The document discusses glaucoma, a progressive optic nerve disease characterized by elevated intraocular pressure (IOP) and irreversible vision loss if untreated. It covers its classification, causes (primary, secondary, congenital), risk factors, symptoms, clinical features, investigative methods, and treatment options including surgical and laser interventions. Significant attention is given to the pathophysiology, progression, and management of various types of glaucoma.

1. GLAUCOMA
ASHES PANDA
4th YEAR 7thSEM
NSHM COLLEGE OF MANAGEMENT & TECNOLOGY

2. It’s progressive disease of optic nerve which characterised by loss of
retinal neurones & action (i.e. - RNFL)
A common eye condition in which the fluid pressure inside the eye rises
to a level higher than healthy for that eye.
If untreated, it may damage the optic nerve, causing the loss of vision
or even blindness
Definition :

3. • Usually with a charecteristics loss of visual function.
• Damage to a optic nerve is irreversible prosses
• Usually caused by raised IOP acting on the nerve head
• Normal IOP is 15-21 mm of hg
• It is a heterogenous group of diseases in whitch optic nerve is damage.
• IOP is the most common risk factor for development of glaucoma
• Vision loss is irreversible
• It is the secound leading causes of BLINDNESS.
• In its early stages it affects peripheral visual field only but as it advances
it affects central vision and results in loss of visual acuity,
About:

4. • SECRATION OF AQUEOUS HUMOR:-
CILLIARY BODY
• ROUTE OF DRAINAGES-
-Trabecular (Conventional) Outflow (90%)
-Uveoscleral (Un conventional) Outflow (10%)
Aqueous production & drainage

5. CILIARY PROCESSES
↓
AQUEOUS IN THE POS. CHEMBER
(THROUGH PUPIL)
↓
ANT. CHAMBER
↓
TRABECULAR MESHWORK
↓
SCHLEMM’S CANAL
↓
COLLECTOR CHANNELS
Trabecular (Conventional) Outflow
(90%):

6. CILIARY PROCESSES
↓
AQUEOUS IN THE POS. CHEMBER (THROUGH PUPIL)
↓
ANT CHAMBER
↓
CILIARY BODY
↓
SUPRACHOROIDAL SPACE
↓
VENOUS CIRCULATION OF CILIARY BODY CHOROID AND SCLERA
 (The normal level of IOP is essentially maintained bye the formation and outflow of the
aqueous humour )
Uveolscleral (Un conventional) outflow
(10%) :

7. Cont. (Uveolscleral Pathway)

8.  (A)Congenital/Developmental glaucoma
1)primary congenital glaucoma
(without associated anomalies)
2)developmental glaucoma
(with associated anomalies)
Classification of glaucoma:

9.  B)Primary Glaucoma
1)Primary open angle glaucoma(POAG)
2)Primary angle clousure glaucoma(PACG)
Cont.

10.  (C) Secondary glaucoma
1) Exfoliative (pseudoexfoliative)Glaucoma
2) Pigmentary glaucoma
3)Traumatic glaucoma
4) Neovascular glaucoma
5)Uveitic glaucoma
Cont.

11. This type of glaucoma occurs in babies when there is incorrect or
incomplete development of the eye's drainage canals during the
prenatal period.
This is a rare condition that may be inherited.
(A)Congenital/Developmental
glaucoma

12.  Glaucoma associated with iridocorneal dysgenesis.
 Glaucoma associated aniridia
 Glaucoma associated with ectopia lentis syndromes
 Glaucoma associated with phakomatosis.
 Miscellaneous conditions
About:

13. • 1) Isolated congenital glaucoma ( <1mounth) :
Isolated maldevelopment of the trabecular meshwork .
No other developmental ocular anomalies or ocular diseases
that can raise IOP.
• 2) Infentile glaucoma (1mounth - 3 years)
It’s rare developmental defect in the iridocorneal filtration
angle of the anterior chamber that prevents aqueous fluid from
properly draining from the eye .
This obstruction increases the IOP which , if untreated
damage the optic nerve.
.
• 3) Juvenile glaucoma (3 years – 35 years)
Primary glaucoma occuring later in childhood or early adult
hood.
Classification of congenital glaucoma:

14. Maldevelopmental of the angle structures
Impaired aqueous outflow
Raised IOP
Damage optic nerve
Pathogenesis:

15. 1. Photophobia, blepharospasm, lacrimation & eye rubbing are often
together. These are thought to be caused by limitation of corneal
nerves, which occurs as a result of the elevated IOP.
2. Corneal sign
Oedema, enlargement, descemet’s breaks(Haab’s straie)
3. Sclera becomes thin.
4. Anterior chamber become deep
5. Iris may show iridodonesis & atrophic
patches in late stages.
6. Lens become flat due to stretching of
zonules & may even subluxate.
7. Axial myopia may occur because of
increase in axial length which may give
rise to anisometropic amblyopia.
8. IOP is raised which is neither marked nor acute.
Clinical features:

16. 9) Optic disc may show variable cupping.
Cont.

