Study material mbbs

1. Myopia
(shortsightedness)
Presented by :- Gauri Shankar Saini
19037

2. Introduction
It is a type of refractive error in which parallel rays of light
coming from infinity are focused in front of the retina when
accomodation is at rest .

3. Etiology
• Etiologically myopia may be of following types;-
1. Axial myopia :- result from increase in anteroposterior
length of the eyeball.it is the commonest form. 1mm
increase in axial length result in -3D of myopia.
2. Curvatural myopia occurs due to increased curvature of the
cornea,lens or both.one mm decrease in radium of
curvature of cornea results in -6D of myopia.

4. Contd.
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 accommodationoccurs in patients
with spasm of accommodation.

5. Grading of myopia
• American optometric association (AOA) has defined three grades of
myopia:-.
Low myopia, when the error is ≤ -3D.
Moderate myopia when the error is between -3D to -6D.
High myopia, when the error is ≥-6D.

6. Clinical varieties of myopia
1. Congenital myopia
2. Simple or developmental myopia
3. Pathologicalor degenerative myopia
4. Secondary myopia

7. Congenital myopia
• Age of onset:- present since birth,it is diagnosed by the age
of 2-3 years.
• Anisometropia is usually present.
• Magnitude and progression:- high degree of error, about 8 to
10 D is usually present which mostly remains constant.
• Fundus examination may show myopic crescent.
• Convergent squint may develop in order to preferentially see
clear at its far point (10-12 cm).

8. Simple myopia
• It is the commonest variety.
• It is considered as a physiological error not associated with any
disease of the eye.
• Prevalence is 20-40% of population.
• Age of onset:- occurs at school going age So it is also called school
myopia.

9. Etiology
• Mechanism of development:- it results from normal
biological variation in the development of eye which may or
may not be genetically determined.
• Axial type of simple myopia may signify just a physiological
variation in the length of eyeball or it may be associated with
precocious neurological growth during childhood.
• Curvatural type of simple myopia is considered to be due to
underdevelopment of eyeball.

10. Predisposing/ precipitating factors
• Role of genetics:- prevalence of myopia is in children
Both parents myopic (20%)
One parent myopic (10%)
No parent myopic (5%)
• Theory of of excessive near work in childhood.
• Limited outdoor activities
• Role of diet.

11. Clinical features
• Poor vision for distance
• Asthenopic symptoms.
• Half shutting
• A change in in psychological outlook of the uncorrected
myopic children.

12. Signs
• Prominent eyeballs.
• Anterior chamber is slightly deeper.
• Pupils are somewhat large and a bit sluggishly reacting.
• Fundus is normal is normal rarely temporal myopic crescent
may be seen.
• Magnitude and progression:- simple myopia usually occurs
between 5-15 years of age and it keeps on increasing till
about 21 years of age at a rate of about -0.5±0.30 every year.

13. Pathological myopia
• It is a rapidly progressive error which starts in childhoodat 5-
10 years of age and results in high myopia (>-6D) during early
adult life which is usually associatedwith degenerative
changes.
• Etiology :- heredity and general growth process.

14. Etiology
1. Role of heredity:-
• Familial in most of cases
• Race ;- more common in certain races like Chinese,
Japanese,Arabs and Jews, uncommon among negroes
,nubiansand Sudanese.
• Sex:- more common in women
• Genetic autosomal dominant
• Sex linked recessive inherited disorder status is being given
to high myopia (>6D ).

15. Role of general growth
• Lengthening of the posterior segment of the globe
commences only during the period of active growth and
probably end with the termination of the active growth.
• Therefore the factors such as nutritional deficiencies,
debilitating disease, endocrine disturbances and indifferent
general health) which affect the general growth process will
also influence the progress of myopia.

16. Clinical features
1. Defective vision
2. Floaters :- these occurs due to degenerated liquified
vitreous.
3. Difficulties in night vision
4. Photophobia
5. Flashes of light may be reported occasionally.

17. Signs
• Prominent eyeballs:- especially in unilateral cases, the
elongation of eye balls mainly affects the posterior pole and
surrounding areas, the part of the eye anterior to the
equator may be normal.
• Cornea is large
• Anterior chamber is deep.
• Pupils are slightly large and react sluggishly to light.
• Magnitude of refractive error increases rapidly and finally
may vary from -10 D to -40 D.

18. Cont.
• Fundus examination reveals:-
1. Optic disc appears large and pale and at its temporal edge
a characteristic myopic crescent is present

19. Degenerative changes in retina and choroid
• Chorioretinal atrophic patches at the macula with a little
heaping up of pigment around them.
• Foster- fuchs ‘ spot ( dark red circular patch due to sub
retinal neovascularizationand choroidal hemorrhage) may
be present at the macula.
• Cystoid degeneration may be seen at the periphery.
• Lattice degeneration and or snail track lesions
• Total retinal atrophy in central area

20. Posterior staphyloma
• Due to ectasia of sclera at posterior pole may be apparent as
an excavation with the vessels bending backwardover its
margins.

21. Degenerative changes in in vitreous
• Include:-
1. Liquefaction
2. Vitreous opacity
3. Posterior vitreous detachment appearing as weiss reflex.

22. ERG
• It may reveal sub normal electroretinogram due to
chorioretinal atrophy.

23. Complications
• Retinal detachment
• Complicated cataract
• Vitreous haemorrhage
• Choroidal haemorrhage
• Strabismus fixus convergence
• Primary open angle glaucoma

24. Secondary myopia
• It is caused by others eye disease/ factors which are not
recognised as population risk factors for myopia.
1. Index myopia
2. Curvatural secondary myopia
3. Positional secondary myopia
4. Consecutive myopia
5. Pseudomyopia
6. Myopia of prematurity
7. Drug induced myopia

25. Treatment
1. Optical treatment:-comprises prescription of appropriate
concave lens,so that clear image is formed on the retina.
• Basic rule of correcting myopia is converse of that in
hypermetropia,i e the minimum acceptance providing
maximum vision should be prescribed.in very high myopia
undercorrection is always better to avoid the problem of
near vision and that of minification of images.

26. Contd
• Mode of prescription of concave lens are spectacles and
contact lenses.
• Contact lenses are justified in cases of high myopia as they
avoid peripheral distortionand minification produced by
strong concave spectacle lenses.

27. Contd
2. Low vision aids (LVA)
3. General measures
• Visual hygiene
• Claririty of the print should be good and continuousreading
especially in night hours.
• Balanced diet rich in vitamin and proteins.
• Early management of associating debilitating diseases.

28. Surgical treatment
1. Radial keratotomy:- making deep 90% thickness radial
incision in the periphery cornea leaving about 4 mm
central optical zone.
On healing flatens central cornea thereby reducing refractive
power.( Refractive error btw -1.5 to -6D).
2. Photo refractive keratectomy:-
Photo ablation of excimer laser:-

29. Contd.
• Which can accurately ablate corneal tissue to an exact depth
with minimal distortion of normal tissue.
• Myopia is treated by ablating the central anterior corneal
surface so that it becomes flatter.
• Approximately 10 micron of ablation corrects 1 D of myopia.

30. LASIK
• Laser in situ keratomileusis
• Currently most frequent performed refractive procedures.
• Can correct myopia up to -10 D.
• Automated microkeratone is used to raise corneal flap.
• Excimer laser applied to stromal bed and flap again
repositioned.

31. Thank you