ophthalmology

1. PRIMARY OPEN ANGLE
GLAUCOMA(POAG)
SREELAKSHMI VENUGOPALAN
ROLL NO 66

2. CONTENTS
 INTRODUCTION
 ETIOPATHOGENESIS
 CLINICAL FEATURES
 CLINICAL ASSESMENT AND INVESTIGATION
 DIAGNOSIS
 MANAGEMENT

3. INTRODUCTION
 Primary open angle glaucoma also known as chronic simple glaucoma of
adult onset characterized by:
• Slowly progressive raised intraocular pressure(>21mmHg)
• Open normal appearing anterior chamber angle
• Optic disc cupping.
• Specific visual field defects.

4. ETIOPATHOGENESIS
 PREDISPOSING AND RISK FACTORS
1. Intraocular pressure
2. Family history- 10% in siblings,4% in the offsprings, polygenic inheritance
3. Age- increases with increasing age, 5th and 7th decades
4. Race- more severe in black people than white
5. Myopes are more predisposed
6. Central corneal thickness-thinner CCT
7. Diabetics
8. Cigarette smoking
9. High blood pressure
10. Thyrotoxicosis – Graves’ ophthalmic disease
11. Corticosteroid responsiveness.

5.  PATHOGENESIS OF RISE IN IOP

6.  PATHOGENESIS OF GLAUCOMATOUS OPTIC NEUROPATHY
• Mechanical theory
• Vascular insufficiency theory

7. CLINICAL FEATURES
 SYMPTOMS
 Usually asymptomatic
 Non specific symptoms
 Headache and eye pain
 Difficulty in reading and close work
 Delayed dark adaption
 Significant loss of vision and blindness
 Scotoma

8.  SIGNS
I. ANTERIOR SEGMENT SIGNS
 Early stage normal anterior segment
 Late stages pupil reflex becomes sluggish, cornea shows slight haze
 Thin CCT-risk factor

9. II. INTRAOCULAR PRESSURE CHANGES
 Exaggeration of the normal diurnal variation
 Diurnal variation test-repeated observations of IOP every 3-4 hours
 A variation of IOP over 5 mmHg is suspicious and over 8 mmHg is diagnostic of
glaucoma.
III. GLAUCOMATOUS OPTIC NERVE HEAD CHANGES
 Optic disc imaging techniques include;
1. Confocal scanning laser topography(CSLT)
2. Optical coherence tomography(OCT)
3. Scanning laser polarimetry

10. A – Normal slight morning rise
B - Morning rise is seen in 20% cases
C - Afternoon rise is seen in 25% cases
D - Biphasic variation seen in 55% cases

11.  GLAUCOMATOUS CHANGES IN THE OPTIC DISC
A. Early glaucomatous changes
 Vertically oval cup- due to loss of neural rim tissue.
 Asymmetry of the cups
 Large cup-cup disc ratio >0:4 (normal 0.3:0.4)
 Splinter haemorrhages
 Pallor areas
 Atrophy of retinal nerve fibre layer- wedge shaped dark areas
arising from the optic nerve head.

12. A & B – Normal optic disc.
C & D – Early glaucomatous
changes.

13. B. Advanced glaucomatous changes in the optic disc
 Marked cupping (cup size 0.7 to 0.9)
 Thinning of the neuro retinal rim –seen as crescenteric shadow adjacent to
the disc margin.
 Nasal shifting of the retinal vessels – BAYONETTING SIGN
 Pulsations of the retinal arterioles – pathognomic sign
 Lamellar dot sign- pores in the lamina cribrosa become slit shaped.

14. A and B – BAYONETTING SIGN (vessels being
Broken of at the margin), marked cupping
C – Marked cupping in OCT examination

15. C. Glaucomatous optic atrophy
 Neural tissue of the disc is destroyed
 Optic nerve head appears white and deeply excavated

16.  Pathophysiology of disc changes
Mechanical Vascular
Raised IOP
Forces lamina cribrosa backwards
Squeezes the nerve fibres
Disturb axoplasmic flow
Ischemic atrophy of the nerve fibres
Large caverns or lacunae are formed
(cavernous optic atrophy)

17. IV. VISUAL FIELD DEFECTS
 Anatomical basis of field defects
Distribution of retinal nerve fibres
• Fibres from the nasal half of retina come as superior
and inferior radiating fibres (SRF & IRF)
• Fibres from macular area come as papillomacular
bundle (PMB)
• Fibres from the temporal retina arch above and below
the macula and PMB as superior and inferior arcuate
fibres (SAF & IAF)

18. Arrangement of nerve fibres within optic nerve head
• Superior and inferior arcuate nerve fibres occupy
the superior and the inferior temporal portions of the
optic nerve head,
Most sensitive to glaucomatous damage
• Macular fibres are more resistant to the glaucomatous
damage and explain the retention of the central vision
till the end.

19.  Nomenclature of glaucomatous field defects
 Initially observed in Bjerrum’s area( 10-20 degrees from fixation) and
correlate with optic disc changes
1. Isopter Contraction- mild generalized constriction of central as well as
peripheral fields. Earliest visual field defect
2. Baring of blind spot-exclusion of blind spot from the central field due to
inward curve of the outer boundary of 30 degree central field.

