all what you have to know about

1. Glaucoma, what you have to know about!!

2. Glaucoma, Definition
GLAUCOMA IS A GROUP OF PROGRESSIVE
DISORDERS CHARACTERIZED BY RETINAL
GANGLION CELL (RGC) APOPTOSIS AND A
SPECIFIC OPTIC NEUROPATHY ASSOCIATED
WITH CUPPING OF THE OPTIC DISC.

3. Glaucoma, pathophysiology
There are three mechanistic theories to explain why
glaucomatous optic neuropathy develops
1. THE PRESSURE-DEPENDENT BIO-MECHANICAL MECHANISM
High IOP deform the lamina cribrosa to physically
ganglion cell death and
tissue remodeling
A structure
where nerve
fibers forming the
optic nerve exit
the eye

4. Glaucoma, pathophysiology
ganglion cell death and tissue remodeling
2. THE VASCULAR/AUTOREGULATORY MECHANISM
Malfunctioning
autoregulatory
mechanisms
3. TO GENETIC FACTORS THAT COERCE PREPROGRAMMED CELL DEATH (APOPTOSIS

5. Glaucoma (Definition)
Optic neuropathy refers to damage to
the optic nerve due to any cause.
Case 1 Case 2
Case 3
Case 4 – Area of pallor more than that of cupping in both
optic discs

7. • Normal visual field extends 50° superiorly,
60° nasally, 70° inferiorly and 95° temporal
Glaucoma (Definition)
• Standard automated perimetry remains
the most widely used method to access the
visual deficit by glaucoma

8. Raised IOP up to 40-70 mmHG . Acute Angle Closed (AACG)
Glaucoma (Definition)

9. Term Definition
Ocular hypertension (OHT) elevated intraocular pressure (IOP) greater than 21 mmHg with
open anterior chamber angles, normal visual fields and healthy
optic discs (nerve heads)
Glaucoma Suspect One or more of the following :
IOP > 20 mmHg;
possible RNFL defect;
Inter-eye asymmetry in CD ration
Early glaucoma RNFL loss/ optic disc features consistent with GLAUCOMA in
absence of VF loss
OR
VF defect consistent with glaucoma in the absence of optic
disc/RNFL changes,,
Glaucoma (Definition)
Treat with
prostagland
in analogue
if IOP more
than 32
mmHg

10. Glaucoma (Definition)

11. Glaucoma, Epidemiology
Global causes of Visual Impairment
Global estimates of visual impairment: 2010, S.P.Mariotti, D. Pascolini, Br J Ophthalmol. 2012 May;96(5):614‐8

12. Global causes of Blindness
Global estimates of visual impairment: 2010, S.P.Mariotti, D. Pascolini, Br J Ophthalmol. 2012 May;96(5):614‐8
Glaucoma, Epidemiology

13. Qatarstatusoflowvisionandblindness
Glaucoma, Epidemiology

14. • January – May 2009
• 3149 Participants (97.3%)
Glaucoma, Epidemiology

15. Methods:
Prevalence and causes of blindness, low vision and status of cataract in 50
years and older citizen of Qatar-a community based survey 3000 participants
Rapid Assessment for the
Avoidable Blindness (RAAB)
Results:
• Bilateral blindness was 1.28%
• Low vision (3.66%)
• Unilateral blindness (3.61%)
Glaucoma, Epidemiology

16. Qatar status of Low Vision
Glaucoma cause 16 % of low vision cases
in Qatar while it represents only 2 % of
global low vision
Glaucoma, Epidemiology

17. Qatar status of Blindness
Causes of Bilateral Blind in Qatar
Cataract, untreated
18%
Phthisis/ globe abnormality
5%
Corneal pathology
21%Glaucoma
39%
Diabetic retinopathy
3%
ARMD
3%
Other post segment / CNS
11%
Glaucoma, Epidemiology

18. SLIDE 18SLIDE 18
• Fifty percent of glaucoma in the community
remains undiagnosed
Glaucoma, Screening
Glaucoma, what you have to know about!!
• Previously undetected cases are largely
identified at routine sight tests by community
optometrists.

