1. esodeviations
An esodeviation is a latent or manifest convergent misalignment of the visual axes.

2. General consideration
Esodeviations are the most common type of strabismus.
Accounting for more than 50% of ocular deviations in the pediatric population.

3. Classification according to fusional capability
Esophoria is a latent esodeviation that is controlled by fusional mechanisms.
Intermittent esotropia is an esodeviation that is intermittently controlled by fusional mechanisms but becomes manifest under certain conditions, such as fatigue, illness, stress, and covering 1 eye.
Esotropia is an esodeviation that is not controlled by fusional mechanisms, so the deviation is constantly manifest.

4. Etiology Innervational. Anatomical. Mechanical. Refractive. Genetic.
Accomodative.

5. Types of esodeviation Pseudoesotropia.
Infantile (congenital) esotropia.
Accomodative esotropia.
Nonaccomodative acquired esotropia.
Incomitant esotropia.

6. pseudoesotropia
Is the false appearance of esotropia when the visual axes are actually aligned accurately.
Flat, broad nasal bridge.
Prominent epicanthal folds.
A narrow interpupillary distance.

7. Infantile esotropia
Classic congenital (essential infantile) esotropia.
Nystagmus and esotropia.
1-Ciancia syndrome.
2-Manifest latent nystagmus.
3- nystagmus blockage syndrome.

8. Classic congenital (essential infantile) esotropia
Few children with classic congenital esotropia are actually born with an esotropia.
Documented presence of esotropia by age 6 months has been accepted as a defining element of congenital esotropia.

9. A family history of esotropia or strabismus is often present.
But well-defined genetic pattern are unusual.
Other than strabismus, children with congenital esotropia are usually normal.
But up to 30% of children with neurologic and developmental problems, including cerebral palsy and hydrocephalus have esotropia.

10. Common findings Equal visual acuity. Alternate fixation.
Cross fixation.
Large angle esotropia , more than 30 prism.

11. Amblyopia may be present when a constant deviation of 1 eye is present.
There may be an apparent abduction deficit because of cross-fixation.
The child ability to abduct each eye may be demonstrated with the doll`s head maneuver, by ratating the child, or by observation with 1 eye patched.

12. Inferior oblique muscle overaction and DVD occur in more than 50% of patients, but are not commonly recognized until age 1 year or older.
Asymmetry of monocular horizontal smooth persuit is normal in infants up to age 6 months.
Patients with congenital esotropia have persistent monocular smooth persuit asymmetry that does not resolved.

18. pathogenesis The cause of congenital esotropia remains unknown.
There are 2 conflicting theories.
Worth`s sensory concept was that congenital esotropia resulted from a deficit in a supposed fusion center in the brain.
According to this theory, the goal of restoring binocularity was considered hopeless.

19. Chavasse disagreed with Worth`s theory and believed the primary problem was mechanical and potentially curable if the deviation could be eliminated in infancy.
Several studies report favorable sensory results in some infants operated on between months of age.
These encouraging results became the basis for the practice of early surgery for congenital esotropia.

20. management Cycloplegic refraction usually reveals 1-2 D of hyperopia.
Significant astigmatism or myopia may be present and may require correction.
Occasionally early onset accomodative ET may be present and requires spectacle correction.
A small-angle esotropia or intermittent may be more likely to respond to hyperopic correction than a large-angle, constant esotropia.

21. Ocular alignement is rarely achieved without surgery in a child with early-onset esotropia.
Surgery should be undertaken only after correction of significant refractive error and treatment of amblyopia.
Failure to correct these problems may compromise stable surgical alignment of the eyes.

22. Most ophthalmologists agree that surgery should be undertaken early.
The eyes should be aligned by age 24 months to optimize binocular cooperation.
Surgery can be performed in healthy children between ages 4 and 6 months to maximize binocular function such as stereopsis.

23. The Congenital Esotropia Observational Study (CEOS) demonstrated that patients with a constant and stable esotropia of at least 40 P who present between age 2 and 4 months are unlikely to improve spontaneously.
Smaller angles may be observed, as they may improve spontaneously.

24. Surgical procedures
Bilateral medial rectus recess is the most acceptable procedure.
Recess-resect of horizontal rectus of 1 eye is an alternative.
More than 2 muscle surgery in 1 cession may be done if the angle of deviation would be more than 50 PD.

