This document provides an overview of glaucoma, including: - Glaucoma is a group of optic neuropathies characterized by optic disc changes and visual field defects, often caused by elevated intraocular pressure. It is a leading cause of blindness worldwide. - There are several types of glaucoma including open-angle glaucoma, closed-angle glaucoma, and normal tension glaucoma. Risk factors include age, family history, ethnicity, corneal thickness, and eye pressure. - Examination techniques for diagnosing glaucoma include visual acuity testing, tonometry, gonioscopy, examination of the optic disc, and visual field testing. Perimetry helps assess severity and

1. Glaucoma
Dr. Rajeev Kumar Aadivasi
Surgery is multiplication of all steps so
don’t put negative in any step.

2. • OHT
• POAG
• PACG
• NTG
• Secondary Glaucoma

3. Definition
• Glaucoma is a group of acute / chronic, progressive,
multifactorial optic neuropathies associated with
characteristic disc changes and characteristic visual field
defect for which elevated IOP is one of primary risk
factor. (which if left untreated can lead to irreversible
blindness)
• Glaucoma Suspect- Individuals presenting with
concerning optic nerve appearances with normal IOP &
either normal visual fields or borderline visual field loss.

4. Introduction
• Glaucoma is not a single disease, rather it is a large group of
disorder that are characterized by widely diverse clinical and
histopathological manifestation.
• Common denominator of glaucoma is a characteristic optic
neuropathy.
• Glaucoma is the second leading cause of blindness in the world
accounting for upto 8% of total blindness.
• In India , glaucoma is the leading cause of irreversible blindness
with atleast 12 million people affected and nearly 1.2 million people
blind from the disease. More than 90 % of cases of glaucoma
remain undiagnosed in the community.
• 3-4 times higher in blacks
Source: https://www.nhp.gov.in/disease/eye-ear/glaucoma

5. Epidemiology
• POAG is the most prevalent type of glaucoma in individuals
of European and African ethnic origin,
• In a meta-analysis of those older than 70 years of age
having a prevalence of 6% in white populations, 16% in
black populations and around 3% in Asian populations. It
affects both genders equally.
• Glaucoma affects 2–3% of people over the age of 40 years;
50% may be undiagnosed.
• Primary open-angle glaucoma (POAG) is the most common
form in white, Hispanic/Latino and black individuals;
• On a worldwide basis, primary angle closure (PAC)
constitutes up to half of cases, and has a particularly high
prevalence in individuals of Asian descent,

6. Classification
• Primary:
a. Congenital
b. Open angle
c. Closed angle
• Secondary: Aetiological
a. Steroid induced
b. Pseudo exfoliation Syndrome
c. Pigmentary Glaucoma.
d. Neovascular
e. Post-traumatic
f. Lens induced
g. Iridiocorneal Endothelial syndrome
h. Inflammatory – corneal ulcer, iridocylitis
i. Epidemic dropsy
j. Vitreous haemorrhage/I.O. tumor
k. Aphakic glaucoma .....

7. Causes of Raised IOP in Glaucoma
1. Hypersecretory Glaucoma - Excess
secretion of aqueous humour, -
epidemic dropsy.
2. Obstruction of flow of aqueous
humor from posterior chamber to
anterior chamber, - pupillary block
glaucoma.
3. Blockage of angle - due to peripheral
anterior synechiae /apposition in PACG.
4. Blockage of aqueous outflow- due
to sclerosis of the trabecular meshwork
in POAG.
5. High episcleral venous pressure -
Sturge Weber syndrome.

