BV OSCE Flashcards
Types of esotropia
- Primary
- Consecutive
- Secondary
Consecutive esotropia
Rarely develops spontaneously
. Constant/intermittent
. Most likely cause previously xot and has had surgery (over liberal surgery, deliberate to guard against re-divergence)
. If px has bsv try prisms
. Refer for surgery/btxa
Secondary esotropia
. The esotropia is secondary to a pathology such as (corneal opacity, macular lesions, glaucoma, optic atrophy, retinoblastoma)
. As children have a lot of accommodation, they tend to be esotropic when they get a pathology
. Surgery and/or btxa-adjustable sutures technique
. Leave slightly sot to guard against xot
Primary esotropia
- Constant – constant tropia (accommodative, non-accommodative)
- Intermittent – if patient has a phoria occasionally (related to accommodative effort, related to distance, related to time)
Constant Esotropia with an accommodative element
. Fully accommodative – deviation is totally corrected by correction of hypermetropia
. Partially accommodative- when there is a residual deviation president even with full hyperopic correction
Constant SOT with a partially accommodative element
. Partially accommodative esotropia
. Sot worse when accommodate – angle of esotropia larger at near
. Associated with hyperopia
. Size of sot decreases with hyperopic rx and in the distance
. Unilateral-amblyopia common
. Bsv present when fully corrected
Management: fully correct hypermetropia/leave if cosmesis good
-treat amblyopia
-refer- surgery/bxta in order to restore bsv/cosmesis
Infantile esotropia (congenital esotropia)
. Congenital esotropia
. Onset sot before 6 months
. Approx. 40% of children with neurological and developmental problems
. Cross fixation- uses le to look right and re to look left
. Angle usually greater than 30d so unlikely to gain bsv
. Usually alternating sot – no amblyopia
. May have small vertical deviation
. Look for dissociated vertical divergence (dvd) and manifest latent nystagmus (mln) and chp to reduce nystagmus, because of cross fixation (re turn to the re to adduct to re)
. Inferior oblique overaction common
Okn test in infantile esotropia: temporal to nasal (normal), nasal to temporal (weak)
Management: surgery (improve cosmesis, restore reduced bsv), consider age of surgery (functional vs cosmetic)
Dissociated vertical divergence (DVD):
-Presents before 2 years
-Eye drifts upwards spontaneously (fatigue) or after being covered
-Usually bilateral, often asymmetric
Nystagmus blockage esotropia
. Very rare
. Congenital, manifest (nystagmus present all the time), horizontal nystagmus
. Sot developed by trying to stop nystagmus
. Nystagmus amplitude increases on abduction
. Chp towards fixing eye to reduce nystagmus
. Sot variable angle
. Management: refer
Nystagmus (manifest latent):
-Nystagmus is present when both eyes open but nystagmus amplitude increases on dissociation (one eye covered)
-Amplitude increases on abduction
-Vision better on adduction
Non-accommodative esotropia
. Most common is infantile SOT
. Onset between 6 months- 2 years
. Refractive error insignificant
. Near deviation approximately equal distance deviation
. Amblyopia common
MANAGEMENT:
-amblyopia treatment
-surgery (improves cosmesis, restore reduced BSV)/BTXA
-consider age of surgery (functional vs cosmetic)
Late onset esotropia
. Usually after 4/5 years old
. Between 2-8 years olds
. Late onset means they have bsv
. May have been intermittent originally
. Diplopia present early stages rapidly moves to suppression if not corrected
. Normal retinal correspondence and sensory and motor fusion present
. Correcting refractive error has no effect
Management:
-Surgery once deviation stable
-Any signs of neurological problems, papilloedema, motility problems, nystagmus refer
-Refer hes for surgery/btxa
- Primary intermittent esotropia
They will have phoria in some positions
Fully accommodative esotropia
. Aetiology: uncorrected hyperopia
. Onset 2-3 years
. No SOT at all distances when fully corrected
. Associated with uncorrected hypermetropia (2D-7D), high AC/A
. Cover test (with full Rx- well controlled SOP all distances, without Rx-esotropia unilateral or alternating)
. BSV good with Rx
. Nil amblyopia
MANAGEMENT: if Rx fully corrects deviation surgical option not necessary especially when BSV is normal. If only a partially accommodative deviation, then surgery or prism may be required to correct)
Convergence excess esotropia
. Aetiology: high AC/A ratio greater than 6:1, every time they accommodate, they converge too much
. Onset 2-5 years
. Usually hyperopic, occasionally has emmetropia and rarely myopia
. Cover test
-no accommodation needed in distance so SOP (phoria) and BSV
-at near with light SOP as no accommodation with light
-SOT at near with accommodative target
-without hyperopic Rx SOT all distances
-MANAGEMENT: correct Rx fully if hypermetropic, under correct myopic
-bifocals- stops Px accommodation at near (minimum amount of plus to control near)/wear for 6 months and reduce by +0.50DS every 6 months
-exercises- improve negative fusional vergence
-surgery-bilateral medial rectus recession
Near esotropia
. With cover test (SOT at near, SOP and BSV at distance)
. Often nil significant refractive error
. Normal AC/A
. Normal ocular motility
. Often have equal VA as intermittent so might have amblyopia
-MANAGEMENT: surgery only (bilateral medial rectus recession)
Distance esotropia
. With cover test (SOT at distance, SOP or straight at near)
. Often no significant refractive error
. Normal AC/A
. Normal motility
. Often in elderly
. Exclude VI nerve palsy
MANAGEMENT: surgical only (asymmetrical lateral rectus resections,
Ipsilateral medial rectus recession)
Cyclic esotropia
. Rare- also known as alternate day squint
. Esotropia alternates day by day
. Constant esotropia on “squinting day” with no demonstrable binocular function
. Bsv with little or no esophoria on straight day
HISTORY of SOT
. Which eye?
