Glaucoma: Causes, Types, Symptoms, Risk Factors, Diagnosis and Treatment
1.
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 .
8. AQUEOUS PRODUCTION AND DRAINAGE
SECRATION OF AQUEOUS HUMOR:-
cilliary body
ROUTE OF DRAINAGES-
-TRABECULAR OUTFLOW(90%)
-UVEAL-SCLERAL OUTFLOW(10%)
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 )
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.
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
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
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
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
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:-
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
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
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
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
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:-