Ocular anatomical and physiological changes. It gives a basic review of ocular changes. #meroeye,

1. Anatomic and Physiologic
changes of eye with Age
Moderator:
Niraj D joshi
Kapil Gautam
3rd year, B.Optometry
IOM, MMC

2. Presentation Layout
Introduction of ageing
Anatomic and physiologic changes in different structures of eye
& clinical implications
Systemic diseases of old age and ophthalmic manifestations
Over-view of ocular changes with increase in age

3. What is ageing ?
The gradual, irreversible biological changes that occur
over the course of the time, that do not result from disease
or other accidents
As a person ages, anatomy & physiology undergo many
changes, that become more apparent with increasing age
Ageing is a progressive physiological process,
characterized by degeneration of tissues and organ systems
with consequent loss of functional reverse of the these
systems
Similarly ageing results anatomical and physiological
changes in eye

4. General ageing changes
Mostly affect appearance
Seldom affect performance
Some need monitoring with age
◦ Lens
◦ Aqueous humor
◦ Retina
◦ Macula

6. Anatomical and physiological
changes & clinical co-relation

7. Periorbital area is the 1st to demonstrate visible signs of
aging
Epidermal thinning and decrease in collagen causing the
skin to lose it’s elasticity
Loss of fat, coupled with gravity and muscle pull leads to
wrinkling.
Skin and soft tissue atrophy
Peri-orbit and Eyelid

8. The elderly eye resembles an eye with Horner’s syndrome
showing ptosis, enophthalmos & miosis
It has been suggested that such changes are caused by an
increase of parasympathetic tone over sympathetic tone with
age

9. Clinical Implications
Hyperfunctional lines
Pull on the skin by underlying facial
musculature
Age induced changes in the collagen of the
dermis
Glabellar rhytids

10. Orbital septum dehiscence, leads to
herniation of intraorbital fat
Action of gravity produces downward
displacement of fat
Mostly herniation of lower eyelid fat
Baggy eyes
Herniation of orbital fat

11. Involutional / Senile ptosis
Prolapse of fat, overstretch of the
orbital septum lead to dehiscence
of levator aponeurosis
Ptosis
Aka Aponeurotic Ptosis

12. Lax and redundant of eyelid tissue
◦ Gravity
◦ Loss of elastic tissue in the skin
◦ Weakening of connective tissue of eyelid
Dermatochalasis
-Ptosis and dermatochalasis may obstruct the
visual field, especially the superior visual field
and sometimes peripheral
-Can be successfully treated with a surgical
procedure called blepharoplasty

13. Common occurrence
Affects only the lower eyelid
Senile entropion
Etiological factors
Affects only the lower eyelid
Horizontal elongation of the lid due to lengthening of both
medial and lateral canthal tendon
Vertical lid instability due to weakening of
capsulopalpebral fascia (lower lid retractor)
Over-riding of preseptal orbicularis on the pretarsal
portion of muscles
Relative enophthalmos due to orbital fat atrophy

14. Commonest variety
Involves only the lower lid
Etiological factors
Horizontal laxity of eyelid
Medial canthal tendon laxity
Lateral canthal tendon laxity
Disinsertion of lower lid retractors
Senile ectropion

15. Enophthalmos is the posterior displacement of the
eyeball within the orbit due to changes in the volume of
the orbit (bone) relative to its contents (the eyeball and
orbital fat)
Age related enophthalmos is due to loss of orbital fat
and a weakening of Tenon’s fascia
Enophthalmos

16. White eyelashes
In the elderly as an ageing process,
Production of melanin pigments in the
hair follicles decrease
Poliosis

17. Papillomas
Squamous
Papillomas
Seborrheic
keratosis
Papillomas
Derived from squamous cells.
Occur mostly around lid
margin
Usually similar color to
surrounding area
Derived from basal cells.
Appears as yellowish or
brownish sessile growth with
irregular surface

18. Represents lipid deposits in histiocytes
in the dermis of the lid
Most commonly near the inner
canthus of the eyelid, more often
on the upper lid than the lower lid
Xanthelasma

