Primary open angle glaucoma (POAG) is characterized by adult onset, elevated intraocular pressure (IOP) above 21 mmHg with an open iridocorneal angle, optic disc cupping, and visual field loss. Risk factors include older age, family history, higher IOP, and certain medical conditions. POAG is caused by reduced outflow of aqueous humor from the eye due to thickening of the trabecular meshwork. Diagnosis requires evidence of optic nerve damage and visual field loss in addition to elevated IOP. Treatment aims to lower IOP and prevent further vision loss through medications, laser trabeculoplasty, or surgery.

1. Primary open angle glaucoma
POAG , also referred to as chronic simple glaucoma is generally a
bilateral, but not always symmetrical disease, characterized by:
 Adult onset
 IOP>21 mmHg
 An open angle of normal appearance
 Characteristic optic disc cupping
 Visual field loss

2. Predisposing and risk factors
1. Intraocular pressure( IOP)- most imp risk factor
2. Age - most cases >40 years, unusual <40years
3. Race - blacks >whites
4. Family history and inheritance – sibling > offspring
5. Diabetes mellitus
6. Reduction in perfusion pressure (BP-IOP)
7. Myopia
8. Retinal diseases like central retinal vein occlusion, retinal
detachment and retinitis pigmentosa
9. Thyroid disorders
10. Cigarrete smoking
11. Steroid usage – topical (>6 weeks) , systemic

3. Pathogenesis of rise in IOP
• Rise in IOP occurs due to decrease in the aqueous
outflow
• Reduced aqueous outflow facility occurs due to failure
of aqueous outflow pump mechanism
Thickening and sclerosis of trabecular meshwork with faulty
collagen tissue
Narrowing of intertrabecular spaces
Deposition of amorphous material in the juxtacanalicular
space
Collapse of schlemm’s canal and absence of giant vacuoles in
the cells lining it

4. Epidemiology of POAG
Affects about 1 in 100 of the general population (of either sex) above
the age of 40 years
Forms about one third cases of all glaucomas
PREVALENCE

5. Clinical features
Symptoms
 Insidious and asymptomatic disease
 Gradual painless loss of vision
 Mild headache, eye ache
 Visual field defect(SCOTOMA)
 Frequent change in presbyopic glasses
 Delayed dark adaptation
 Significant loss of vision and blindness

6. Signs
1. Anterior segment signs
- corneal haze
- sluggish pupil
2. Intraocular pressure changes
Repeated observations of IOP(
every 3-4 hour), for 24 hour(
diurnal variation test)
Different patters of diurnal
variation of IOP
Morning rise in IOP- 20% of cases
Afternoon rise in IOP-25% of cases
Biphasic rise in IOP-55% of cases
Variation in IOP of over 5 mm Hg
(Schiotz) is suspicious and over 8
mm of Hg is diagnostic of glaucoma
Fig.Patterns of diurnal variations of IOP: A, normal slight morning rise; B, morning rise seen in 20% cases of POAG; C, afternoon rise seen in 25% cases of POAG; D,
biphasic variation seen in 55% cases of POAG

7. 3. Optic nerve head evaluation
Normal optic nerve head
 Neuroretinal rim – tissue
between the outer edge of the
cup and disc margin. A normal
rim is orange or pink in colour
and follows the
 ISNT rule
 Rim-disc ratio
 Cup-disc ratio- normal vertical
C/D ratio= 0.1-0.4, although it
varies with the size of the disc
 Asymmetry between 2 eyes
is < 0.2
 Blood vessels

9. A
Normal optic disc (A, Diagrammatic depiction; B, Fundus photograph)
B

10. Early glaucomatous changes include :
Vertically oval, large cup
Asymmetry of >0.2 between 2 eyes
Large cup i.e., 0.6 or more (normal cup
size is 0.3 to 0.4)
Pallor of the disc
Splinter haemorrhages
Atrophy of RNFL
C
D
FIG.optic disc showing early glaucomatous changes
(C, Diagrammatic depiction; D, Fundus photograph)

11. Advanced glaucomatous changes
 Marked cupping (cup size 0.7 to 0.9)
 Thinning of neuroretinal rim
 Nasal shifting of retinal vessels (Bayonetting sign)
 Pulsations of the retinal arterioles
 Lamellar dot sign
Glaucomatous optic atrophy
All the neural tissue of the disc is destroyed and the
optic nerve head appears white and deeply excavated

12. Optic disc showing advanced glaucomatous changes (A, diagramatic depiction; B, fundus photograph) and
glaucomotous optic atrophy (C, diagramatic depiction; D, fundus photograph
A
B
D
D

