Introduction

Acute-onset strabismus with diplopia in children is most frequently perceived as an alarming sign. It has diverse aetiologies, ranging from mild and reversible to serious and potentially life-threatening. Comprehensive population-level statistics on the exact distribution of causes of acute-onset strabismus are still lacking. The most common causes of acute acquired comitant esotropia (AACE) in children include accommodative esotropia (31%), which is typically associated with uncorrected hyperopia and is often precipitated by systemic illness or minor trauma. Decompensated monofixation syndrome or esophoria accounts for approximately 27% of cases, while idiopathic aetiologies represent about 19%. Intracranial pathology, including brain tumours and hydrocephalus, is responsible for roughly 6% of cases.
In recent years, excessive near work and increased digital device use have also been proposed as potential contributing risk factors [1, 2].

This study aims to present cases of acute-onset strabismus associated with diplopia in children, emphasising diagnostic and therapeutic approaches to provide practical guidance for clinicians. It highlights the importance of detailed history-taking, thorough patient evaluation, and interdisciplinary collaboration, especially in atypical presentations or cases with neurological symptoms.

Patient 1: partially accommodative esotropia

A nine-year-old boy presented with acute-onset binocular horizontal diplopia, first noted two days earlier at school. He experienced balance loss but denied trauma or systemic symptoms. His history included neonatal hypotonia, with no prior ophthalmologic evaluation.

The patient presented to the paediatric emergency department, where a non-contrast head computed tomography (CT) scan was performed with no prior ophthalmologic consultation. The CT findings were unremarkable. Best-corrected visual acuity was 0.05 and 0.6 in the right (OD) and left (OS) eyes, respectively, expressed as the logarithm of the minimum angle of resolution (logMAR). Cycloplegic refraction revealed significant hyperopia: +5.5/–1.5 × 5° OD and +6.25/–1.5
× 170° OS. Esotropia measured 20 prism dioptres (PD) at distance and near PD was 12.

Accommodative esotropia was diagnosed. Spectacle correction was prescribed, but the improper eye alignment persisted, suggesting partially accommodative esotropia. Only prismatic correction eliminated diplopia. Surgical correction was performed due to persistent strabismus. After the surgery, at 12 years of age, the patient no longer exhibited strabismus while wearing appropriate optical correction.

This case supports cycloplegic refraction as the initial diagnostic approach in acute esotropia without neurological signs, especially when uncorrected hyperopia is suspected, prior to neuroimaging.

Patient 2: acute acquired non-accommodative esotropia

A 2.5-year-old child presented with sudden-onset left esotropia, first noticed by the parents after returning from daycare. Four days after symptom onset, the child was evaluated by a community ophthalmologist. Mild hyperopic correction (+1.25 D in both eyes) was prescribed, and right-eye occlusion therapy for 4 hours daily was initiated. Orthoptic exercises were also recommended.

However, the refractive error was within the physiological range for age and unlikely to account for the deviation. Furthermore, orthoptic exercises have no established efficacy in the management of AACE.

Given the acute presentation, a neurological assessment was performed, which revealed no abnormalities. Brain magnetic resonance imaging (MRI) ordered by the neurologist was unremarkable. Perinatal history was noncontributory.

Six weeks after onset, the patient was referred to our department. Visual acuity with correction was 0.5 binocularly and 0.7 monocularly (logMAR). Cycloplegic autorefraction confirmed mild hyperopia (OD +1.50/–0.50 × 80°,
OS +1.25/–0.75 × 66°), consistent with age-related physiological refractive status. With correction, esotropia measured
12–17° at distance and 15–20° at near distance. Ocular motility was normal. Cover testing demonstrated comitant left esotropia of 30–34 PD at distance and 35–40 PD at near distance. The anterior segment and fundus examination were normal. The findings were consistent with AACE in an otherwise healthy child without significant refractive error.

Bilateral medial rectus recession (5.5 mm) was performed later that year, followed by bilateral lateral rectus resection (5.0 mm) one year later due to residual deviation. Postoperatively, alignment was orthotropic with full motility, symmetric fusion, and measurable stereopsis.