20. 3. Small wing shaped paracentral scotoma (B)
 Earliest clinically significant field defect
 Appear above or below the blind spot in Bjerrum’s area
4. Seidel’s scotoma (C)
 Paracentral scotoma joins the blind spot
 Sickle shaped scotoma
5. Arcuate of Bjerrum’s scotoma ( D)
 Extension of Seidel’s scotoma either above or below the fixation
point

21. 6. Ring or double arcuate (E) - two scotomas join together
7. Roenne’s central nasal step (E) -two arcuate scotomas run in different arcs and
meet to form a sharp right angled defect at the horizontal meridian.
8. Peripheral field defect ( F)- The peripheral nasal step of Roenne’s results from
unequal contractions of the peripheral isopter

22. 9. Advanced glaucomatous field defects
 Tubular vision (G)-visual field loss gradually spreads centrally as well as
peripherally, small island of central vision
 Temporal island of vision (H)- islands of vision progressively diminish in
size , leaving the patient with no light perception

24. CLINICAL ASSESMENT AND INVESTIGATION
A. HISTORY & OCULAR EXAMINATION WITH SLIT LAMP BIOMICROSCOPY
 To look out signs of glaucoma and to rule out secondary glaucoma
B. SPECIFIC EVALUATION TECHNIQUES
1. Applanation Tonometry
2. Central corneal thickness
3. Diurnal variation test
4. Gonioscopy
5. Perimetry
6. Optic nerve head evaluation
7. Nerve fibre analyzer
8. Provocative tests- Water drinking test

25. DIAGNOSIS
1. Primary open angle glaucoma
 Raised IOP (>21mmHg)
 Definite glaucomatous optic disc cupping
 Visual field changes
2. Ocular Hypertension
 IOP constantly >21mmHg
 No optic disc cupping
 No visual field defects
3. Normal tension glaucoma (NTG)
 Typical glaucomatous cupping with or without visual field changes
 IOP constantly < 21mmHg

26. MANAGEMENT
 Aim of the treatment – Lower intraocular pressure to a level
where visual loss does not occur.
 Therapeutic choices include
1. Medical therapy
2. Argon or diode laser trabeculoplasty
3. Filtration surgery

27. MEDICAL THERAPY
Antiglaucoma drugs
• IOP Dependent
Neuroprotective agents
• IOP independent method of treating retinal
ganglion cells.

28.  Antiglaucoma drugs
1. Prostaglandin analogues-
 Decrease the IOP by increasing the uveoscleral outflow of aqueous
 LATANOPROST(0.005%)
 TRAVOPROST (0.004%)
 BIMATOPROST (0.03%)
 TAFLUPROST(0.015%)
 UNOPROSTONE(0.15%) BID
2. Topical beta blockers-
 Lower IOP by reducing the aqueous secretion due to effect on beta-2 receptors in the
ciliary processes.
 TIMOLOL MALEATE (0.25, 0.5%;1-2 times/day)
 BETAXOLOL(0.25%; 2 times/day)
 LEVOBUNOLOL(0.25, 0.5%;1-2 times/day)
 CARTEOLOL( 1%;1-2 times/day)

29. 3. Adrenergic drugs
 Lower the IOP by increasing the aqueous outflow by stimulating alpha receptors in
the aqueous outflow system
 EPINEPHRINE HYDROCHLORIDE (0.5, 2%; 1-2 times/day )and DIPIVEFRIN
HYDROCHLORIDE (0.1% 1-2 times/day)
 BRIMONIDINE - selective alpha 2 adrenergic agonist
4. Carbonic anhydrase inhibitor
 Lower IOP by decreasing aqueous production by altering ion transport along the
ciliary process epithelium.
 Topical- DORZOLAMIDE 2% 2-3 times/day or
BRINZOLAMIDE 1% BD
 Oral- ACETAZOLAMIDE and METHAZOLAMIDE

30. 5. Rho kinase inhibitors-
 Lower IOP by relaxing the cytoskeleton of trabecular meshwork and schlemm’s
canal cells
 RIPASUDIL(0.4%)
 NETARSUDIL(0.02%)-neuroprotective role
6. Miotics, PILOCARPINE (1,2,4%;3-4 times/day)
 Pilocarpine contracts longitudinal muscle of ciliary body and open spaces in
trabecular meshwork, thereby mechanically increasing aqueous outflow.
7. Hyperosmotic agents
 MANNITOL 1-2gm/kg body weight

32.  LASER TRABECULOPLASTY
 Done using argon laser or diode laser and selective trabeculoplasty.
Indications-
 When the IOP is uncontrolled despite of medical therapy
 As primary therapy where there is non compliance to medical therapy

33.  Role of Argon in ALT
 Hypotensive effect caused by increasing outflow facility
 Producing collagen shrinkage on the inner aspect of the trabecular meshwork
and opening intratrabecular spaces
 Complications
1. Transient acute rise of IOP
2. Transient inflammation
3. Others like haemorrhage, uveitis, peripheral anterior synechiae and reduced
accommodation
 Selective laser trabeculoplasty- Selective photothermolysis
 Targets selectively pigmented trabecular meshwork cells
 Pressure lowering effect.

34.  SURGICAL THERAPY
Indications
1. Uncontrolled glaucoma.
2. Noncompliance of medical therapy or non availability of ALT/SLT.
3. Failure of medical therapy.
4. Eyes with advanced disease.
Types of Surgery
1. Trabeculectomy
2. Filtration surgery- External and Internal