13. 4. Visual field defects
Anatomical basis :
Distribution of retinal
nerve fibres
1. Papillomacular bundle(PMB)
2. Arcuate fibres
Superior arcuate fibers(SAF)
Inferior arcuate fibers(IAF)
3. Radiating fibres
Superior radiating fibers(SRF)
Inferior radiating fibers(IRF)
Arrangement of nerve fibres
within the optic nerve-arcuate
fibres occupy temporal portion
of the disc and are most
susceptible to damage
Distribution of retinal nerve fibres
Arrangement of nerve fibres within optic
nerve head

14. Nomenclature of glaucomatous field defects
 Isopter contraction
 Baring of blind spot
 Wing shaped paracentral
scotoma-earliest clinically
significant field defect
 Seidel’s scotoma – paracentral
scotoma joins the blind spot to
form a sickle shaped scotoma
 Arcuate or Bjerrum’s scotoma
 Ring or double arcuate scotoma
 Roenne’s central nasal step
 Perpheral field defects
 Advanced glaucomatous field
defects
Field defects in POAG: A, baring of blind spot; B,
superior paracentral scotoma; C, Seidel's scotoma;
D, Bjerru-m's scotoma; E, double arcuate scotoma
and Roenne's central nasal step

15. Criteria to grade glaucomatous field defects
• The criteria to label early, moderate and severe glaucomatous field defect
from the HFA central 30-2 test, single printout is depicted in Table

16. Assessing visual field glaucomatous
field defects
Camparing individual single field
printouts
Overview printout
Progression analysis software( GPA IN
HFA machines and peritrend in octopus
perimeter)
Visual field index(VFI)
• For proper understanding of Table
evaluation of the Humphrey single
field printout described should be
revised

17. INVESTIGATIONS
1. Tonometry
2. Central corneal thickness(CCT)
3. Diurnal variation test
4. Gonioscopy
5. Documentation of optic disc changes
6. Slit-lamp examination of anterior segment
7. Perimetry to detect the visual field defects
8. Nerve fibre layer analyzer (NFLA)
9. Provocative tests
Water drinking test

18. TONOMETRY
• The intraocular pressure (IOP) is measured with the help of an
instrument called tonometer
• Indentation tonometery
• Schiotz tonometer
• Applanation tonometry
• Goldmann tonometer
• Perkin’s applanation tonometer
• Pneumatic tonometer
• Pulse air tonometer
• Tono-Pen
Schiotz tonometer
Perkin’s hand-held
applanation tonometer

19. Technique of Schiotz tonometry
Technique of applanation tonometry
End point of applanation tonometry. (A) too small; (B) too
large; (C) end point.

20. Gonioscopy
 The technique of biomicroscopic examination of the angle of the
anterior chamber using a goniolens.
 The angle structures seen from behind forward are:
1. Root of the iris
2. Ciliary body band
3. Scleral spur
4. Trabecular meshwork
5. Schwalbe’s line

22. PERIMETRY
• The visual field is a three-dimensional area of
a subject’s surroundings that can be seen at
any one time around an object of fixation
• Perimetry
• It is the procedure for estimating extent of the
visual fields
• Kinetic versus static perimetry
• Peripheral versus central field charting
• Peripheral field charting
 Central field charting
• Confrontation method
• Perimetery: Lister’s, Goldmann’s and automated
• Campimetry or scotometry
• Goldmann’s perimetry
• Automated field analysis
• Manual versus automated perimetry
• Manual perimetry
• Automated perimetry
Extent of normal visual field

23. • MANUAL PERIMETRY
• Confrontation method
• Lister’s perimeter
• Campimetry (scotometry)
• Goldmann’s perimeter
Lister’s perimeter.
Bjerrum’s screen
Goldmann’s perimeter

24. • AUTOMATED PERIMETRY
• Automated perimeters are computer assisted and test visual fields by a
static method
• Commonly used automated perimeters are: Octopus, Field Master and
Humphrey field analyser
Humphrey field analyser (automated
perimeter)

25. • Advantages of automated perimetry over manual perimetry
• Interpertation of automated perimetry print out field charts
• Automated perimeter variables
• Testing strategies and programmes
• Automated perimeter variables
• Background illumination
• Stimulus intensity
• Stimulus size
• Stimulus duration
• Testing strategies and programs
• Suprathreshold testing
• Threshold testing
• Full threshold testing
• Fast Pac
• SITA (Swedish Interactive Threshold Alogarithm)
Stimulus intensity scales compared

