Approach to the pediatric patient with acute vision change

INTRODUCTION — An acute change in vision may result from numerous diseases and injuries. A systematic approach is necessary to reach a correct diagnosis and to identify serious underlying etiologies. The patient’s age, underlying disease conditions, visual history, and history of possible injury must be determined. The extent of the visual impairment, the rapidity of its onset, and the association with other systemic findings are vital pieces of information.

This topic will review the causes of vision change (eg, diplopia, blurry vision). The approach to a child with vision loss is discussed separately. (See "Diagnostic approach to acute vision loss in children".)

CAUSES OF DIPLOPIA — When a child complains of diplopia, a prompt evaluation should be initiated. Younger children may not be able to complain of diplopia. Instead, they may squint, cover one eye with their hand, or use an abnormal head posture for viewing. Diplopia may be binocular or monocular (see "Overview of diplopia", section on 'Diplopia'):

●Binocular diplopia is present with both eyes open and absent when either eye is closed. Binocular diplopia reflects conditions in which the visual axes are misaligned. In general, most patients will close the eye with the poorer vision or, if vision is equal, the eye with the dysfunctional muscle. Binocular diplopia will be discussed here.

●Monocular diplopia is present if the diplopia occurs when a person is viewing with only one eye. This condition is less common and is typically caused by corneal surface irregularity, crystalline lens anomalies, or refractive error.

The extraocular muscles are innervated by cranial nerve III except for the superior oblique (cranial nerve IV) and the lateral rectus (cranial nerve VI) muscles (figure 1). Any condition that results in palsy of the third, fourth, or sixth cranial nerves can cause binocular diplopia [1].

Other potential etiologies include:

●Conditions associated with transient loss of control of eye movements (eg, ocular migraine, seizures, drug intoxication [eg, ethanol, benzodiazepines, sedative-hypnotic medications])

●Mass lesions of the orbit (eg, orbital tumors, hematoma, or infection)

●Ocular muscle weakness, restriction, or malfunction (eg, myasthenia gravis, tick paralysis, botulism, orbital floor fracture with entrapment)

●Decompensated phoria (tendency for eyes to converge or diverge), a form of acquired strabismus in which a child with an ocular phoria has worsened to a fixed ocular tropia (a persistent ocular misalignment) that is manifest and can cause acute, constant, or intermittent diplopia (see "Evaluation and management of strabismus in children")

Third cranial nerve palsy — Third nerve palsy in children often is congenital (intrauterine or birth-related events) but may occur after postnatal trauma, infection, inflammation, tumor, or childhood migraine (table 1). (See "Third cranial nerve (oculomotor nerve) palsy in children", section on 'Etiology'.)

Patients with acquired third nerve palsies usually complain of the sudden onset of binocular horizontal, vertical, or oblique diplopia, oftentimes with an ipsilateral ptosis. Children with congenital third nerve palsies may not complain of diplopia because they ignore or suppress the second image or because they have superimposed amblyopia; often they are brought to medical attention by their parents/caregivers, who have noticed ptosis or strabismus. Patients with third nerve palsy may have one or more of the following findings (see "Third cranial nerve (oculomotor nerve) palsy in children", section on 'Clinical manifestations'):

●Ptosis (picture 1)

●Primary position exotropia (eye turned out) which worsens with gaze toward the paretic medial rectus muscle (figure 2)

●Ipsilateral hypertropia (eye is turned up) or hypotropia (eye is turned down), depending on which of the extraocular muscles is most affected

●Complete third nerve palsies usually are associated with a large-angle exotropia and hypotropia (eye is down and out)

Fourth cranial nerve palsy — The most common causes of fourth nerve palsies in children are congenital, traumatic, and idiopathic. Fourth nerve palsies may also accompany intracranial mass lesions (eg, tumor, abscess, hemorrhage) (table 2). (See "Fourth cranial nerve (trochlear nerve) palsy", section on 'Causes of isolated fourth nerve palsy'.)

Children with fourth nerve palsies may complain of binocular (ie, present with both eyes open) vertical, torsional diplopia. Objects viewed in primary position or especially in down-gaze may appear double (eg, when going down a flight of stairs so that the child does not know which step to select).

