2. Myopia: it is a refractive condition in
the eye where the incident parallel rays
of light gets focused in front of the
retina when accommodation is at rest
3. High myopia – autosomal recessive or
X linked
Moderate myopia – autosomal
dominant
Congenital stationary night blindness –
autosomal dominant or X linked
4. Is seen in
Stickler’s syndrome
Ehlers Danlos syndrome
Marfan’s
Noonan’s syndrome
Down’s syndrome
Knobloch’s syndrome with occipital
encephalocele
5. If a person who had been an emmetrope
earlier says he can view near objects better
and is seen to have myopia suspect
diabetes. This is because due to hyper
glycemia the lens becomes swollen and the
person becomes myopic.
Also arsenic poisoning, sulpha, B complex
usage and smoking
6. Axial myopia- due to increase in axial length
Index myopia due to changes in the refractive
index- E.G. nuclear sclerosis in old age
Congenital myopia (also called developmental
myopia) – here the child is born with
abnormally long eye. Immediately after birth
the error will be -10 D or even more. This is
usually stationary
Curvature myopia due to increase in corneal
curvature
8. Plus signs added to the above categories
Lacquer cracks
Myopia with choroidal neovascularization
Fuchs’ spot
9. This type of myopia starts very early –
around five to ten and progress up to or even
beyond 25 years of age.
The degenerative changes start late and
becomes marked around the age of 50.
More common in women
10. If the refractive error is more than – 6 D and
/or the axial length is > 26.5mm it is called
high myopia.
If degenerative changes are seen in the
retina it is called pathological myopia or
degenerative myopia.
11. Tessellated fundus
Chorio retinal atrophy either diffuse or focal
Macular changes
Posterior staphyloma
Changes in the periphery
12. The disc appears larger
The physiological cup also is larger but the
neuro retinal rim will be normal. With this we
can differentiate it from glaucomatous
cupping
13. Essentially atrophic and seen on the
temporal border of the disc. Rarely it can
surround the disc.
Here the pigmentary epithelium stops short
of the disc and the choroid is atrophic
On the nasal side the retina may be drawn on
to the disc – called super traction crescent
14. This is progressive
Thinning of choroid
Loss of choroidal blood vessels
Loss of photoreceptors and RPE due to loss
of blood supply
15. This is usually seen around the disc
May extend to the macula
Then entire posterior pole
FFA: Hyper fluorescence in the late phase
ICGA: reduction in the number of choroidal
blood vessels
OCT: thinning of the choroid in the area of
atrophy
16.
17. Well defined lesions which appear like
healed choroiditis patches esp. in the macula
and around the disc
Loss of chorio capillaries, outer retina and
RPE
As the lesion advances bare sclera is seen
CNV, macular retinoschisis, retinal breaks
with detachment occur more often
18. Lacquer cracks: due to breaks in the Bruch’s
membrane. Difficult to see with
ophthalmoscope. In ICGA cracks appear as
hypo fluorescent linear lesions.
When cracks appear hemorrhage can occur.
If it is minimal it will disappear soon. If it is
thick it will persist and cause defects in the
outer retina, leading on to visual loss
19. If it occurs close to the fovea vision will be
grossly affected
It is a risk factor for choroidal
neovascularisation
This is due to stretching of the sclera
20. Raised pigmented lesion usually in the visual
axis .
Proliferation of pigment epithelium with
hemorrhage
21. Cause for CNV (usually type 2)in young
individuals
Risk factors: Patchy chorio retinal atrophy,
steep posterior staphyloma and lacquer
cracks
Even after treatment prognosis is poor as
there will be degenerative changes around
the CNV
22. If there is sub retinal exudation it should be
considered as active lesion
OCT: absence of Bruch’s membrane,
disruptions in the ellipsoid zone, absence of
external limiting membrane and retinal
thickening
OCTA: lacy wheel pattern, numerous
capillaries with a halo around the lesion.
Treatment – anti VEGF
23. Dome shaped macula within the posterior
staphyloma
If horizontal ridges are seen from the disc to
the macula in a case of posterior staphyloma
this should be suspected.
Vitreo macular traction, choroidal or scleral
thickening (seen with OCT), hypotony and
retinal resistance to scleral deformation
24. Reduction in visual acuity and
metamorphopsia
Atrophic changes will be seen in the RPE
Retinal detachment
And CNV can occur
25. Due to -tangential vitreous traction from
contraction of cortical vitreous and epiretinal
membrane
Antero posterior traction because of
staphyloma
Poor adhesion due to RPE atrophy
OCT will be needed to differentiate from
lamellar hole, macular detachment and
macular retinoschisis
26. Vitrectomy with ILM peeling along with gas
tamponade
This will remove pre macular traction creating
factors like vitreous attachment, epiretinal
membrane, the scaffold for cellular
proliferation.
Facilitates in increasing the flexibility of the
retina
If there is a detachment macular buckle can be
tried
27. When posterior staphyloma is present foveal
retinal detachment and retinoschisis can
ensue due to vitreous traction
The splitting of retina is due to higher rigidity
of the inner retina (rigid ILM and retinal
vessels)compared to the outer retinal layers
28. Split is at the level of external limiting
membrane
Stiff vessels may cause retinal micro folds
also
Vitrectomy has to be done
29. This is due to the stretching of the thin retina
Best seen with binocular ophthalmoscopy.
A crescentic shadow of about 2 -3 D will be
seen temporal to the disc with change in the
course of the vessels.
Above the age of 50
Absence of normal choroidal flush shows that
this may be due to ischemia
30. Lattice degeneration- abnormal thinning in the
peripheral retina.
Oval or straight patches
Single or multiple
Usually binocular
31. Pigment clumps are usually seen
Sclerotic vessels form crossed hatch pattern –
hence the name lattice degeneration
Atrophic holes may be seen
Tears and holes also may form leading on to
retinal detachment
32. May seen in normal eyes also
Usually seen in myopes
Ehlers Danlos
Marfan’s and Stickler’s
33. Snail track degeneration – pin point white dots
in rows
? May be early lattice
Cystoid degenerations may also be seen in the
periphery
34. It is corrected with minus or concave lenses.
Can be corrected with spectacles or contact
lenses. With contact lenses side vision will
be better. This is essential in high myopia.
Laser corrections are also done.
35. It is better to slightly under correct myopia
by about 0.25 D, but if they have exophoria
full correction must be given
The concave lenses act as base out prisms
and hence it reduces the amount of
convergence and accommodation needed for
near vision
36. This can be done with orthokeratology lenses. These
lenses worn overnight will displace the epithelium
and cause thinning of the cornea in the center
thereby correcting the myopia during the day time.
But the peripheral vision still remains blurred and
this may be the reason for the reduction in the
growth of the eye.
Very diluted atropine drops are also used to prevent
progression of myopia
37. AIOS Times Issue 1,2019
Duke Elder’s Refraction