19. Lacrimal papilla becomes
prominent with age
Eversion of lower puncta
due to laxity of the lids,
cause epiphora
Adult dacryocystitis may occur commonly between 40 to 60
years of age
Predominantly seen in females
May occur in both acute and chronic form (chronic more
common)
Lacrimal passages

20. Lacrimal gland dysfunction, meibomian gland disease &
goblet cell dysfunction results in dry eye
Tear volume decreases as much as 60% by age 65 yr from
that at age 18 yr
Dry eye syndrome affects 75% of people over age 65 yr
Tear secretion

21. Degeneration
Decrease in no. &height of epithelial cells
Shortening of inferior fornix
No. of mucus cell decreases leading to dry eye
Conjunctiva

22. Elastotic degeneration of collagen fibers of the
substantia propria of conjunctiva with
little or no vascularization
Coupled with deposition of amorphous hyaline
material
Pinguecula
Pterygium
Degenerative and hyperplastic condition
Subconjunctival tissue proliferates as
vascularised granulation tissue under
epithelium encroaching the cornea

23. Normal ageing change that may be exacerbated by posterior
lid margin disease
Mechanical stress on the conjunctiva precipitate by the dry
eye is a potential initiating mechanism
Conjunctivo-chalasis

24. Cornea
• Paracentral epithelium as well as the nasal and
temporal limbal epithelium become thinner
• Central epithelium seemed to remain constant
(Investigative Ophthalmology and visual science, August 2014,vol
55(8))
Epithelium
• Thickness of 8 to 10 μm remains constant
• Calcific deposition at the periphery
Bowman’s
layer
• Stromal keratocyte density decreases
• Rigidity increases
• Increase in stromal interfibrillar spacing
Stroma

25. • Thickness increases
• Hassel-Henle bodies increases
Descemet’s
membrane
• Decrease in endothelial cell density
• Decreases from 6000 cells/mm2 at birth to 3000
cells/mm2 in older age
• Defect left is filled by enlargement of the
remaining cells(polymegathism) resulting into
pleomorphism
• Cells vary in diameter from 18 to 20 μ at birth to
40μ or more in the aged
Endothelium

26. Other changes include
Change in Corneal toricity (curvature)
Cornea flattens
Change from WTR astigmatism to ATR
astigmatism
Decrease in corneal luster
Touch (pressure) sensitivity is greatest in the center of cornea,
& falls with age

27. Clinical Implications

28. Arcus senilis
• Stromal lipid deposition
• Starts in superior & inferior perilimbal cornea
• Progress circumferentially to form a band of 1mm
wide
• Occurs bilaterally in 60% of persons between 40 and
60 years of age and in nearly all individuals over the
age 80
• Pigmented line of iron deposition commonly seen
at the junction between middle and lower third of
the cornea
Hudson stahli line
Not detrimental to visual functioning

29. • Rounded wart like excrescences of hyaline
material projecting into AC around the corneal
periphery
• Arise from Descemet’s membrane
Hassel Henle bodies
Vogt’s White Limbal Girdle
• Very common, bilateral, age-related
condition present in 50%of people aged
between 40-60.
• Arc like whitish crescentic lines composed
of chalk like flecks located at limbus at 9 &
or 3 o’clock (more common nasally)

30. Crocodile Shagreen
• Anterior/posterior polygonal opacities in
the corneal stroma
• Named so because of their resemblance to
crocodile skin
• Frequently involve anterior 2/3rd of cornea
Krukenberg’s spindle
• Deposition of uveal pigment on the corneal
endothelium

31. Sclera
• Becomes thicker and more rigid
• Loses it’s white color and becomes
yellower with fatty degeneration
• Calcium deposited between the
collagen fibres results in scleral plaque
• Senile hyaline scleral plaques
consisting of calcium deposition
within the scleral collagen

32. Anterior Chamber
Depth and volume decreases causing :
Increment in the refractive power of eye
(increase in myopia)
More interference with aqueous outflow