8. c d
a b
a. Pre-trabecular - membrane over
trabeculum
b. Trabecular - ‘clogging up’ of trabeculum
c. Post trabecular – raised episcleral veinous
pressure
Open-angle
d. With pupil block - seclusio pupillae and
iris bombé
e. Without pupil block - peripheral anterior
synechiae
Angle-closure
Cause of Secondary glaucomas

9. Factors associated with Glaucoma
• IOP>21mmHg
• Age
• Race: 4.3times higher in Africans
• corneal thickness < 550microns (there is increase 30-40% chance of developing
glaucoma per 40 microns thinner cornea)*
• Positive family history
• Moderate association
– Myopia
– Sex F:M-2:1 for NTG
– Diurnal variation of IOP
• Weaker association
– DM
– Migraine and other vasospasm disorder - NTG
– Sleep Apnea - NTG
– Systemic Hypertension
*

10. Mechanism of Optic Nerve damage
• Mechanical- elevated IOP
• Vascular- insufficient blood supply to the ONH.
• Neurochemical
– A third proposed mechanism of neuronal injury is
one of a neurochemical nature. Glutamate
excitotoxins (excitatory neurotransmitters), NO,
Endothelins

11. Trophic
insufficiency

12. Anatomy
a - Uveal meshwork
b - Corneoscleral meshwork
c - Schwalbe line
d - Schlemm canal
e - Collector channels
f - Longitudinal muscle of
ciliary body
g - Scleral spur
c - Iris outflow
a - Conventional outflow (85–90%)
b - Uveoscleral outflow
Physiology
Mean aqueous
humor production
rate - 2.2 to 3.1 μL
per minute. ( ~1.5
μL/min during the
night and 3 μL /min
during the day)
1. Ultrafiltration
2. Diffusion
3. Active secretion
• 80–90 percent of
total aqueous
humor
formation.
Aqueous outflow

13. Ultrastructure of the trabecular
meshwork
• The trabecular meshwork comprises of sheets of connective
tissue lined by endothelium
• Fenestrated with pores of size ranging from 75 to 5 µm
• The extra cellular matrix comprises of endogenous
metalloproteinases which are responsible for ECM turnover
and maintenance of aqueous outflow
1. Uveal meshwork
2. Corneoscleral meshwork
3. Juxtacanalicular meshwork

14. Examination Techniques

15. Examination Techniques
• Visual Acuity Testing
• Pupillary response
• IOP (done before gonioscopy)
• Pachymetry – ( Ultrasonic or optical)
• Slit-Lamp Biomicroscopic Examination
– Cornea
– AC, Angle (Gonioscopy)
– Iris
– Lens
– Vitreous
– Retina
– Disc
• Documentation by Imaging and functional test.
• Stereo disc photography

16. Intra-Ocular Pressure
• Definition-
• Normal IOP 10-21mmHg
Circardian variation in IOP > 8 mm Hg
Asymmetry of IOP > 5 mm Hg

17. Tonometry
• Indentation Tonometry
– Schoitz
• Applanation Tonometry
– Goldmann
– Perkins
– MacKay-Marg
– TONO-Pen
– Pascal Dynamic Contour Tonometry ( accurately measure the true IOP irrespective of the corneal
thickness.)
• iCare (The tonometer measures the deceleration of the probe and the rebound time, and calculates
the IOP from these parameters.)
• Non-contact Tonometry (air puff tonometry)

18. Goldmann
Contact applanation
Perkins
Portable contact applanation
Pulsair 2000 (Keeler)
Air-puff
Schiotz
Portable non-contact applanation
Non-contact indentation
Contact indentation
Tono-Pen
portable contact applanation
Icare® TA01i
Rebound tonometer
The Mackay–Marg Tonometer
Applanation-type device
The pneumatic tonometer
Pascal Dynamic Contour Tonometry
Tonometers

19. Schwalbe line
Schlemm canal
Trabeculum
Scleral spur
Ciliary body
Angle structures

20. Gonioscopy
Gonioscopy can be used for:
1. Diagnostic
• Angle access is narrowed with appositional closure (occludable):
configuration with imminent risk angle of an acute closure glaucoma.
• Occluded angle: Primary angle closure glaucoma.
• Angle is occluded with s/o secondary angle closure glaucoma, for example
due to neovascularization in rubeosis iridis.
• Open angle: open angle glaucoma.
• Angle open but with inflammatory cellular deposits, erythrocytes, or
pigment in the trabecular meshwork: secondary open angle glaucoma.
• Traumatic angle recession
• Blood in Schlemn’s cannal
• Trabecular dysgenesis
• Patency of trabeculectomy, shunt
2. Therapeutic – laser trabeculoplasty, laser goniopuncture, goniotomy,
3. Indentation gonioscopy to detect appositional closure, break the
acute ACG attack

