Esotropia

An overview

1. ESOTROPIA
DR.PRAKRITI YAGNAM.K

3. •Definition :
•Inward deviation of eye
•May be concomitant or inconcomitant
•Concomitant –Variability of angle of deviation is within 5
prism diopters in different horizontal gaze positions
•Inconcomitant–Angle differs in various positions of gaze
as a result of abnormal innervation or restriction

4. •Concomitant esotropia :
•Usually constant and present in early childhood or infancy
•Therefore often associated with amblyopia , poor binocular
fixation and poor stereopsis
•Fusional divergence helps to keep esotropia in check but innate
divergence amplitude in humans is weak ( 6 –8 PD ) resulting in poor control

5. Classification :
Accomodative Non accommodative
Refractive Non refractive Mixed Early onset
Microtropia
Basic
Distance esotropia
Fully Partial With excess Convergence excess
Divergence insufficiency
Convergence. AccomodationSensory
Consecutive
Cyclitic
Acute

6. Accomodative esotropia :
Esodeviation due to excess convergence as a result of sustained
accommodative effort
Near vision
AccomodationConvergence
Ciliary muscle contraction and To fixate bifoveallyon the target
altering curvature of crystalline lens
Quantitative relation –AC/A ratio
Normal is 3 –5 PD

7. •Refractive accommodative esotropia :
•Excessive hypermetropia ( +2 to +7 D )
•AC / A ratio is normal
•Presents at ages 18 months to 3 years ( Range 6 months to 7 years )
•Fully accommodative –hypermetropia with esometropiawhen refractive error is uncorrected
•After optical correction –deviation eliminated and BSV present in all directions

9. •Partially refractive –Deviation reduced but not eliminated by
full correction of hypermetropia
•Amblyopia with bilateral congenital superior oblique weakness
present
•Supressionof squinting eye is present
•Sometimes ARC develop

11. Pathogenesis :
Uncorrected hyperopic error
Retinal blur
Excessive accommodative effort
Accomodative convergence with poor divergence amplitude
Esotropia

12. -In children who do not make an effortto clear retinal blur by
accommodative effort or if hypermetropia is too high. To overcome with
accommodation
Uncorrected hypermetropia
B/L ametropia but no esotropia

13. •Clinical features :
•Age of onset –Infancy to late childhood
•Size of deviation –20 to 60 PD
•Amblyopia , stereopsis and binocularity may be compromised
•Complete evaluation to rule out any other neurological causes of acquired esotropia

14. Diagnosis :
-Cycloplegic refraction and measurement of baselines at distance and near
Older children –Cyclopentolate 1%
Younger children –Atropine E/O

15. Management :
-Goals–Good alignment
Equal vision
Good stereopsis
Emmetropization
-Full hyperopic correction is given
-Aim is to reduce esotropia by 8 to 10 PD to develop peripheral fusion
-Amblyopia –full patching regime

16. Regular followup is
essential
Cycloplegic refraction ,
magnitude of deviation
and presence of fusion
is checked in each visit
Tapering of hyperopic
correction in steps of
0.5 D over a period of
6 –8 months

17. Miotics given –phospholine iodide and pilocarpine
Reduce accommodative effort
Reduce AC
Indication–children who cannot wear spectacles or lenses
Diagnostic use –to determine if esotropia will respond to hypermetropicoptical
correction
Side effects –brow ache , nausea , abdominal cramps , diarrhea , iris cysts , lens opacities ,
RD

18. Surgery :
Not recommended in
fully accommodative
refractive esotropia
Can be done in partially
accommodative
esotropia for residual
deviation after hyperopic
correction
Surgery done is bilateral
MR recession

19. Determining the target angle of surgery :
-Standard surgery for distance –Surgery for residual esotropia measured
with full hyperopic correction in place
-High rates of under corrections are seen
Augmented surgery
-Average of near deviation with and without correction
-Average of near deviation without correction ( largest deviation )
-Distance deviation with correction ( smallest deviation )

20. Prism adaptation :
Full hyperopic correction
Base out prisms for residual correction
assessed for 2 weeks
esotropia increased stabilized
prisms increased till stabilised

21. •This stabilized angle is taken as target angle for surgery
•Goal is to achieve binocular fusion
•If distance vision is normal and near deviation is about 8 to 10
PD bifocals are used
•After surgery also hyperopic correction is given because surgery
is aimed at correcting non accommodative component

