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Summary Table

Category	Key Points
Risk Factors	Family history of strabismus or amblyopia, prematurity, low birth weight, uncorrected refractive errors (especially hyperopia), cerebral palsy, Down syndrome, hydrocephalus, congenital cataracts, retinoblastoma
Etiology	Imbalance of extraocular muscles, refractive errors (accommodative type), cranial nerve palsies (CN III, IV, VI), orbital pathology, sensory deprivation (cataract, corneal opacity), neurological disease
Patient Presentation	Child brought in by parents with "crossed eyes," "wandering eye," or "lazy eye"; head tilt or face turn; squinting; closing one eye in bright light; complaints of double vision (in older children and adults)
Classic Physical Exam	Asymmetric corneal light reflex (Hirschberg test), positive cover-uncover test, abnormal eye movement on extraocular motility testing, possible head tilt/turn (compensatory posture)
Key Diagnostic Results	Hirschberg test showing displaced light reflex, cover test confirming deviation, cycloplegic refraction revealing significant hyperopia (in accommodative esotropia), reduced visual acuity if amblyopia present
Management	Refractive error correction with cycloplegic refraction first, occlusion therapy (patching) or atropine penalization for amblyopia, surgical realignment for non-accommodative deviations, prism therapy for small deviations
Keywords	"Crossed eyes," "wandering eye," "lazy eye," "asymmetric red reflex," "abnormal corneal light reflex," "head tilt," "epicanthal folds" (distractor for pseudostrabismus), "hyperopia and esotropia," "amblyopia"

1. Pathophysiology

Strabismus is the misalignment of the visual axes, where the eyes fail to fixate on the same target simultaneously. Each eye is controlled by six extraocular muscles innervated by three cranial nerves:

CN III (oculomotor) supplies the medial rectus, superior rectus, inferior rectus, and inferior oblique
CN IV (trochlear) supplies the superior oblique
CN VI (abducens) supplies the lateral rectus

Any disruption to muscle function, innervation, or the central neural mechanisms of binocular fusion can produce misalignment.

In adults with newly acquired strabismus, the brain receives two non-corresponding images and the patient experiences diplopia (double vision). This is why adult-onset strabismus is almost always symptomatic and prompts a workup for cranial nerve palsy, thyroid eye disease, or intracranial pathology.

In children, the immature visual cortex cannot tolerate diplopia, so the brain actively suppresses the image from the deviated eye. While this eliminates the double vision, prolonged suppression during the critical period of visual development (birth to roughly age 7 to 8) prevents the affected eye from forming proper cortical connections. The result is amblyopia, a permanent reduction in visual acuity that is not correctable by lenses alone after the critical period closes. This is the single most important reason strabismus must be detected and treated early.

A common form, accommodative esotropia, illustrates the link between refraction and alignment. A hyperopic (farsighted) child must accommodate excessively to see clearly. Accommodation is neurologically linked with convergence; therefore excessive accommodation triggers excessive convergence, pulling the eyes inward. The eyes cross because the brain is trying to focus, not because the muscles are intrinsically weak. Correcting the hyperopia with glasses can completely eliminate the deviation in pure accommodative esotropia.

2. Classification of Clinical Manifestations

Classification	Type	Clinical Features
By direction	Esotropia	Eye deviates inward (most common in children)
	Exotropia	Eye deviates outward (often intermittent, worse with fatigue or distance vision)
	Hypertropia	Eye deviates upward
	Hypotropia	Eye deviates downward
By onset	Congenital/Infantile	Onset before 6 months of age, large angle deviation, often requires surgery
By onset	Acquired	Onset after 6 months, often associated with refractive errors or neurological disease
By comitance	Comitant	Deviation angle is the same in all directions of gaze (typical of childhood strabismus)
By comitance	Incomitant	Deviation varies with gaze direction (suggests cranial nerve palsy, restrictive disease, or muscle pathology)

3. Diagnostic Workup

Test	Purpose	Findings
Hirschberg corneal light reflex	Initial screening	Asymmetric light reflex; nasal displacement = exotropia, temporal displacement = esotropia
Cover test	Detects manifest strabismus (tropia)	Covered eye remains aligned; uncovered eye shifts to fixate
Alternate cover test / Cover-uncover test	Detects latent deviation (phoria) and total deviation	Eye shifts when cover is moved between eyes
Krimsky test	Quantifies deviation in young children	Prism placed to center light reflex
Cycloplegic refraction	Detects hyperopia driving accommodative esotropia	Significant hyperopia (typically over +2.00 D)
Visual acuity	Detects amblyopia	Reduced acuity in the deviated eye
Extraocular motility testing	Detects incomitance and cranial nerve palsy	Limited movement in field of action of paretic muscle
Fundus examination / Red reflex	Rules out organic causes	Leukocoria suggests retinoblastoma or cataract; this is a red flag
Neuroimaging (MRI/CT)	Reserved for acquired or incomitant cases	Identifies tumor, demyelination, aneurysm, or orbital pathology

The workup begins with the Hirschberg test as the best initial screening tool. A penlight is held about 30 cm from the patient, and the position of the corneal light reflex is observed. In normal alignment, the reflex falls symmetrically and slightly nasal to the center of each pupil. Displacement of the reflex indicates deviation:

If the light reflex falls temporally on one eye, that eye is esotropic (turned in)
If it falls nasally, the eye is exotropic (turned out).