On examination, an ipsilateral hypertropia (the involved eye is deviated upward) is present because the action of the superior oblique muscle (to move the eye down and in) is weak. The deviation is greater when gaze is in the direction that utilizes the involved muscle. Thus, a right fourth nerve palsy causes greater hypertropia in left gaze and when using an ipsilateral head tilt. The patient may adopt an anomalous head position to avoid diplopia because torsional and vertical diplopia often improve with head tilting to the side opposite the paralyzed muscle (picture 2). (See "Fourth cranial nerve (trochlear nerve) palsy", section on 'Clinical manifestations'.)

Sixth cranial nerve palsy — Dysfunction of the sixth cranial nerve (abducens nerve) can result from lesions occurring anywhere along its path between the sixth nucleus in the dorsal pons to the lateral rectus muscle within the orbit. The lesions may be congenital or acquired (table 3). (See "Sixth cranial nerve (abducens nerve) palsy", section on 'Etiologies'.)

Patients with sixth nerve palsies typically complain of binocular (ie, requires both eyes to be open) horizontal diplopia that worsens with gaze toward the paretic lateral rectus muscle. However, children may not complain of diplopia. Early in the course, strabismus may be present only in the gaze toward the paralyzed side, but with time, the strabismus (ie, esotropia) may be present when gazing straight ahead (primary position) and even in the opposite gaze. The degree of esotropia and abduction deficit are markers of severity of the paresis or palsy and/or secondary contracture of the ipsilateral medial rectus muscle.

The ocular examination typically reveals a primary position esotropia (eye turned in), worse in gaze toward the paretic muscle (lateral incomitance), and an ipsilateral abduction deficit. The face often is turned toward the paralyzed side to avoid the gaze toward the symptomatic lateral rectus muscle. Other manifestations depend upon the location of the lesion along the course of the nerve (table 4). (See "Sixth cranial nerve (abducens nerve) palsy", section on 'Clinical manifestations'.)

Migraine — Migraine headaches are a relatively common cause of visual change in children. Migraine with brainstem aura (formerly basilar-type migraine) is typically occipital, associated with visual disturbances, and accompanied by blurred or tunnel vision, dizziness, ataxia, diplopia, and vomiting. Headache and nausea after such an episode are the rule, but occasionally may be absent. (See "Types of migraine and related syndromes in children" and "Migraine with brainstem aura".)

Recurrent painful ophthalmoplegic neuropathy, formerly called ophthalmoplegic migraine, occurs primarily in children and affects the third cranial nerve causing ptosis, pupillary dilation, diplopia, and blurred vision. It may be due to recurrent bouts of demyelination and can take days to weeks to resolve. (See "Overview of craniofacial pain", section on 'Recurrent painful ophthalmoplegic neuropathy'.)

Seizures — Seizures may also present with visual changes, for example, diplopia, which sometimes manifest as a migraine-like episode. Visual disturbances may also be the only clinical manifestation of childhood occipital epilepsy, but are more commonly associated with more typical seizure activity [2].

Toxic ingestion — Children who are intoxicated with benzodiazepines, sedative-hypnotic agents, ethanol, or opioids may have disconjugate gaze and double vision. (See "Benzodiazepine poisoning" and "Ethanol intoxication in children: Clinical features, evaluation, and management" and "Opioid intoxication in children and adolescents", section on 'Clinical manifestations'.)

Cavernous sinus thrombosis — Cavernous venous sinus thrombosis typically presents with diplopia in association with orbital pain, chemosis, and proptosis (figure 3). Diplopia is variably seen with other types of cerebral venous thrombosis. Underlying etiologies include prothrombotic states, either congenital (eg, antithrombin III deficiency) or acquired (eg, hyperviscosity syndrome); oral contraceptive usage; sinusitis or intraocular infection; Crohn disease [3]; or malignancy. (See "Cerebral venous thrombosis: Etiology, clinical features, and diagnosis".)