22. •Non refractive accommodation :
•Esotropia with greater deviation for near
compared to distance
•With full hyperopic correction distance angle
can be controlled but significant residual near
angle is present
•AC/A ration is high
•For 1 D increase in accommodation there is
large increase in convergence
•Independent of refractive error
•Frequently hypermetropia coexists
sometimes myopia

25. Diagnosis :
-Cycloplegic refraction
-Measurement of AC / A ratio by heterophoric or
gradient method

26. Management :
Bifocal glasses
-Bifocal add for residual near esotropia ( < 10 PD )
-Add relaxes accommodation thus reduces convergence
-Aim –to promote fusion and to reduce near angles
-Maximum can be added is +3 D
-Ideal is executive type bisecting the pupil
-Can be gradually reduced

27. Miotics :
Phospholine iodide 0.125 %
Ciliary spasm
Reduces peripheral accommodative demand and convergence
Surgery :
-Bilateral MR recession with posterior fixation suture ( or )
-Bilateral Fadenprocedure

28. Convergence excess Hypoaccomodativeconvergence
-Increased convergence -Weak accommodation
with normal accommodation
Increased effort
-AC/A ratio is normal
Over convergence
-Normal NPA -Remote NPA
-Straight eye with BSV for distance
-Esotropia for near with suppression
-Straight eyes through bifocals

30. Treatment :
•Refractive error correction
< 6 years –full cycloplegic refraction
> 8 years –without cycloplegia maximum plus is
prescribed
( manifest hypermetropia treated )
•Convergence excess –bifocals to relieve
accommodation and then accommodative
convergence
Bifocals –executive type
strength of lower segment is gradually
reduced and eliminated

31. •Surgery :
•Near deviation > far deviation –Bilateral MR recession
•Near and far deviation same with equal vision in BE –Unilateral MR recession with LR resection
•In residual amblyopia –surgery in amblyopic eye done
•In partially accommodative esotropia –surgery is best delayed to avoid consecutive esotropia
•So aim is to correct residual squint with glasses
•Undercorrection –MR posterior fixation sutures –Faden operation

32. •Early onset esotropia :
•-Infantile or congenital esotropia
•Idiopathic
•Develops within six months of life
•There will be no significant refractive error
•No limitation of ocular movements
•Uptofour months infrequent episodes of
convergence are normal but ocular alignment
thereafter is abnormal

33. •Signs :
•Large angle of deviation ( 30 prism diopters )
and stable
•Fixation is alternating in primary position
•Cross fixation is seen in sidegaze –Left eye
in right gaze and vice versa
•Refractive error is normal for the age ( +1 /
+2 D )
•Inferior oblique overaction may be present or
develops
•DVD develops in 80 % by the age of three
years

35. -Nystagmus is present
and is horizontal and
latent
Other associations :
•Mild amblyopia
•Apparent limitation of
abduction due to cross fixation
•Absent or reduced binocular vision
•Absence of nervous system disorders

37. Etiology :
•Multiple causes can lead to misalignment
•Worth–Congenital absence of fusional potential at cortical levels
Restoring binocularity is not possible
•Chavasse–Primary motor dysfunction
Poor fusion and lack of high gradestereopsis
Sensory adaptation to abnormal visual stimulation during early
binocular development caused by motor misalignment

38. Helveston–Combination of fusional and motor components
Risk factors :
•Prematurity
•Family history of strabismus
•Prenatal or gestational complications
•Genetic factors
No gender predilection is seen

39. Abduction limitation is elicited by Dolls head manoever
Gentle spinning of child
Vestibular movement to opposite direction of spin
Refixation saccade in same direction
Full abduction is elicited
-Due to limited abduction and tight medial recti children cross fixate

40. -These manifest after one year of age combinedly or individually
Classic triad for motor abnormality :
Inferior oblique overactionDissociated Vertical DeviationLatent nystagmus

41. IO overaction :
•Seen in 70 % of patients
•Overelevation of eye is supra adduction
DVD :
•Seen in 75 % of patients
•Elevation of non fixing eye when covered or with
visual inattention

43. •3. Latent nystagmus :
•Seen in 50 % of patients
•Predominantly horizontal jerk nystagmus elevated by occlusion of either eye
•Slow phase is towards side of occluded eye
•Also show persistent smooth pursuit asymmetry throughout life
•Temporally directed smooth pursuit eye movements are slow and lag behindfixation target compared to nasally directed movements

44. Evaluation :
•Visual acuity
•Ocular preference detection
•Measuring deviation by cover tests or Krimpsky tests
•Ocular mobility examination
•Sensory evaluation
•Fundus evaluation