33. Trabecular Meshwork
• Increased pigmentation of the trabecular meshwork
• Increase in the resistance to the outflow of aqueous humor
• Cellularity of the trabecular meshwork decreases with age
• Accumulation of extracellular sulfated proteoglycans with
accompanying changes in collagen / microfibril

34. All of these changes may result in a decrease in aqueous
outflow facility
These changes have been implicated in the pathogenesis
of primary open angle glaucoma

35. Uvea
• Pupil tends to become small and the iris less reactive and
more difficult to dilate pharmacologically
Senile miosis is due to
• Atrophy of the dilator muscle fibers or
• ‫۔‬Increased rigidity of the iris blood vessels
• ‫۔‬Or both
• Causes decreased retinal blur circles and decreased retinal
illuminance

36. • Small difference in the diameter of the pupil in the dark and
light adapted state
• Less Reactive to light
• Slight increase in latency of pupillary response

37. • Pigment loss
• May cause iris transillumination
• Shape and tone changes
• Hyperplasia and proliferation of the ciliary
body non- pigmented epithelium
• Bruch’s membrane thickens
• Produces small, homogenous, focal deposits
of anomalous hyaline materials known as
Drusen
Iris
Choroid
Ciliary Body

38. • Changes in ageing lens can be grouped as
Lens
Anatomical changes
Physiological changes
Biophysical changes
Biochemical changes
Changes in crystalline

39. Anatomical changes
• Lens weight and thickness increases
• Axial thickness increases by about 28% by age 70 over that which
existed at age 15 to 20 years
• Nuclear thickness remains constant
• Cortical thickness increases anteriorly by o.6mm and posteriorly
by 0.4 mm
• Flattening of anterior lens surface and conical bulging of the
posterior lens surface

40. • Epithelial cells become flatter and density decreases
• Lens capsule thickens
• Total loss or partial degradation of number of plasma
membrane and cytoskeletal proteins
• Cholesterol: phospholipid ratio decreases

41. • Changes to cellular junctions
• Alteration on cation permeability
• Membrane potential changes from -5omv to -20 mv
• Sodium concentration increases
• Na+:K+ permeability ratio increases by six folds
• Free calcium level increases
• Ca ATPase inhibited
Physiological changes

42. • UV and visible light absorption increases
• Increase yellow pigmented proteins
• Increase fluorescence property of lens
• Light transmission and lens transparency decreases
• Amount of light reaching the retina in a normal 60 yr old is
only about 1/3rd of that reaching the retina of 20 year old
Biochemical changes

43. • Overall metabolic activity of the lens decreases
• Decrease glycolytic activity
• Decrease level/activity of antioxidants
Biophysical changes
Change in crystalline
• Loss of alpha, gamma protein & beta protein become
more polydisperse
• Act as scatter points for light
• Increased solubility

44. • Amplitude of accommodation decreases as near point
changes with age
• Near point increases with age
• Difficulty in near vision
• Condition is known as presbyopia
Changes in accommodation

45. 1.Changes in the elastic properties of lens capsule
2.Sclerosis or hardening of the lens substance
3.Weakening of the ciliary muscle
Pathophysiology of Presbyopia

46. Clinical Implications

47. • The precipitation, denaturation, coagulation or
agglutination of soluble proteins is responsible for lens
opacification: old concept
• Exact pathogenesis of cataract formation is not clear
• Biochemical changes have been suggested
Senile Cataract

48. Affects equally persons of either sex usually above the
age of 50 years
Usually bilateral but almost always one eye is affected
earlier than the other
It is broadly divided into two types
Cortical/soft
cataract
Nuclear/hard
cataract
Cuneiform Cupuliform/ Posterior sub capsular
cataract

49. Cortical (Cuneiform)
cataract
Nuclear CataractCortical (Cupuliform)
cataract

50. Posterior sub capsular opacity has a more profound effect on
vision.
In PSCC near vision is impaired more than distance vision
• Pt with cortical cataract frequently complain of glare due
to light scattering
• Nuclear cataract is often associated with myopia due to
increase in refractive index of nucleus

51. Risk factors affecting onset, type,
maturation of senile cataract
Heredity
Hypertension
Renal failure
Myopia
Smoking
Alcohol use
Use of steroids
Diabetes
Dietary factors
Exposure to UV
radiation

