Historically, AACE has been classified into three types depending on clinical features and apparent etiology: a) Type I (Swan): refers to an esotropia following the interruption of fusion by monocular occlusion or vision loss (1); b) Type 2 (Burian-Francesschetti): esotropia associated with physical or psychological stress and mild hyperopia with no other known cause; and c) Type 3 (Bielschowsky): esotropia that occurs in adolescents and adults, related to different degrees of uncorrected myopia.
Since then, findings from a number of reports suggested other etiologies of AACE such as accommodative spasm, decompensating esophoria, age-related distance esotropia, decompensated monofixation ocular syndrome, myasthenia gravis and neurological disorders (3).
It is important to be conscious about the infrequent, but possible, presence of central nervous system pathologies in these patients. Comitancy in AACE did not exclude the possibility of an underlying serious neurological disorder (4). In our patient neurological examination and neuroimagen findings were negative.
Epidemic keratoconjunctivitis (EKC) is a relatively common eye infection caused by human adenoviruses (5). Clinical signs of EKC include lid swelling, conjunctival injection, follicles, chemosis, pseudomembranes and subepithelial infiltrates. Most patients completely recover without any complications in a few weeks, however in some cases subepithelial infiltrates may persist for months (6).
Orbital involvement in viral infection is extremely rare. There are some reports of adenoviral conjunctivitis that caused orbital inflammation and caused extraocular motility restriction and diplopia (7). Our case did not present proptosis nor limited extraocular motility.
Our patient also developed subepithelial infiltrates but these did not cause a severe loss of vision; therefore, we consider that the cause of the strabismus was the prolonged occlusion of the eye due to edema and palpebral ptosis during several days, which disrupted the corrective fusional movements and lead to esotropia. Besides, the patient probably had to make an effort to use exclusively the eye of + 1.75 D of hyperopia without the aid of glasses, which probably caused abnormal convergence impulses that resulted in an acquired comitant esotropia. Therefore, considering all signs mentioned above this case could be classified as a Swan type (1).
Patient had no history of previous strabismus, however a latent deviation could manifest as an esotropia as a result of an interruption of the fusion mechanism that previously worked correctly and maintained the alignment of the eyes (8).
It is known that patients with esophoria initially use divergence fusional reserves in order to compensate it, but sometimes stress situations, physical illnesses, close working distance or even aging can reduce these reserves provoking an unmasked large angle AACE (9). In this case, fusional divergence amplitude at distance and at near were slightly lower than normal. So we cannot discard that the esotropia could have been triggered by a decompensated esophoria that had not been previously diagnosed (9).
In patients with AACE surgical treatments are important because spontaneous recovery is uncommon. The prognosis for binocular recovery is relatively good because given the late-onset of esotropia, and most patients have already established binocular single vision and stereopsis before the onset of strabismus (10, 11). The surgery performed in our patient allowed us to achieve orthotropy and stereoacuity.