25. Botulinum toxin
Botulinum toxin injection into the medial rectus muscles have been used in the treatment of congenital ET.
Multiple injections may be required and the long term sensory and motor outcomes have not been shown to be superior to those from incisional surgery.

26. The goal of treatment
The goal of treatment in congenital esotropia is to reduce the deviation to orthotropia or as close to it as possible.
Ideally, this results in normal sight in each eye and in the development of at least some degree of sensory fusion that will maintain motor alignment.
Approximately 1/3 of children will require multiple surgeries.

27. Alignment within 8P of orthtropia frequently results in the development of the monofixation syndrome.
This syndrome is characterized by peripheral fusion, central suppression, and favorable appearance and is a successful surgical result.
This small angle strabismus generally represents a stable, functional surgical outcome even though bifoveal fusion is not achived.

29. Accomodative esotropia
Accomodative esotropia is defined as a convergent deviation of the eyes associated with activation of the accomodative reflex.
All accomodative esodeviations are acquired.

30. Characteristics
Onset generally between 6 months and 7 years, averaging 2.5 years of age.
Usually intermittent at onset, becoming constant.
Often hereditary.
Sometimes precipitated by trauma or illness.
Frequently associated with amblyopia.
Diplopia may occur but usually disappears as patient develops facultative suppression scotoma in the deviating eye.

31. Types Refractive accomodative esotropia.
Nonrefractive accomodative esotropia.
Partially accomodative esotropia.

32. Refractive accomodative esotropia
The mechanism of refractive accomodative esotropia involves 3 factors.
1- uncorrected hyperopia.
2- accomodative convergence.
3-insufficient fusional divergence.

33. The uncorrected hyperopia forces the patient to accommodate to sharpen the retinal image.
Thus inducing increased convergence.
If the fusional divergence mechanism is insufficient, esotropia results.
The angle of esotropia is generally 20 to 30 PD and approximately equal at distance and near fixation.
The average amount of hyperopia is D.

34. Treatment
Correction of the full amount of hyperopia,as determined under cycloplegia.
Any concomitant amblyopia should be treated as well.
A gradual reduction of hyperopia correction may be possible over time.
This reduction stimulates gradual increased fusional divergence amplitude.
It can be result to discontinuation of spectacle therapy in the future.

35. Parents must understand the importance of full-time wear of spectacle correction.
The esodeviation, without glasses, may even increase initially after the correction is worn.
It is helpful to explain that the glasses help to control the strabismus, not cure it.

36. Miotic therapy
Miotic agents such as echothiophate iodide has been suggested as a substitute for glasses.
Because of potential ocular and systemic side effects, their use is usually confined to children who are uncooperative in wearing glasses at all or who spend long hours playing in the water.

37. Surgical correction
May be required when a patient fails to regain fusion with glasses.
Those who subsequently develops a nonaccomodative component.
However, the ophthalmologist must rule out latent uncorrected hyperopia before proceeding with surgery.

39. High accomodative convergence/ accomodative esotropia
Patients with high AC/A have abnormal relationship between accomodation and accomodative convergence.
Excess convergence tonus results from accomodation, and esotropia develops in the setting of insufficient fusional divergence.
The angle of esotropia is greater at near.
It can be reduced by D bifocal lenses.

40. Using of accomodative target in measurement of the angle of esotropia is critical.
This type of esotropia may be seen in patients with high hyperopia, normal hyperopia, emmetropia, or even myopia.
In these latter groups the disorder is also called nonrefractive accomodative esotropia.
The refractive error in these patients averages D.

41. Management of high AC/A esotropia
Bifocals.
Long-acting cholinesterase.
Surgery.
Observation.

42. Bifocals Is the most commonly used treatment.
They should be prescribed in the executive or 35-mm flat-top style with a power of or D.
The top the segment should cross the pupil.
Conventional bifocals are preferred.
An ideal response is esophoria for near and distance fixation.
An acceptable response is esophoria for distance and less than 10 P of esotropia for near fixation.

43. Long-acting choinesterase inhibitors
Starting the maximum strength (0.125% echothiophate iodide drops) in both eyes once daily for 6 weeks.
If such treatment is effective, strength or frequency should be decreased to the minimum effective dose.
Parents must be warned about the potentially serious side effects of these drugs.

44. Side effects
Deletion of pseudocholinesterase from the blood, which makes the patient highly susceptible to depolarizing muscle relaxants such as succinylcholine.
Pupillary cysts: some ophthalmologists prescribe phenylepherin 2.5% drops twice daily concurrently to reduce the risk of cyst formation.