17. • Reduced visual acuity
• Bupthalmos
• Corneal diameter >12mm
• Corneal oedema
• Haab’s striae
• Elevated IOP
• Optic atrophy
Examination :

18. a) IOP measurement
b) Corneal diameter measurement
c) Slit lamp examination
d) Ophthalmoscopy
e) Gonioscopy
Investigation :

19. • Goniotomy for clear cornea.
• Trabeculotomy for hazy cornea
• Trabeculectomy & shunt procedures only when goniotomy or
trabeculotomy fails.
Treatment:

20. In Primary Open Angle Glaucoma, the angle in eye where the iris
meets the cornea is as wide & open as it should be, but the eye’s
drainage canals become clogged over time , causing an increase in
internal eye pressure & subsequent damage to the optic nerves.
1)Primary Open Angle
Glaucoma(POAG)

21. • Slowly progressive raised IOP (>21 mm Hg)
• Visual field loss as damage progresses
• Optic disc cupping
• Glaucomatous optic nerve damage
• An open anterior chamber angle
About :

22. • Certain rise of IOP that occures due to decrease of aqueous outflow.
• Aqueous outflow reduce due to -
-thickening of trabecular meshwork
-sclerosis of trabecular meshwork
-narrowing of intertrabecular spaces
-trabecular meshwork stiffening
Pathogenesis of rise in IOP :

23. • High eye pressure (>21 mm/Hg)
• Family history of glaucoma
• Thin cornea
• Suspicious optic nerve appearance with increased cupping (size of
cup, the space at the center of optic nerve, is larger than normal)
• High myopia (very severe nearsightedness)
• Diabetes
• Eye surgery or injury
• Use of corticosteroids (for example, eye drops, pills, inhalers, and
creams)
Risk factors :

24. Symptom –
1) In very early stage patient is asymptomatic
2) Headache & eye ache
3) Scotoma
4)Frequent changes in near addition
5) In late stage- delayed dark adaptation may develop
Clinical features :

25. Sign-
1) In late stage –
Pupil reflex becomes sluggish
May slight haze cornea
2) Glaucomatous field defect in perimetry
3) Fundus findings-
a. Glaucomatous cupping
b. Peripapillary splinter haemorrhage
c. Disc pallor (pale colour)
d. Glaucomatous optic atrophy
Cont .

26. e. Bayoncting sign-
discontinuation of blood vescles at optic cup
margin.
f. Thinning of neuroretinal
rims – in normal case
Inferior(I) > Superior(S)
Nasal (N) > Temporal(T)
Cont .

27. • Pachymetry
• Tonometry
• Visual field analysis (VFA)
• OCT disc profile
• Diuranal variation-
- Measurement of IOP from morning to evening
- Difference between higher & lower value of IOP
(higher IOP – lower IOP) >5mm/hg suspect
>8mm/hg confirm
Investigation:

28. • Gonioscopy -
Cont.
SHAFFER’
S
GRADING
SYSTEM
ANGLE
WIDTH
(DEGREE)
CONFIGARATION
STRUCTURE
VISIBLE
GONIOSCOPY
IV 35 - 45 WIDE ANGLE Schwalbe’s Line
Trabecular Meshwork
Scleral Spur
Ciliary Muscle Band
III 20-35 OPEN ANGLE Schwalbe’s Line
Trabecular Meshwork
Scleral Spur
II 20 MODERATELY
NARROW
Schwalbe’s Line
Trabecular Meshwork
I 10 VERY MUCH
NARROW
Schwalbe’s Line
0 0 CLOSED ANGLE No angle structure seen

29. Diagram of
SHAFFER’S GRADING SYSTEM 
• Provocative test-
water drinking test-
fasting about 8hr. , then 1lit. Water drink , First check- the IOP
15 min. gap measure the value & Second check- the IOP 1hr. gap measure
the value .
(maximum IOP – Minimum IOP) is more than 8mm/hg(>8mm/hg)
then abnormal condition.
Cont.

30. • Trabeculectomy-
A superficial flap of sclera is dissected anteriorly to the
trabecular meshwork & a section of trabecular meshwork is removed
underneath the flap .
This alternate outflow pathway is created to increase passage
of aqueous from the ant. Chamber to the subconjunctival space ,
creating & filtering bleb &
there by lowering IOP.
Treatment:

31. • Cyclophotocoagulation (CPC) :
It’s a laser procedure that reduces production of aqueous
humour in CPC .
A laser to destroy of the parts of cilliary body which
products aqueous humour if successful this will reduce the
production of fluid &
decreasing the IOP in eyes .
Cont.

