This document provides information about glaucoma, including: - Glaucoma is characterized by loss of vision due to damage to the optic nerve, usually caused by elevated intraocular pressure. Vision loss from glaucoma is irreversible. - While elevated IOP is a major risk factor, not all glaucoma involves high pressure, and many people with elevated pressure never develop glaucoma. - There are several types of glaucoma including open-angle glaucoma (POAG), angle-closure glaucoma (PACG), and secondary glaucomas caused by underlying conditions. - Treatment depends on the type but may involve medications, laser treatment, or surgery to lower

2. INTRODUCTION
 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 mnn 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
 Vission 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,

3. Intraocular pressure is not the only factor
responsible for glaucoma!
 95% of people with elevated IOP will never have the
damage associated with glaucoma.
 One-third of patients with glaucoma do not have
elevated IOP.
 Most of the ocular findings that occur in people
with glaucoma also occur in people without
glaucoma.

4. EPIDEMIOLOGY
 Globally estimated 8.4 million people who are blind on
the result of glaucoma
 These number are set to increases to 11.2 million by
2020
 It is the secound leading causes of BLINDNESS globally
 The highest prevelance of open angle glaucoma occures
in AFRICA.(WWW.SCIENCEDIRECT.COM)
 Global prevelance of glaucoma -2%of those over the age
of 40 years and 10% of those over 80 years of age
 Glaucoma blindness-
- global 8.0%
-india 12.8%

5.  Primary open-angle glaucoma (POAG) is the most
common type of glaucoma, accounting for over 70% of
cases.
 Ocular hypertension affects 3-5% of the population
over 40 years of age .

6. from google

7. Population distribution of IOP

8. AQUEOUS PRODUCTION AND DRAINAGE
 SECRATION OF AQUEOUS HUMOR:-
cilliary body
 ROUTE OF DRAINAGES-
-TRABECULAR OUTFLOW(90%)
-UVEAL-SCLERAL OUTFLOW(10%)

9. TRABECULAROUTFLOW:-
CILLIARY BODY
POSTERIOR CHAMBER
ANTERIOR CHAMBER
TRABECULAR MESHWORK
SCLEMNS CANEL
COLLECTOR CHANELS
EPISCLERAL VEIN

10. UVEOLSCLERALOUTFLOW
CILLIARY BODY
POST. CHAMBER
ANT. CHAMBER
CILLIARY BODY
SUPRA CHOROIDAL SPACE
VENOUS CIRCULATION OF CILLIARY BODY
 (The normal level of IOP is essentially maintained bye the formation and outflow
of the aqueous humour )

11. CLASSIFICATION of glaucoma
 (A)Congenital/Developmental glaucoma
1)primary congenital glaucoma
(without associated anomalies)
2)developmental glaucoma
(with associated anomalies)

12.  (B)PRIMARY GLAUCOMA
1)POAG
2)PACG
3)Primary mixed
mechanism glaucoma
(C) SECONDARY GLAUCOMA
Phacomorphic glaucoma
Phacolytic glaucoma
Pigmentary glaucoma
Traumatic glaucoma
Cilliary block glaucoma
Neovascular glaucoma
Glaucoma in aphakia

13. Absolute glaucoma
• The end stage of glaucoma is referred to as absolute
glaucoma.
• There is no functioning vision, the pupillary reflex is
lost and the eye has a stony appearance.
• The condition is very painful and is treated by
destructive processes.

14. CONGENITAL/DEVELOPMENTAL
GLAUCOMA
 A rare condition
 Manifest without associated anomalies
Bupthalmhos and cloudy cornea

15. Congenital Glaucoma
Buphthalmos,
glaucomatous
cupping, and
cloudy cornea
OD
Normal OS
Haa’s bstriae

16. PATHOGENESIS
 Maldevelopmental of the angle structures
 Impaired aqueous outflow
 Raised IOP
 Damage optic nerve

17. CLASSIFICATION
I. Primary developmental/congenital glaucoma
II. Developmental glaucoma with associated congenital
ocular anomalies
III. Developmental glaucoma with associated systemic
anomalies
IV. ISOLATED CONGENITAL
GLAUCOMA:-
ISOLATED CONGENITAL GLAUCOMA

18. V. INFANTILE CONGENITAL GLAUCOMA:-
-synonymous with congenital glaucoma
-1 months to 3 years
VI. JUVENILE GLAUCOMA:-
-Primary glaucoma occuring latter in
childhood
-3years to 18years

19. EPIDEMIOLOGY
-1 in 10,000 births
-65% of patients are boys

20. CLINICALFEATURES
SYMPTOMS:-
-Photophobia
-Lacrimation
-Blepharspasm
-Irritation
-Cloudy cornea
-Red eye
-Poor vission and pain