. Direction of strabismus
. How often (constant/intermittent/regularity) constant=no bsv
. How long has it been there for (likelihood of amblyopia)
. When do parents notice (during a particular activity)
. Is vision good
. Birth history (premature/weight)- forceps damage lr
. Previous ocular history (any pathology), any treatment (surgery)
. Gh
. Fh (strabismus, amblyopia, refractive error)
Investigation of SOT
- VA- amblyopia common in constant except if alternating, uncommon intermittent
Consecutive esotropia – often have amblyopia
Secondary esotropia- vision likely to be poor
Infantile SOT – allow CHP to achieve best VA - Cover test- enable differentiation of different types of SOT
With and without Rx
Near and distance
With a light and accommodative target at near if SOT
Look for DVD and MLN - Ocular motility
IO and SO underaction with a V pattern, especially in constant esotropias - near point of convergence
Important indicator of control for near - measurement of angle
Consider age, level of vision – PCT best test to measure deviation
If poor vision, use krimsky- prism placed over fixing eye
Prism reflection test (PRT)- uncooperative and has SOT
Hirschberg’s test-babies (near and distance) - controlled binocular acuity test (CBA)
Patient looks target Snellen chart/budgie stick at near
Performed at distance using LogMAR
Point where they become manifest (double) – CBA is one before
Differential diagnosis using CBA
-In convergence excess SOT- near SOT will occur as patient accommodates to read further down the chart
-Near SOT- near SOT there all the time so not affected by accommodation
-fully accommodative SOT- near with Rx- No SOT patient remains SOP all the way down the chart
- measure AC/A ratio
Convergence excess esotropia has highest AC/A - measure binocular function
Sensory fusion (to assess diplopia, suppression, and ARC)
Motor fusion
Stereopsis - post-operative diplopia test
In patient with suppression this test must be performed to avoid diplopia
. measured with prisms
. prims placed before deviated eye
. base opposite the deviation then base in same direction
. prism increased until patient reports diplopia
. if complains of diplopia after small correction then not a good candidate for surgery - refraction
. refraction carried under cycloplegia
. >12months- use cyclopentolate 1%
. 6-12 months with light irides- use cyclopentolate 0.5%
. 6-12 months with dark irides- use cyclopentolate 1%
. 3-6 months – use cyclopentolate 0.5%
. atropine 1% to achieve full cycloplegia in patients with darkly pigmented irides
-glasses prescribed when indicated and worn full time for at least 1 month to enable accurate diagnosis - fundus and media examination
Management of esotropia (SOT) stage 1
. Refraction
. Fundus and media examination
. Correction of ametropia
. Even when you refer give hyperopic rx
. Amblyopia therapy particularly if they under 7 years of age if has sot and suppression> 5 years old must have sbisa before treating as can cause tractable diplopia
Management of esotropia (SOT) stage 2
Improve alignment of visual axis
. restore BSV
. enhance ARC
. no potential for BSV consider surgery (self-esteem, mood, quality of life)
Management options
1. conservative
Observe-monitor
Optical (prisms, manipulation Rx)
Orthoptic exercises
- non-conservative- refer to HES
Surgery
Botulinum Toxin
Conservative optical management
- Hyperopic glasses
-relax accommodation and therefore convergence
-order full plus in all accommodative SOT - Prisms
-Base out prisms
-resolve diplopia
-investigate BSV before surgery
-assess risk of diplopia post-op - Exercises
-improve negative relative convergence (look through the cats by cutting holes in the cats tummy)
-used in intermittent SOT
-lend prism bar- Base IN exercise - Surgery
-angle > near (both medial rectus recessions)
-angle>at distance (both lateral rectus recessions)
-near angle=distance angle (MR recession and LR resection on one eye) - Botox
-neurotoxin which paralyses muscle into which it is injected
-paralyzes the muscle within 5-7 days, recovery of muscle function up to 3 months
-injected into medial rectus for esotropia
-antagonist (lateral rectus) has the advantage
-eye moves out
Advantages: useful as results are temporary:
-consecutive SOT- as already had surgery
-residual SOT-reducing deviation might allow patients to regain control
-secondary deviation-when vision poor
-useful to confirm is post-op diplopia suggests intractable diplopia
Secondary exotropia
-XOT follows visual impairment from a pathology
