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 Table of Contents  
Year : 2018  |  Volume : 56  |  Issue : 1  |  Page : 23-25

Cotrimoxazole-induced angle closure attack: A paradoxical treatment

1 Department of Ophthalmology, PIMS, Puducherry, India
2 Department of Ophthalmology, JIPMER, Puducherry, India

Date of Web Publication4-Jun-2018

Correspondence Address:
Dr. Subashini Kaliaperumal
No. 23, 3rd Cross, VM Garden, Shanmugapuram, Puducherry - 605 009
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/tjosr.tjosr_26_18

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An elderly female came to the Emergency with acute onset diminution of vision, redness, and pain in both eyes for a day. Examination revealed best-corrected visual acuity of OU–finger counting at half meter, corneal edema, shallow anterior chamber, and very high intraocular pressures in both eyes. Further history revealed intake of oral cotrimoxazole a day before the presentation. B-scan revealed shallow choroidal effusion inferotemporally OU. Thus, a diagnosis of drug induced, “nonpupillary block” glaucoma was made. This case report describes how a cycloplegic relieved the angle closure attack in contrast to the standard treatment of pilocarpine and laser iridotomy. The case is also reported to make ophthalmologists aware of this unusual complication of a very commonly prescribed antibiotic.

Keywords: Choroidal effusion, co-trimoxazole, cycloplegic, nonpupillary block glaucoma, shallow anterior chamber

How to cite this article:
Selvaraj R, Kaliaperumal S, Sangaraju S. Cotrimoxazole-induced angle closure attack: A paradoxical treatment. TNOA J Ophthalmic Sci Res 2018;56:23-5

How to cite this URL:
Selvaraj R, Kaliaperumal S, Sangaraju S. Cotrimoxazole-induced angle closure attack: A paradoxical treatment. TNOA J Ophthalmic Sci Res [serial online] 2018 [cited 2020 May 26];56:23-5. Available from: http://www.tnoajosr.com/text.asp?2018/56/1/23/233718

  Introduction Top

Acute attack of angle-closure glaucoma in both eyes can happen in selected conditions. Drug-induced angle closure glaucoma is one such. Others include snake bite reaction. It is a well-known fact that mechanism involving angle closure is “pupillary block.” However, “nonpupillary block” mechanisms do prevail as in intake of sulfa drugs. This case reports the sequelae of events following intake of cotrimoxazole.

  Case Report Top

A 55-year-old female came to the emergency with acute onset diminution of vision in both eyes for a day. She had associated history of redness, pain, watering, and colored halos. She did not have any systemic comorbidities.

Examination revealed best-corrected visual acuity of OD–finger counting at half meter, OS– finger counting at ¼ meter. Both eyes showed circumcorneal congestion and diffuse corneal edema. Anterior chamber was shallow with Van Herick–Grade 1 and lens-iris diaphragm pushed anteriorly. Pupil was vertically oval and dilated [OD-[Figure 1]a and [Figure 1]b, OS – [Figure 2]a and [Figure 2]b. Intraocular pressure by Goldman Applanation was OD-47 mmHg and OS-43 mmHg. Gonioscopy and Ophthalmoscopy were not possible due to the corneal edema.
Figure 1: (a) Diffuse illumination of the right eye showing minimal congestion, shallow anterior chamber on day 1 of presentation. (b) Slit photo of right eye showing minimal congestion, shallow anterior chamber on day 1 of presentation

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Figure 2: (a) Diffuse illumination of left eye showing congestion, corneal clouding, fixed dilated pupil, and shallow anterior chamber. (b) Slit photo of the left eye showing congestion, corneal clouding, fixed dilated pupil, and shallow anterior chamber

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Having made a diagnosis of acute angle closure attack in both eyes, she was treated with intravenous mannitol, oral acetazolamide 250 mg QID and topically with 0.5% timolol eye drops BD and 2% pilocarpine eye drops QID. LASER iridotomy was attempted but could not be done due to poor constriction of pupils.

On further probing, the patient revealed intake of two doses of 960 mg of oral cotrimoxazole for fever and cold with myalgia a day before the presentation after which, the B-scan done revealed shallow choroidal effusion inferotemporally in both eyes [Figure 3].
Figure 3: B scan of the right eye showing shallow choroidal detachment

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In light of the above findings, pilocarpine was discontinued and instead atropine 1% eye ointment was started. Corneal edema began to clear, and anterior chamber started to deepen. Visual acuity improved to 6/60 in OD and 4/60 in OS. Intraocular pressure recorded was 9 and 11, respectively.

The revised diagnosis was “nonpupillary block” glaucoma. The presence of choroidal effusion further correlated with it, and so was treatment with topical steroids and cycloplegics. This was followed by deepening of anterior chamber, clearing of corneal edema, and reduction in intraocular pressure without any topical antiglaucoma medication.

The case discloses to the practicing ophthalmologists, the entity of nonpupillary block angle closure glaucoma and its management with atropine which is usually a contraindication in angle closure attacks.

  Discussion Top

Angle-closure glaucoma is most commonly caused by relative pupillary block mechanism. Angle-closure attacks may also occur in predisposed eyes following intake of drugs such as topiramate, hydrochlorothiazide, and sulfa drugs.