26. • Test programmes- The standard test programmes used with static threshold
strategy on the Humphrey’s Field Analyser (HFA) can be grouped as below
A. Central field tests
• Central 30 - 2 test,
• Central 24 - 2 test,
• Central 10 - 2 test,and
• Macular test
B. Peripheral field tests
• Peripheral 30/60-1,
• Peripheral 30/60-2,
• Nasal step, and
• Temporal crescent
C. Speciality tests
• Neurological-20,
• Neurological -50,
• Central 10-12, and
• Macular test
D. Custom tests

27. • Evaluation of Humphrey single-field
print-out
I. Patient data and test parameters
II. Reliability indices
III. Gray scale simulation of the test data
is depicted in zone III or part III of the
printout
IV. Total deviation plots
V. Pattern deviation plots
VI. Global indices
VII. Glaucoma hemifield test (GHT)
VIII.Actual threshold values

28. DIAGNOSIS
1. Primary open angle glaucoma (POAG)
raised IOP(>21 mm of Hg) associated with definite glaucomatous optic disc
cupping and visual field changes
2. Ocular hypertension or glaucoma suspect
patient has an IOP constantly more than 21 mm of Hg but no optic disc or visual
field changes
3. Normal tension glaucoma (NTG) or low tension glaucoma (LTG)
diagnosed when typical glaucomatous disc cupping with or without visual field
changes is associated with an intraocular pressure constantly below 21 mm of Hg

29. Triad of abnormalities in disc, field and intraocular pressure (IOP) for the diagnosis
of glaucoma.

30. Management
 The primary aim of treatment is to prevent functional impairment of vision.
 It is important to perform a good baseline evaluation with which future progress
can be compared and documented
The initial data should include: visual acuity, slit-lamp examination of anterior segment,
tonometry (preferably with applanation tonometer); optic disc evaluation (preferably with
fundus photography), gonioscopy and visual field charting
GRADING- American Academy of Ophthalmology (AAO) grades severity of
glaucoma damage into mild, moderate and severe

31. Therapeutic choices
1. Medical therapy
2. Argon or diode laser trabeculoplasty
3. Filteration surgery

32. Medical therapy
The initial therapy of POAG is still medical, with surgery as the last
resort
Basic principles of medical therapy of POAG
Identification of target pressure
Treatment regimes :
Single drug therapy
 One topically instilled anti-glaucoma drug is chosen after considering
patient’s medical history and socio-economic background. If the initial drug is
ineffective or intolerable, it is to be replaced.
Combination therapy
 If one drug is insufficient to control the IOP, then a combination therapy is
advised
Monitoring of therapy by disc changes and field changes and
tonometry is most essential on regular follow-up

33. ANTI-GLAUCOMA DRUGS
• Classification
• A. Parasympathomimetic drugs (Miotics)
• B. Sympathomimetic drugs (Adrenergic agonists)
• C. β-blockers
• D. Carbonic anhydrase inhibitors
• E. Hyperosmotic agents
• F. Prostaglandins
• G. Calcium channel blockers

35. Prostaglandin analogues
 Mechanism of action: uveoscleral outflow
 Indication : first line therapy
 Preparations :
1. Latanoprost (0.005%) - PG F2-α analogue, OD dosage, additive
effect with timolol.
2. Bimatoprost (0.03%) - decreases outflow resistance, OD dosage.
3. Travoprost (0.04%) – PG F2-α analogue, OD dosage.
4. Unoprostive isopropyl (0.12%) – dolosanoid related structure
similar to PG F2-α, BD dosage.

36. Side effects
 Systemic
1. Upper respiratory tract symptoms (flu like )
2. Headache and precipitation of migraine in susceptible individuals
3. Muscle and joint pains
4. Skin rash

37.  Ocular Side Effects
1. Conjunctival hyperaemia and
foreign body sensation
2. Eyelash lengthening, thickening,
hyperpigmentation, increase in
number
3. Iris hyperpigmentation
4. Increase in severity and recurrence
of herpetic keratitis
5. Anterior uveitis
6. Cystoid macular edema

38. β–adrenergic antagonists
 Mechanism of action – block β receptors in ciliary processes
aqueous production
 Indication – used as first line therapy for patients who cant PG
analogues.
 Preparations
1. Timolol maleate(0.25%,0.5%) – non selective β blocker, BD
dosage
“short term escape” and “long term drift”
2. Betaxolol(0.25%,0.5%) – cardioselctive (β1) bocker, BD dosage,
useful in asthmatics, less effective than timolol.
3. Levobunolol(0.5%) – non selective β blocker
4. Carteolol(1%, 2%) – lesser incidence of bradycardia
5. Metipranolol(0.1%, 0.3%, 0.6%)