21. CLINICALFEATURES
SIGNS:-
Corneal oedema
Corneal enlargement
Haab’s straie
Sclera thin and blue
A.chamber deep
Iridodonesis
Optic disc-variable cupping & atrophy

22. INVESTIGATION
a) IOP measurement
b) Corneal diameter measurement
c) Slit lamp examination
d) Ophthalmoscopy
e) Gonioscopy

23. TREATMENT
A. MEDICAL TREATMENT :-
-Not very effective.
-It is a surgical diseases .
-Acetazolamide & beta-blockers use till
surgery is taken

24. TREATMENT
B.SURGICAL TRATMENT:-
-Goniotomy
-Trabeculectomy
-Filteration surgery
-Glaucoma drainage devices
tr T TRABECULECTOMY

25. Images of surgical treatment
 GONIOTOMY

26. POAG
(PRIMARY OPEN ANGLE GLAUCOMA)
 POAG is a commonly disease of a adult onset
 It is a charecterized by
-IOP >21 mm of hg
-open anterior chamber
angle
-optic dics cupping
-optic dics damages
-specific visual field damages

27.  POAG is a bilateral disease
 IOP is the major risk factor
 Also known as chronic simple glaucoma
 Most prevalence of all glaucoma
 Most common glaucoma

28. PREDISPOSING&RISKFACTORS
 IOP –most common risk factors
 Age-most case >40 years
 BP-Diastolic pressure <55 mm of hg
 Retinal diseases-CRVO,RD,RP
 Diabetes melitus
 Central corneal thickness

29. PATHOGENESIS OF RISE IN IOP
 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

30. EPIDEMIOLOGY
 POAG affects about 1 in 100 of general population
 Forms about one third cases of all glaucoma

31. CLINICALFEATURES
-SYMPTOMS
-Asymptomatic diseases
-Gradual painless loss of vision
-Mild headache
-Visual field defect
-Changes in presbyopic glasses
-Delayed dark adaptation

32. SIGNS
 Ant.segment signs:-
-normal
-corneal haze
-lazy pupil reflex
 Iop changes:-
-Initial stages IOP normal
-Doing DIURNAL variation test
-In later stages,IOP is permanently raised
-Range of IOP between 30 to 45 mm of hg

33. ONH evaluation:-
 Early glaucomatouas changes
-Large cup
-Asymetry of >0.2 between two eyes
-Cup ratio 0.6 or more
-pallor disc
-vertical oval cup
-splinter haemmorages
 Advavce glaucomatous chamges:-
-Cup size 0.7 to 0.9
-Neuroretinal rim thinning
-Nasal siftting of retinal vessels
-Lamellar dot signs

34. Visual field deffects:-
 In glaucoma ,visual field defects observed in
BJERRUM’S area ....
-Retinal paracentral scotoma
-Roenn’s nasal steep
-Seidel scotoma
-Arcuate scotoma

35. INVESTIGATIONOFPOAG
 1)GONIOSCOPY:-
-Wide open angle of ant.chamber
-structure seen ROI,SS,SL,CBB,TM
 TONOMETRY :-
-Tonometry shoul be preferred over
Schitze tonometry
-IOP <21 mm of hg
PROGRESSIVE CUPPING:-
CD=0.3 to 0.4
normal fundus

36.  CD=0.5 CD=0.5 to 0.7
optic dics margine
NRR
 CD=0.9 CD=1.0
0.9
CD=1.0

37. Cup-to-disk ratio

38. MANAGEMENT
 Aim of treatment to prevent impairment of vision
 Require careful & regular periodic supervision by
ophthalmologist
 Theraputic choices:-
-Medical therapy:-
-Parasympathomimetic drugs
-Prostaglandine
-Topical beta blockers
-Carbonic anhydrase inhibitors
• Argon or diode laser trabeculoplasty :-
Action:- outflow by causing shrinkage
of TM
Technique:-40-50 spots on the anterior half of TM
over 180 using a Goniolens

39. SURGERYFORPOAG
 Fileration surgery
 Trabeculectomy
 Trabeculectomy

40. PACG
PRIMARY ANGLE CLOSURE GLAUCOMA
 It refers to occlusion of the TM by the peripheral iris
abstructing aqueous outflow
 Narrow angle/acute glaucoma
 Much more rare
 IOP is ries very queckly
 It is caused by a rapid or sudden increase in eye
pressure

41. CLASSIFICATION
 (1)Primary angle closure suspect:-
-Normal IOP,optic disc & visual field
-No peripheral anterior synechiae
 (2)Primary angle closure:-
-Optic nerve damage from an
episode of severe IOP elevation
-ITC in three or more quadrants
 (3)Primary angle closure glaucoma:-
-Shows three or more quadrents of
ITC with rised IOP.
-Normal disc & field