45. surgery
Some ophthalmologists advocate surgery for high AC/A esotropia.
Surgery can normalize the AC/A ratio in these patients.
It can be used in some patients, usually adoalecents.

46. Observation
Many patients will show a decrease in the near deviation with time and ultimately develop binocular vision at both distance and near fixation.
Some ophthalmologists will observe the near deviation as long as the distance deviation allows for the development of fusion or if the patient is asymptomatic.

48. For the long-term management of both refractive and nonrefractive accomodative esotropia, it is important to remember that measured hyperopia usually increases until age 5-7 years.
Therefore, if the esotropia with glasses increases, the cycloplegic refraction should be repeated and the full correction prescribed.
After age 5-7 years, hyperopia may decrease, and the full cycloplegic refraction in place will thus blur vision and the prescription will need to reduced.

49. If glasses or drugs correct all or nearly all of the esotropia, the clinician may begin to reduce the strength of glasses or drugs to create a small esophoria when the patient reaches age 5 or 6.
This reduction may stimulate the fusional divergence mechanism to redevelop normal magnitude.

50. Partially accomodative esotropia
These patients show a reduction in the angle of esotropia with glasses but have a residual esotropia despite treatment of amblyopia and provision of full hyperopic therapy.
Sometimes, it results from decompensation of a fully accomodative esotropia.
In other instances the child may have had an esotropia that subsequently developed an accomodative element.

51. An interval of weeks to months between the onset of accomodative esotropia and the onset of treatment often results in some residual esotropia.
Hence, prompt treatment of accomodative esotropia may offer substantial benefits.

52. Patients with pure refractive accomodative esotropia who have been made orthotropic with glasses are less likely to develop a nonaccomodative component to their esodeviation than patients with the type of accomodative esotropia with a high AC/A ratio.

53. Treatment of partially accomodative esotropia
Amblyopia management.
Prescription of the full hyperopic correction.
Surgery for the nonaccomodative portion of esotropia.

54. Nonaccomodative acquired esotropia
Basic acquired esotropia.
Acute esotropia.
Cyclic esotropia.
Sensory deprivation esotropia.
Divergence insufficiency.
Spasm of the near synkinetic reflex.
Surgical consecutive esotropia

55. Basic acquired esotropia
Esotropia that develops after age 6 months and that is not associated with an accomodative component.
The amount of hyperopia is not significant.
The near deviation is the same as the distance deviation.
Although most children with this form of esotropia are otherwise healthy, CNS lesions must be considered.
Therapy consists of amblyopia treatment and surgical correction as soon as possible.

56. When planning surgery for patients with acquired esotropia, some ophthalmologists advocate prism adaptation.
Prism adaptation is a process of prescribing the full hyperopic correction if indicated and adding press-on prism to neutralize any residual esodeviation.
The patient wears the glasses with the press-on prisms for 1 or 2 weeks and is then reexamined.

57. If the esodeviation increases with the prisms, new prisms are prescribed to neutralize the deviation.
In some patients, the deviation continues to increase and more prism is required to correct it.
Surgery is then planned for the full prism-adapted deviation.

58. Acute esotropia Occasionally, an acquired esotropia is acute in onset.
The patient is aware of deviation and frequently has diplopia.
Artificial disruption of binocular vision, (patching of an eye) for any reason is one of the known cause of acute ET.

59. Neurologic evaluation may be indicated.
Most patients with acute onset of esotropia have a history of normal binocular vision.
Therefore the prognosis for restoration of single binocular vision is good.
Treatment consists of use of prisms during the period of observation and later on performing surgery.

60. Cyclic esotropia
Is a rare condition, with an incidence of 1:3000-1:5000 strabismus cases.
Onset typically occurs during the preschool years.
The esotropia is present intermittently, usually every other day (48-hour cycle).
Variable cycles and 24-hour cycles have also been documented.

61. Fusion and binocular vision are usually absent on the strabismus day, with marked improvement on the straight day.
Diplopia is unusual but may be seen in older patients who are not able to develop suppression.
Occlusion therapy may convert the cyclic esotropia into a constant one.
Surgery is usually curative.

62. Sensory deprivation esodeviation
Monocular vision loss from various causes
Cataract, corneal scarring, optic atrophy, or prolonged blurred or distorted retinal images, may cause an esodeviation.
Anisometropia with amblyopia is common in this type of esotropia.

