Myopia

1. MYOPIA AND
HYPERMETROPIA

2. MYOPIA
• Myopia or shortsightedness is a type of refractive error in which
parallel rays of light coming from infinity are focused in front of the
retina when accommodation is at rest.

3. Etiological dassification
1. Axial myopia results from increase in anteroposterior length of the
eyeball. It is the commonest form.
2. Curvatural myopia occurs due to increasedcurvature of the cornea,
lens or both.
3. Positional myopia is produced by anterior placement of crystalline
lens in the eye.
4. Index myopia results from increase in the refractive index of
crystalline lens associated with nuclear sclerosis.
5. Myopia due to excessive accommodation occurs in patients with
spasm of accommodation.

4. Grading of myopia
American OptometricAssociation (AOA) has defined three grades of
myopia:
• Low myopia, when the error is s-3D.
• Moderate myopia, when the error is berween-3D to -6D.
• High myopia, when the error is >-6D.

5. Clinical varieties of myopia
1. Congenital myopia.
2. Simple or developmental myopia.
3. Pathological or degenerative myopia.
4. Acquired or second.ray myopia which occurs secondary to some other
disease/ factors are as follows:
• post-traumatic,
• post-keraritic,
• drug-induced,
• pseudomyopia,
• space myopia,
• night myopia, and
• consecutive myopia.

6. CONGENITAL MYOPIA
• Present since birth, the congenital
myopia, is usually diagnosed by the age
of 2- 3 years.
• Most of the time the error is unilateral
but rarely, it may be bilateral.
• High degree of error, about 8 to 10D, is
usually present, which mostly remains
constant.
• Convergent squint may develop in
order to preferentially see clear at its
far point (which is about 10- 12cm).

7. • Associations may include other congenital anomalies such as-
• Cataract,
• microphthalmos,
• aniridia,
• Megalocornea
• congenital separation of retina.
• Early correction of congenital myopia is desirable.

8. Simple myopia
Most common type of myopia which progresses during the childhood
and adolescence and rarely exceed 5 to 6 D.
- It generally begins b/w ages 7 to 8 years and stop to progress by the
age of 21 years and the BCVA is always normal (6/6).
- It is considered as a physiological error not associated with any
disease of eye .

9. Clinical features-
• It rarely present at birth. Most of such patients are rather born
hypermetropioc but during development the normal mark is
overshooted and child becomes myopic.
• There is no effective method for halting the progress of this so called
“SCHOOL myopia” once it has started.

10. Symptoms-
1- Poor vision for distance (shortsightness)
2-Asthenopic symptoms- occurs with small degree of myopia . Strain
develops due to dissociation between convergence and accommodation.
3-Change in psychological outlook- These children take the poor far-vision
indoor for granted and concentrated their energy in to indoor activities.

11. Signs-
1- Eyes are typically large and some what
prominent.
2- A/C deep
3- Pupil are large size (and a bit sluggish reaction)
4- Fundus –is normal; rarely may show myopic
crescent at the temporal margin of the disc.
5- The error does not exceed 6 to 8 diopters.

12. Pathological myopia
Pathological myopia is essentially a degenerative and progressive condition which manifest in early
childhood.
Etiology- It is unequivocal that the pathological myopia results from a rapid axial growth of the
eyeball which is out side the normal biological variations ( i.e. 20 to 30 D)of development.
- To explain the spurt in axial growth , various theories have been put forward. So far no
satisfactory hypothesis has emerged to explain the etiology of pathological myopia . However , it
is definitely linked with
(i) Heredity and
(ii) General growth process.

13. (i) Role of hereditary- the condition has a strong hereditary tendency and is more common in
women than in man.
- Autosomal dominant pathological myopia has been linked to genes 18p11.31 and 12q2123.
(ii) Role of general growth process- Lengthening of the posterior segment of the globe commences
only during the period of active growth and probably ends with the termination of the active
growth. Therefore , the factors ( such as nutritional deficiency, debilitating diseases, endocrinal
disturbances, general health etc) which effect the general growth process may also have some
influence on the progress of myopia.

14. Etiological hypothesis- summarized
More growth of retina.
Stretching of sclera
Genetic Factors General growth process
* Increase axial length
* Degeneration of choroid
* Degeneration of retina
* Degeneration of vitreous

15. Clinical features
Symptoms-
1- Defective vision- The inability to see distant object clearly and holding the book too close to the
eye while reading are the usual complaints of parents. Further due to progressive degeneration
changes an uncorrectable loss of vision may occurs.
2- Muscae volitantes – Floting black opacities in front of the eyes are also complained of by many
patients. Theses occur due to degenerated liquified vitreous.