Orbital fractures — Blunt orbital trauma (eg, baseball striking the orbit) may cause fracture of the orbital floor ("blowout fracture") with entrapment of orbital fat and sometimes the extraocular muscles, typically the inferior rectus muscle (image 1). Visual impairment may be limited to double vision when looking in a certain direction, particularly upward and limitation of upward gaze in the affected eye (picture 3). Inspection may show enophthalmos as well. Careful examination of the globe for associated injuries (eg, corneal abrasion, hyphema, corneal or scleral laceration) is also necessary. (See "Orbital fractures", section on 'Orbital floor fracture'.)

Orbital cellulitis — Orbital cellulitis can present with double vision in the setting of periorbital swelling and tenderness, erythema, proptosis, pain upon extraocular movement, and rarely, with advanced disease, acute vision loss from compressive optic neuropathy. Orbital cellulitis is most commonly caused by an extension of acute bacterial sinusitis although it may complicate ophthalmic surgery, orbital trauma, and infections of the tear ducts, teeth, or middle ear. (See "Orbital cellulitis", section on 'Clinical manifestations'.)

Graves' ophthalmopathy (orbitopathy) — This condition is also known as thyroid-related ophthalmopathy. Diplopia may occur in children and adolescents with Graves' disease because of initially increased inflammation and accumulation of hydrophilic glycosaminoglycans in the extraocular muscles and retro-orbital connective and adipose tissue (figure 4) and later restrictive connective tissue changes in the extraocular muscles. Other clinical findings include one or more of the following: a sense of irritation in the eyes; excessive tearing that is often made worse by exposure to cold air, wind, or bright lights; eye or retro-orbital discomfort or pain; blurring of vision; and occasionally loss of vision. (See "Clinical features and diagnosis of thyroid eye disease", section on 'Clinical features'.)

Myasthenia gravis — Myasthenia gravis (MG) is a rare cause of diplopia in children. The clinical manifestations vary from subtle blurring of vision to severe diplopia. As with all symptoms of myasthenia, the symptoms vary depending on how much use of the muscles is available. Weakness of the eye muscles in MG can also produce ptosis, the degree of which is variable, switching from one eye to the other on separate examinations and occasionally increasing with sudden exposure to bright light. Most patients with MG do not complain of eye pain or headache. Fatigability and variability of clinical findings are characteristic.

Physical examination may reveal unusual eye movements that do not conform to the anatomy of one nerve or muscle. The pupils are always spared in MG, helping in the differentiation from other disorders, such as botulism. The diagnosis and treatment of myasthenia gravis is discussed separately. (See "Ocular myasthenia gravis".)

Tick paralysis — There are more than 800 known species of argasid (soft-shelled) and ixodid (hard-shelled) ticks, and over 40 individual tick species are capable of producing salivary toxins that can cause paralysis in humans and animals. The tick species that cause most cases of human tick paralysis in the United States and Canada are Dermacentor andersonii (the Rocky Mountain wood tick), and D. variabilis (the American dog tick). Tick paralysis occurs four to seven days after a female tick has been feeding on the human host. Paralysis may involve the ocular muscles causing diplopia. It is typically associated with paresthesias, fatigue, and muscle weakness, which progresses to unsteady gait and ascending complete paralysis. However, unilateral and isolated paralysis has also been described. (See "Tick paralysis", section on 'Tick vectors' and "Tick paralysis", section on 'Clinical manifestations'.)

Botulism — Botulism, acquired from food sources or wound infections contaminated with one of eight strains of Clostridium botulinum, is marked by symmetric cranial nerve involvement. Blurred vision and diplopia typically occur in the setting of a symmetric descending muscular weakness. The patient retains normal mental status and does not have fever or sensory abnormalities. (See "Botulism", section on 'Clinical manifestations'.)

Miller Fisher syndrome — Children with Miller Fisher syndrome have external ophthalmoplegia which may cause diplopia in association with ataxia, muscle weakness, and areflexia. This specific form of Guillain-Barré syndrome is sometimes associated with Campylobacter infection. (See "Guillain-Barré syndrome in children: Epidemiology, clinical features, and diagnosis", section on 'Pathogenesis' and "Guillain-Barré syndrome in children: Epidemiology, clinical features, and diagnosis", section on 'Miller Fisher syndrome'.)