This test is fast and tolerated well by uncooperative children.

The cover test confirms the presence of a manifest deviation (tropia). The examiner covers one eye and watches the uncovered eye. If the uncovered eye shifts to take up fixation, a tropia exists. The alternate cover test (cover-uncover test) then quantifies the total deviation including any latent component (phoria), and combined with prism bars provides a measurement in prism diopters used to plan surgery.

Before any conclusions are drawn, every child with suspected strabismus must undergo cycloplegic refraction. Cycloplegic agents (cyclopentolate or atropine) paralyze the ciliary muscle, eliminating accommodation and revealing the true refractive error. This is the single most important step in distinguishing accommodative from non-accommodative esotropia, because accommodative esotropia can be treated with glasses alone, whereas non-accommodative forms require surgery.

A fundus examination with red reflex testing is mandatory in any child with strabismus. Leukocoria (white pupillary reflex) raises concern for retinoblastoma, congenital cataract, or persistent fetal vasculature, all of which can present as strabismus due to sensory deprivation. Missing this is a high-stakes error.

For acquired strabismus, sudden-onset diplopia, or incomitant deviations, neuroimaging is the most accurate next step to rule out intracranial pathology. A new sixth nerve palsy in an adult, for example, can reflect raised intracranial pressure or a compressive lesion.

Strabismus diagnosis is confirmed by the combination of cover-uncover testing with prism quantification and cycloplegic refraction. There is no single laboratory test; the diagnosis is clinical.

4. Management & Treatment

Treatment Modality	Indication	Details
Optical correction (glasses)	Accommodative esotropia, significant refractive error	Full hyperopic correction based on cycloplegic refraction; bifocals if high accommodative convergence
Occlusion therapy (patching)	Amblyopia in deviated eye	Patch the better-seeing eye 2 to 6 hours daily; duration depends on age and severity
Atropine penalization	Amblyopia, alternative to patching	Atropine 1% drops to better-seeing eye, blurs near vision and forces use of amblyopic eye
Prism lenses	Small-angle deviations, diplopia in adults	Fresnel or ground-in prisms
Surgical correction	Non-accommodative deviation, residual deviation after glasses	Recession (weakening) and resection (strengthening) of extraocular muscles
Botulinum toxin injection	Selected acute palsies, small deviations	Temporary chemodenervation of antagonist muscle
Treatment of underlying cause	Cranial nerve palsy, thyroid eye disease, intracranial mass	Address the primary pathology

The first step in management is full correction of any refractive error, prescribed on the basis of cycloplegic refraction. In a hyperopic child with esotropia, fitting glasses with the full hyperopic correction may completely resolve the deviation within weeks. The child wears the glasses full-time, and the alignment is reassessed. If the deviation fully corrects with glasses, the diagnosis is fully accommodative esotropia and no surgery is indicated. If only part of the deviation corrects, the residual is termed partially accommodative esotropia, and the non-accommodative component may eventually require surgery.

The next priority is treatment of amblyopia, which must be addressed before or alongside any surgical plan. The mainstay is occlusion therapy, where the better-seeing eye is patched to force the brain to use the amblyopic eye. Typical regimens involve 2 to 6 hours of patching per day, titrated to severity and age, with weekly to monthly follow-up to monitor progress and prevent reverse amblyopia. Atropine penalization is an alternative; atropine 1% drops are placed in the better-seeing eye once daily, blurring near vision and forcing the child to use the amblyopic eye. Compliance is often better with atropine, and outcomes are comparable for moderate amblyopia.

Surgery is reserved for non-accommodative or residual deviations after refractive and amblyopia treatment have been optimized. The principle is to weaken overacting muscles (recession, in which the muscle is detached and reattached posteriorly) and strengthen underacting muscles (resection, in which a portion of the muscle is removed). Surgery is performed under general anesthesia, typically as a day-case procedure. Timing matters: infantile esotropia is generally operated on between 6 and 24 months of age to give the best chance of developing some binocular function.