-nil fusion causes eye to drift
-usually constant, unilateral
-more likely in older patients
-Management: treat amblyopia, refer HES, treat underlying condition
Consecutive exotropia
-XOT follows previous esotropia/phoria
-often constant
-may occur spontaneously (no BSV & amblyopia)
-often after surgery for eso deviation (over correction by surgeon)
-management: under 8 years (refer) to prevent loss of BSV or amblyopia
Primary exotropia
-Initial defect was the XOT
-Constant or intermittent
Primary constant exotropia
-XOT under all viewing conditions
-ensure nil pathology or neurological disease particularly <2 years
-consider refer to HES
-amblyopia may develop if occur early
MANAGEMENT:
-treat amblyopia
-BOTOX-into lateral rectus muscle
-surgery- MR AND LR in affected eye, adjustable sutures in px with diplopia
Intermittent near XOT
more common in adults than children
-more likely to complain of diplopia
-may complain of problems for near work (headaches, diplopia, asthenopia symptoms)
-cover test (near xot, distance controlled (phoria)
Management:
-under correct hyperopic rx
-prism- base in
-surgery-bilateral medial rectus resection
Intermittent non-specific XOT
-intermittent XOT/BSV at any distance of viewing
-can present in any age group
-diplopia unlikely-usually suppression occurs
-Management- refer for surgery
Intermittent distance XOT
-near=BSV
-distance-intermittent or constant XOT
-most common in children
-suppression normally occurs when manifest-diplopia rare
-may close one eye in bright light
Distance XOT split into
1. True distance XOT
-near BSV
-distance XOT
- simulated distance XOT
-want to break into XOT at near but controlled by accommodation (high AC/A Ratio), which is eliminated by +3.00DS causing them to become manifest at near
-controlled at near by fusion which is eliminated using patching
Differential diagnosis- carry CT after 45 minutes of occlusion if deviation controlled at near after occlusion, then true, if near manifest after occlusion than simulated
Management:
-prism- base in relieving
-minus lenses-particularly those with high AC/A
-surgery
Investigation of exotropia
- history
-age of onset-how young
-frequency (constant-intermittent)
-symptoms (when? Near-distance)
-family history
-POH (glasses, amblyopia, secondary XOT, consecutive XOT)
-GH - VA
-amblyopia (common in constant, common in consecutive XOT)
-secondary exotropia from ocular pathology and amblyopia equals reduced VA - cover test
-enables differentiation of different types
-do at near, distance
-accommodative target and a light
-if XOP present then note size of deviation
-record fixing eye/alternating
-CT with +3.00DS after occlusion to determine real or simulated distance XOT - ocular motility
- XOT manifest on elevation
-consecutive XOT look for surgery scars - near point convergence
-important indicator of control for near - BSV
-sensory fusion
-stereopsis at distance which they are controlled
-fusional reserves - measure angle of deviation using PCT
- measurement of suppression
-post-op diplopia test which simulates to patient what it’s like to have surgery - cycloplegic refraction and fundus and media examination
Principles of management
Functional cure-restore BSV
Reconstructive cure- NO BSV- improve cosmesis
-refraction, fundus, and media
-correction of ametropia
-amblyopia therapy particularly under 7 years of age
-Rx- under correct hyperopia (as plus relaxes accommodation and eyes move further)
-Rx- full minus
- prisms (base in – near XOT)
-presbyopia
-orthoptic exercise to improve near point of convergence such as dot card
-surgery (reconstructive, functional surgery to restore BSV)
-consider refer for all under 8
3rd nerve palsy
Anatomy: originates in the pons at the oculomotor nucleus-passes through the circles of willis - runs parallel to the posterior communicating artery (PCA)-through the cavernous sinus and splits in the superior and inferior divisions
Superior division innervates (superior rectus and the levator), and inferior division innervates (medial rectus, inferior rectus, and inferior oblique)
Causes: posterior communicating artery aneurysm, trauma (closed head injury), vascular (diabetes and hypertensive), inflammation or infection, congenital
Symptoms: sudden onset of unilateral ptosis, ocular pain, headache, diplopia
Features of total 3rd CN palsy
-affected eye is down and out (exotropia and hypotropia)
-pupil maybe dilated
-ptosis
-accommodation is reduced or absent
-limited elevation and depression and adduction
-normal abduction