52. • Changes in the collagen fibrils and hyaluronic acid
components causing harmless floaters
• Condensation of the vitreous gel, enhancement of
fibrillary structure of vitreous, increased mobility of
fibrillary structures
• Liquefaction increases
• Index of refraction of the vitreous increases (↑
hypermetropia)
Vitreous

53. Clinical Implications

54. • Degenerative change
• Usually associated with collapse and opacities in the
vitreous which may be seen subjectively as black floaters in
front of the eyes
Senile vitreous liquefaction (Synchysis)

55. Vitreous attachments to the retina weakens
Separation of the cortical vitreous from the retina anywhere
posterior to vitreous base
PVD with vitreous liquefaction and collapse is of common
occurrence in majority of normal subjects above the age 65
years
Occurs in eyes with senile liquefaction, developing the hole
in posterior hyaloid membrane
Posterior Vitreous Detachment

56. • Synchytic fluid collects
between the posterior hyaloid
membrane and internal
limiting membrane of the
retina, leading to PVD along
with collapse of the remaining
vitreous gel
• May cause traction on the
peripheral retina and
occasionally a retinal tear

57. • Small, white rounded bodies suspended in the vitreous gel
• Formed due to accumulation of calcium containing lipids
• Unilateral, asymptomatic
• Seen in old patients with normal vitreous
Asteroid Hyalosis

59. • Diffuse thickening of the internal limiting membrane of the
retina and diminution of neural elements with gliosis in the
peripheral retina
• Disorganization in the area of the ora serrata, and the RPE may
migrate into the sensory retina in this area
• Reduction of nuclei in the outer nuclear layer of the retina with
age
Retina
The important areas that changes with age are RPE and
the Photoreceptor

60. Why does the retina shows changes with age?
• The retina undergoes considerable stresses during a
person’s lifetime
• There is a much lower turnover in the retina
• The retinal photoreceptor and ganglion cell are part of
CNS and therefore donot replicate in life
So they are vulnerable to accumulative changes with age

61. The loss of foveal reflex that is
often seen with age is due to
thickening of inner limiting
membrane

62. • Loss of cells as well as pleomorphic changes in cell
• Loss of melanin granule which are anti-oxidants
• Decrease in number of cells in the posterior pole
• Accumulation of lipofuscin in Bruch’s membrane
Retinal pigment Epithelium

63. • Para foveal rods do reduce by around 30%
• Reduced dark adaptation
Photoreceptors
Loss of rods before cones in the macula with an
accompanying decline in scotopic sensitivity
compared to photopic sensitivity

64. Macula
• Retinal macular microcirculation reduces with age
• Decrease in number of cells seen in the foveal ganglion
cell layer
• Decrease in choroidal circulation with age increase in the
severity of AMD (age related macular degeneration)
associated with risk for the development of SRNVM
(subretinal neovascular membrane)

65. Clinical Implications

66. • Debris from the overlying retina accumulate in Bruch’s
membrane
• Basal laminar deposits accumulate mainly in the macular
areas, which eventually manifest as drusen
• Drusen looks like specks of yellowish white materials
under the retina
Age Related Macular Degeneration

67. Drusen
SoftHard
• Small solid round deposits
with distinct margins
• Seen in 80%of normal
individual & is more
common with age
• May precede atrophy of
RPE,choroid &outer retina
• Do not constitute a sight
threatening risk
• Larger, paler &have
indistinct border
• May precede RPE
changes &
neovascularization
• Are indication of
significant risk of Macular
Degeneration

68. Risk factors
Ageing
Hypertension
Cardiovascular
risk factors
Female sex
Hyperopia
Exposure to
sunlight
Family history
Genetic
factors
Smoking

69. Corpora amylacea
• Corpora amylacea may be observed in the peripapillary
retinal nerve fiber layer, optic nerve head and optic nerve
as an aging process
• These bodies appear to be accumulations of intracellular
organelles, including neurotubules, mitochondria and
dense bodies