Conversion disorder — Conversion disorder describes neurological symptoms such as visual changes, weakness, abnormal movements, or blackouts that are not consistent with a neurological disease process and are not feigned. Psychogenic visual symptoms range from intermittent blurred vision to complete blindness. Apparent visual field defects and double vision (due to spasm of convergent eye movements) can also occur. (See "Functional neurological symptom disorder (conversion disorder) in adults: Terminology, diagnosis, and differential diagnosis".)

A large number of tests exist to help provide evidence of internal inconsistency in visual testing. At the bedside, the following are useful:

●Inability to sign name or touch fingers together in the presence of complete blindness suggests a psychogenic problem (blind people should be able to do this if otherwise unaffected)

●Optokinetic nystagmus in the presence of complete blindness (and the absence of cortical blindness)

●Tubular visual field defect, for example, tunnel vision of the same width as examined at 1 m and 2 m

●Convergence spasm leading to hyper-adduction of one eye during convergent testing; this can give the appearance of a sixth nerve palsy

CAUSES OF BLURRY VISION — In children, acutely blurred vision is most commonly caused by conjunctivitis or corneal abrasion. Other less common conditions include keratitis, hyphema, and retinal artery or vein occlusion.

Conjunctivitis — Conjunctivitis causes unilateral or bilateral eye discharge, conjunctival redness, tearing and blurry vision. Conjunctivitis in children is most commonly infectious. Etiologies commonly include non-typable Haemophilus influenza, Streptococcus pneumoniae, and many different viruses, the most severe of which is adenovirus. Onset is variable, but usually occurs over one or two days, and vision is not greatly impaired. Infectious conjunctivitis may be associated with corneal abrasions due to eye rubbing. Conjunctivitis must also be differentiated from infectious keratitis (inflammation of the cornea). (See "Conjunctivitis", section on 'Classification and epidemiology'.)

Allergic conjunctivitis is an IgE mediated Type I hypersensitivity reaction which is sometimes associated with asthma and eczema. Allergic conjunctivitis is suggested in children with itching, tearing, conjunctival edema, hyperemia, watery discharge, burning, and photophobia with occasional eyelid edema (picture 4 and picture 5 and picture 6). It is typically bilateral, but may be unilateral. There is usually exposure to an allergen such as pollen, dust mites, mold or animal dander. (See "Allergic conjunctivitis: Clinical manifestations and diagnosis", section on 'Clinical manifestations'.)

Corneal abrasion — Corneal abrasions should be suspected when a child presents with acute onset severe eye pain, photophobia, tearing, blurred vision, and inability to open the eye. Some patients may not be able to recall a specific event. A younger child may just start crying and holding the eye. Contact lens wearers are at increased risk for developing infectious keratitis. Corneal abrasions may be caused by superficial ocular foreign bodies that are trapped under the eyelids, particularly the upper lid, and cause injury during blinking. (See "Corneal abrasions and corneal foreign bodies: Clinical manifestations and diagnosis", section on 'Clinical manifestations'.)

Keratitis — Microbial keratitis (inflammation of the cornea) can be visually threatening and is characterized by severe foreign body sensation, pain, photophobia, and blurred vision. It can develop after severe conjunctivitis, corneal herpes simplex virus infections, and corneal abrasions. Contact lens wearers are at increased risk. Staphylococcus species are the leading cause of bacterial keratitis while herpes simplex virus and adenovirus are common pathogens in patients with viral keratitis. Patients suspected of microbial keratitis warrant prompt referral to an ophthalmologist. (See "The red eye: Evaluation and management", section on 'Infectious keratitis' and "Herpes simplex keratitis", section on 'Clinical manifestations'.)

Hyphema — Hyphema, a suspension of red blood cells in the anterior chamber without the formation of a clot usually occurs in children after blunt trauma to the eye, such as being struck with a ball and may also be associated with other eye injuries although spontaneous hyphema has been described in young children with intraocular juvenile xanthogranuloma. (See "Traumatic hyphema: Clinical features and diagnosis", section on 'Spontaneous hyphema'.)

