Clinical Optometry

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C A S E R E P O RT

A Rare Case of Esotropia Induced by Short-Term

Use of 0.01% Atropine for Myopia Control
Umesh Belbase 1, *, Santosh Chhetri 1,
*, Nita Sunam Gamal 2
, Anup Subedi 3
,
Mario Cantó-Cerdán 4,5
1
Department of Optometry, Metro Eye Care Lumbini, Butwal, Nepal; 2Department of Pediatric Ophthalmology, Lumbini Eye Institute & Research
Centre, Bhairahawa, Nepal; 3Department of Optometry, Himalaya Eye Hospital, Pokhara, Nepal; 4Department of Optometry, Vissum (Miranza),
Alicante, Spain; 5Grupo de Investigación En Optometría (Gioptom), University of Alicante, Alicante, Spain
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*These authors contributed equally to this work

Correspondence: Santosh Chhetri, Metro Eye Care Lumbini, Butwal, Nepal, Email [email protected]

Abstract: This report a case of intermittent esotropia in an 8-year-old boy with high axial myopia, which manifested within just three
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months of initiating 0.01% atropine treatment, despite minimal axial elongation. After discontinuation of atropine and introduction of
multifocal soft contact lenses, normal binocular visual function was restored. This case emphasizes the importance of monitoring
binocular parameters during low-dose atropine treatment for myopia control.
Keywords: LDA, binocular vision, multifocal soft contact lenses, progressive myopia

Introduction
Myopia is a leading cause of visual impairment globally, with increasing prevalence, particularly among children.1 Low dose
atropine 0.01% (LDA), has emerged as an effective intervention to slow axial elongation in progressive myopia while
minimizing side effects.2 Despite its efficacy and safety profile, rare adverse effects such as accommodation dysfunction and
binocular vision disturbances have been reported.3,4 Understanding the full spectrum of LDA-associated complications is critical
for clinicians managing pediatric myopia, especially in cases with pre-existing binocular dysfunction or high accommodative
demand. We report a rare case of acquired esotropia in a child that was treated with short-term LDA treatment. The esotropia
resolved, and fusion was restored in the child after discontinuation of LDA and the use of multifocal soft contact lenses.

Case Report
An 8-year-old boy presented to Metro Eye Care Lumbini with a primary complaint of gradually blurring distance vision in both
eyes for the past three months. Upon examination, it was noted that both parents had high myopia. The patient’s presenting visual
acuity was 20/80 in the right eye (RE) and 20/60 in the left eye (LE) with his previous glasses, prescribed six months earlier
(−8.00/-2.00×180; LE −7.00/-1.00×180) . Following both dry and cycloplegic retinoscopy, the new prescription was −10.00/
−2.00×180 (20/25) in the right eye and −9.00/−1.00×180 (20/25) in the left eye. With the new prescription, a small exophoria of 2
prism diopters (PD) at near and orthophoria at distance were observed, with other binocular parameters within the normal range.
The axial length was recorded as 26.46 mm in the right eye and 26.15 mm in the left eye, reflecting an increase of 0.56 mm in the
right eye and 0.48 mm in the left eye compared to measurements taken six months earlier (Figure 1). Due to the significant
increase in axial length, treatment with 0.01% atropine sulfate eye drops at night was initiated.
Following a three months of follow-up period, the patient occasionally complained of binocular double vision. The
cover test revealed comitant intermittent esotropia in the right eye with poor control, measuring 18 prism diopters (PD) at
near and 6 PD at a distance. The accommodative convergence to accommodation (AC/A) ratio, assessed via the gradient
method, was high (7:1). Stereoacuity was absent, and uncrossed diplopia at both distance and near vision was observed
on the Worth Four Dot test. Although Magnetic Resonance Imaging (MRI) of the brain and orbit was recommended,

Clinical Optometry 2025:17 365–368 365

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 Belbase et al

Figure 1 Line chart showing axial length changes in the right eye (RE) and left eye (LE) across three visits: prior to treatment (rapid progression phase), during 0.01%
atropine treatment, and after switching to multifocal soft contact lenses.

financial constraints led to the acquisition of a Computed Tomography (CT) scan of the brain and orbit, which revealed
no abnormalities. Axial length progression was minimal, measuring 26.50 mm in the right eye and 26.19 mm in the left
eye three months after atropine treatment. With the multifocal contact lens (center-distance, +2.50 diopter), the prism bar
cover test showed 2 PD esophoria at near and 4 PD exophoria at distance (Figure 2), with a normal AC/A ratio. The
multifocal soft contact lenses effectively resolved diplopia and restored binocular fusion. Consequently, atropine
treatment was discontinued, and multifocal soft contact lenses were prescribed as an alternative, alongside divergence
therapy. Three months post-atropine cessation, axial lengths were 26.54 mm in the right eye and 26.22 mm in the left eye.
While wearing multifocal soft contact lenses, prism bar cover testing revealed 2 PD esophoria at near and 4 PD
exophoria at distance, with normal binocular vision. Given the stable binocular function and effective control of axial
elongation, the multifocal soft contact lenses were continued as part of an ongoing myopia control strategy.