32. • Argan laser Trabeculectomy (ALT):
A 514 mm argan laser beam focused through a gonio lens to treat
the boarder between ant. & pos. trabecular meshwork .
A full treatment consists of 100 spots over the entire 360 degree
of the trabecular meshwork.
This may be devided between 2 sessions consisting 50 spots over
180 degree.
Aqueous outflow improves after the procedure.
IOP reduction obtained is usually in the 7-10 mm/hg .
It’s not repeatable procedure as it cause extensive scaring of the
Trabecular Meshwork.
Side effects- Transient iritis
Corneal opacities
Hyphema
Peripheral ant. Synechiae
Cont.

33. • Selective laser trabeculoplasty (SLT)
Uses 532nm Nd. Yag laser .
The laser energy 100 times lower than ALT .
SLT selectively target pigmented cells while leaving the
rest of the trabecular meshwork tissue intact for this reason it can be
applied to 360 degrees of the meshwork in one treatment and
It considered safe to be repeated.
Cont.

34. Difference between ALT & SLT
ALT
(Argan Laser
Trabeculectomy)
SLT
(Selective Laser
Trabeculoplasty)
Energy High Low
Peak Power Very low Very high
Pulse
duration
Long Very short
Tharmal
damage
High Low
Repatable No Yes

35. This is a closed angle type of glaucoma, i.e the iris is Found to be
blocking the drainage of the eye through the trabecular meshwork &
the eye pressure to rise .
2)Primary Angle Closure
Glaucoma(PACG)

36. • Age- 40 years & older
• Gender – female are more commonly affected than male
• genetically
• Eye injury & eye surgery
• Axial length – short eye size to have shallow ant.chember .(in
hypermetropic case )
Risk factos:

37. • Pupillary block –
Pupil is the pathway between anterior & posterior
chamber, if pupil is blocked than pressure of the pos. chamber will
increase resulting bulge out of iris ( iris bombe) .
Mechanism :

38. • Non pupillary block-
1)Plateau iris –
This caused by a large or anteriorly positioned ciliary
body that leads to mechanical obstruction of trabecular meshwork.
Plateau iris has been considered an abnormal
anatomic variant of the iris .
Cont .

39. 2)Phacomorphic mechanism –
The increase in lens thickness from an
advanced cataract, a rapidly intumescent lens, or a traumatic
cataract can lead to pupillary block and angle closure.
Cont .

40. 6 different stages are there –
1) Latent primary angle closure glaucoma
2)Subacute angle closure glaucoma
3) Acute angle closure glaucoma
4) chronic primary angle closure glaucoma
5) absolute glaucoma
Clinical features :

41. 1) Latent primary angle closure glaucoma
• Symptoms- asymptomatic
• Sign- Narrowing of the ant. Chamber
Fundus appears normal
• Treatment- peripheral iridotomy
Cont .

42. 2)Subacute angle closure glaucoma
• Cause - physiological mydriasis
shallowing of ant. Chamber
• Symptoms- headache
eye pain
colour hallows in light
blurring of vision
• Sign- Narrowing of the ant. Chamber
Fundus appears normal
• Treatment- peripheral iridotomy
Cont.

43. 3) Acute angle closure glaucoma
• Cause- Ectopic lens
(when your lens moves from where it should be)
Uveitis
(inflammatory cells are moving into the ant. Chamber from
uvea)
• Symptom- severe headche,
eye pain
nausea,
vomiting
redness,
blurring of vision
photophobia,
watering
Cont.

44. • Sign- eyelid oedema
conjuntival congestion
corneal oedema
change in iris colour
uveitis (inflammatory cells are moving into the ant. Chamber
from uvea)
IOP is more than 30 mm/hg
• Treatment- yag peripheral iridotomy
trabecular surgery
clear lens extortion
Cont.

45. 4) Chronic primary angle closure glaucoma
• Synechia - It is an eye condition where the iris
adheres to either the cornea or lens.
It can be caused by ocular trauma, iritis
or iridocyclitis.
• Anterior synechia- in this case iris adheres to
the cornea.
• Posterior synechia- in this case iris adheres to
the lens.
Cont.

46. 5) Absolute glaucoma
End stage of glaucoma , when pressure of eye is always 40
mm/hg or more .
Symptom- orbital pain , severe headache
loss of peripheral vision, watering
redness
Sign- eyelid oedema, change in iris colour
Management- trabeculectomy,
Enucleation ( eye is remove)
Cont.