Upon physical examination, a hyphema appears as a layering of red blood cells in the anterior chamber that may be apparent upon visual inspection or may require slit lamp examination for detection (microhyphema) (picture 7 and picture 8 and figure 5). (See "Traumatic hyphema: Clinical features and diagnosis", section on 'Evaluation'.)

A rapid overview summarizes the important clinical features and initial management of a traumatic hyphema (table 5).

Branch retinal artery occlusion — The central retinal artery, a branch of the ophthalmic artery, enters the eye near the optic disc and branches into many segments. When one of the segments becomes occluded mild visual impairment may occur based on which branches have been occluded. It may present as painless monocular vision field loss, typically with preservation of central vision. Branch retinal artery occlusion (BRAO) is rare in pediatrics, but may be associated with hypercoagulable states, vasculitis, and congenital heart disease. Funduscopic exam shows retinal whitening along the distribution of the occluded vessel. Prompt referral to an ophthalmologist is warranted. (See "Central and branch retinal artery occlusion", section on 'Branch retinal artery occlusion'.)

Branch retinal vein occlusion — Branch retinal vein occlusion (BRVO) is very rare in children but may present as a scotoma or painless visual field defect with blurred or gray vision corresponding to the region of retinal vein occlusion. The supratemporal visual fields are frequently affected. Intraretinal hemorrhages, cotton wool spots, and disc swelling are seen on funduscopic exam. (See "Retinal vein occlusion: Epidemiology, clinical manifestations, and diagnosis", section on 'Clinical manifestations'.)

Conversion disorder — Blurry vision without an organic basis may reflect a manifestation of a conversion disorder. (See 'Conversion disorder' above.)

EVALUATION — A careful history and physical examination frequently provide the key information to diagnose the cause of vision change.

History — Important historical information includes the following:

●Type of vision change – Blurry vision typically accompanies infection or injury to the conjunctiva or cornea. Binocular diplopia is seen in patients with cranial nerve III, IV, or VI palsy; transient abnormality of control of eye motion; orbital mass lesion (eg, orbital cellulitis); or weakness or malfunction of the orbital muscles.

●Trauma – Blurred vision after eye trauma and associated with pain and photophobia suggests corneal abrasion or hyphema. Blunt trauma to the orbit with diplopia upon upward gaze indicates an orbital blowout fracture with muscle entrapment. Head trauma may trigger ocular migraine or a concussive syndrome with diplopia.

●Systemic symptoms – Children with infectious conjunctivitis may also have fever, rhinorrhea, otitis media, or viral pharyngitis. Patients with seasonal allergies may have excessive tearing, sneezing, and itchy eyes. Depending upon etiology, diplopia may be accompanied by focal neurologic deficits, fever, altered mental status, or muscle weakness. (See 'Causes of diplopia' above.)

●Photophobia – Patients with traumatic hyphema, foreign bodies, corneal abrasions, conjunctivitis, or migraines commonly complain of photophobia.

●Headache – Diplopia and headache suggests an intracranial mass lesion or migraine.

●Eye pain – Patients with conjunctivitis, keratitis, hyphema, or corneal abrasion typically complain of significant superficial eye pain.

●Contact lens wear – Contact lens wear is a risk factor for microbial keratitis, especially with soft lenses and when lenses are used improperly (poor hygiene, overnight wear, contaminated solutions). (See "The red eye: Evaluation and management", section on 'Bacterial keratitis'.)

●Timing – Sudden onset of painless loss of vision in a focal field of vision suggests branch retinal artery or vein occlusion.

●Past medical history – Conditions that predispose to specific types of vision change include thrombotic disorders (cavernous sinus thrombosis, branch retinal artery or vein thrombosis), migraine (transient vision loss), and psychiatric illness (conversion disorder).

●Family history – Patients with causes of blurred vision will have a family history of the same disorder.

●Social history – Children with conversion disorder may have significant psychosocial stress related to school or family issues.

Physical examination — Patients with suspected globe rupture or laceration should not undergo lid retraction or other procedures that may apply pressure to the eye. In addition, topical drops (eg, fluorescein, anesthetic drops) should not be applied except by an ophthalmologist. (See "Open globe injuries: Emergency evaluation and initial management", section on 'Physical examination'.)

