advanced 3 TRI A EXAM Flashcards
1
Q
Amblyopia definition and types?
A
- Developmental condition characterised by reduced vision in one eye, VA worse than 0.2 logMAR or corrected VA difference of 0.2 logMAR or worse, which is not due to abnormalities of fundus or pathology of visual pathway, but due to sensory impediment to visual development e.g.
- Stimulus Deprivation Amblyopia: Result of manifest strabismus
- Strabismus Amblyopia : result of manifest strabismus
- Anisometropia Amblyopia : result of difference in refractive errors between two eyes
- Ametropic Amblyopia : result of high degree of bilateral uncorrected refractive error
- Meridional Amblyopia : result of uncorrected astigmatism
2
Q
What do all patients have to undergo before commencement and after commencement of treatment?
A
- pupil check, cycloplegic refraction, fundus and media examination
3
Q
Stimulus deprivation amblyopia?
A
- Although there is less robust evidence of the effectiveness of occlusion in cases of stimulus deprivation amblyopia , patients with SDA usually need more aggressive occlusion regardless of age.
4
Q
When will patching have no effect?
A
- If fundus has hypoplasia (not enough cells in fovea during development)
5
Q
Mechanisms of amblyopia:
A
- Light deprivation: no stimulus to retina
- Form deprivation: retina receives a defocused image
- Abnormal binocular interaction: non-fusible are formed on the fovea
6
Q
Prevalence of Amblyopia:
A
- 2-5% in the UK
7
Q
Severity of Amblyopia:
A
- MILD – 0.2 - 0.3 logMAR
- MODERATE - >0.3 – 0.7 logMAR
- SEVERE - 0.7+ logMAR
8
Q
Why do we treat Amblyopia?
A
- Having amblyopia greatly increases risk of blindness / significant visual loss in later life.
- Amblyopia nearly doubles the lifetime risk of BVI (Leeuwen et al 2007).
9
Q
What is the pass mark for visual school screening in Scotland?
A
- 0.2 logMAR Keeler or 0.1 logMAR Sonksen
- 0.1 logMAR Kays pictures
- Or referred if manifest dev / sig phoria / OM defect / reduced conv + 20 ^ / No co-op
10
Q
What is the definition of anisometropia??
A
- Difference of 1D or more between two eyes
11
Q
What are the types of anisometropia?
A
- Mixed anisometropia: One eye refractive error is myopic, and one eye refractive error is hypermetropic.
- Simple hypermetropic astigmatism
- Simple myopic astigmatism
12
Q
How to transpose rx?
A
- Add the sphere and cylinder powers to determine the new sphere power.
- Change the sign of the cylinder.
- Change the axis by 90 degrees
13
Q
How much refractive error risks amblyopia?
A
- Children with >+3.50DS increased risk of amblyopia & squint
14
Q
How much refractive error do you give for anisometropia?
A
- Give full Rx in amblyopia
14
Q
How much refractive error do you give for hypermetropia?
A
- In Accommodative ET – full +
- XT or X - <+3.00DS left uncorrected
- without strabismus – give if above expected for age
14
Q
How much refractive error do you give for myopia?
A
- Weakest – that gives best corrected VA
14
Q
Refractive adaptation VA average improvement?
A
- Amblyopic VA - average improvement of 0.24 logMAR with refractive adaptation alone in 18 weeks. Stewart & MOTAS et al. (2004) = 2 visits
- 15% did not require occlusion after refractive adaptation. Stewart et al. (2007)
14
Q
Recommended time length to achieve maximum VA in refractive adaptation?
A
- Recommended time length to achieve maximum VA 18-22 weeks (Paediatric Eye Disease Investigator Group (2012)
- Greatest change in first 12 weeks. Asper et al. (2018)
- Continued VA improvement up to 30 weeks (Paediatric Eye Disease Investigator Group (2006)
- Refractive adaptation phase: review within 3 months of prescribing glasses to establish full-time glasses compliance and improvement in visual acuity.
14
Q
Refractive Adaptation : how much cases of amblyopia with glasses alone?
A
- Resolution of amblyopia with refractive correction alone (average 32%) Asper et al. (2018)
14
Q
Effect of Age and Type of Amblyopia on Refractive Adaptation Period?
A
- Children with amblyopia between the ages of 3 and 8 years, regardless of the type of amblyopia, can benefit from refractive adaptation treatment (Stewart & MOTAS et al. (2004)
14
Q
What are the patching recommendations for moderate amblyopia ?