This case demonstrates that acute-onset esotropia may
occur in otherwise healthy children without clinically significant hyperopia. Physiological refractive error does not necessitate optical correction in such cases, and orthoptic exercises have no proven benefit. After exclusion of neurological pathology, timely surgical management may lead to favourable functional outcomes and preservation of stereoscopic vision.

Patient 3: infection as a cause of acute-onset diplopia
associated with strabismus

A nine-year-old girl presented to the ophthalmology clinic with sudden vertical strabismus in the OD, nystagmus, and severe frontal headache lasting two days. She also reported ear pain. A month prior, she had fractured her right arm but denied a head injury. Her medical history included astigmatism, and her father had a history of strabismus. Examination revealed cycloplegic autorefraction measurements of +1.0/–2.0 × 169° OD and +1.5/–1.0 × 171° OS, with monocular visual acuity of 0.15 OD and 0.0 OS (logMAR). Due to the vertical strabismus and neurological symptoms, she was referred for further evaluation to a paediatric hospital. Laboratory and serologic testing identified neuroborreliosis and concurrent human herpesvirus (HHV)-6 and HHV-7 infections.

The patient was treated with cefotaxime, acyclovir, and dexamethasone, resulting in complete resolution of strabismus, nystagmus, and systemic symptoms. This case highlights the importance of considering infectious aetiologies in acute-onset strabismus with neurological features.

Patient 4: acute-onset esotropia with diplopia in paranasal sinusitis

A 16-year-old girl presented to the ophthalmologist with acute-onset OS esotropia and binocular diplopia following a 10-day upper respiratory infection complicated by paranasal sinusitis. She had been undergoing antibiotic therapy for two days prior to the evaluation. Her medical history included myasthenia gravis in her grandmother’s sister.

Ophthalmic examination revealed left esotropia, mild proptosis, and soft tissue swelling. The clinical findings were consistent with an inflammatory sixth nerve palsy secondary to sinusitis with orbital involvement, a recognised complication of paranasal sinus disease in the paediatric and adolescent population. Oropharyngeal exam showed erythema with purulent discharge on the posterior pharyngeal wall. Contrast-enhanced CT confirmed sinusitis with fluid accumulation but no extraocular muscle involvement.

The patient underwent endoscopic sinus surgery and was treated with cefotaxime, clindamycin, and systemic corticosteroids. Postoperatively, cycloplegic refraction was –2.5/−0.25
× 9° OD and –2.75/−0.5 × 15° OS with visual acuity with correction 0.0 OD and 0.1 OS (logMAR). The OS esotropia of 30 PD was more apparent at distance. In case of persistent diplopia, alternating eye patching was recommended.

A follow-up appointment was scheduled three months after completion of neurological and otolaryngological care; however, the patient did not attend. During a telephone consultation, her father reported that diplopia had resolved.

This case illustrates that acute-onset esotropia, caused by sixth nerve palsy especially in adolescents, can occur secondary to sinusitis with orbital involvement, and that prompt surgical and medical management can lead to complete resolution of ocular symptoms.

Patient 5: acute-onset exotropia due to hydrocephalus secondary to a pineal gland tumour

A 12-year-old girl presented to the emergency department with sudden-onset OS exotropia first noted three hours prior. Over the preceding two weeks, she had exhibited a leftward head tilt and neck pain but denied visual acuity changes or diplopia. Visual acuity was 0.05 OD and 0.15 OS (logMAR). The patient had no prior ocular treatment and was generally healthy. On further questioning, the parents reported two episodes of vomiting and headaches over the past two weeks. Family history included esotropia in an older sister.

Examination revealed an outward and slightly downward deviation of the OS, limited ocular motility, and a larger left pupil with sluggish light reaction, which suggested third nerve palsy. Cycloplegic autorefraction indicated hyperopia (OD +2.0/–0.5 × 165°, OS +2.25/–0.75 × 170°). Fundus examination showed mild vessel tortuosity in the OS, with no nystagmus present.

Given the atypical strabismus and associated neurological symptoms, the patient was referred for further evaluation, leading to a diagnosis of hydrocephalus secondary to a pineal gland tumour, suggesting Parinaud syndrome.

This case underscores the importance of urgent neuroimaging in patients with atypical acute-onset exotropia and neurological or systemic symptoms.

Discussion

This case series describes diplopia associated with acute-onset strabismus in the paediatric population, emphasising the critical role of a detailed medical history in guiding physical examination and subsequent investigations, including neuroimaging.