19. SLIDE 19SLIDE 19
World Glaucoma Week (March)
Glaucoma, Screening
Glaucoma, what you have to know about!!

20. • DM – HTN
• Ocular hypertension (OHT) is a very important risk factor for OAG,
although OAG can occur with or without raised eye pressure.
Glaucoma, risk factors
• Age : >= 40 ys old (2% of people older than 40 years and
rising to almost 10% in people older than 75 years )
• Positive family history ( first degree relatives )

21. Glaucoma, Clinical Assessment
IOP at or below
target
Progression
(increased optic nerve damage
and/or visual field change)
Outcome Monitoring Intervals of
IOP, optic nerve head
and visual field
Yes No (means not detected
or not assessed )
No change in
treatment plan
6 to 12 (months)
Yes Yes Review target IOP and
change treatment plan
2 to 6 (months)
Yes Uncertain No change in
treatment plan
2 to 6 (months)
NO NO Review target IOP and
change treatment plan
2 to 6 (months)

22. When glaucoma cause red eye
Angle Closed Glaucoma
Secondary Glaucomas
Post glaucoma surgeries
Glaucoma medications

23. Angle Closed Glaucoma
ACUTE form (an ophthalmic emergency!)
Angle Closed Glaucoma
SUBACUTE form which has the same etiologic factors except that episodes of
elevated intraocular pressure are of short duration and are recurrent.
PRIMARY ( no cause )
SECONDARY
Angle Closed Glaucoma classification

24. Angle Closed Glaucoma , pathophysiology

25. Angle Closed Glaucoma , Pathophysiology

26. Angle Closed Glaucoma, pathophysiology

27. Primary Angle Closed Glaucoma, Risk factors
Hyperopia
Female & old
Asian

28. Very high IOP Corneal edema
Halos (subacute form)
Decrease vision
Angle Closed Glaucoma (ACG), signs

29. Angle Closed Glaucoma
Differential diagnosis of red eye
Incidenc
e
Bi/unilateral pain VA Pupil
Acute Angle
Closure
Glaucoma
- Unilateral Yes, often with
headache,
nausea, and
vomiting
Decrease dilated & react poorly
to light
Bacterial &
viral
conjunctivitis
+++ Uni or
Bilateral
May have a mild
burning sensation Normal Normal
Corneal
erosions/abr
asions
++ Unilateral Yes with
photophobia,
tearing, and FB
sensation
Depend in
location
and size of
abrasion
Incidence: +++ very often, ++ often, + occasionally, – rarely

30. Diagnostic criteria for ACG in population based research
Country Symptoms IOP Gonioscopy Disc damage Field loss
Greenland + (with PT or
IOP)
+ absolute
requirement
− −
Alaska + + (with visual
fields)
absolute
requirement
+ + (with IOP)
China + + + − −
Tibet + + + − −
Japan − + (with
gonioscopy)
+ (with IOP) − −
+ = additional feature sufficient for diagnosis combined with absolute requirement
Angle Closed Glaucoma , Diagnosis

31. Secondary Glaucoma
Thick cataractous lens push forward the iris and block the angle
PHACHOMORPHIC GLAUCOMA
A mature cataract that progresses; the lens becomes swolle
n from the osmotic effect of degenerated lens protein.

32. Secondary Glaucoma
neovascularization of the angle secondary to diabetic
retinopathy
NEOVASCULAR GLAUCOMA

33. A preservative is an additive agent that extends the shelf-life of a drug.
They can cause superficial punctate keratitis, corneal erosion, conjunctival
allergy, conjunctival injection, and anterior chamber inflammation.
Adverse reactions to glaucoma eye drops containing preservatives
Glaucoma medications SIDE EFFECTS

34. Adverse reactions to main agents in glaucoma eye drops
Use of a prostaglandin analogue as first line treatment for OHT & early to moderate COAG. Latanoprost,
Bimatoprost, Travoprost
Glaucoma medications SIDE EFFECTS
Pilocarpine
(Epinephrine, brimonidine

35. Adverse reactions to main agents in glaucoma eye drops
Glaucoma medications SIDE EFFECTS
Brimonidine
(Combigan/alphagan)
prostaglandin analogue
Latanoprost, 1996 (Xalatan
Travoprost 2001 (Travatan)
Bimatoprost 2001 (Lumigan)
Tafluprost 2012 (Taflotan )
Carbonic
anhydrase
inhibitors
Brinzolamide
dorzolamide

36. SLIDE 36
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YOUR
ATTENTION