70. Retinal Vessels
• Exhibit changes associated with aging, these include
widespread loss of cellularity in the peripheral capillaries of
elderly persons
• Arteriosclerotic changes occur in retinal vessels with aging
includes
- thickening and hyalinization of the vessel wall
- hyperplasia of the muscular layer and fibrinoid
necrosis of the vessel wall

71. Degenerations
dPeripheral retinal degenerations a/w ageing
• Typical and reticular peripheral cystoid degeneration(TPCD)
• Paving stone (cobblestone) degeneration
• Lattice degeneration
• TPCD appears as
microscopic
cystoid spaces in
the inner to outer
plexiform layers
• In the peripheral
retina near ora

72. Peripapillary Atrophy
• Peripapillary atrophy (PPA) is a clinical finding associated
with chorioretinal thinning and disruption of the retinal
pigment epithelium (RPE) in the area surrounding the
optic disc.
• Area of hyper and hypopigmentation that may encircle the
optic disc margin, commonly more visible in the temporal
disc area

73. Tigroid /Tessellated
• There is a overall loss of choroidal melanocytes and
choroidal and RPE atrophy in old individuals
• Tigroid fundus show lesser amounts of pigment in the REP,
allowing streaks of underlying normal choroidal
pigmentation to become visible and give the characteristic
appearance

74. Optic Nerve
• Thickens as a result of impairment of exchange of nutrients
and other metabolites between the capillaries and nerve
fibers
• Loss of nerve fiber bundles and accumulation of
proteoglycans within the optic nerve

76. • The horizontal rectus EOMs are displaced inferiorly in the
elderly relative to the globe center
• This displacement presumably reflects an inferior location
of the corresponding pulleys, partially converting
horizontal rectus EOM force to depression
• This may contribute to the observed impairment of
elevation in older people and predispose them to a
characteristic pattern of Incomitant strabismus
Extra Ocular Muscles

77. Oculomotor System
• Under scotopic conditions, aging people have difficulty with
fixation causes increase in exodevition
• Supraduction decreases with age
•  positive fusional vergence but same negative fusional
vergence
•  accommodation with  AC/A ratio
•  stereopsis

78. Systemic diseases in ageing eye represent more
significant problem for anatomical & physiological
changes
Systemic disorder a/w ophthalmic disorder are
Hypertension - causes retinopathy, choroidopathy
and optic neuropathy
Diabetes mellitus- causes proliferative and non-
proliferative retinopathy
GCR- causes AION
Strokes – may causes hyperfusion of the optic nerve
and retina
Systemic diseases

79. An unwanted or harmful reaction experienced
following the administration of a drug of
combination of drugs
Elderly pt are more likely to experience due to age
related changes
E.g. NSAIDs = gastrointestinal bleeding
Beta- blockers = bradycardia, hypotension
Adverse drug reactions in elderly
people

80. General ageing changes..
Sclera- thinner, pigment change
Aqueous Humor – intraocular pressure
Vitreous Humor – thins, opacity
Cornea – Arcus senilis (Ca++, cholesterol deposit, sensitivity
Iris – muscles weaken, Smaller pupil
Lens - Size and thickness, Elasticity
Conjunctiva – Dry eye
Summary

81. More general ageing changes
Retina- Discolor, blood vessel changes
Optic nerve – Boundaries less defined, fewer capillaries
Macula – little or on foveal reflex, Drusen lipofuscin
deposits, pigmentation
Lids - Orbicularis oculi muscle weakens
Lacrimal glands/tears – Production
Orbital – Fat loss, Enophthalmos

82. Refraction – lens and ciliary muscles
Results in presbyopia
Age 40+
Acuity and contrast
Decreases after age 50
Glare
Due to lens and vitreous humor
Dark
Pupil and lens

83. More performance changes
Vitreous humor
Haziness
Flashing lights
Moving spots
Color
Discrimination of cones
Dark adaptation
Pupil and lens
Rate of sensitivity recovery decreased 0.02 log
unit/min per decade
Visual field
Size 1 to 3 degrees per decade

84. THANK YOU
CET articles
References