Bilateral transient myopia induced by oral acetazolamide in the early postoperative period after phacoemulsification

Kalina, Paul H. MD; Kalina, Andrew G. BA

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JCRS Online Case Reports 8(2):p e00016, April 2020. | DOI: 10.1097/j.jcro.0000000000000016
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Transient myopia has been reported with many medications, including tetracycline, aspirin, metronidazole, ganglionic blocking agents, Tamiflu, and sulfonamide-derived drugs, such as acetazolamide, topiramate, hydrochlorothiazide, and chlorthalidone.1–18 Clinical presentation occurs 1 or 2 days after medication, with decreased distant vision and myopic refractive shift.11 Angle-closure glaucoma may or may not be present.1,2,6,7,11,18 Serous choroidal detachment has also been noted.11,19,20 This case report describes acute transient myopia after administration of oral acetazolamide without associated angle-closure glaucoma. To our knowledge, this is the first report of the condition occurring in a patient with bilateral pseudophakia.


A 62-year-old healthy man with no ocular history, including pseudoexfoliation, presented for cataract surgery. His presurgical refraction was −1.50 +0.25 × 28 in the right eye and +1.00 +1.00 × 15 in the left eye. The biometric data obtained from the swept-source optical coherence tomography biometer are summarized in Table 1. The patient had uneventful phacoemulsification with placement of a 1-piece, monofocal, nontoric posterior chamber intraocular lens in his right eye. Having reported no contraindications to sulfonamide medications, he received a 500 mg acetazolamide sequel orally within 30 minutes postoperatively as per the standard postoperative procedure. The eye healed uneventfully, with an uncorrected distant visual acuity (UDVA) of 20/20−2. Refraction was plano +0.25 × 170. The patient reported great satisfaction with his vision and use of over-the-counter reading spectacles.

Table 1.:
Biometric data obtained with swept-source optical coherence tomography.

Three weeks later, cataract surgery was performed in a similar manner on the left eye. As with his first surgery, the patient received a single 500 mg acetazolamide sequel postoperatively. At his visit the next day, the patient was noticeably anxious. He stated that both eyes had done very well the previous day, but on awakening, his distant vision was markedly decreased in both eyes. No pain, redness, or other associated issues were reported except that he now read without spectacles. The UDVA was 20/100 in the right eye and 20/125 in the left eye. Refraction improved distant vision to 20/20 in the right eye with −2.50 sphere and 20/20 in the left eye with −3.00 +0.75 × 90. The eyes were orthophoric. Pupils showed normal reactions and the corneas were clear with secure incisions. The anterior chambers were neither flat nor obviously shallow centrally, but did appear shallow peripherally. Intraocular lenses, discs, and retinas were within normal limits bilaterally. Applanation intraocular pressure was 15 mm Hg in the right eye and 20 mm Hg in the left eye. Gonioscopy revealed normal, open angles but with a suggestion of slight narrowing. No choroidal detachments were visible by ophthalmoscopy. Cyclopentolate 1% produced no improvement in vision or angle appearance. Optical coherence tomography of the retinas and optic nerves was normal. B-scan ultrasound was also normal. Because of uncontrollable circumstances and the patient's high level of anxiety, neither biometric data nor ultrasound biomicroscopy (UBM) could be obtained during this time. Based on the clinical examination, the working diagnosis was an acute bilateral myopic shift from an idiosyncratic ocular reaction to oral acetazolamide.

A detailed review of the findings was completed with the patient. The presumed association between his acute symptoms and acetazolamide was explained, as well as the expectation that, given the one-time administration of medication, his vision would improve as the idiosyncratic reaction resolved. He was instructed to continue prednisolone 1% and ofloxacin eyedrops and return for re-examination in a few days or sooner if new issues arose. Four days later, visual acuity and refractive error were significantly improved in both eyes. The UDVA was 20/20−2 in the right eye and 20/25−2 in the left eye. Refraction was −0.25 sphere in the right eye and −0.75 +0.25 × 90 in the left eye. Intraocular pressure was 14 mm Hg in both eyes. Anterior and posterior segment examinations were normal. Two weeks later, UDVA was 20/20 in both eyes. Refraction was −0.25 sphere in the right eye and +0.25 sphere in the left eye.