63. Obstacles preventing clear retinal images must be identified and remediated as soon as possible.
Symmetric inputs must be accomplished at an early age if irreversible amblyopia is to be avoided.
Any secondary amblyopia should be treated before surgery if it is possible.
Surgery for residual esotropia may be indicated.

64. Divergence insufficiency
The characteristic finding of divergence insufficiency is an esodeviation, generally in adults, that is greater at distance than at near.
The deviation does not change with vertical or horizontal gaze.
Fusional divergence is reduced.
Divergence paralysis may represent a more severe form of divergence insufficiency.

65. Divergence paralysis Can be divided into 2 form:
1- primary isolated form.
2- secondary form associated with other neurologic problems, such as pontine tumors or severe head trauma.

66. Primary isolated form Is frequently a benign condition.
Symptom resolve in 40% of patients within several months.

67. Secondary divergence paralysis
May obtain relief from symptoms with treatment of the underlying neurologic disorder.
Management of diplopia consist of base-out prism and sometimes surgery.

68. Spasm of the near synkinetic reflex
Patients can present with varying combinations of excessive convergence, excessive accomodation, and miosis.
The etiology is generally thought to be functional, but rarely, it can be associated with organic disease.
Patients may present with acute, persistent esotropia alternating at other times with orthotropia.

69. The characteristic movement is the substitution of a convergence movement for a gaze movement on horizontal versions.
Monocular abduction is normal in spite of marked abduction limitation on version.
Pseudomyopia may occur.
Treatment consist of cycloplegic agents such as atropin or homatropin, plus lenses for patients with significant hyperopia and bifocals.

70. Surgical consecutive esodeviation
Esodeviation following surgery for exodeviation frequently improves spontaneously.
Treatment includes base-out prisms, plus lenses or miotics, alternate occlusion, and finally surgery.
Unless the deviation is very large or symptomatic, surgery should be postponed for several months because of the possibility of spontaneous improvement.

71. A slipped or lost lateral rectus
Produces varying amounts of esotropia.
A slipped muscle should be suspected in the case of consecutive esotropia with a large abduction deficit following surgery on a lateral rectus muscle.
Surgical exploration and reattachment of the muscle is required.
Transposition procedures may be necessary when lost muscles cannot be found.
For slipped muscle, advancement of the muscle is required.

72. Incomitant esodeviation
The term incomitent esodeviation is used when esodeviation varies in different fields of gaze.

73. Sixth nerve (Abducence) paralysis
Congenital 6th nerve palsy is uncommon.
Congenital 6th N. palsy is thought to be caused by increased ICP associated with the birth process and usually resolves spontaneously.
6th N palsy occurs much more frequently in childhood than in infancy.
Older patients may complain of double vision and often have a face turn toward the side of paretic 6th N. to avoid diplopia.

74. Approximately 1/3 of these cases are associated with intracranial lesions and may have associated neurologic finding.
Other cases may be related to infections or immunologic processes.
Spontaneous benign lesions usually resolve over several months.

75. Characteristics Usually equal vision of both eyes.
The esotropis increases in gaze toward the paretic muscle.
Saccadic velocities show slowing of the affected LR muscle.
Active force generation tests weakness of that muscle.
Versions show limited or no abduction of the affected muscle.

76. Work-ups
A careful history to define any antecedent infections, head trauma, or other factors.
CT scan and MRI are indicated when neurologic signs or symptoms are present.

77. Patching of sound eye to prevent amblyopia of deviated eye in children.
Fresnel Press-ON prisms to correct the diplopia in primary position.
Correction of any concurrent refractive error specially hyperopia in children.
Botux injection into the antagonist MRM may align the eye temporarily.
Spontaneous resolution may occur in more than half of the patients with traumatic palsies.

78. Surgery
Is indicated when spontaneous resolution does not take place after 6 months or more of follow-up.
In patients with some LR muscle function, a large recession of ipsilateral MR muscle with resection of the LR muscle.
In cases of total paralysis, muscle transposition may be required.

79. Other forms of incomitant esodeviation
Medial rectus muscle restriction may result from thyroid myopathy, medial orbital wall fracture, or excessively resected MRM.
Incomitant esodeviation also may be seen in Duane syndrome, Mobious syndrome and other special forms of strabismus.