A
- 2 hours = 6 hours patching for <7 year olds (PEDIG 2003)
- 2 hours + near tasks = 2 hours without near tasks (PEDIG 2008)
- When baseline acuity is 0.6 to 0.7, more hours may improve acuity faster (PEDIG 2003)
14
Q
What are the patching recommendations for severe amblyopia ?
A
- 6 hours = full time patching for <7 year olds (PEDIG 2003)
- high dose rate achieved a successful outcome more rapidly but did not improve outcome
14
Q
Compliance?
A
- Compliance better when starting VA better (refractive adaptation)
- Dose rates of 2-6 hours resulted in same final outcome
- Regular supervision / contact with orthoptist improves compliance and may shorten treatment phase.
14
Q
What are types of occlusion?
A
- Total occlusion – occlusive patch, blenderm, frosted lens
- Partial occlusion – bangerter foil (< 0.05 logMAR difference in VA improvement between 2 hours patching and 0.3 BF. BF better tolerated, PEDIG 2010)
- Full time occlusion – all waking hours/24 hours
- Part time occlusion – specific periods of time/certain activities
14
Q
How many hours for 1 line VA improvement?
A
- log unit (1 chart line) improvement per 120 hours of occlusion (MOTAS 2004)
- 224 hours gave 0.1 logMAR increase in VA (white and walsh 2022)
14
Q
Max hours for occlusion ?
A
- 252 hours occlusion = 80 % done (MOTAS 2004)
- 504 hours occlusion required to reach outcome VA (MOTAS 2004)
14
Q
Age and patching?
A
- Amblyopia improves with optical correction alone in about one fourth of patients aged 7 to 17 years, although most patients who are initially treated with optical correction alone will require additional treatment for amblyopia.
- For patients aged 7 to 12 years, prescribing 2 to 6 hours per day of patching with near visual activities and atropine can improve visual acuity even if the amblyopia has been previously treated.
- For patients 13 to 17 years, prescribing patching 2 to 6 hours per day with near visual activities may improve visual acuity when amblyopia has not been previously treated but appears to be of little benefit if amblyopia was previously treated with patching.
- PEDIG 2005
14
Q
When are patching/atropine patients reviewed?
A
- Review every 6-8 weeks after commencement of treatment to monitor improvement and / or adjust the prescribed hours of occlusion. If acuity fails to improve by at least 4 letters each visit the occlusion dose should be increased i.e. from 2 to 4 to 6 hours.
14
Q
Atropine, how does it work?
A
- Paralyses the ciliary muscles to optically defocus the non-amblyopic eye
- Effect lasts for longer than other cycloplegics – up to 14 days
- Greater effect for near VA than distance
- Daily atropine Vs Weekend atropine
14
Q
Atropine in severe amblyopia?
A
- Average 4.5 lines improvement if treated with weekend atropine and full Rx
- Average 5.1 lines improvement if treated with weekend atropine and plano lens (PEDIG 2009)
- 2 hours patching (1.8 lines improvement) vs weekend atropine (1.5 lines improvement) – (7 – 12 year olds in this study)- PEDIG 2009
14
Q
Atropine + Optical Penalisation?
A
- Non responders – could add optical penalisation although no great improvement in VA found when compared to atropine alone (about ½ line).
14
Q
Atropine in moderate amblyopia?
A
- Mean VA after 4 months 0.2 logMAR (PEDIG 2004)
- Penalisation with 1% atropine has been shown to be as effective as occlusion in moderate amblyopia (0.30-0.70 LogMAR) at 6 months– PEDIG 2003
14
Q
Patching and quality of life?
A
- Questionnaire - focus group of patients, orthoptists and ophthalmologists
- Children were hardly troubled by the patch when playing games on the computer, watching TV or colouring (item 5), whereas parents thought that they were really troubled (Fig. 1e).
- Almost all children (54), could play well with other children when wearing the patch (item 6).
- Most all children (57) were not laughed at or bullied by other children when wearing the patch (item 10), and almost all parents agreed (Fig. 1j)
- Children’s quality of life during occlusion therapy is affected less than their parents think
14
Q
Suppression and patching?
A
- All patients aged 6 and above with no motor fusion should be evaluated with Sbisa bar or Bagolini filter bar prior to amblyopia treatment and monitored closely. If diplopia occurs then treatment should be stopped immediately. It should be noted that the Bagolini filter bar (filters 1-16) and Sbisa bar (filters 1-17) are not equivalent . Monitoring of suppression should be undertaken using the same bar at each visit
- Filter 7 is most often used as the point at which treatment is stopped
14
Q
who is atropine not suited towards?