42. RISK FACTORS
 Age:- -60 years- pupillary block
 -young non pupillary block
 Gender:-Female > Male
 Family history:-Genetic factors
 Race:-Asians
 Refraction:-Typically hypermetropic

43. CAUSES
 Angle beteween iris and cornea is closed
 Increase IOP suddenly
 Completely block the canals,which stops fluid flowing
 Some health condition can also cause ACG:-
-Cataract
-Ectopic lens
-Diabetic retinopathy
-Tumors

44. MECHANISMOF ACG
 1)Relative pupil block:-70% of case
-Iris hase large arc of contact
with anterior surface of lens
 2)Iris bombe formation:-Responsible for few atypical
case
 3)Appositional angle closure:-mechanism along with
pupillary block with iris bombe.
Relative pupilary blok:-

45. IRIS BOMB

46. Iris
bombe

47. CLINICALFEATURES
Symptoms:-
-Rapidly progressive impairement of vision
-Painful eye
-Red eye
-Nausea
-Vomitting
-photophobia
-Haloes

48. Signs:-
-Reduce visual acuity
-Cornea cloudy,& oedemotous
-Pupil oval,fixed,modaretly dilated
-Eye feels hard on palpation
-Elevated IOP 50-100 mm of Hg
-Aqueous flare & cells
-Optic disc oedema & hyperaema

49. MANAGEMENT
 1)Medicine:-
-Acetazolamide
-Topical steroids
-Topical beta blockers
 2)Surgical management:-
-Peripheral laser iridotomy
-Peripheral iridotomy
 INITIAL MANAGEMENT :-
-Immediately on attack:
-Pilocarpine
-beta blockers
-Topical corticosteroid

50. -If patient in pain:-
-Topical ketorolac
-Systemic pain medication
-If patient in vomitting:-
-Intramascular metoclopromide
-If patient in comfortable:-
-Laser iridoctomy in fellow eye

51. SECONDARYGLAUCOA
 Group of disorder in which the raised IOP is assosiated
with a primary ocular or systemic diseases.

52. CLASSIFICATION
 (A)Depending on the mechanism of rise in
IOP:-
i)Secondary open angle glaucoma:-
-In which aqueous outflow
may be blocked by
pretrabucular membrane or
trabecular closing.
ii)Secondary angle closure:-
which may be or may not be
assosiated with pupil block

53.  (B)Depending on the cavsative primary
diseases:-
-Lens induced glaucoma
-Inflamatory glaucoma
-Neuvascular glaucoma
-Cilliary block glaucoma
-Traumatic glaucoma
-Glaucoma in aphakia
-glaucoma with assosiated with intra ocular
haemorrhage

54. LENSINDUCED(phacogenic)
 Pacomorphic –(due to swollen lens)
 Phacotopic-(anterior lens displacement)
 Phacolytic
 Lens partical glacucoma
 Phacoanaphylactic glaucoma

55. Figure 1: (a) Traumatic anterior dislocation of lens with pupillary block glaucoma; (b)
lens particle glaucoma; (c) phacomorphic glaucoma; (d) phacolytic

56. PHACOMORPHICGLAUCOMA
 Causes:-
-Intumesent lens
-ant.subluxation of lens & spherophakia
 Pathogenosis:-
-swollen lens pushes iris forward
 Treatment:-
-Medical:-control of IOP by-
- iv mannitol
-acetazolamide
-topical beta blockers
-LASER iridotomy

58. PHACOLYTIC GLAOCOMA
 Pathogenesis:-
-T.M is clogged by the lens
proteins,macrophages .
-Deep anterior chamber and aqueous may
contain fine white protein particles.
 Clinical features:-
-Symptoms:-
-pain,nausea,vomitting
-rapidly progressive
impairement of vision

59.  Signs:-
-Lid oedematous
-Congunctiva-chemosed & congested
-Cilliary vessel congested
-A.C very shallow
-Iris may be discolored
-Optic disc oedematous & hyperaemic
 Management:-
-Medical therapy to lower the IOP
-Extraction of the hypermature
catarctous lens with PCIOL
implantation

60. Phacolytic glaucoma

61. NEUVASCULAR GLAUCOMA
 Result due to formation of neuvascular membrane
involving the angle of anterior chamber
 Etiology:-
Neuvascularization of iris following retina
isvhaemia features of –
-PDR
-CRVO
-Sickle-cell retinoparhy

62.  Clinical Profile:-
- Pre-glaucomotous stage
-Open angle glaucoma stage
-Secondary angle closure glaucoma
 Treatment:-
-Panretinal photocoagulation
-Medical therapy not affective
-Arteficial filtration shunt.