21. Gonioscopy
• Optically
– Direct Gonioscopes
• Koeppe
• Barkan
• Swan-Jacob
– Indirect Gonioscopes
• Goldmann
• Posner
• Zeiss
• Imaging
– UBM
– Anterior Segment OCT
– Scheimpflug
photography
– Ret Cam Gonioscopy
– Gonio-photography

22. Koeppe direct gonioscopy with Haag Streit stereoscopic
viewer suspended from the ceiling
The Koeppe lens magnifies the image 1.5x

23. Goldmann Zeiss
• Single or triple mirror
• Contact surface diameter 12 mm
• Coupling substance required
• Suitable for ALT
• Not suitable for indentation gonioscopy
• Manupulation gonioscopy can be done
• Four mirror
• Contact surface diameter 9 mm
• Coupling substance not required
• Not suitable for ALT
• Suitable for indentation gonioscopy
Goniolenses

24. Posner, Sussman, and Zeiss lenses (top to bottom).

25. Differentiates ‘appositional’ from ‘synechial’ angle closure
Press Zeiss lens posteriorly
against cornea
Aqueous is forced into
periphery of anterior chamber
The lower the initial pressure, the easier the examination; if the pressure is extremely high, indentation
may be difficult. As the IOP nears 40 mmHg, the ability to move the peripheral iris is lost. (J -2559)
Indentation gonioscopy

26. Indentation gonioscopy in iridocorneal contact
• Part of angle is forced open
During indentation
• Part of angle remains closed by PAS
• Complete angle closure
Before indentation
• Apex of corneal wedge not visible

27. Van Herick Method
Closed angleabsent peripheral AC
Slit angle AC depth = Slit-like
Grade 1 angle AC depth <1⁄4 corneal
thickness
Grade 2 angle AC depth = 1⁄4 corneal
thickness
Grade 3 angle AC depth = 1⁄4 to 1⁄2
corneal thickness
Grade 4 angle AC depth = Corneal
thickness

28. 3 2 1
0
4
• Ciliary body easily visible
Grade 4 (35-45 )
Grade 2 (20 )
Grade 1 (<10 )
• Upto trabeculum visible
• Schwalbe line and perhaps
top of trabeculum visible
• High risk of angle closure
• Iridocorneal contact present
• Apex of corneal wedge not visible
• Angle closure possible but unlikely
• Use indentation gonioscopy
to know appositional closure
Grade 0 (0 )
• Upto scleral spur visible
Grade 3 (25-35 )
0
1 2 3
4
Shaffer grading of angle width1960

29. Spaeth’s system of descriptive grading included three components:
(1) angular width of angle recess,
(2) Peripheral iris configuration, and
(3) insertion site of the iris root

30. RPC System of Grading of angle
Grade 0 — Closed
Grade 1 — Schwalbe’s line
Grade 2 — Anterior (non pigmented) TM
Grade 3 — Posterior pigmented TM
Grade 4 — Scleral spur
Grade 5 — Ciliary body band
Grade 6 — Root of iris

31. Diagnostic gonioscopy in POAG

32. Horizontal
raphe
Retinal nerve fibres
Papillomacular
bundle
Horizontal
raphe

33. Examination of the optic nerve
• Methods
1.slit-lamp biomicroscope with a handheld lens/
contact lens
2.Direct Ophthalmoscopy
3.Indirect Ophthalmoscopy
4.Fundus Photography
5.Posterior segment ocular imaging
6.Visual field