47. • Tonometry
• Pachymetry
• Gonioscopy
• Visual field analysis (VFA)
• OCT disc profile
Investigation:

48. • Peripheral iridotomy:
It creates a hole in the outer edge of the iris, leading to
an opening of the angle in the majority of cases. After the angle is
widened from the procedure, the Trabecular meshwork is exposed
and fluid outflow is enhanced.
• Lens extraction- alone or in combination with trabeculectomy.
• Trabeculectomy
Treatment :

49. It refers to any form of glaucoma in which there is an identifiable
cause of increased eye pressure (IOP), resulting in optic nerve
damage and vision loss.
(C) Secondary glaucoma

50. 1) Exfoliative (pseudoexfoliative)Glaucoma
2) Pigmentary glaucoma
3)Traumatic glaucoma
4) Neovascular glaucoma
5)Uveitic glaucoma
Etiological classification:

51. 1) Exfoliative (pseudoexfoliative) Glaucoma
• It is caused by the abnormal accumulation of protein in the drainage
system.
• It occurs when a flaky, dandruff-like material peels off the outer
layer of the lens within the eye.
• The material collects in the angle between the cornea and iris and
can clog the drainage system of the eye, causing eye pressure to rise.
Cont.

52. 2) Pigmentary glaucoma
• It occurs when the pigment granules that are in the back of the iris
(the colored part of the eye) break into the clear fluid produced
inside the eye.
• These tiny pigment granules flow toward the drainage canals in the
eye and slowly clog them, causing eye pressure to rise.
3)Traumatic glaucoma
• Injury to the eye may cause traumatic glaucoma. This form of open-
angle glaucoma can occur immediately after the injury or develop
years later.
• It can be caused by blunt injuries that bruise the eye (called blunt
trauma) or by injuries that penetrate the eye.
Cont.

53. 4) Neovascular glaucoma
• It is caused by the abnormal formation of new blood vessels on the
iris and over the eye's drainage channels.
• The new blood vessels block the eye’s fluid from exiting through the
trabecular meshwork (the eye’s drainage canals), causing an
increase
in eye pressure.
• It occurs generally in diabetes case.
Cont.

54. 5) Uveitic glaucoma
• Uveitis is swelling and inflammation of the uvea, the middle layer of
the eye.
• Uveitis can cause increased IOP when inflammatory debris
obstructs the trabecular meshwork resulting in decreased fluid
outflow from the eye .
• Increased eye pressure in uveitis can result from the inflammatory
process itself or the medication (steroids) used to treat it.
Cont.

55. When a patient has an IOP constantly more than 21mm/hg but no
optic disc & visual field changes.
Risk factors:
IOP consistently > 30mm/hg
Central corneal thickness < 550 µm
Vertical cup disc ration of more than 0.7
Ocular Hypertension :

56. It is a form of glaucoma in which damage occurs to the optic nerve
without eye pressure exceeding the normal range. In general, a
"normal" pressure range is between 12-22 mm Hg.
Normal tension glaucoma:

57. • Prostaglandins
Increase the aqueous outflow of the fluid by uveoscleral pathway.
Eg- Latanoprost, Bimatoprost,
Travoprost , Tafluprost
Side efects- Mild rubbing & stinging of eye
Darkening of iris,
Blurry vision
Doses- Once a day
Management of glaucoma :

58. • Miotic or Cholinergic agent
These increase the outflow of the fluid by Uveoscleral
pathway & reduce the fluid(Aqueous) production.
Eg- Pilocarpine
Side effects- Headache, blurry / dim vision
Eye ache, small size pupil
Doses- 4 times / day
Cont.

59. • Bita blockers
Reduction the production of fluid from eye.
Eg- Timolol, betaxolol
Side effects- Breathing problem
Slow heart rate
Low BP
Doses- 1 to 2 times / day ( depending on condition)
Cont.

60. • Alpha aderergic agonists
Reduce the production of aqueous humour & increase
outflow of the fluid in eye.
Eg- Apraclonidine, Brimonidine
Side effects- Irregular heart rate, High BP
Redness, Itching of eye
Doses- 2 to 3 times /day
Cont.

61. • Rho kinase inhibitors
The medicines lower the eye pressure by suppressing the
rhokinase enzymes responsebles for fluid increase.
Eg- Netarsudil (Rhopressa)
Side effect- Redness, eye discomfort
Deposits forming of the cornea
Doses- 1 time/ day
Cont.

62. • Carbonic anhydrase inhibitors
Reduce production of fluid in eye.
Eg- Dorzolamide, Brinzolamide
Side effects- Mettalic test
Friquent urination
Tingling in the fingers & toes
Doses- 2 to 3 times / day
Cont.

63. THANK YOU