45. DD :
•Bilateral congenital sixth nerve palsy
•Sensory esotropia due to organic eye disease
•Nystagmus blockage syndrome
•Mechanical limitation of eye movements –Duanes syndrome ,
Mobius syndrome or strabismus fixus

46. Pseudoesotropia
Congenital fibrosis syndrome
Infantile Myasthenia Gravis
Esotropia secondary to neurological diseases like hydrocephalus ,
intracranial tumors

47. Initial treatment :
•Amblyopia and significant refractive error correction
is done
•Surgical correction is done within one year maximum
within two years
Goal :
-Alignment of eyes to within 10 prism diopters associated
with peripheral fixation and central suppression
-Residual small angle is stable but bifoveal fusion is not
achieved

48. •Recession of bilateral medial recti
•Unilateral MR recession + LR resection
•Large angles –Recession of 6.5mm. Or
more
Procedure :
Subsequent treatment :
Under correction –Further recession of MR
Resection of one or both lateral
recti or surgery of other eye

49. Inferior oblique
overaction :
At age of 2 years
and other eye within 6 months
Disinsertion ,
recession and myectomy
DVD :
Superior rectus recession
Botulinum toxin can
be used as an alternate treatment

50. Surgery outcomes :
•Classified by Von Noordes
•Subnormal binocular vision –optimal treatment result
•Microtropia –desirable treatment result
•Small angle deviation esotropia / consecutive ( < 20 PD ) –cosmetically acceptable
•Large angle deviation -Cosmetically unacceptable with residual esoor exotropia more than 20 PD

51. Regular followup done
postoperatively to evaluate amblyopia ,
consecutive exotropia
or residual esotropia
If consecutive or
residual deviations are large resurgery is
planned
If residual esotropia is
small full hyperopic spectacle correction
can be given
Infantile esotropia can
develop good vision but binocularity is poor

52. Microtropia :
•Small angle ( < 10 prism diopter ) squint
•Symptoms are rare unless with
associating decompensated
heterophoria
Signs :
•Prominent association with anisometropia or hypermetropicastigmatism of more ametropic eye is
seen
•Normal motor fusion is seen
•ARC is present with abnormal
binocular single vision

54. •Monocular fixation is eccentric to
fovea in deviating eye and central
suppression scotoma is present
•Stereopsis is reduced
•Types :
•With identity and without identity
•Diagnosis :
•-4 prism diopter base out test

55. With identity Without identity
-Point used for fixation by deviating eye -Do not correspond
is similar tofovea of straight eye
under binocular viewing conditions
-In cover test no movement of -Small movement of deviating
squinting eye when it takes up eye when it takes monocular
monocular fixation fixation
Treatment :
-Refractive error and amblyopia correction

56. Four prism diopter base out test :
-This test distinguishes bifovealfixation from foveal suppression ( CSS )
With bifovealfixation
The prism is placed base out in front of right eye
deviation of image away from fovea temporally
corrective movement of both eyes to the left
Left eye converges or re fixates to fuse the images

57. In left microtropia :
Patient fixates a distance target with both eyes
4 PDbaseoutprismplaced infrontof left eye
Image moves temporally and falls within the CSS
No movement of either eyes is seen
Now prism is placed infrontof right eye Adducts to maintain fixation
Left eye also moves to the left ( Heringslaw )
Image falls within CSS
No subsequent refixation is seen

59. Convergence excess :
•Near esotropia –non accommodative convergence excess
•Usually seen in older children and young adults
Signs :
•No significant refractive error
•Orthophoria or small esophoria with BSV for distance
•Esotropia for near

60. -NORMAL OR LOW AC/A
RATIO
-NORMAL NPA
TREATMENT :
-BILATERAL MR RECESSION

62. Distance esotropia :
•In healthy young adults with
myopia
Signs :
•Intermittent or constant
esotropia for distance
•Minimal or no deviation for
near
•Normal bilateral abduction
•Fusional deviational
amplitude may be reduced

63. Absence of
neurological
disease
Treatment :-Prisms until
spontaneous
resolution
-Surgery in
persistent
cases

65. Acquired basic esotropia :
-Occurs after six months of age
-No hyperopia is seen
-No discrepancy in near –distance deviation
-May be associated with neurological disease or myasthenia gravis
-Associated with amblyopia

67. Management :
-Amblyopia therapy
-Extraocular surgery for deviation

68. Acute ( late onset ) esotropia :
•At around 5 –6 years
Etiology :
•ICSOL , orbital lesions , psychological stress or emotional problems
•Underlying sixth nerve palsy must be excluded

