This document provides information on primary open angle glaucoma (POAG), the most common type of glaucoma. It defines POAG as a chronic, progressive optic neuropathy caused by conditions that lead to optic nerve damage and vision loss, with the main risk factor being elevated intraocular pressure (IOP). The document discusses the epidemiology of POAG, symptoms, signs, diagnostic tests, treatment options including medications and surgeries like trabeculectomy, and provides details on mechanisms and risk factors of the disease.

1. PRIMARY OPEN ANGLE
GLAUCOMA
-Dr. Saurabh Kumar
(Intern, PMCH Dhanbad)
Department of EYE
Tue,(17/12/2019)

2. Definition-
Chronic, progressive optic neuropathy
caused by a group of ocular
conditions,which lead to damage of
optic nerve with loss of visual
function,commonest risk factor being
raised IOP.

3. Epidemiology :
1 in 100 of general population
>40 yrs. Of age
1/3rd cases of all glaucomas

4. POAG:
 Also called as Chronic Simple Glaucoma
 Adult onset
 Open angle of normal appearance
 IOP : >21 mmHg
 Characteristic OPTIC DISC CUPPING
 Visual field loss.

5. Predisposing & Risk factor:
 Intraocular Pressure (m/imp)
 Age >40 yrs.
 Race : Blacks > Whites
 Family history & Inheritance : Siblings > Offsprings
 Diabetes Mellitus
 Reduction in perfusion pressure
 Myopia
 Retinal vein occlusion, Retinal detachment, Retinitis
pigmentosa
 Thyroid disorders
 Cigarrete smoking
 Steroid usage

6. Pathogenesis : rise in IOP
 Thickening & sclerosis of Trabecular Meshwork
 Narrowing of Intertrabecular spaces
 Amorphous material deposition in
Juxtacanalicular Space
 Collapse of Schlemm’s Canal
Pathogenesis : Retinal Ganglion Cell death
 Blockage of transport of GF(Neurotrophins) from
Brain to RGC.

7. Symptoms :
 Insidious & asymptomatic onset
 Gradual painless loss of vision
 Headache, Eyeache
 Visual field defect (SCOTOMA)
 Frequent change in presbyopic glasses
 Delayed dark adaptation
 Significant loss of vision & blindness

8. Signs :
 Anterior segment signs:
-Corneal haze
-Sluggish pupil
IOP changes:
-Morning rise (20%)
-Afternoon rise (25%)
-Biphasic rise (55%)
Variation in IOP over 5mmHg is suspicious,
& over 8mmHg is diagnostic Of Glaucoma.

9. Optic nerve head evaluation :
 Vertically oval Cup
(loss of neural rim tissue in Inf & Sup. Poles)
 Assymmetry of cups (>0.2)
{N’mlly : Cup/Disc diam .=0.3}
 Large cup (>0.6)
 Splinter Hemorrhage
 Pallor areas
 Atrophy (Retinal nerve fiber layers)
{seen with RED FREE light}
Early changes :

10. Advanced changes:
 Marked Cupping (0.7-0.9)
 Neuroretinal Rim thinning
N’lly ; I S N T Rule
 Nasal shifting of Retinal vessels
(Bayonetting sign)
 Retinal arteriols Pulsations
 Lamellor Dot Sign
(slit shaped pores in lamina cribrosa)

11. Localised RNFL loss :
Localised Wedge shaped dark area

12. Five Rules for assement of
the Optic Disc in Glaucoma:
 Observe the scleral Ring to identify the
limits of the optic disc and its size.
 Identify the size of the Rim.
 Examine the RNFL.
 Examine the Region of parapapillary atrophy.
 Look for Retinal &optic disc haemorrhage.

13. Visual Field Defects :
 Isopter contraction
 Barring of Blind Spot
 Small wing shaped Paracentral Scotoma
 Seidel Scotoma
 Arcuate/Bjerrum’s Scotoma
 Ring/Double Arcuate Scotoma
 Roenne’s central nasal step
 Peripheral field defects

14. Visual Field Defects :

15. Investigations:
 Tonometry (Applanation > Schiotz)
 Central Corneal Thickness
 Diurnal variation test
 Gonioscopy
 Optic disc changes documentation
 Slit lamp
 Perimetry
 Nerve Fibre Layer Analyser
 Provocative test (water drinking test)
 Slit Lamp +78D /90D Indirect Opthalmoscopy is useful in diagnosing early
Glaucoma since Optic disc changes occur before loss of Visual field is visible.

16. Tonometry

17. Treatment :
 Aim : To lower IOP to a level where further visual loss does not occur.
 1) Prostaglandn analogue (Inc. Uveoscleral outflow) :
LATANOPROST (causes pigmentation of eyelids)
TRAVOPROST
BIMATOPROST
 2) B - blocker (topical) (Dec. Aq. Humour secretion) :
TIMOLOL MALEATE
LEVOBUNOLOL (longest action)
BETAXOLOL

18. 3) a Agonists (Inc. Aq. Outflow)
BRIMONIDINE (2nd Drug of choice)
4) CA Inhibitors (Dec. Aq. Production)
DORZOLAMIDE {bitter taste}
BRIZOLAMIDE
5) Cholinergic drug (Inc. Aq outflow)
PILOCARPINE

19. Argon/Diode Laser Trabeculoplasty :
 Indications:
1) avoidance of polypharmacy
2)avoidance of surgery
3) primary therapy in patients
with non compliance
 Mech of action : Inc. outflow by causing
shrinkage of trabecular meshwork.
40-50 spots on the Ant. half of trabecular
meshwork over 180* using a Goniolens.

20. Surgical management :
Indications-
 Uncontrolled Glaucoma despite maximal
medical (3 drugs) & laser trabeculoplasty.
 Non-compliance of medical therapy
 Advanced disease requiring a very low target
IOP

21. Trabeculectomy
 Creation of a fistula b/w the angle of anterior
chamber & sub-tenon’s space which allows egress
of aqueous from AC to a drainage bleb.

22. Procedure :
 Conjunctival flap
 Partial thickness scleral flap
 Excision of trabecular tissue
 Peripharal IRIDECTOMY
 Closing using 10-0
monofilament sutures.
 Subconj. inj. Dexamethasone
& Gentamycin

23.  Diverting Aqueous Humor into the subconjunctival space,
forming a filtering bleb under Upper eyelid.

24. THANK YOU
Have A Nice Day
Regards - saurabh