Features of superior division 3rd CN palsy
-congenital most common
-superior rectus and levator affected
-eye hypotropic with ptosis
-CHP- chin up, face turn to unaffected side
-muscle sequelae- O/A of IO, IR and SO
Features of inferior division 3rd CN palsy
-medial rectus, inferior rectus and inferior oblique, sphincter pupillae and ciliary muscle affected
-eye exotropic, intorted, hypertropic
-muscle sequelae- O/A of LR, SR and SO
-accommodation affected
Pupil involvement
-3rd cranial nerve runs parallel to the PCA
-aneurysms on PCA will cause pupil dilation
-in 62-83% of total 3rd CNP pupil is spared, pupil sparing = ischemia
-pupil involvement = compressive lesion
-Ptosis then diplopia spared
Treatment: emergency refer to HES, children under 8 (amblyopia therapy), occlusion patch if diplopia, surgery
4th cranial nerve palsy
Anatomy: the trochlear nerve originates in the nucleus in the mid brain at the level of the inferior colliculus and proceed posteriorly and crossover before making their way
to the eye (longest and thinnest nerve)-passes through the circle of willis
Innervates SO, longest, and thinnest nerve so easily damaged in soft head or body trauma
Congenital or acquired (trauma, vascular aetiology)
Bilateral unless proven otherwise
Unilateral 4th CN palsy
-affects SO
-eye hypertropic and esotropic
-may control hypertropia with CHP- chin depression, face turn to affected eye, head tilt to unaffected side
-adaptation to torsion
-unilateral hyperdeviation in PP
-no reversal on OM/BHTT
Bilateral 4th CN palsy
Brown’s syndrome-V eso pattern
-significant extorsion- vertical/torsional diplopia the greatest symptom
-CHP-chin depression
-reversal of hypertropia on dextrodepression and laevodepression
6th cranial nerve palsy
Anatomy: the abducens nerve originates in the nucleus in the pons ventral to the floor of the fourth ventricles-moves vertically and a 90-degree bend over the petroclinoid ligament to the lateral rectus
-6th cranial nerve has a long course, compression as the nerves passes over petrous temporal bone due to raised ICP, aneurysms, space occupying lesion
-innervates lateral recuts prone to damage due to raised intra-cranial pressure
-lateral rectus pulls eyes out and the greatest effect on distance fixation
Acquired:
-more common in adults
-caused by microvascular, trauma, neurological such as MS
Congenital rare
-transient in new-borns
-related to traumatic birth
-often resolves
-Duanes syndrome: congenital absence of the 6th CN
Symptoms: horizontal diplopia, headache
Clinical features
-esotropia greater for distance
-limitation of abduction on the affected side
-adoption of AHP- face turn to the affected side to achieve binocularity
-unilateral or bilateral
-field of BSV displaced to the unaffected side
Muscle sequelae
-UO of LR
-OA of MR
Management in children
-establish cause: MRI and referral to neuro
Important BSV not lost and prevent amblyopia (encourage CHP, BTXA to MR)
Management in adults
-occlusion in patients with recent onset and large angle esotropia
-Fresnel prisms
-surgery to resolve diplopia in PP
Summary of nerve palsies
3rd CN palsy with pupil involvement- lesion that compresses the 3rd CN supply and also compresses parasympathetic nerve fibres which travel along its surface
- signs: complete ptosis, diplopia, hypotropia and exotropia, restricted parasympathetic supply inhibits constriction, anisocoria (unequal pupil size) increase in bright light, affected pupil is dilated and unreactive and near reflex also absent
-cause: enlarging aneurysm on PCA, trauma, tumour
-without pupil involvement: generally vascular in origin related to diabetes or HTN
congenital 3rd CN palsy (IR, IO, SR, MR)
-causes: familial, perinatal trauma, familial migraine
-characteristics: hypotropia, exotropia, intact pupil reflexes, ptosis, limitation of elevation, depression, adduction
acquired 3rd CN palsy (IR, IO, SR, MR)
-causes: tumours, trauma, inflammation, and vascular lesions of the brain
-symptoms: sudden onset of unilateral ptosis, ocular pain, headache, diplopia
-characteristics: pupil sparing suggests ischaemia, pupil involvement suggest compressive lesion, exotropia, hypotropia, ptosis, limitation of elevation, depression, adduction
4th CN palsy (SO)
-causes: congenital or acquired (tumours, trauma, inflammation)
-characteristics: vertical diplopia, hypertropia, CHP to lower eye
Acquired 6th CN palsy
-causes: tumours, trauma, inflammation, and vascular lesions of the brain, high ICP
-symptoms: horizontal diplopia, headache