39. side effects
 Systemic
1. Cardiovascular effects – bradycardia, arrhythmia, heart failure,
syncope
2. Respiratory reactions – bronchospasm and airway obstruction,
especially in asthmatics
3. CNS effects – depression, anxiety, confusion, drowsiness,
disorientation
4. Others – nausea, diarrhoea, decreased libido, skin rashes, alopecia

40.  Ocular
1. Conjuctival hyperaemia
2. Superficial punctate keratopathy
3. Corneal anaesthesia

41. Contraindications
1. Bronchial asthma
2. Chronic obstructive pulmonary disease
3. Heart blocks
4. Congestive heart failure
5. Cardiomyopathy

42. Parasympathomimetics
 Classification
1. Agonists (direct acting) – pilocarpine
2. Cholinesterase inhibitors (indirect acting) :
 Reversible – physostigmine
 Irreversible – echothiophate iodide, demecarium, diisopropyl-
fluoro-phosphate
3. Dual action - e.g. carbachol

43.  Mechanism of action trabecular outflow
 Preparations
1. a) Pilocarpine e/d(1%,2%,4%)BD-QID dosage
b) ocuserts(pilo-20,pilo-40)
c)Pilocarppine gel(4%)HS
2. Carbachol(0.75%,1.5%,3%)BD-TDS dosage, may be useful in
pilocarpine sensitivity
3. Echothiophate iodide(0.125%)OD-BD dosage, intense miosis, more
GI side effects
4. Demecarium bromide(0.125%,0.25%)
5. Physostigmine(0.5%)

44. Side effects
 Systemic
1. Increased salivation, increased gastric, abdominal cramps,
diarrhoea
2. Increased sweating, anxiety
3. Bradycardia

45.  Ocular
1. Miosis leading to decrease visual acuity in cases of posterior polar cataracts,
impairment of night vision
2. Brow ache, head ache
3. Myopia
4. Keratitis
5. Iritis, iris cyst, posterior synechiae
6. Lenticular opacities
7. Retinal detachment

46. Carbonic anhydrase inhibitors
 Mechanism of action aqueous humor production
 Indications : useful as short term therapy, especially in acute cases

47.  Preparations
Oral
1. Acetazolamide tablet (diamox 250mg, IV
diamox5-10mg/kg)BD-QID dosage
2. Dichlorphenamide(50mg) BD-TDS dosage
3. Methazolamide(50 mg) BD-TDS dosage
Topical
1. Dorzolamide(2%) BD-TDS dosage, additive
effect with timolol
2. Brinzolamide (1%)BD-TDS dosage, less
stinging sensation

48. Side effects
 Systemic
1. Paraesthesias, numbmness, lethargy, depression, malaise
2. Metabolic acidosis, hypokalemia, increased serum urate level
3. Urinary frequency
4. Anorexia, cramps, flatulence, weight loss, diarrhoea
5. Sulfonamide related – blood dyscrasias, renal calculi, steven-Johnson
syndrome
Topical agents are less likely to induce systemic side effects

49. Ocular
1. Induced myopia, blurred vision
2. Stinging senstaion
3. Conjunctivitis, keratitis
Ocular side effects are seen with topical agents

50. Adrenergic agonists
 Mechanism of action aqueous outflow by both α and β
receptor stimulation, aqueous production due to stimulation
of α receptors

51.  Classification and preparations
Non selective(α and β receptor stimulation)
1. Epinephrine(0.5%,1%,2%), BD dosage
2. Dipivefrine (0.1%) – prodrug of epinephrine, increased corneal panetration
α2 adrenergic agonists
 Apraclonidine (0.5%,1%)BD-TDS dosage, used prophylactically for prevention
of IOP elevation following laser trabeculoplasty, YAG laser iridotomy and
posterior capsulotomy
 Clonidine (0.125%,0.25%) BD dosage, centrally acting anti-hypertensive agent
 Brimonidine(0.2%)BD-TDS dosage
Clinically, nonselective adrenergic agents have been replaced by α2 adrenergic
agonists because of their improved efficacy and side effect profile

52. Side effects
 Systemic
1. Hypertension(nonselective agents), hypotension(α2 adrenergic
agonists)
2. Headache, fatigue, syncope
3. Anxiety, insomnia, depression

53.  Ocular
1. Eyelid retraction, lid edema, dermatitis
2. Conjuctival hyperaemia, irritation, allergy, follicular conjuctivitis
3. Mydriasis
4. Cystoid macular edema in aphakics

54. Hyperosmotic agents
 Mechanism of action plasma tonicity
osmotic gradient dehydrated the vitreous
 Indications
To control acute episodes of elevated IOP