16. 3- Eye strain and headache- may occurs due to an imbalance between
accommodation and convergence in myopia.
4- Flashes of light
5-Night blindness- may be complained by very high myopes having marked
chorio-retinal degenerative changes.

17. Signs-
1- Prominent eyes- appearing elongated and even simulating an
exophthalmos. (The elongation is probably not due to stretching but to a primary
degeneration of the coats of the eye including the posterior half of the sclera; the
part of eye Anterior to the equator may be normal).
2-Cornea – large size
3- A/C- Deep
4- Pupil- Large size
5- Refractive error- May progress until mid 30s and frequently results in
myopia of 10-20D.

18. 5- Fundus examination-
A- Optic disc-
(i) Large and pale
(ii) Temporal crescent
(iii) Nasal Supertraction crescent

19. B- Degenerative changes in retina and choraid-
(i) Tigroid appearance of fundus- due to visible prominent large choroidal
vessels following atrophy of RPE and choriocapillaris.
-In late stages White atrophic patches seen due to total disappearance of
choroidal tissue (Post. pole).

20. (ii) Foster- fuchs’ spot- Dark red circular patch due to subretinal
neovascularization and choroidal haemorrhage , may be present at macula.

21. (iii)Cystoid degeneration- may be seen at the periphery
(iv)Total retinal atrophy – at central area
(v) There may be associated lattice degeneration / Snail track lesion.
(vi) Retinal hole/ tear, hemorrhage and even Retinal detachment.

22. C- Posterior staphyloma- In high degree of myopia, the sclera may bulge out at the
posterior pole to form a posterior staphyloma.
D- Degenerative changes in vitreous- it includes:
-Liquefaction
-Vitreous opacities
-Posterior vitreous detachment(PVD)(Weiss’ ring)

23. E- Visual field- show concentric and in some cases ring scotoma may be seen.
F-Electroretinogram (ERG)- subnormal

24. Complications-
- Retinal tear / R. D
- Hemorrhage
- Complicated cataract
- Nuclear sclerosis
- POAG (common association)

25. Treatment of myopia
1- Optical Correction
2-Contact lenses
3-Surgical correction
4- General health
5- Low vision aids
6- Genetic Counseling

26. 1- Optical correction- Concave lenses
(Problem of high minus glass-
Minification of object, bright image, distortion of image,
reduced fiel of vision, eye appears smaller behind the glass)
Basic rule of correction of myopia
- The minimum acceptance providing maximum vision.
- Children- below 8 years of age- full correction
-Adults-
* < 30 yrs of age- accept their full myopic
* > 30yrs – Undercorrected distance vision
- Irrespective of age , full correction can rarely be tolerated in
case of high myopia (more then -10 D).

27. 2- Contact lenses- Have most important role in myopic correction.
Advantage: * Less minification of image
* Image distortion can be eliminated
* Field of vision is increased
* Glass free

28. 3- Surgical correction- For pt. who do not wish to use glasses , refractive surgery to
correct the myopia is an option.
-Radial keratotomy (RK)
-Photorefrective keratectomy(PRK)
-Intra corneal ring (ICR)
-Laser-assisted in situ keratomileusis(LASIK)
-Phakic lens implantation(ICL)
-Refractive lens exchange(Fukala’s operation)

29. 4- General health-The general health of a myopic child should be attended to.
Nutritious diet, out door activities and regular exercises should be
encouraged.
- Advised to do near work in good illumination .
- Avoid blunt ocular trauma .

30. 5-Low vision Aid- in pathological myopia low vision aids may be of some help
to the patient, particularly in reading.
6-Genetic counseling- Genetic counseling may stop hereditary propagation of
the disease in the family.
-Two highly myopic adults with degenerative myopia should never, from the
medical point if view, have child.

31. HYPERMETROPIA
Hypermetropia is also known as ‘far sight’. In this
dioptric condition of the eye, with the
accommodation at rest, incident parallel rays come to
a focus posterior to the light sensitive layer of the
retina.

32. Etiology types of hypermetropia
a. Axial
b. Curvarural
c. Index
d. Positional
e. Due to absence of crystalline lens.
f. Consecutive hypermetropia

33. Axial hypermetropia
• It is the commonest form, and in this condition, the total refractive
power of eye is normal but there is an axial shortening of eyeball.
• About 1 mm shortening of the antero-posrerior diameter of the eye
results in 3 dioptres of hypermetropia.

34. Curvatural hypermetropia
• It is the condition in which the curvature of cornea, lens or both is
flatter than the normal resulting in a decrease in the refractive power
of eye.
• About l mm increase in radius of curvature results in 6 dioptres of
hypermetropia.

35. Index Hypermetropia
• It occurs due to decrease in the refractive index of the lens in old age
due to cortical sclerois.
Positional Hypermetropia
• It results from posteriorlyplaced crystalline lens.