For adults with acquired strabismus, the priority is to identify and treat the underlying cause. A pupil-sparing third nerve palsy in a vasculopathic adult is often microvascular and resolves over weeks to months; observation with prisms for diplopia is appropriate. A pupil-involving third nerve palsy is treated as a posterior communicating artery aneurysm until proven otherwise and requires urgent neuroimaging and vascular evaluation.

The next best step in any child presenting with strabismus is to perform a complete eye examination including red reflex and fundus to rule out organic disease (especially retinoblastoma), followed by cycloplegic refraction. Glasses come before patching, patching comes before surgery, and surgery comes after stable refractive correction.

Contraindications and cautions include avoiding atropine penalization in children with known hypersensitivity, and timing surgery carefully in children who are still developing accommodative control.

5. Differential Diagnosis & Distractors

Differential Diagnosis	Why It's Similar	Key Discriminator
Pseudostrabismus	Child appears to have crossed eyes due to wide nasal bridge, prominent epicanthal folds, or narrow interpupillary distance	Hirschberg corneal light reflex is symmetric, and cover test is negative; reassurance is sufficient
Sixth nerve palsy	Causes esotropia	Esotropia is incomitant, worse on gaze toward the affected side; abduction is limited; often acquired with sudden onset
Third nerve palsy	Causes ocular misalignment with the eye "down and out"	Associated ptosis and possible pupillary involvement; multiple muscle groups affected
Fourth nerve palsy	Causes vertical and torsional deviation	Compensatory head tilt away from the affected side (Bielschowsky head tilt test positive); hypertropia worsens on contralateral gaze and ipsilateral head tilt
Duane retraction syndrome	Limited eye movement mimics paralytic strabismus	Globe retraction and palpebral fissure narrowing on adduction; congenital and non-progressive
Brown syndrome	Limited elevation in adduction looks like inferior oblique paresis	Restriction is mechanical (superior oblique tendon sheath), present from birth, no overaction of antagonist
Retinoblastoma	Can present as strabismus due to vision loss in the affected eye	Leukocoria (white pupillary reflex), abnormal red reflex; this is the can't-miss diagnosis
Congenital cataract	Sensory strabismus from poor vision	Absent or abnormal red reflex, opacity visible on slit lamp; requires urgent surgery
Thyroid eye disease (in adults)	Restrictive strabismus with diplopia	Proptosis, lid retraction, lid lag; thyroid function tests abnormal; orbital imaging shows enlarged extraocular muscles sparing tendons
Myasthenia gravis	Variable diplopia and ptosis	Fatigability, worse at end of day; ice-pack test positive; acetylcholine receptor antibodies
Intermittent exotropia	Outward deviation that may be missed on examination	Worse with fatigue, illness, or distance fixation; child closes one eye in bright sunlight

6. Traps & High-Yield Pearls

The most common way a question on strabismus is missed is by failing to rule out organic and life-threatening causes before treating the misalignment. A child with new strabismus and an abnormal red reflex has retinoblastoma until proven otherwise, and the correct next step is referral for urgent ophthalmologic evaluation, not patching or glasses. Equally, an adult with sudden-onset diplopia and a third nerve palsy with pupil involvement has an aneurysm until proven otherwise, and the correct next step is urgent neuroimaging with vascular study, not prism glasses.

The second classic trap is confusing pseudostrabismus with true strabismus. A young infant with prominent epicchanthal folds may look cross-eyed, but the corneal light reflex is symmetric and the cover test is negative. The correct answer here is reassurance, not referral for surgery.

The third trap is missing the link between hyperopia and esotropia. If a vignette describes a hyperopic child with esotropia, the next best step is full cycloplegic refraction and prescription of hyperopic glasses, not surgery. Surgery in a child whose deviation would have resolved with glasses is a serious management error.

The fourth trap is forgetting amblyopia. Treating the deviation without addressing the amblyopic eye allows permanent vision loss. Patching or atropine penalization comes alongside refractive correction, and both come before any surgical decision.

The fifth trap is confusing comitant and incomitant strabismus. Comitant deviation in a young child is usually idiopathic or accommodative and follows the standard pediatric pathway. Incomitant deviation, especially of new onset in an older child or adult, points to a cranial nerve palsy or restrictive disease and demands a workup for intracranial, vascular, or systemic pathology.

The core competency being tested is recognizing strabismus as a clinical sign, not a diagnosis in itself, and sequencing the workup correctly: rule out organic disease (red reflex, fundus), correct refractive error (cycloplegic refraction and glasses), treat amblyopia (patching or atropine), and only then consider surgery. Mastery of this sequence, together with the ability to identify the red flag presentations of leukocoria, pupil-involving third nerve palsy, and acquired incomitant deviation, is what separates a correct answer from a near-miss distractor.

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