-signs: esodeviation that is greater at distance, isolated abduction deficit, abnormal CHP
Nystagmus
-A rhythmic oscillation of the eyes, which can be physiological or pathological, it can be symmetrical, asymmetrical, unilateral, or bilateral
-can be horizontal, vertical, torsional or a combination
-Benign idiopathic (congenital) nystagmus is secondary to visual deficit such as retinal dystrophies and neurological deficit such as intra-cranial lesions
-manifest nystagmus: present when both eyes are open may increase when one eye is covered
-latent nystagmus: when one eye is covered, steady fixation with both eyes open
-null zone: the eye position where the nystagmus intensity (amplitude x frequency) is least
Description: observe Px in PP for 20 secs classify by position, type, rate, plane, and null zone
Types of nystagmus
- Cerebellar jerk nystagmus: Nystagmus is jerky with large amplitude and low frequency; nystagmus increases when eyes look in the direction of fast phase
Signs: headaches, limb weakness, disturbed speech - down-beat nystagmus: nystagmus in pp with the fast phase downwards. Lateral gaze accentuates the nystagmus. Causes: stroke, MS, alcohol
- see-saw nystagmus: torsional nystagmus in pp. When one eye elevates and intorts and the other depresses and extorts. Typical lesion in chiasmal region
- congenital pendular nystagmus: horizontal/vertical and rotary. Nystagmus decreases on convergence and increases on covering of one eye, AHP
Anterior segment: congenital cataract, Aphakia, albinism
Posterior segment: ON hypoplasia, foveal hypoplasia
Symptoms of nystagmus:
uncontrolled eye movements, visual problems, dizziness, reduced depth perception or balance problems
Management options for nystagmus
glasses to ensure best possible corrected vision, contact lenses as they move with eye, low vision aids such as magnifiers to help with reading, prisms, drugs such as cannabis, BOTOX, surgery
Treatment to reduce AHP:
surgery to EOMs to move null zone to primary position, prisms to move visual environment to null position
Myasthenia Gravis
-ocular fatigue
-systemic fatigue
-diurnal variation as the day progresses (so might be better on wake)
-weakness increases after exercise
-common in younger females and older males
-lack of facial expression
Ocular signs and symptoms
1. Ptosis: initial signs, usually bilateral and asymmetrical, increases with fatigue, frontalis over-action is often seen in attempt to elevate eye, lid retraction in an attempt to elevate the eye
Investigating ptosis: request Px to elevate their eyes for 1-2 minutes, severity of ptosis increases when eyes return to PP
Cogan’s lid twitch:
-request px to depress eyes for 15 secs, on return to PP lid initially elevate above ptotic level before returning to normal position
Gorelick’s sign:
-in asymmetrical cases hold the more ptotic lid and the ptosis on the opposite side will increase
- diplopia: variable may change horizontal to vertical, px may report that images separate further as fatigue increases, may mimic palsies, and change which muscle is affected
- orbicularis weakness: can usually close eyes, may not be able to bury eye lashes, unable to stop examiner opening eyes with gentle pressure
Treatment: ptosis props, occlusion such as frosted lens, surgery is contraindicated due to instability
Duane’s retraction syndrome
-congenital
-females>males
-abnormal horizontal eye movements (unilateral more common)
Aetiology
-neurogenic: abnormal innervation to LR
-myogenic: fibrosis or inelasticity of the LR and MR muscle inserts abnormally
Clinical signs
-complete or less often partial absence of abduction
-partial loss adduction (sometimes)
-deviation in PP (Eso/Exo)
-CHP: face turn affected side for distance, face turn to unaffected side for near
-poor convergence
-A or V pattern
-reduced binocular function
-up or down shoot on adduction
-globe retraction on adduction
Classification of Duane’s syndrome
. Type A- loss Abduction>adduction
. Type B- loss abduction only
. Type C- loss adduction>abduction
Type A
-limitation on ABDuction with less marked limitation of ADDuction
-may have esotropia
-widening of palpebral fissure on ABDuction and narrowing and globe retraction on ADDuction
Type B
-limitation of ABDuction, normal ADDuction
-may have associated esotropia
-widening of palpebral fissure on ABDuction and narrowing and globe retraction on ADDuction
Type C
-limitation of ADDuction>ABDuction
-usually exotropic
-globe retraction on ADDuction
Associated developmental defects