69. Signs :
•Sudden onset of diplopia and esotropia which is comitant
•Normal ocular motility without significant refractive error
Treatment–Prisms or occlusion of one eye to obliviate diplopia
•If etiology can be delineated it is managed
•If deviation is stable for six months or more B/L MR recession or
resection –recession procedure of affected eye is done

71. Secondary ( sensory ) esotropia :
•Unilateral reduction in vision that
interferes or abolishes fusion
Causes :
. Corneal scarring
•Cataract
•Optic atrophy
•Optic N. hypoplasia
•Macular scarring
•Retinoblastoma

73. Esodeviation is more common in
children while exo is common inadults
Oblique muscle overaction is common
Severe degree of recalcitrant amblyopia
not responding to treatment is common
Management :Treatment of cause
Amblyopia therapy

74. -Strabismus correction
Functional –if amblyopia treatment is successful
Cosmetic –chances of recurrence with time is
common
Surgery on amblyopic eye is preferable
-Oblique muscle dysfunction must be dealt with

75. Consecutive esotropia
:
Surgical overcorrection of
exodeviation
Due to loss or slipping of
lateral rectus muscle
-Complication in surgery
to oblique muscles –
more common in SO
weakening

77. Management :
-If deviation is large in immediate postoperative period with restrictive
ocular motility –lost or slipped muscle
MRI of orbit with EOM is done
Immediate exploration of and retrieving done
Muscle transposition surgery is done

78. Small overcorrections resolve over time
due to establishment of normal fusional
divergence phenomenon
Base out prisms , plus lenses and miotics
can aid in fusional divergence
If persistent diplopia is present alternate
occlusion of eyes is done
Constant significant deviation over 3 –6
months requires resurgery

79. Cyclic esotropia :
Rare condition
Alternating manifest
esotropia with
suppression and BSV lasting for 24 -48 hours
Develops esotropia in
trophic phase alone
Remaining times there
will be straight gaze
Possible factor –
repetitive circadian
rhythm

80. Diagnosis :
Based on typical
history
Examination is done
in both phases
Repeated
examinations are
necessary
Usually progressive
and finally becomes
constant over several
months to years

82. Management :
If significant hypertropia is present –refractive correction
Surgery is effective
even in cyclic phase –performed for maximum angle of deviation

83. High myopic esotropia :
High myopia
Instability of muscle pulleys that stabilize SR and LR
Nasal displacement of SR and
Inferior displacement of LR
Esotropia with hypotropia
Heavy eye syndrome

85. Key to diagnosis –MRI
-Shows distorted muscle paths
-Displacement of SR muscle nasally –mechanical adduction and limitation
of abduction
-Displacement of LR inferiorly –mechanical depression with limitation of
elevation
-Orbital connective tissue degeneration and associated abnormalities are seen

87. •Management :
•Surgery –Large recession –resection procedures
•Disinsertion of medial rectus muscle
•Modified Jensen procedure with transposition of superior rectus
•inferior rectus
•Loop myopexyof Lateral rectus and Superior rectus muscles
with or without frontal muscle split performed along with medial rectus recession

88. •Other variants
•Traditional scleral fixation of sutures
•Use of silicone bands around two muscles
•Injection of botulinum toxin into medial rectus muscle along with myopexy

89. Divergence insufficiency :
Constant or
intermittent
Greater for distance
than near by atleast 10 PD
Normal versions and
ductions
Bifoveal fixation is
lost for distance but present for nearAC /A ratio is low

90. CAUSES :
SUPRANUCLEAR
CONDITION
VERGENCE DISORDER
DEGENERATIVE
CONNECTIVE
TISSUE DISORDER
OF EXTRAOCULAR
MUSCLES

91. Nystagmus blockage syndrome :
•Condition with congenital nystagmus and straight eyes who may use accommodative convergence to damp their nystagmus leading to esotropia
•Therefore in inattention–orthotropia + manifest nystagmus
•Near fixation –esotropia + dampened nystagmus
•The clinical nystagmus is inversely proportional to esotropia

92. •Characteristic sign –Appearance of nystagmus on attempted abduction of either eye with a head turn in the direction of abducted eye
•Pupillary constriction during esotropicphase is seen
•Surgery :
•Bilateral MR recession with or without posterior fixating sutures
Or
•-Unilateral recession –resection procedures

93. THANK YOU !!!