This case report is unique and offers important insights in that it is the first report, to our knowledge, of drug-induced myopia in a patient with bilateral pseudophakia during the early postoperative period after phacoemulsification. A literature search identified a report by Fan et al. in which a single pseudophakic eye also developed drug-induced myopia from acetazolamide; however, the other eye was phakic.11 The patient in their report also had associated angle-closure glaucoma and choroidal detachments, which are common on presentation but were not present in our patient.1,2,6,7,11,19–21

Importantly, despite receiving oral acetazolamide after each surgery within the same time frame, the patient only experienced the myopic shift following his second procedure. Previous authors have theorized that this pattern of response depends on an allergic reaction or sensitization to the drug.6,7,11,12,21,22 However, there are other reports in which re-exposure to Hygroton, promethazine, and acetazolamide failed to produce any reaction, which theoretically negates such a mechanism.23,24 The controversy surrounding this issue was discussed with our patient, and the idea of a rechallenge with acetazolamide was raised; however, the patient declined for several understandable reasons. The issues of sensitization and re-exposure are important, especially for individuals who take acetazolamide to mitigate adverse effects associated with high altitude.22 Until further research is performed, this case report suggests that regardless of lens status, ideally a multidose trial of acetazolamide (or related medication) should be performed before usage at high altitude to identify any potential adverse visual effects for the individual.

Previous investigations have proposed a variety of possible mechanisms for drug-induced myopia as follows: anterior chamber shallowing from decreased aqueous production, changes in crystalline lens thickness (due to altered metabolism, increased curvature, influx of fluid, and altered index of refraction), and ciliary body edema with forward displacement of the iris–lens diaphragm.7,11 Galin et al. found that the decrease in aqueous humor production from acetazolamide did not change the anterior chamber depth.8 Conflicting data have been reported on lens thickness. Ultrasonographic studies by Pallin and Ericsson attributed anterior chamber shallowing entirely to increased lens thickness.25 Schroeder implicated both anterior chamber shallowing and increased lens thickness.26 Studies by Bovino and Granstrom found the anterior chamber to be shallow, but lens thickness unchanged.5,27 They hypothesized that anterior chamber shallowing and myopic shift were related to ciliary body edema with forward displacement of the lens–iris diaphragm. Postel et al. identified by UBM the presence of supraciliary choroidal effusion causing forward rotation of the ciliary body and lens–iris diaphragm.7 Krieg suggested that drug-induced myopia is related to a disturbance in eicosanoid metabolism that results in ciliary body edema and anterior rotation of the iris–lens diaphragm.24 Our case report fully supports the mechanism of forward displacement of the iris–lens diaphragm. The patient's induced myopia was symmetric at −2.50 diopters, which corresponds to approximately 1 mm of the anterior lens shift. Given the preoperative anterior chamber depths, biometric data at the time of the myopic shift would have been extremely beneficial in strengthening this conclusion. Unfortunately, such data were unable to be obtained. Choroidal detachments were not visible by indirect ophthalmoscopy or B-scan ultrasound. However, with the lack of UBM imaging, we cannot comment on the presence of anterior choroidal effusion and ciliary body rotation. The occurrence of myopic shift in bilateral pseudophakia refutes the hypothesis associated with increased lens thickness.

In conclusion, we report a case of acetazolamide-induced myopia in a patient with bilateral pseudophakia and an absence of angle-closure glaucoma or choroidal detachment. This reaction necessitates sensitization to the drug, which underscores the importance of obtaining a thorough exposure history. These case findings fully support the hypothesis that the myopic shift results from ciliary body edema producing anterior displacement of the iris–lens diaphragm and refute any potential mechanism pertaining to altered lens parameters. Although cycloplegia proved to be ineffective, the idiosyncratic reaction did resolve within a few days upon discontinuation of the inciting medication. Finally, we would like to highlight the importance of patient counseling and reassurance, as sudden refractive change and vision decrease can incite significant anxiety.


  • In phakic eyes, acute transient myopia has been described after oral acetazolamide administration. Associated findings have included anterior chamber shallowing, angle-closure glaucoma, and serous choroidal detachment. This clinical condition appears extremely rare in pseudophakic eyes with only one unilateral case reported in the literature.
  • Previous investigations have proposed a variety of possible mechanisms for this condition, including decreased aqueous production, changes in crystalline lens thickness, and ciliary body edema with forward displacement of the iris–lens diaphragm.


  • This is the first report, to our knowledge, of acute transient myopia after administration of oral acetazolamide in both pseudophakic eyes of a patient in the very early period after cataract surgery.
  • This case refutes potential mechanisms pertaining to altered lens parameters and supports the hypothesis that the myopic shift results from anterior displacement of the iris–lens diaphragm due to ciliary body edema.


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