A
- atropine is not suitable for aphakic / pseudoaphakic children, patients with Down’s syndrome or those with a known history of cardiac disorders, raised IOP, narrow angles or known hypersensitivity to atropine or any component of the preparation
14
Q
When and how to stop occlusion?
A
- Amblyopia treatment should be tapered once optimum equal visual acuity obtained has been reached to reduce the risk of recurrence or reversing amblyopia.
- No significant improvement in the amblyopic eye when occlusion dosage increased after 2 consecutive visits with full compliance with treatment and no change in refraction and fundus exam.
- Failure to improve, or deterioration of acuity, within 4-6 months of the commencement of amblyopia therapy (when compliance is good), should prompt re-refraction and re-examination of fundus and possible further investigations.
- Complaints of binocular diplopia.
14
Q
Patching and quality of life?
A
- Questionnaire - focus group of patients, orthoptists and ophthalmologists
- Children were hardly troubled by the patch when playing games on the computer, watching TV or colouring (item 5), whereas parents thought that they were really troubled (Fig. 1e).
- Almost all children (54), could play well with other children when wearing the patch (item 6).
- Most all children (57) were not laughed at or bullied by other children when wearing the patch (item 10), and almost all parents agreed (Fig. 1j)
- Children’s quality of life during occlusion therapy is affected less than their parents think
14
Q
The theory behind infantile esotropia?
A
- Generally unknown – multifactorial
- Monkey studies with prism glasses during critical period – become ET
o At birth fusion is immature
o Similar input from both eyes during critical period for BV connections – striate cortex
o Loss of binoc connections in ocular dominance columns (not linked to accom due to not develpoing BIN)
o Lack of disparity sensitivity
o Retinal disparity cues main influence on ocular alignment
o Cues present reduces prevalence of misalignment
14
Q
What are the types of infantile esotropias?
A
- Essential Infantile Esotropia, Nystagmus blockage syndrome, accommodative infantile SOT, 6th NP, Secondary SOT
15
Q
Characteristics of Infantile Esotropia? (13)
A
- Stable ET >30^BO (some increase in size) (pretty large angle)
- N=D angle
- No sig refractive error, + makes no difference
- Onset <6 months, generally 3-4 months
- Alternating – dense amblyopia rare (amblyopia in 41-35% > post sx)
- Cross fixation – bilateral abduction limitation (look L with Reye that’s squinting)
- Poor BSV prognosis
- LMLN (latent manifest latent nystagmus)– intensity increases on occlusion – possible rotary component, see with SL or when close one eye >2 years old
- DVD - >2yrs old
- IO o/a (up and in)
- Asymmetric motion VEPs
- Asymmetry of OKN (N-T abnormal)
- AHP:
a. Compensate for nystagmus (latent or manifest)
b. Compensate abduction limitation
c. Compensate for DVD (tilt) (can get with DVD or without)
16
Q
Investigations for infantile esotropia?
A
- Case history
- Refraction
- VA
- CR
- CT
- Prism reflections/Krimsky/PCT
- Pupils
- Conv
- OM
- VOR tests: Doll’s head or Spinning Baby (stimulation of semi-canals = conjugate deviation in opposite direction) to check abduction full
- OKN – BIN then Monoc, (symmetry of OKN develops 4-6 months), if asymmetric = 85% chance strabismus occurred first 6 months. Connection to latent nystagmus development. Hand-help drum held at eye level, rotated about 20° per second , Too slow – pursuit system takes over , Too fast – cannot fix on stripes.
- DVD- dissociated vertical deviation. See DVD…
17
Q
DVD what is it and how to test?
A
- Progressive elevation of the eye under the cover. Fixation required.
- Incidence in Infantile Esotropia as high as 51-90% patients (Lang 1968) Progressive elevation of the eye under the cover
- Extorsion and latent nystagmus may be associated features.
- Nearly always bilateral – can be very asymmetric, > in distance
- Unsightly hypertropia - inattention or poor health/fatigue (can’t have bilateral hypertropia if looks assymetric)
- Elevation similar on ab- and ad-duction – can be spontaneous on versions (nose) – looks like IO o/a
- A patterns more common
- SO o/a possible
- BSV weak if present at all
- Bielschowsky Darkening Wedge test. Fixate light, non fixing eye occluded with frosted occluder. Nuetal density or sbisa bar introduced over fixating eye. As light entering fixing eye is reduced, occluded eye starts to move down. As density of the bar is reduced, the occluded, eye will start to elevate. Difficult as need prolonged fixation with kids.