Reduced ambient light and parent/caregiver presence facilitate cooperation in the child. Once an open globe is excluded, topical analgesia may be provided, as needed, for photophobia. If the patient is unable to open the eye secondary to pain or photophobia from a suspected corneal abrasion gently open the eye using digital traction on the upper and lower eyelids while avoiding pressure on the globe.

The clinician should perform a complete ocular examination, starting away from the patient and evaluating each of the anatomical components of vision in turn. Potentially frightening or painful procedures (eg, bright illumination of the injured eye, funduscopic examination, lid retraction) should be performed later in the evaluation. Key aspects of the examination include (see "The pediatric physical examination: HEENT", section on 'Eyes'):

●Patient level of consciousness and ability to cooperate with the examination

●Inspection of the orbit and surrounding structures

●Visual acuity of each eye independently

●Extraocular movement

●Confrontational visual fields

●Pupillary appearance and response to light (including the swinging flashlight test (figure 6))

●Evaluation of anterior chamber depth and presence of visible hyphema using a penlight

●Direct funduscopic examination

●Eversion of the eyelids

●Slit lamp examination of the eye (in the older patient and by experienced clinicians)

In children younger than two to three years of age, visual behavior (table 6) rather than visual acuity is assessed. The goal is to determine whether visual behavior is normal for age and whether vision is equal between the two eyes. Visual behavior can be tested in all children. Even newborn infants demonstrate visual fixation if an appropriate target (eg, the human face) is used. (See "Vision screening and assessment in infants and children".)

In addition to monocular or binocular diminished visual acuity, key abnormal findings include:

●Squinting, covering one eye or voluntarily keeping it closed, or tilting the head to one side suggest diplopia in the child who cannot express this complaint.

●Periorbital swelling (eye trauma, orbital infection).

●Signs of an open globe (eg, eccentric or peaked pupil (picture 9 and picture 10), obvious laceration, protruding intraocular foreign body, or evidence of extrusion of ocular contents (picture 11 and picture 12 and picture 13 and picture 14)). If present, a stiff, protective shield should be applied and an ophthalmologist should be consulted immediately. (See "Open globe injuries: Emergency evaluation and initial management", section on 'Initial emergency assessment and treatment'.)

●Proptosis (orbital infection and/or mass).

●Conjunctival injection (conjunctivitis, keratitis, corneal injury).

●Blood (hyphema) or pus (hypopyon) in the anterior chamber.

●Pain on extraocular movement (orbital infection).

●Abnormal funduscopic examination – regional retinal pallor (branch retinal artery occlusion), abnormal vessels, retinal hemorrhage, papilledema (idiopathic intracranial hypertension, intracranial mass lesions).

●Evidence of conversion disorder – patients with hysterical blindness carefully avoid falling or bumping into things. Optokinetic reflex is intact. Additionally, a mirror placed in front of the patient's eyes can be tilted in different directions and a seeing patient's eyes will move [4].

●Fluorescein staining identifies corneal defects (eg, corneal abrasion or keratitis), but is contraindicated in the patient with an open globe.

●Slit lamp examination is best for identifying microhyphema, hypopyon, iritis, and lens abnormalities. (See "Slit lamp examination".)

It is important to remember that visual acuity improves with age. The normal visual acuity for a toddler is 20/50 and gradually improves to the normal adult acuity of 20/20 by age five or six years.

Diagnostic studies — The need for ancillary studies varies depending upon whether the visual change is diplopia or blurred vision and the likely conditions suggested by the history and physical exam. In most healthy children with migraine conjunctivitis, corneal abrasion, or keratitis, extensive testing is not necessary.

●Diplopia – Potential studies include:

•Computed tomography (CT) of the head or magnetic resonance imaging (MRI) (cranial nerve palsy).

•MRI with MR venography (cavernous sinus thrombosis). (See "Cerebral venous thrombosis: Etiology, clinical features, and diagnosis", section on 'Neuroimaging'.)

•Orbital CT (orbital cellulitis or blowout fracture). (See "Orbital fractures", section on 'Imaging' and "Orbital cellulitis", section on 'Diagnosis'.)