36. Absence of crystalline lens
• It can be either congenital or acquired and it leads to aphakia
(absence of lens)- a condition of high hypermetropia.
Consecutive hypermetropia
• Overcorrected myopia after refractive surgery, implantable contact
lens
• Underpowered IOL in cataract surgery

37. Clinical types of hypermtopia
a. Simple hypermetropia
b. Pathological hypermetropia
c. Functional hypermetropia

38. SIMPLE HYPERMETROPIA
• It is the commonest form
• It results from normal biological variations in the development of the
eyeball
• It includes-
 Axial hypermetropia
 Curvatural hypermetropia

39. PATHOLOGICAL HYPERMETROPIA
• It results due to congenital or acquired conditions to the eyeball
which are outside the normal biological variations of development
It is of 2 types-
 Congenital
 Acquired

40. CONGENITAL PATHOLOGICAL
HYPERMETROPIA
• Microphthalmos
• Microcornea
• Congenital posterior subluxation
of lens
• Congenital aphakia
Microphthalmos
Microcornea

41. ACQUIRED PATHOLOGICAL HYPERMETROPIA
• Senile hypermetropia
• Curvatural
• Index hypermetropia
• Positional hypermetropia
• Aphakia
• Consecutive hypermetropia
• Retrobulbar orbital tumours, by pushing the posterior wall of the
eyeball anteriorly

42. Functional hypermetropia
• It results from paralysis of accommodation as seen in patients with
3rd nerve palsy and internal ophthalmoplegia

43. Hypermetropia: Variation with age
• At birth, the eyeball is relatively short, having +2 to +3
hypermetropia, which is gradually reduced.
• By the age of 5-7 years, the eye is emmetropic and remains so till the
age of about 50 years.
• After 50 years of age, senile hypermetropia is due to changes in the
crystalline lens, with a hypermetropia of +2 to +3

44. Clinical features
Symptoms
• Asymptomatic. A small amount of refractive error in young patients is
usually corrected by mild accommodative effort without producing
any symptom.
• Asthenopic symptoms- These include:
i. tiredness of eyes
ii. frontal or frontotemporal headache
iii. Watering
iv. mild photophobia

45. • Defective vision with asthenopic symptoms. When the amount of
hypermetropia is such that it is not fully corrected by the voluntary
accommodative efforts, then the patients complain of defective vision
which is more for near than distance and is associated with
asthenopic symptoms due to sustained accommodative efforts.
• Defective vision only. Wh en the amount of hypermetropia is very
high, the patients usually do not accommodate (especially adults) and
there occurs marked defective vision for near and distance.

46. Signs
• Size of eyeball may appear small
as a whole especially in high
hypermetropia.
• Cornea may be slightly smaller
than the normal.
• Anterior chamber is
comparatively shallow.
• Retinoscopy and
autorefractometry reveals
hypermetropic refractive error.
Shallow anterior chamber

47. • Fundus examination reveals a small optic disc which may look more
vascular with ill-defined margins and even may simulate papillitis.
• The retina as a whole may shine due to greater brilliance of light
reflections (shot silk appearance).
• A-scan ultrasonography (biometry) may reveal. A short
anteroposterior length of the eyeball in axial hypermetropia.

48. GRADING OF HYPERMETROPIA
Hypermetropia can be classified as : -low (up to 2 D)
- moderate (2.25–5D)
- high (more than 5D)
and rarely exceeds 6–7 D, which is equivalent to a 2 mm shortening of the
optic axis.

49. Complications
• Recurrent styes, blepharilis or chalazia may occur,
• Accommodative convergent squint
• Amblyopia
• Predisposition to develop primary narrow angle glaucoma.

50. Treatment
Optical treatment.
Basic principle of treatment is to prescribe convex (plus) lenses, so that
the light rays are brought to focus on the retina.
Fundamental rules for prescribing glasses in hypermetropia include:
• Total amount of hypermetropia should always be discovered by
performing refraction under complete cycloplegia.
• The spherical correction given should be comfortably acceptable to
the patient. However, the astigmatism should be fully corrected.

51. • Gradually increase the spherical correction at 6 months interval till
the patient accepts manifest hypermetropia.
• ln the presence of accommodative convergent squint, full cycloplegic
correction should be given at the first sitting.
• If there is associated amblyopia, full correction with occlusion therapy
should be started.

52. SURGICAL TREATMENT
• Conductive keratoplasty/corneal refractive therapy
• Laser thermal keratoplasty
• Photorefractive Keratectomy and their variants
• Hyperopic LASIK
• Phakic IOLs
• Refractive lens exchange

53. THANK YOU