- Reversed Fixation Test: Used to differentiate DVD from Hypertropia (BD^) record e.g. RE > DVD than LE
- Measurement is difficult, Manifest component measured with SPCT (simultaneous prism CT bring prism bar + occluder in at the same time which measures manifest only) first, Alt PCT – each eye fixing to record asymmetry, May be impossible to reverse the movement, Can use synoptophore.
18
Q
Differential dx of dvd?
A
- IO o/a
- CT = constant degree of elevation and no torsion (compared to progressive elevation and intorsion on refixation in DVD)
- OM = Greatest elevation on adduction and V pattern more likely (whereas DVD elevation equal in all POG and A pattern more likely, and SO o/a possible)
- Latent nystagmus = not often present (dvd usually present)
- Beilshowsly darkening wedge test = negative ( + in DVD)
19
Q
Management of DVD?
A
- Persistent and frequent spontaneous elevation, intervention not often required
- Non surgical: Suggestion of manipulating Rx to make fix with most affected eye (if out of critical period)
- Surgical – depends on:
o Associated IO o/a – Anterior transposition, moves insertion of IO back from equator so it goes agaisnt elevation, io recess not effective =)
o DVD unilateral or bilateral
o Amount of asymmetry
o A-pattern with o/a SO
o Fadens on SR to stop eye pulling up, or max SR recess + fadens (depends on severity)
o IR resection if DVD reoccuring only
20
Q
DHD what is it and how to test?
A
- Asymmetric or unilateral slow outward deviation – spontaneous or after dissociation (looks likr intermittent distance XT)
- Characteristics:
- XT spontaneous or after dissociation
- Obvious asymmetry
- Hard to neutralise with PCT
- Positive response to Bielschowsky dark wedge test (becomes ET under cover as density increases)
- Other components of DVD/DTD present (torsional)
21
Q
Differential dx of DHD?
A
- Intermitttent XT = Other components of DSC evident, asymmetry and +ve darkening wedge test
- Uncorrected anisometropia – smaller XT with less myopic or more hypermetropic eye = Refraction
- Overcorrection of hypermetropia (seen in accommodative ET) = Refraction (resolved after + reduced)
- Paralytic strabismus - 2° deviation > 1 ° = Ocular movements
22
Q
Management of DHD?
A
- DHD can be treated alone with lateral rectus muscle recession. DHD can be treated as above, but combined with medial rectus muscle recessions or posterior fixation sutures to simultaneously treat the esotropia. The esotropia can be treated alone, possibly with a reduced surgical dosage (Wilson, saunders and berland, 1995).
23
Q
Management for infantile esotropia?
A
- Full refractive correction
- If angle small, no treatment needed
- Unilateral muscle surgery (LR) recession – amount based on size of deviation and presence of any underlying strabismus
- Correct refractive error
o Generally not associated with significant refractive error
o <+2.00DS unlikely to benefit
o Significant myopia, hypermetropia and astigmatism give correction
o Careful assessment of effect of prescription on deviation before Sx planning
- Correct refractive error
- Restore visual acuity
o Consider fixation pattern as well as formal VA assessment (testing available for age group not sensitive for small degrees of amblyopia)
o Occlusion preferred if fixation preference / VA reduction
- Restore visual acuity
24
Q
Surgery in infantile esotropia?
A
- Bilateral MR recession
- 6mm R & L correct up to 45∆
- Staged surgery
o Maximum amount initially then further surgery on un-operated muscles - Enhanced surgery
o >6mm but <8mm
o Higher incidence of consecutive XT
o Restriction of adduction - Selective surgery
o More than 2 muscles to correct full angle in one procedure
o >70∆ give BT first into BMR - 25-45∆ = Bilateral MR recession 3-6mm
- 50-60∆ = Bilateral MR recession 5mm & single LR resection 5-7mm
- > 70∆ = BT injection of both MR first, Then reassess
25
Q
What is the best timing for infantile esotropia surgery?
A
- Later gives better motor outcome, Earlier gives better BSV potential!
- Retrospective review assessed at 6/11 months, 12-17 motnhs, 18-27 months - Muz & Sanac 2020
26
Q
Botulinum Toxin in Infantile strabismus?
A
- Success rates of 31% (residual <10∆)
- mean follow-up 24 months
- Significant improvement in deviation size
- Niyaz et al. 2021
27
Q
Surgery vs Botulinium Toxin for Infantile Esotropias?
A
- Botox = Very large angles – initial treatment with BT (one or two injections) gives smaller stable ET to then surgically manage but delay before eyes aligned – reduces likelihood of BSV
- de Alba Campomanes (2010)– BT results less effective than surgery for >35∆
- Ideally surgery before 10 months old
- BMR Sx more effective for Infantile ET than BTxA, BTxA was more likely to undercorrect and lower success rate.