•Serum thyroid stimulating hormone (TSH), free thyroxine (T4), and triiodothyronine (T3) (Graves’ ophthalmopathy). (See "Clinical manifestations and diagnosis of Graves disease in children and adolescents", section on 'Diagnostic evaluation'.)

•Botulinum toxin (food borne botulism). (See "Botulism", section on 'Clinical manifestations'.)

•Immunologic and electrophysiologic studies (myasthenia gravis).

•Cerebrospinal fluid examination and electromyography (Miller Fisher syndrome). (See "Guillain-Barré syndrome in children: Epidemiology, clinical features, and diagnosis", section on 'Cerebrospinal fluid' and "Guillain-Barré syndrome in children: Epidemiology, clinical features, and diagnosis", section on 'Electrodiagnostic studies'.)

•No specific studies are typically needed for transient diplopia associated with toxic ingestion or seizures. However, additional studies are typically indicated to further evaluate for the underlying toxin or cause of the seizure. (See "Approach to the child with occult toxic exposure", section on 'Ancillary studies' and "Seizures and epilepsy in children: Clinical and laboratory diagnosis".)

●Blurred vision – Potential studies include:

•Orbital CT if an open globe or other serious ocular injury is likely in a patient with traumatic hyphema. (See "Traumatic hyphema: Clinical features and diagnosis", section on 'Diagnostic imaging'.)

•Carotid duplex ultrasound, MR angiography, or CT angiography should be ordered for patients with vascular risk factors (diabetes, sickle cell disease, systemic lupus erythematosus), if branch retinal artery or vein thrombosis is suspected. These patients also warrant screening for inherited thrombophilia. (See "Thrombophilia testing in children and adolescents", section on 'Children with venous thromboembolism'.)

DIAGNOSTIC APPROACH — The algorithms provide a diagnostic approach to the child with acute diplopia (algorithm 1) or blurry vision (algorithm 2).

In patients with diplopia, orbital trauma and upward gaze diplopia indicate an orbital fracture with inferior rectus muscle entrapment. Careful assessment of eye position, the presence of deficits in extraocular movement, and differentiation of whether the diplopia is on vertical or horizontal gaze identifies the presence of palsies of the third, fourth, or sixth cranial nerve. Exophthalmos suggests Graves’ ophthalmopathy while generalized weakness is associated with diplopia caused by botulism, Miller Fisher syndrome, myasthenia gravis, or tick paralysis. Ocular pain with proptosis raises significant concern for orbital cellulitis and cavernous sinus thrombosis. Diplopia caused by seizures, migraines, or toxic ingestion are typically transient and associated with typical features of these conditions.

In children with acute onset of blurry vision, trauma suggests the presence of a corneal abrasion or hyphema. Ocular pain without trauma is characteristic of conjunctivitis, superficial corneal foreign body, or keratitis. Branch retinal artery or vein occlusion is typically painless.

Patients with visual complaints that do not have an organic basis and in whom bedside or specialty evaluation reveals internal inconsistency, have conversion disorder.

In contrast to acute blurry visions, subacute or chronic blurry vision most commonly is caused by uncorrected refractive error, either myopia, high hyperopia, or astigmatism. Evaluation and management of refractive errors in children are discussed separately. (See "Refractive errors in children".)

SUMMARY

●An acute change in vision may result from a variety of conditions:

•Binocular diplopia occurs when the visual axes are misaligned and warrants prompt evaluation. Pathophysiology includes palsies of the third, fourth, or sixth cranial nerves; conditions associated with transient loss of supraoptic control of eye movements; mass lesions of the orbit; or ocular muscle weakness or malfunction. (See 'Causes of diplopia' above.)

•Acutely blurred vision is most commonly associated with conjunctivitis or corneal abrasion. Other less common conditions include keratitis, hyphema and retinal artery or vein occlusion. (See 'Causes of blurry vision' above.)

●A careful history and physical examination frequently provide the key information to diagnose the cause of vision change. (See 'Evaluation' above.)

●A diagnostic approach to identifying the underlying cause of diplopia and blurred vision are presented in the algorithms (algorithm 1 and algorithm 2).