63. Neuvascular glaucoma

64. TRAUMATIC GLAUCOMA
 Mechanism:-
-Inflammatory glaucoma due to iridocyclitis
-Due to intra ocular haemorrhage
-Lens-induced glaucoma due to shollen lens
-Epithelial grouth
-Angle recession glaucoma
-Angle-closure glaucoma due to anterior
synechia

65. Management:-
 Medical therapy with topical 0.5% timolol and oral
acetazolamide and surgical intervention according to
situation.
 Image of traumatic glaucoma:-

66. GLAUCOMA INVESTIGATION
 Instrument which are use in glaucoma
investigation are:-
-OCT (Disc profile):
-To measure the thickness of RNFL
-VFA:- for visual field test
-Perimetry:-visual field test
-Tonometry:-measure the inner eye pressur
-Opthalmoscopy:-for shape & color of optic nerve
-Gonioscopy:-to see the iridocorneal angler
-Pachymetry:- to measure thickness of cornea

67. Tonometry
Applanation Schiotz Gonioscopy

68. THE VISUAL FIELD
Humphrey automated perimetry

70. PATIENTS
RECORDS

71. CASE:-01
 PT’S NAME:-Vishwanath thakur DATE:-09/10/2018
 REG NO.:-1819-011510 AGE:-55 year
 OCCUPATION:-farmer SEX:-Male
 ADRESS:-west bengal
 C/O:-RE-Trauma by hand
 FINDING:-
Fundus-RE-Total cup,LE-c/d=0:5
V/A:-RE-6/60p ,LE:-6/24p
IOP:-RE-54,LE:-15

72.  INVESTIGATION:-
VFA
APLANATION TONOMETRY
INDIRECT OPHTHALMOSCOPY
 REPORTS:-VFA:-RE-Trabeular vision
LE-generalized depression
A.T:-RE-55,LE-14
I.O:-RE-Total cupping,LE:-c/d=0:5
 CONCLUSIONS:-

73. CASE:-02
 PT’S NAME:- Hiralal manjhi DATE:-12/10/2018
 REG NO.:-1718-017579 AGE:-52y
 OCCUPATION:-bussinessman SEX:-male
 ADRESS:-Purulia,W.B
 C/O:-low vision,headache,
 FINDING:-
Fundus-LE-cupping undialated
V/A:-RE-NOPL ,LE:-6/18P
CORNEA:-RE-Total corneal opacity

74.  INVESTIGATION:-
VFA
OCT (DISC PROFILE)
APLANATION TONOMETRY
INDIRECT OPHTHALMOSCOPY
 REPORTS:-VFA:-LE-advanced field loss
A.T:-RE-18,LE-27
OCT:-LE significant development seen of
inferior quadrent
(LE-vertical C/D=1.00)
 CONCLUSIONS:-

75. CASE:-03
 PT’S NAME:- DATE:-
 ID NO.:- AGE:-
 OCCUPATION:- SEX:-
 ADRESS:-
 C/O:-
 FINDING:-
Fundus
V/A:-RE- ,LE:-

76.  INVESTIGATION:-
VFA
OCT (DISC PROFILE)
APLANATION TONOMETRY
INDIRECT OPHTHALMOSCOPY
 REPORTS:-
 CONCLUSIONS:-

77. CASE:-04
 PT’S NAME:- DATE:-
 ID NO.:- AGE:-
 OCCUPATION:- SEX:-
 ADRESS:-
 C/O:-
 FINDING:-
Fundus
V/A:-RE- ,LE:-

78.  INVESTIGATION:-
VFA
OCT (DISC PROFILE)
APLANATION TONOMETRY
INDIRECT OPHTHALMOSCOPY
 REPORTS:-
 CONCLUSIONS:-

79. CASE:-05
 PT’S NAME:-REENA DEVI DATE:-04/09/2018
 REG NO.:-Reg1819-011281 AGE:-30 years
SEX:-female
 OCCUPATION:-House wife ADRESS:-Ranchi
 C/O:- -painless loss of vision,-Mild headache
-Changes in presbyopic glasses
 FINDING:-
Fudus-Cupping
V/A-RE-6/6P,LE-6/6P
NCT-RE-22,LE-10

80. • INVESTIGATION:- -VFA
-OCT (DISC PROFILE)
-INDIRECT OPHTHALMOSCOPY
-APLANATION TONOMETRY
 REPORTS:-
VFA:-Normal
OCT:-Vertical C/D=RE-0.71,LE-0.72
I.O:-Cupping
A.T:-RE-23,LE-13 (mm of Hg)
 CONCLUSIONS:-