- 69% Sx success versus 36% BTxA success (deviations >30∆)
- However, Similar results with Sx and BTxA in deviations <30∆
- Song et al 2023
28
Q
Prognosis for bimedial recession infantile esotropia following correction?
A
- Success 50% - 85% (orthophoria within 10∆)
- Generally accepted that satisfactory alignment can be obtained but bifoveal BSV unlikely
o Subnormal BSV
o Microtropia
o Residual ET with ARC - 39% alignment remained stable following early surgery
- 31% initially stable but later decompensated and required additional surgery
- Hiles et al. 1980
29
Q
What is Nystagmus Blockage Syndrome – Infantile Esotropia?
A
- Rare Esotropia that results from the use of convergence to block/abolish manifest nystagmus and improve VA.
- High incidence of neurological disorders (Hoyt 1977)
- 12/15 ET patients with ocular or oculocutaneous albinism (von Noordon 1988b)
30
Q
What are characteristics of nystagmus blockage syndrome infantile SOT? (12)
A
- Congenital horizontal nystagmus (no change on occlusion)
- Nystagmus increases on abducted and blocked when adducted
- Non accommodative ET, variable
- Visual attention increases ET and reduces nystagmus.
- Inattention reduces ET and increases nystagmus
- Face turn to side of fixing eye + convergence – looks like bilateral ET
- ET unilateral – amblyopia
- Pseudo-sixth nerve palsy (MR contracture could give +FDT)
- Pupil miosis during ET
- ET eye remains adducted when BO^ in front of fixing eye
- High incidence of neurological disorders
- DVD rare
31
Q
Differential Dx of nystagmus blockage infantile SOT?
A
- Essential Infantile SOT = amblyopia uncommon (NBS COMMON) , angle of dev static and large (NBS variable and spasmodic increase) , latent nystagmus (congenital nystagmus), force duction test may be limited (usually full in NBS) , DVD common (NBS = DVD rare) , not usually nuerological abnormalities (IS with NBS), results of surgery predictable (NBS = unpredictable).
32
Q
Accomodative Infantile SOT?
A
- Fully Accommodative ET
- moderate + rx
- onset < 6months
- Only seen very occasionally
- Baker and Parks 1980: Early-onset ET only present at near – most hypermetropic – half high AC/A ratio
- BV unstable compared to accommodative ET of later onset
- High incidence of strabismic amblyopia
- Management: Careful as risk of consecutive XT due to weak BV
33
Q
Sixth Nerve Palsy Infantile SOT?
A
- Explanation for limited abduction in ET
- Isolated palsy considered rare – can be caused by neurological disorders such as hydrocephalus.
34
Q
Secondary Infantile SOT Aetiology + Characteristics? (3 + 4)
A
- Vision loss so severe that fusion is disrupted
o Trauma
o Retinal detachment
o Cataract
Characteristic - VA loss often unilateral
- Age of visual loss determines deviation- Shortly after birth = ET or XT, In childhood = ET, Later childhood and Adulthood = XT
- Diplopia (intractable)
- Large angle
35
Q
Characteristics of Early Onset SOT?
A
- Age = (6 months – 2 years old)
- Characteristics: N=D, Amblyopia common, Poor BSV prognosis, Dev may increase c time, Surgery often needed.
36
Q
Investigations of Early Onset Esotropia?
A
- Case History
- VA (reduced in dev eye?)
- CT
- OM (check no lateral incomitance – same size L + D version)
- PODT
- BSV Potential: Prisms (split ^ between EE, come back in 1 wk and may have BSV!)
- Synoptophore
- BTxA
- Neuroradiological Investigation
37
Q
What are the Aims in management of Early Onset SOT?
A
- Obtain optimum or equal VA
- Restore normal BSV if possible
- Early onset = Although previous BSV experience, rarely able to recover – strabismic amblyopia high
- Improve cosmetic appearance if no potential for BSV
38
Q
Management of Early onset SOT?
A
- Same as for constant esotropia with accommodative element
- Refraction
- Treat amblyopia
- Assess for BSV potential
o Botulinum Toxin A
o PAT
o PODT - Surgery:
- BSV potential
o Aim to correct ET fully - Poor BSV potential
o Only indicated if cosmesis poor
o Undercorrect leaving residual ET 5-8∆
39
Q
What are characteristics of late-onset esotropia?
A
- Onset 2-8+ years
- N = D
- Intermittent – constant large angle
- Diplopia
- NRC
- OM normal
- Minor injury or short period of uniocular occlusion preceding the onset
