, MD and David L. Epstein, MD, MMM
Angle-closure glaucoma secondary to acute myopia is a relatively rare condition that an ophthalmologist may see a handful of times during an entire career, but it is a distinct entity that can be puzzling diagnostically. Acute transient myopia due to an idiosyncratic reaction to systemic drugs that have no cholinergic or parasympathomimetic activity is well known, but in only the rarest instances has the episode been accompanied by shallowing of the anterior chamber.1–11 More than 20 different drugs of several different kinds, but most commonly diuretics12–14 and sulfa-type drugs,2,4,7,10,15–17 have induced acute transitory myopia. Other drugs reported include tetracycline,3 aspirin,5 corticosteroids,18 bromocriptine,19 prochlorperazine,20 and promethazine.21 More recently, topiramate has been implicated in cases of angle-closure glaucoma associated with acute myopia and suprachoroidal effusions.22
Sometimes, there is no past history of drug exposure. Typically, however, the patient has taken some medication weeks or months previously, such as a diuretic or sulfonamide antibiotic, without notable visual side effects, but after discontinuing the medication for a while and then taking it again, an acute reaction develops. Characteristically, within a few hours or a few days after resuming the medication, the patient experiences blurring of vision for distant objects due to the development of several diopters of myopia. Visual acuity can be restored to normal with a suitable refraction but not by anticholinergics. There is no miosis and no evidence of cyclotonia.
Good evidence, including ultrasonographic measurements,8,13 indicates that swelling of the crystalline lens is responsible, at least in part, for the myopia in most cases and that it is reversible.4 However, others have attributed at least some of the myopia to the forward movement of the crystalline lens.7,10,11 We have seen one patient in whom accumulation of anterior choroidal fluid was implicated not only in the pathogenesis of secondary angle-closure glaucoma but also in the induced myopia.11 The choroidal effusion presumably caused forward rotation of the ciliary body, which led to forward movement of the entire crystalline lens due to loss of zonular tension and angle closure. The latter presumably occurred from direct mechanical pressure of the ciliary body on the iris because laser iridectomy was without effect. The forward position of the crystalline lens could explain about half of the myopic shift. A similar case of induced myopia and angle closure has been reported in which one eye had a pseudophakos, and therefore, presumably lens swelling was ruled out as a cause of the myopia, which was attributed to the forward shift in the intraocular lens position.10 This condition has also been observed commonly in young women, often during the first few months of pregnancy.
When the suspect drug is discontinued, the myopia disappears spontaneously within a few days. In all cases, similar changes have occurred in both eyes, except for an instance of unilateral aphakia that, in contrast to the aforementioned, there was no change in the refraction of the aphakic eye. Either crystalline lens swelling or forward positioning of the crystalline lens or both may be involved in the etiology of the induced myopia.
Only in rare cases does crystalline lens swelling and/or forward shift of the crystalline lens cause sufficient shallowing of the anterior chamber to induce bilateral angle-closure glaucoma from pupillary block, and it is usually subacute rather than acute. When the process resolves in a few days, the myopia disappears, the anterior chambers return to normal depth, and the angles reopen to their former width. The following case is another example.
ACUTE BILATERAL TRANSITORY MYOPIA ASSOCIATED WITH OPEN-ANGLE GLAUCOMA
Joel S. Schuman, MD, FACS
I have seen a patient with bilateral transitory myopia associated with open-angle, rather than angle-closure, glaucoma. At the initial presentation, the patient, a 36-year-old woman, reported blurred vision after awakening. She had a low-grade fever (100°F) and a flu-like syndrome of aches, pains, and malaise. She did not recall taking any unusual medications, only loratadine (antihistamine) and nonsteroidal anti-inflammatory drugs. She had no hypertension or diabetes, and a blood glucose was normal.
On examination, visual acuity was 20/200 OU, refracting to 20/25 OU with -2.00 D in each eye. IOPs were 23 and 24 mm Hg, and her angle was open in each eye to ciliary body band. Her examination otherwise was completely unremarkable. She was given her prescription and sent home. When she returned 3 weeks later, visual acuity was 20/20 without correction, and IOPs were 15 mm Hg in each eye. Angles were again open, and her examination was unchanged except that her axial anterior chamber depth seemed slightly greater than on the previous visit.
Two months later, the patient presented again with the same constitutional and ophthalmologic complaints. Vision was again correctable to 20/25 with -2.00 D sphere, but this time her IOPs were 36 and 38 mm Hg, although her angles were still open to scleral spur. She denied taking any new medications, but during the examination recalled that she had taken quinine for leg cramps just before the previous episode, and again before the current episode. This was the 31st quinine tablet she had ever taken, though she had only 2 recognized episodes of blurred vision.
Ultrasound biomicroscopy showed her angles to be open to ciliary body band, confirming the gonioscopy, but also revealed very anterior ciliochoroidal effusions bilaterally (Figure 37-1). On follow-up examination 2 weeks later, the IOPs had returned to the mid-teens, the patient was again emmetropic, and ultrasound biomicroscopy demonstrated that the angles were now significantly wider than previously. The effusions were gone (Figure 37-2). An A-scan ultrasound at the time of the myopia compared with one taken after its resolution showed deepening of the anterior chamber and thinning of the crystalline lens with the resolution of the episode.
Figure 37-1. Ultrasound biomicroscopy during an episode of acute bilateral transitory myopia associated with open-angle glaucoma demonstrates anterior ciliochoroidal effusion with narrowing of the angle inlet, but the angle is open to ciliary body band.
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