INFANTILE ESOTROPIA Flashcards

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1
Q

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 BE 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
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2
Q

What are the types of infantile esotropias?

A

Essential Infantile Esotropia, Nystagmus blockage synd rome, accommodative infantile SOT, 6th NP, Secondary SOT

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3
Q

Characteristics of Infantile Esotropia? (13)

A
  1. Stable ET >30^BO (some increase in size) (pretty large angle)
  2. N=D angle
  3. No sig refractive error, + makes no difference
  4. Onset <6 months, generally 3-4 months
  5. Alternating – dense amblyopia rare (amblyopia in 41-35% > post sx)
  6. Cross fixation – bilateral abduction limitation (look L with Reye that’s squinting)
  7. Poor BSV prognosis
  8. LMLN (latent manifest latent nystagmus)– intensity increases on occlusion – possible rotary component, see with SL or when close one eye >2 years old
  9. DVD - >2yrs old
  10. IO o/a (up and in)
  11. Asymmetric motion VEPs
  12. Asymmetry of OKN (N-T abnormal)
  13. AHP: a. Compensate for nystagmus (latent or manifest)
    b. Compensate abduction limitation
    c. Compensate for DVD (tilt) (can get with DVD or without)
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4
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…
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5
Q

DVD what is it?

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
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6
Q

How to test DVD?

A
  • 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.
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7
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
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8
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 to Bielschowsky dark wedge test (becomes ET under cover as density increases)
  • Other components of DVD/DTD present (torsional)
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9
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
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10
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).
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11
Q

Management for infantile esotropia (non surgical)?

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
    1. 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
    1. 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
      O If not tolerting can give BTX to MR for amblyopia help to align visual axis
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12
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
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13
Q

What is the best timing for infantile esotropia surgery?

A
  • Later gives better motor outcome, Earlier gives better BSV potential!
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14
Q

Botulinum Toxin in Infantile strabismus?

A
  • Success rates of 31% (residual <10∆)
  • mean follow-up 24 months
  • Significant improvement in deviation size
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15
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
  • 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, equal results with Sx and BTxA in deviations <30∆ (good)
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16
Q

Barriers stopping giving BSV or ABSV with surgery for infantile eso?

A
  • Surgery waiting list long
  • Hard to find paediatric strabismus surgeons
  • Hard to find anesthiologists
17
Q

Prognosis for bimedial recession infantile esotropia following correction?

A
  • Success 50% - 85% (orthophoria within 10∆)
  • Satisfactory alignment can be obtained generally, but foveal 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
18
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
19
Q

What are characteristics of nystagmus blockage syndrome infantile SOT?

A
  1. Congenital horizontal nystagmus (no change on occlusion)
  2. Nystagmus increases on abducted and blocked when adducted
  3. Non accommodative ET, variable
  4. Visual attention increases ET and reduces nystagmus.
  5. Inattention reduces ET and increases nystagmus
  6. Face turn to side of fixing eye + convergence – looks like bilateral ET
  7. ET unilateral – amblyopia
  8. Pseudo-sixth nerve palsy (MR contracture could give +FDT)
  9. Pupil miosis during ET
  10. ET eye remains adducted when BO^ in front of fixing eye
  11. High incidence of neurological disorders
  12. DVD rare
20
Q

Differential Dx of nystagmus blockage infantile (NBS) 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).
21
Q

Accomodative Infantile SOT?

A
  • Fully Accommodative ET ( Only seen very occasionally )
  • moderate + rx
  • onset < 6months
    *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
22
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.
23
Q

Secondary Infantile SOT Aetiology + Characteristics?

A
  • Vision loss so severe that fusion is disrupted
    O Trauma, Retinal detachment or Cataract
    Characteristics
  • 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