Timing of symptom onset is a pivotal diagnostic feature. Acute strabismus is characterised by a sudden appearance of symptoms within hours or days, whereas chronic strabismus develops gradually over weeks or months, making it less noticeable [3, 4].

Patient age significantly influences the potential aetiology of acute-onset strabismus. In younger children, particularly those under six years old, non-paralytic ophthalmic causes such as refractive errors and accommodative disorders are prevalent [5, 6]. Conversely, in older children and adolescents, neurological aetiologies – including acute cranial nerve palsies, idiopathic intracranial hypertension, and intracranial pathologies like brain tumours – are more common [3, 7].

A key step in evaluation is differentiating ophthalmic from neurogenic strabismus. This begins with recognising “red flags”, including systemic symptoms such as new-onset headaches, fever, altered consciousness, vomiting, seizures, nystagmus, balance disturbances, or paresis. The presence of these symptoms necessitates urgent neurological consultation and a brain MRI. Neurogenic strabismus may also present with restricted ocular motility and atypical clinical features, such as vertical strabismus [8, 9].

Neuroimaging is warranted in paediatric patients with strabismus, accompanied by ophthalmic signs such as optic disc swelling or abnormal pupillary responses, even in the absence of systemic symptoms [3]. The American Academy of Ophthalmology (AAO) recommends immediate imaging – preferably MRI – in all cases of non-isolated acute strabismus with concerning features [3, 10].

For sudden-onset esotropia without neurological symptoms, ophthalmic evaluation should be prioritised to identify potential causes such as uncorrected hyperopia, thus preventing unnecessary neurological investigations.

Acute-onset strabismus associated with facial pain, fever, and purulent nasal discharge should raise suspicion for orbital complications secondary to sinusitis or otitis, warranting urgent otolaryngology consultation. Diagnostic imaging, such as MRI or CT scans of the orbits and paranasal sinuses, can help identify orbital complications, including cellulitis or abscesses [11, 12]. Effective treatment of acute sinus or middle ear infections is a priority before considering surgical interventions to correct strabismus, which should only occur after the acute phase has resolved and the patient’s condition has stabilised [13].

Awareness of prognosis for diplopia associated with strabismus in paediatric patients is vital for physicians and families. However, outcomes vary considerably depending on strabismus subtype, angle of deviation, and timing of intervention. In AACE of ophthalmic origin, surgical success rates are generally favourable when intervention is timely [1].
The AAO Preferred Practice Pattern notes that residual
or recurrent deviation requiring further intervention remains a possibility and underscores the importance of long-term
follow-up [10]. Neurological strabismus has a less favourable prognosis, with only 56% achieving alignment post-surgery [14].
It should be noted that neurological strabismus derives from a cohort of patients with cortical visual impairment, a heterogeneous group that includes cases secondary to prematurity and hypoxic-ischaemic injury – conditions associated with diffuse cerebral damage and intrinsically poorer visual and motor prognosis. This percentage should therefore be interpreted with caution when applied to other forms of strabismus.

Follow-up is essential for all patients, to monitor ocular alignment, binocular vision, and risk of amblyopia. Patients with well-aligned eyes who show no signs of amblyopia may be reviewed less frequently, with the frequency of visits decreasing with age. The onset of new or changing symptoms indicates an increase in follow-up frequency [10].

Conclusions

Sudden-onset diplopia associated with strabismus in children requires prompt and systematic clinical evaluation. Early recognition and accurate diagnosis are critical to preserving binocular vision and preventing long-term complications such as amblyopia. A detailed medical history and comprehensive physical examination are essential for identifying “red flags”, including neurological signs or increased intracranial pressure, which necessitate urgent neuroimaging.
In the absence of systemic or neurological symptoms, ophthalmic causes – particularly uncorrected refractive errors –
should be considered first, with cycloplegic refraction and ocular alignment testing guiding management. Awareness of the varied aetiologies, from benign ophthalmic disorders to serious neurological or infectious conditions, allows for individualised, evidence-based care, timely intervention, and improved functional outcomes.

Disclosures

The authors declare no conflict of interest.

This work received no external funding.

Approval from the Bioethics Committee was not required.

References