Figure 2 Line chart showing near and distance deviation (in prism diopters) across three visits: initial assessment (orthophoria at distance, small exophoria at near), during
0.01% atropine treatment (development of esodeviation), and after switching to multifocal soft contact lenses (improvement in deviation). Positive values indicate
esodeviation; negative values indicate exodeviation.

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 Belbase et al

Discussion
Atropine sulfate 0.01% has been demonstrated to have minimal side effects in children initiating treatment for
progressive myopia.5 We report a rare complication associated with the short-term use of LDA, wherein an 8-year-old
boy developed acquired esotropia during the course of treatment.
Aman and Guyton4 reported esotropia onset following a gradual increase in atropine concentrations over a six-year
period to manage progressive myopia. Similarly, Kothari et al3 described three patients who developed convergence
excess esotropia following the use of 0.01% atropine after undergoing surgery for intermittent exotropia; in two of these
cases, esotropia persisted despite discontinuation of atropine, with only partial recovery in accommodation and fusion.
Unlike previous cases, our patient had no history of strabismus surgery or an increasing atropine dosage.
A recent report by Englisch et al6 described a case of reversible esophoria decompensation in a child following an
increase in atropine concentration from 0.01% to 0.025%, despite initial tolerance at the lower dose. Their case supports
a dose-dependent effect of atropine on binocular function, particularly in patients with convergence excess. Although our
case involved esotropia even at 0.01%, both cases highlight the importance of monitoring binocular vision when
initiating or adjusting atropine therapy.
Several factors could explain the development of acquired esotropia in our patient. Initially, a child with high myopia
developed esotropia, likely due to the combined effects of excessive convergence demand and atropine-induced
accommodative lag. With spectacle correction, the high-minus lenses increased the strain by making near objects appear
closer.7 Additionally, the patient’s working distance was notably shorter, further contributing to binocular stress. These
factors likely triggered the onset of esotropia.
Furthermore, atropine, is a cycloplegic agent, interferes with accommodation. However, LDA may induce only partial
cycloplegia, allowing for residual accommodation. This retained accommodative effort can trigger excessive conver­
gence through the AC/A ratio relationship,8,9 thereby increasing esodeviation.10 In contrast, full and sustained cyclople­
gia, such as that achieved with 1% atropine, completely suspends accommodation, eliminating the accommodative
component of esotropia, as observed in patients with fully refractive accommodative esotropia.11
Multifocal soft contact lenses present an effective alternative to atropine by creating peripheral myopic defocus,
which slows axial elongation.12 Unlike atropine, these lenses preserve normal accommodation and reduce the risk of
inducing binocular vision disorders.13 In our case, the multifocal soft contact lenses restored fusion and reduced
esodeviation, highlighting their effectiveness in children with binocular dysfunction or atropine intolerance.
Finally, the anticholinergic effect of atropine partially inhibits peripheral accommodation, which may lead to enhanced
central accommodative effort and, consequently, increased accommodative convergence, potentially contributing to the
development of esotropia. Esotropia has also been documented with the use of systemic anticholinergics, including
scopolamine patches for motion sickness,14 medications like amitriptyline and oxybutynin for nocturnal enuresis, and
haloperidol with benztropine mesylate for Tourette syndrome.15,16 In most reported cases, patients had underlying neurolo­
gical conditions or preexisting esophoria, and the esotropia typically resolved after discontinuing the medication.

Conclusion
While LDA is widely regarded as an effective and safe option for controlling progressive myopia, it may trigger esotropia and
binocular disruptions. If esodeviation occurs, discontinuing atropine and introducing alternative approaches for myopia control
may be necessary to maintain normal binocular function. Close monitoring and assessment of binocular vision parameters are
essential to balance effective myopia control and preserve binocular function. Further research is needed to determine the
effect of LDA on accommodative convergence in cases of high myopia and to evaluate the impact of alternative approaches,
such as multifocal soft contact lenses, bifocal glasses, or progressive addition lenses, in such scenarios.

Ethics and Consent Statement

Formal institutional review board approval was not required to publish the case details at our institution. However,
written informed consent was obtained from the patient’s parents for the clinical examination, treatment, and publication

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 Belbase et al

of this case report. All clinical procedures were conducted in accordance with institutional ethical standards and the
principles outlined in the Declaration of Helsinki. The patient’s identity has been anonymized to ensure confidentiality.

Acknowledgments
We would like to thank the patient and their family for their cooperation and consent to share this case.

Funding
The authors declare that their work is not funded by any Institution, Organization, or Government.

Disclosure
The authors report no conflicts of interest in this work.

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