Acute acquired comitant esotropia is an uncommon presentation of esotropia with diplopia and minimal refractive error, presenting in previously orthophoric children and adults. It is a rare entity with three widely accepted subtypes. Swan type occurs following a unilateral occlusion or vision loss.1–7 Franceschetti type is associated with mild hypermetropia, absence of an accommodative component, and an idiopathic etiology.2–5 Bielschowsky type develops in individuals with uncorrected myopia2–6 who prefer excessive near work, which increases tonicity in the medial rectus muscles while disrupting the normal balance of converging and diverging forces of the eye.3 Given the marked rise in hand-held device use in recent years, particularly in the adolescent demographic,9,10 acute acquired comitant esotropia of the Bielschowsky type may become more prevalent. Limiting children's media use could serve as a prophylactic measure. Other treatment strategies may include surgery, botulinum toxin injection, prism therapy, ocular occlusion, and behavior modification, depending on etiology.4,7 It is important to note that an underlying neurological illness (eg, brain tumors or cerebellar disease) may present as acute onset esotropia and therefore must be ruled out.2,4,7
We report a case of an adolescent patient with Bielschowsky type acute acquired comitant esotropia, in the setting of exorbitant smartphone use, who experienced a reduction of esodeviation with removal of the inciting stimulus.
A 16-year-old boy initially presented to an optometrist with acute onset horizontal diplopia and a headache. During the prior month, the patient had been on vacation, lost his contact lenses, and used his cell phone more than 8 hours per day. His ocular history was significant for myopia without any history of strabismus, trauma, or recent illness. On examination, cycloplegic refraction demonstrated 5 diopters of myopia in both eyes, which corrected his visual acuity to 20/20 in both eyes. The patient also displayed large angle esotropia with a possible abduction deficit of the left eye.
He was sent to the emergency department with a differential diagnosis of myasthenia gravis, inter-nuclear ophthalmoplegia, sixth nerve palsy, or other intracranial process. Magnetic resonance imaging of the brain and orbits was normal. The patient was subsequently evaluated by a pediatric neurologist and was diagnosed as having intermittent esotropia, but otherwise had normal results. Because of the concern for myasthenia gravis, the patient underwent a Tensilon test, which had inconclusive results. The test and laboratory results, including a myasthenia gravis panel, were also equivocal. For empirical treatment, the patient was prescribed oral pyridostigmine, which he stopped due to intolerance of side effects and lack of improvement.
Approximately 6 weeks after initial symptom onset, the patient was referred to the pediatric ophthalmology clinic. The patient endorsed improvement in his diplopia, which occurred minimally throughout the day. He started wearing a new pair of contact lenses and limited his cell phone use to less than 1 hour per day. His best corrected visual acuity was 20/20 in each eye. His pupils were equally reactive and without a relative afferent pupillary defect. The patient's intraocular pressure was 14 mm Hg bilaterally. Sensorimotor examination, including the Worth 4-dot and Bagolini striated glass test, demonstrated normal binocular fusion and retinal correspondence, with 100 arc seconds of stereoacuity. Bilateral extra-ocular motility was full (Figure 1). Alternate prism cover testing demonstrated a comitant 30 prism diopter esophoria at distance and near with good control (Video 1, available in the online version of this article). Cycloplegic refraction indicated myopic astigmatism of −5.50 +0.50 × 135 in both eyes. Slit-lamp and funduscopic examinations were normal. The patient was discharged from our clinic with a diagnosis of acute acquired comitant esotropia of a benign etiology, and instructions to continue refraining from near work.
Nine-frame motility test indicating full motility.
This case highlights a recently discovered phenomenon of acute acquired comitant esotropia due to prolonged smartphone use, which rapidly improved with cessation of near work. Because our patient lost his contact lenses and had high myopia, he preferred near work consistently during the period of developing esotropia. Lee et al.3 identified 12 patients with acute acquired comitant esotropia without underlying neurological deficits, in the setting of smartphone use averaging more than 6 hours per day over a 4-month period. The patients regressed in 1 month. Similarly, our patient's esotropia resolved to a well-controlled comitant phoria after restricting his cell phone use for a short period.
Acute acquired esotropia, especially in adolescents, prompts neurological assessment to rule out cerebellar or pontine tumors, increased intracranial pressure, and severe head trauma.4 Other etiologies include divergence paralysis from cranial sixth nerve palsy, myasthenia gravis, convergence spasm, restrictive strabismus, and a decompensated monofixation syndrome.7,8 These etiologies present with incomitant deviations, motility deficits, abnormal binocular fusion, or systemic neurological deficits, none of which our patient displayed. Our patient had a comitant deviation and further neurological testing was normal, including neuroimaging and testing for myasthenia gravis.
Smartphone use in adolescents has skyrocketed; approximately, 70% to 75% of teenagers own smartphones.9,10 Sustained near work may induce esodeviations in susceptible children. Further research is needed to help elucidate the correlation of prolonged smartphone use with the development of esodeviation and the level of limitation required for prevention. In conjunction with an increased risk of obesity, depression, sleep disturbance, and developmental delay,10 a potential disruption in visual function should serve as another contributing factor to the limits that parents place on children's media use.
- Schreuders J, Thoe Schwartzenberg GWS, Bos E, Versteegh FG. Acute-onset esotropia: should we look inside?J Pediatr Ophthalmol Strabismus. 2012;49:e70–e72.
- Hoyt CS, Good WV. Acute onset concomitant esotropia: when is it a sign of serious neurological disease?Br J Ophthalmol. 1995;79:498–501. doi:10.1136/bjo.79.5.498 [CrossRef]
- Lee HS, Park SW, Heo H. Acute acquired comitant esotropia related to excessive smartphone use. BMC Ophthalmol. 2016;16:37. doi:10.1186/s12886-016-0213-5 [CrossRef]
- Gilbert AL, Koo EB, Heidary G. Evaluation and management of acute acquired comitant esotropia in children. Semin Ophthalmol. 2017;32:8–13. doi:10.1080/08820538.2016.1228398 [CrossRef]
- Sturm V, Menke MN, Töteberg M, Jaggi GP, Schoeffler C. Early onset of acquired comitant non-accomodative esotropia in childhood. Klin Monbl Augenheilkd. 2012;229:357–361. doi:10.1055/s-0031-1299237 [CrossRef]
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- Chen J, Deng D, Sun Y, et al. Acute acquired concomitant esotropia: clinical features, classification and etiology. Medicine (Baltimore). 2015;94:e2273. doi:10.1097/MD.0000000000002273 [CrossRef]
- Erkan Turan K, Kansu T. Acute acquired comitant esotropia in adults: is it neurologic or not? [published online ahead of print November 27, 2016]. J Ophthalmol. 2016;2856128. doi:10.1155/2016/2856128 [CrossRef].
- Kerr D. Smartphones commandeer 70 percent of teen market. www.cnet.com/news/smartphones-commandeer-70-percent-of-teen-market. Published: October 29, 2013.
- Reid Chassiakos Y, Radesky J, Christakis D, et al. Council on Communications and Media. Children and adolescents and digital media. Pediatrics. 2016;138:e20162593. doi:10.1542/peds.2016-2593 [CrossRef]