. coloboma, lens opacities, heterochromia, deafness, cleft palate
Management
-urgent referral if under 8 (check ocular/systemic association, ensure BSV maintained, treat amblyopia)
-if BSV good and cosmetically acceptable CHP then observe only
-if CHP causing neck problems or poor cosmesis-surgery to enhance abduction ability
-if manifest in primary position, then prism and surgery
Brown’s syndrome
Acquired: trochlear damage (traumatic, inflammatory), SO tendon abnormalities (inflammatory)
signs
-limited elevation of the eye on ADDuction with normal depression in ADDuction
-limited elevation in direction elevation and ABDuction
Symptoms
-pain/discomfort
-diplopia
-CHP
-unable to elevate eye
-90% unilateral
Characteristics
-unilateral, most px have BSV but some has strabismus in PP
-limitation of elevation in ADDuction, ABDuction, and direct elevation
-A or V pattern, CHP head tilt to affected eye or chin elevation in bilateral Brown’s
-down drift of affected eye
-over action of SR
Treatment
Non-surgical- if BSV present and deviation well compensated observe and monitor BSV
Surgical-possible contralateral superior rectus
Thyroid eye disease (TED)/graves ophthalmology
Symptoms
-discomfort: drying of corneal epithelium, proptosis, lid retraction, swollen conjunctiva
-loss of VA: cornea exposure, optic nerve compression
-diplopia: vertical/horizontal due to oedema and EOM fibrosis
Signs
-lid retraction
-lid lag on down gaze
-proptosis oedema
-IR most commonly affected then MR (esotropia and hypotropia)
-CHP to increase BSV
-conjunctival chemosis
-corneal erosion
Graves ophthalmology
-this refers to the inflammatory response and its sequelae in and around the orbit associated with autoimmune thyroid disease
-most associated with hyperthyroidism but does occur with hypothyroidism
Treatment
Active treatment: steroids, surgical decompression, radio therapy, ocular lubricants
Inactive treatment: prism therapy, surgery to increase BSV, lid retraction surgery
Types of convergence anomalies:
Types of convergence anomalies:
1. convergence insufficiency: inability to obtain adequate binocular convergence without undue effort
- Factors causing convergence insufficiency: illness, fatigue, near work, constant distance vision
- Secondary causes of convergence insufficiency: heterophoria, uncorrected refractive error, accommodative insufficiency, pathology such as thyroid eye disease
- Symptoms of convergence insufficiency: headaches, eyestrain, asthenopia, diplopia, blurred vision (XOP decomp) and diplopia
- CT: XOP/XOT at near, orthophoria distance
- Test subjective (when patient reports diplopia) and objectively (watch patients’ eye for convergence to break)
-likely to have low base out fusional reserve at near
-other investigation (measure deviation with PCT, VA, stereoacuity, OM if incomitant refer, fundus and cyclo)
-management: treat any pathology, significant refractive error corrected and exercises such as dot card
- convergence fatigue: inability to maintain convergence overtime
- Symptoms of convergence fatigue: symptoms occur after prolonged near work
- CT: normal at near and distance but after prolonged dissociation with occluded a tropia or phoria might appear at near
- base out at near reduces on prolonged testing - convergence paralysis: the ability to converge closer than infinity is entirely lost
-primary
-secondary (closed head injury, viral illness, occlusive vascular disease)
- at distance closer than infinity (Nil convergence, XOT, crossed dip)
-if no convergence, pupillary response may absent
-nil base out fusional reserves
-management: urgent referral, occlusion, Botox, base in prism to correct XOT - convergence accommodative/spasm
-spasm of convergency usually causes spasm of accommodation and miosis
-convergence spasm (MR may become contracted)
-accommodative spasm (ciliary muscle becomes contracted)
-causes (over treatment of CI, uncorrected hypermetropia)
-signs and symptoms: could result in SOT, blurred vision in distance, pupil miosis, headache, lead on dynamic ret
Differential diagnosis: if px has greater esotropia in the distance, important to rule out 6th nerve palsy (check OT, check pupils normal)
Management: pathology treated, cycloplegic, give full hyperopic correction to relax accommodation, BOTOX
Measurement of Accommodation
- near point assessed with RAF rule in dioptres
- assessed three-times insufficiency vs fatigue
- assessed monocularly and binocularly
If accommodation is normal monocularly but binocularly not, then it suggests convergence insufficiency instead of accommodative insufficiency
