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Case Report
Topiramate-induced secondary angle closure Parveen Rewri, Nirha Chetan Rao, Vijaya Lingam Sankara Nethralaya, Medical Research Foundation, Chennai, Tamil Nadu, India
ABSTRACT Acute angle closure (AAC) is a serious complication of topiramate therapy. A 43-year-old woman developed simultaneous bilateral AAC following use of topiramate. In another centre, patient was treated as a pupillary block angle closure which included oral acetazolamide. On examination at our centre however, a diagnosis of topiramate-induced secondary angle closure was made but delayed recognition lead to iris atrophy and cataract; both changes affected the quality of vision after recovery. In this case report, we highlight the fact that a careful clinical approach can prevent ambiguity in diagnosis and differentiation from primary angle closure. Awareness among health professionals can also help in early recognition thus evading serious ocular complications. Keywords: Acute angle closure crisis, iris atrophy, topiramate
INTRODUCTION Topiramate is a sulfamate-derived drug used as an antiepileptic and for migraine prophylaxis. Acute myopia and acute angle closure (AAC) are serious adverse effects of the drug, which were first reported over a decade ago.[1] So far, over 100 cases have been reported.[2,3] Similar ocular complications have been reported with other sulfa-containing drugs.[4] Topiramate-induced angle closure may present in a variety of ways; in terms of duration, dose and clinical picture, visual and anatomical outcomes.[2-6] We report a case of bilateral secondary angle closure, induced by topiramate use, in which delayed recognition resulted in iris atrophy and cataract.
CASE REPORT A 43-year-old woman consulted her ophthalmologist 2 days after sudden onset of pain, redness and decreased vision in both eyes. She was a known case of migraine and was on oral topiramate 50 mg daily for 9 days, Access this article online Quick Response Code:
Website: www.thejhs.org DOI: 10.4103/1658-600X.126062
Address for correspondence: Dr. Lingam Vijaya, Smt Jadhavabai Nathmal Singhvee Glaucoma Services, Sankara Nethralaya, Medical Research Foundation, 18, College Road, Chennai - 600 006, Tamil Nadu, India. E-mail:
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prior to the onset of ocular symptoms. Her intraocular pressure (IOP) recorded was 50 mmHg in the right eye and 38 mmHg in the left eye, which lead to the diagnosis of acute primary angle closure. She was treated with intravenous mannitol, oral acetazolamide, topical 2% pilocarpine, brimodine and topical prednisolone. On presentation, nearly 72 hours after onset of symptoms, visual acuity was a finger count at 1 meter and 2 meters in the right and left eye respectively. Manifest refraction could not be estimated due to central corneal oedema. Slit-lamp examination showed bilateral conjunctival congestion, corneal oedema with Descemet’s folds, shallow anterior chambers with irido-corneal touch, mid-dilated and sluggishly reacting pupils. The IOP was 28 mmHg in the right eye and 18 mmHg in left eye. Bilaterally, no angle structures were identified even with indentation gonioscopy. On A-scan biometry, axial length was 20.2 - 20.7 mm, central anterior chamber depth was 0.8 - 0.9 mm in the right and left eye respectively [Figure 1a]. Ultrasound biomicroscopy revealed nearly flat anterior chamber [Figure 1b] with supra-choroidal effusion and anterior rotation of ciliary processes in both eyes. As a result, a diagnosis of secondary angle closure was made. Topiramate and pilocarpine were discontinued; and topical prednisolone was continued in addition to homatropine 1% which normalized the IOP with re-formation of the anterior chamber and clearing of corneal oedema. Gonioscopy revealed bilaterally open angles without any peripheral anterior synechiae [Figure 1c]. Slit-lamp examination showed pigment dispersion on corneal endothelium, sectoral atrophy of iris and cataract changes [Figure 1d]. The follow-up Journal of Health Specialties / April 2014 / Vol 2 | Issue 1
[Downloaded free from http://www.thejhs.org on Wednesday, September 17, 2014, IP: 182.71.138.234] || Click here to download free Android application for this jou Rewri, et al.: Unsual complications in case of topiramte induced angle closure
by sustained high IOP, resulting in ischaemia and then infraction of sectors of the iris. The untreated raised IOP and sequel of ischaemia may have deleterious effects on the eye. a
b
c
d
Figure 1: (a) Early raised IOP related corneal oedema and near flat anterior chamber from forward displacement of iris-lens diaphragm. (b) Near flat anterior chamber on ultrasound biomicroscopy. (c) Open angles on four mirror gonioscopy. (d) Iris atrophic changes after resolution of acute angle closure
biometry showed ACD of 2.4 - 2.6 mm in right and left eye respectively. Best corrected distant visual acuity was 6/6p in both eyes. The IOP was 10 mmHg in both eyes without any anti-glaucoma medication.
DISCUSSION Topiramate-associated acute angle closure can mimic pupillary block angle closure, and clinical differentiation between the two is very important. Secondary acute angle closure, related to topiramate, occurs without pupillary block and can also affect eyes with open angles.[1,7] The mechanism understood to date, underlying the myopia and secondary angle closure, is choroidal effusion and forward rotation of the iris-lens diaphragm.[7] Unlike pupillary block, this condition is not aborted with laser peripheral iridotomy. Diagnostic clues in the clinical examination include history of topiramate use, bilateral presentation and preservation of pupillary reaction. Typically topiramate-induced AAC resolves without residual changes. [2,5] However; Aminlari et al., reported resolution with bilateral peripheral anterior synechiae.[6] In our case, iris changes probably resulted from persistent ischaemia. Viet Tran et al., reported high cerebrospinal fluid protein concentrations followed by iris atrophy after 1 month, in a case of topiramateinduced angle closure and suggested inflammation as the possible mechanism of a breakdown of blood tissue barriers.[8] Sudden and persistent raised IOP can produce ischaemic changes in ocular structures. Raised IOP for 2 - 7 days can cause ischaemic changes and synechiae formation.[9] Iris stroma and ciliary body were the first structures to manifest ischaemic changes.[10] Iris sphincter muscle and its vascular supply were affected
Journal of Health Specialties / April 2014 / Vol 2 | Issue 1
Another concern in these patients is the use of acetazolamide, a sulfa-containing carbonic anhydrase inhibitor, commonly used to lower acutely raised IOP. Acetazolamide-induced transient myopia and AAC has also been reported.[4] Topiramate is a weak inhibitor of carbonic anhydrase in the central nervous system,[11] however, cross-reactivity with non-antibiotic sulfonamide is unlikely but theoretically, possibility exists.[12] Health professionals in neurology and ophthalmology should be aware of AAC associated with topiramate, so that serious ocular complications of topiramate therapy are recognized and managed quickly.
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