55. Preparations
1. Mannitol IV(20% solution1-2g/kg over 20-30 minutes), to be used
cautiously in hypertensives
2. Glycerol oral(50% solution1-1.5g/kg, mixed with equal amoount of
water or lime juice), to be used cautiously in diabetics as it is
metabolised to glucose
3. Urea IV – not recommended for routine use
4. Isosorbide – metabolically inert

56. Side effects
 Systemic
1. Expansion of blood volume, congestive heart failure
2. Nausea, vomiting, diarrhoea
3. Electrolyte disturbances
4. Renal failure
 Ocular
1. Rebound increase in IOP
2. Aqueous flare

57. Calcium channel blockers
Mechanism of action
• Might be due to its effects on secretory ciliary epithelium
Preparations
• Verapamil has been tried as 0.125 percent and 0.25 percent eyedrops
twice a day
Indications
• place in the mangement of patients with POAG, where miotics, beta-
blockers and sympathomimetics are all contraindicated
NEUROPROTECTIVE AGENTS

58. Argon or diode laser trabeculoplasty
 Indications
1. Avoidance of polypharmacy(>2 preparations)
2. Avoidance of surgery
3. Primary therapy in patients with non-compliance to medical therapy
 Mechanism of action outflow facility by causing shrinkage of
trabecular meshwork

59. Technique
40- 50 spots on the anterior
half of trabecular meshwork
over 180° using a gonioloens
Complications
1. Acute rise of IOP
2. Uveitis, haemorrhage, PAS

60. Surgical management
 Indications
1. Uncontrolled glaucoma despite maximal medical therapy(3 drugs)
and laser trabeculoplasty
2. Failure of medical therapy and /or laser trabeculaplasty
3. Non-compliance to medical therapy and unavailability of laser
trabeculoplasty
4. Advanced disease requiring a very low target pressure may benefit
from early surgery
5. Primary line of treatment

61. Surgical procedures
 Trabeculectomy
 Full – thickness sclerectomy
 Viscocanalostomy

62. Trabeculectomy
 Creation of a fistula between the angle of anterior chamber and
sub-tenon’s space which allows egress of aqueous from AC to a
drainage bleb

63. Procedure
 Conjunctival flap
 Partial thickness scleral flap
 Excision of trabecular tissue
 Peripheral iridectomy
 Closure using 10-0
monofilament sutures
 Subconj inj dexamethasone
and gentamycin

66. Use of antimetabolites
 5-fluorouracil
 Mitomycin C
Originally advocated for patients with high risk like aphakia,
pseudophakia, neovascular glaucoma, H/O failed operations, now
also being used as a routinely by many surgeons

67. Complications of trabeculectomy
 Post – op shallow AC
 Hyphaema
 Iritis
 Cataract due to accidental injury to the lens
 Endophthalmitis

68. OCULAR HYPERTENSION
Ocular hypertension or glaucoma suspect, either ofthese terms is used when a patient has an
IOP constantly more than 21 mm of Hg but no optic disc or visual field changes
Glaucoma suspect
Defined as an adult having normal open angle on gonioscopy and anyone of the following signs in at least one
eye
 Elevated IOP
 Suspicious disc changes
 Visual field defects
High risk factors
Significant diurnal variation
Significantly positive water drinking provocative test
Splinter haemorrhages over or near the optic disc
IOP constantly more than 28 mm of Hg
Retinal nerve fibre large defects
Parapapillary changes
Central corneal thickness < 555 μm
Significant asymmetry in the cup size of the two eyes
family history
high myopia, diabetes or pigmentary changes in the anterior chamber

69. Treatment
Patients with high-risk factors should be treated on the lines of POAG
Patients with no high risk factors should be annually followed by examination
of optic disc, perimetry and record of IOP

70. • NORMAL TENSION GLAUCOMA
• The term normal tension glaucoma (NTG), also referred to as low tension
glaucoma is labelled when typical glaucomatous disc changes with or
without visual field defects are associated with an intraocular pressure
(IOP) constantly below 21 mm of Hg
• It is believed to result from chronic low vascular perfusion, which makes
the optic nerve head susceptible to normal IOP
• Clinical features
• IOP – NORMAL OR LOWER THEN 21
• OPTIC DISC CHANGES
• Visual field defects
• Differential diagnosis
1. HIGH PRESSURE GLAUCOMAS
• POAG
• GLAUCOMA with intermitent rise in iop
• Previous episodes of glaucoma
2. Non glaucomatous optic neuropathies
• Congenital optic disc anomalies
• Acquired optic neuropathies

71. • Treatment
• Medical treatment to lower IOP
• Trabeculectomy
• Systemic calcium channel blockers
• Monitoring of systemic blood pressure