Dynamic retinoscopy (objective test) MEM method
Accommodative disorders
- accommodative insufficiency/fatigue
- Aetiology: high hyperopia, illness, trauma, children with down’s syndrome
- Symptoms of accommodative insufficiency: blurred vision at near, asthenopia, micropsia
-if accommodative fatigue then symptoms after prolonged near work
- Signs of accommodative insufficiency: XOP or SOP at near (because of effort to accommodate), reduced near point accommodation for age, dynamic ret (shows lag), reduced accommodative facility
- Management: correct hyperopia, exercises, and downs syndrome (bifocals) - accommodative paralysis
Aetiology: head injury, trauma
-no accommodation can be exerted, blurred vision for distances closer than infinity
- Management: urgent refer - accommodative inertia: difficulty changing focus, blur when changing from near and distance but clear
-associated with presbyopia and developing cataract
-symptoms: complains of blurred vision when changing from near to distance
-management: full hyperopic correction, orthoptic exercises (flippers, jump accommodation)
Heterophoria (latent strabismus)
when both eyes are uncovered the visual axis are directed towards the fixation target
-when the eyes are dissociated the eyes deviate from the fixation point
-can be concomitant (angle of deviation same in all directions of gaze) or incomitant (angle of deviation differs in different directions of gaze)
-can be decompensated (patient usually symptomatic) or compensated (patient symptom free)
Classification of exophoria
-Divergence excess exophoria (D>N) - exophoria which is increasing in the distance
-convergence weakness exophoria-exophoria which is larger at near (N>D) – failure to converge so px is exophoric
Classification of esophoria
-Divergence weakness esophoria– esophoria which is larger in the distance
-convergence excess esophoria – esophoria which is larger at near
Cause of decompensation
-under corrected refractive error so esophoria (uncorrected hypermetropic refractive error) and exophoria (uncorrected myopic refractive error)
-surgery
-pathology
Symptoms of heterophoria: due effort to maintain BSV (headache, eyestrain, and asthenopia) or due to failure to maintain BSV (diplopia, blurred vision)
Investigation of heterophoria
-History (when did they start, how regular, are they progressing, do they become worse when doing particular activity, can they be stopped)
-GH
-POH (cataract surgery, strabismus, surgery)
-VA
-CT
-OT
-convergence (RAF rule repeat 3 times to make ensure convergence insufficiency not convergence fatigue)
-accommodation (near point), dynamic ret
Main reason for treating heterophoria
alleviate symptoms, prevent phoria from breaking down into tropia
1. removal cause of decompensation-long hours of close work, poor illumination or contrast, sudden increase in the amount of close work
2. modifying Rx- full plus for esophoria and hyperopia
Treating convergence insufficiency
Failure to converge to 6cm or failure to reach 10cm comfortably without fatigue
-associated with exophoria at near and asthenopia and diplopia
Exercise for convergence insufficiency
- jump convergence: 2 targets at least 3m apart
-px fixates on near target and focus on it to maintain single image
-swap fixation to distance target to ensure single
-repeat process several times - Dot card
-slim rectangular piece of card with equal spaced dots
-card held to nose at slightly depressed position
-px fixates at the furthest dot and so on and maintain single image
-repeat 3-5 cycles
Treating accommodative anomalies
accommodative insufficiency and fatigue are characterised by reduced amplitude of accommodation in relation to the patients age and signs of fatigue
-treated using exercises
- jump accommodation
-similar to jump convergence
-targets at two distances except target held at nearest point of blur - accommodative push-up
-an accommodative target such as a letter on the budgie stick held at arm’s length
-target moved closer at consistent speed and attempt to maintain BSV
-once image blurs and cannot be kept clear return to original position
-repeat 3-5 times - lens flippers (+/-1.00, +/-1.50, +/-2.00) to increase number of rotations they can see
-suggest 1-2 mins x3/day
Treatment of amblyopia
- occlusion therapy
- optical penalization
- cycloplegic drugs such as atropine
management of amblyopia
-Factors to consider when treating amblyopia: age of onset, duration of amblyopia, type of amblyopia, other pathology, compliance