It is well known that pupillary dilatation can precipitate acute angle closure glaucoma by pupillary block mechanism in individuals with innately narrow iridocorneal angles such as seen with anticholinergic eye drops such as atropine and cyclopentolate.[1] Angle-closure is exacerbated by pupil dilatation caused by alpha agonists and also by the parasympathetic inhibitory effect of ipratropium, often combined with salbutamol in nebulizers or inhalers.[1],[2]

Pilocarpine can induce acute angle closure glaucoma in its own right, as a result of forward displacement of the lens-iris diaphragm.[3]

Tricyclic antidepressants, for example, clomipramine, imipramine, amitriptyline, and selective serotonin reuptake inhibitors may precipitate angle closure. The underlying mechanism is pupillary block caused by pupil dilatation, which is attributed to the significant anticholinergic and serotonergic side effects of the antidepressants.

Sulfa-based agents such as topiramate, acetazolamide, and hydrochlorothiazide are among the few drugs that can induce “nonpupillary block” acute angle closure glaucoma. There are three case reports on cotrimoxazole-induced angle closure glaucoma in literature search, however, no such reports from India. Hence, its mechanism and treatment modalities are described in this article. Quagliato et al. have reported that sulfa-based drugs can cause shallowing of the anterior chamber, choroidal effusion, increased intraocular pressure, swelling of the lens, and retinal edema.[4] The typical presentation is blurred vision due to forward displacement of the lens-iris diaphragm (myopia). The exact mechanism by which sulfa-based agents cause acute angle closure glaucoma is unknown, attributed to idiosyncratic reactions to the drug per SE Ciliary body swelling and anterior choroidal effusion can both cause forward displacement of the iris-lens diaphragm resulting in obstruction to aqueous flow and subsequent acute angle closure glaucoma. It is interesting to note that the mechanism of forward push of lens-iris diaphragm holds good even for intraocular lenses.[5] Both ciliary body swelling and anterior choroidal effusion can also reduce the diameter of the ciliary body ring, leading to zonular laxity that facilitates lens thickening and further decreases the anterior chamber depth.[6]

Since the mechanism is nonpupillary block, peripheral iridotomy may not relieve the attack of angle closure. Topical pilocarpine may increase the surface area of lens-iris touch and may worsen the formation of peripheral anterior synechiae. Paradoxically, cycloplegics are given to reduce the ciliary edema and topical steroids to reduce the choroidal effusion.[7] Both are found to be responsive as reported in this case.

Spadoni et al.[7] reported a case of acute angle closure following intake of trimethoprim with sulfamethoxozole prescribed for Pneumocystis carinii prophylaxis. Although it was diagnosed and the drug intake was stopped within 4 days, the patient had an unfavorable outcome and landed up with cataract and phthisis bulbi 2 months later.

In contrast, our patient stopped the drug after two doses, had a favorable outcome, vision improved, and intraocular pressure dropped to normal, with deepening of anterior chamber. At 1 month follow-up [OD-[Figure 4]a and [Figure 4]b, OS – [Figure 5]a and [Figure 5]b, right eye had a vision of 6/9 with no anterior chamber reaction, clear media and 0.2 as the cup disc ratio. Whereas vision in the left eye did not improve beyond 3/60 with presence of sequelae of uveitis like posterior synechiae and fibrin in the pupillary plane. Disc hazily showed 0.2 cup to disc ratio. Rest of fundus appeared normal.
Figure 4: (a) Right eye showing clear cornea, deep anterior chamber at the end of 1 month. (b) Slit lamp photo of the right eye showing deepening of anterior chamber at the end of 1 month

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Figure 5: (a) Left eye showing sequelae of uveitis with posterior synechiae and fibrin at the pupil, though cornea cleared. (b) Slit photo of left eye showing deepened anterior chamber

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  Conclusion Top

Cotrimoxazole, being a commonly prescribed antibiotic in India, physicians, pediatricians, and especially general practitioners need to be aware of this uncommon idiosyncratic reaction. It is insisted on the ophthalmologists that in a case of bilateral angle closure attack, history of recent drug intake gives a major clue in the diagnosis and treatment since it involves stoppage of the offending drug. Iridotomy may not be effective for drug-induced nonpupillary block angle closure attacks. Rather, atropine and topical steroids have a proven benefit.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Ah-Kee EY, Egong E, Shafi A, Lim LT, Yim JL. A review of drug-induced acute angle closure glaucoma for non-ophthalmologists. Qatar Med J 2015;2015:6.  Back to cited text no. 1
Brooks AM, West RH, Gillies WE. The risk of precipitating acute angle-closure glaucoma with the clinical use of mydriatic agents. Med J Aust 1986; 145:34-6.  Back to cited text no. 2
Lachkar Y, Bouassida W. Drug-induced acute angle closure glaucoma. Curr Opin Ophthalmol 2007;18:129-33.  Back to cited text no. 3
Quagliato LB, Barella K, Abreu Neto JM, Quagliato EM. Topiramate-associated acute, bilateral, angle-closure glaucoma: Case report. Arq Bras Oftalmol 2013;76:48-9.  Back to cited text no. 4
Razeghinejad MR, Pro MJ, Katz LJ. Non-steroidal drug-induced glaucoma. Eye (Lond) 2011;25:971-80.  Back to cited text no. 5
Panday VA, Rhee DJ. Review of sulfonamide-induced acute myopia and acute bilateral angle-closure glaucoma. Compr Ophthalmol Update 2007;8:271-6.  Back to cited text no. 6
Spadoni VS, Pizzol MM, Muniz CH, Melamed J, Fortes Filho JB. Bilateral angle-closure glaucoma induced by trimetoprim and sulfamethoxazole combination: Case report. Arq Bras Oftalmol 2007;70:517-20.  Back to cited text no. 7


  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]


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