-occlusion period: vision 6/9 to 6/24- 2 hours of patching- vision less than 6/24 = 6 hours of patching
-the importance of treating amblyopia: DVLA requirements, pathology to good eye in later life, critical period
-advantages of occlusion: cheap, can specify time, can use in severe amblyopes
-disadvantages of occlusion: poor cosmesis, compliance, allergy to Elastoplast
Optical penalization:
-Blurs VA in better eye sufficient to make the worse eye work
-this treatment is for those who can’t tolerate occlusion therapy
-this is achieved with alteration of spectacle correction or cycloplegic drugs
Near penalization: Encourage use of amblyopic eye for close work- instil cycloplegia usually atropine in good eye to stop accommodation and give +3.00 to good eye
Distance penalization: Encourage use of amblyopic eye for distance, add +3.00 to good eye to blur
Total penalization: Encourage use of amblyopic eye at all distance- strong convex lens or cycloplegic and strong concave lens
-atropine alone does not work for severe amblyopia
Cycloplegic drugs
atropine ointment/drops
Advantages: good cosmesis, as effective as occlusion in treating moderate amblyopia, used when VA doesn’t improve with occlusion therapy
Disadvantages: px may be allergic, interaction with systemic medication, cannot be used in severe amblyopia, constantly blurred vision, not suitable for older strabismic amblyopes
Review: review every 3 months, younger px reviewed more regularly
Treatment for different types of amblyopia
- stimulus deprivation amblyopia:
-treat primary pathology (e.g. cataract)
-full Rx and constant wear
-total occlusion preferable - Strabismic amblyopia
-full time glasses wear
-occlusion or atropine
-consider inverse occlusion if eccentric fixation - anisometropic amblyopia
-full time glasses wear
-no need for occlusion if VA consistently improving
Complications: Intractable diplopia, occlusion amblyopia, failure of VA to improve, increase in angle of deviation, allergy to atropine
Compliance: build up good relationship, explain critical period, explain to child what is happening, ask child which eye to wear patch
Keeler acuity cards:
-working distance 38cm
-usually 15 cards with black and white stripes on right or left side, 1 blank card
-4mm hole in centre where practitioner looks through
-starts with low spatial frequency (wider stripes)
-correctly identifies the same stimulus twice means the child can resolve that card
- Cardiff acuity cards:
-based on vanishing optotypes
-pictures: (duck, house, fish, car, train, boat)
-3 cards for each of the 11 acuity levels (2 out of 3 responses correct move on to next)
-no crowding (nothing surrounding the pictures)
-may overestimate VA
-50cm or 1m depending on age
-present the cards with widest target which is the lowest acuity at eye level
- Peekaboo App:
-preferential looking test
-2 forced choice or 4 forced choices
-child must touch the pattern
-working distance 25-50cm
-VA measured 0.2-1.3 LogMAR
Older children 2 years and above:
-Recognition ability: Ability to detect, resolve and recognise a target
-more sensitive to amblyopia defects
- Kay pictures
-used for children between 2-4 years
-pictures of common objects known to a child
-single or crowding in LogMAR (3m) – 1.0-0.1 LogMAR
-single picture in Snellen (3m or 6m) – 6/6 – 6/60 - Keeler LogMAR crowded test
-used for children between 3-5
-3m
-Flipchart
-6/36-6/3
-screening and uncrowded test
Near vision
Kay pictures near test at 33cm, Lea symbols near vision at 40cm
Contrast sensitivity:
- Cardiff contrast sensitivity test 50cm
-vanishing optotypes
-three cards at each contrast level from 46% to 1% in 12 steps
-12 months onwards - Hiding Heidi
-five contrast levels
-two cards: white and one with “Heidi”
-child must point to where Heidi is
-0 months onwards
-variable working distance
Optometric examination in children History
-RFV
-FLOADs to any concerns/worries
-POH (patching, squint, amblyopia, HES)
-FOH (patching, strab, any ocular conditions in the family)
-Birth history (type of delivery, full-term)
-Medical history, Medications, Allergies
Binocular vision status (CT, OM)
-20 Dioptre base out prim to measure fusion (BO prism is held before either eye at 33cm, eye behind prism should adduct rapidly to restore fusion and abduct on removal)
-4 dioptre base out – test for macula suppression
-sensory fusion (worth 4 dot test, Baglioni lenses)
-NPC to measure convergence
-Stereopsis
-Accommodation (RAF rule, flipper lenses, Accommodative lag, or lead)