34. Particular of Optic disc to be evaluated
1.Disc Size
2.Cup
3.Color
4.Contour of neuroretinal rim
5.Peripapillary Atrophy
6.Vessel Caliber
7.ISNT Rule
8.NFLD

35. Perimetry
• Subjective
– Kinetic :- Confrontation, tangent screen, Goldmann
perimeter
– Static :- Humphrey, Octopus
• Purpose:-
– Diagnosis of glaucoma,
– Differentiation from neurological field defect
– Assessing severity of disease,
– Planning of management and follow up
– Legal issue (Legal blindness is defined as BCVA in the better eye < to 20/200 or a visual
field extent of < 20 degrees in diameter)

36. Advantage of Perimetry
• Advantages of manual kinetic perimetry:
1. Easier for some patients
2. More flexible
3. Better examination of peripheral visual field
• Advantages of automated static perimetry
1. Shorter test duration
2. Reproducible standardized testing conditions
3. No examiner bias
4. Can compare visual fields obtained in different centers
5. Availability of normative data
6. Sophisticated statistical analysis and more accurate monitoring
7. Better data storage capabilities
8. Higher sensitivity
9. Stimuli presentation at random locations and therefore, (1) improved
patient fixation and (2) absence of local retinal adaptation
10. No need for highly trained perimetrists

37. Characteristics of Glaucomatous Field Defect
• Almost always localized
• Begin nasal to the blind spot
• Almost always detectable within the central 30°
• As the arcuate fibers do not cross the horizontal
midline, most glaucomatous visual field loss respects
(i.e. doesn’t cross) the horizontal midline.
• As nasal fibers and the maculopapular bundle are
typically spared until late in the disease process, it is
common to have a central or temporal island of
vision remaining in eyes with advanced glaucoma

38. Progression of glaucomatous visual field defect
• Nasal step
• Enlargement of the blind spot
• Seidel’s scotoma
• Isolated paracentral scotomata (within central 10°)
• Arcuate defects
• Ring scotoma
• Split fixation
• Central and temporal islands
• Clover leaf pattern (typical "clover leaf" pattern fairly characteristic of a fatigue field with high false negatives. Here,
initially the patient performs well and then become progressively less responsive.)
• One of the earliest presentations of glaucomatous visual field loss can be increase in short-term (intra-test) and long-term
(inter-test) fluctuations.
• Bjerrum area, 10-25° from fixation

39. Reliability Indices
1. Fixation Loss
2. False positive
3. False negative
• Are flagged if exceed 33%
4. Short Term fluctuation
• < 2.5 = Good Accuracy

40. Scotoma
• A scotoma is an area of visual loss or depression
surrounded by an area of normal or less depressed vision.
• A scotoma is diagnosed (Anderson’s Criteria) when three
contiguous non edge points on the pattern deviation plot
within Bjerrum's area (non contiguous with blind spot) on
two consecutive visual fields have a probability of <5% of
being normal. At least one of these three points must have
a P<1% of being normal.
• CPSD < 5%
• GHT – Abnormal / outside normal limits
Nasal step can be excluded from Anderson’s Criteria
• The glaucoma hemifield test (GHT) compares the sensitivity of five clusters of points above and
below the horizontal midline which resemble nerve fibre bundle patterns.

41. Pattern deviation
• The Humphrey field analyzer also provides
printouts
• In total deviation , which is the difference
between the measured threshold for each retinal
point tested and the age-corrected normal, and
• In pattern deviation , which is created from the
total deviation by adjusting it an amount equal to
an average of the 17 worst test points.
– This helps eliminate “background noise,” such as the
generalized depression of a cataract.

42. The cumulative defect (Bebie curve) curve

43. Histopathologic data revealed that axonal loss as great as
35% may precede the appearance of kinetic visual-field
defects¹¹, and a 20% loss of large retinal ganglion also may
be present with static visual-field loss of 5 dB¹².
11. Optic nerve damage in human glaucoma. III. Quantitative correlation of nerve fiber loss and visual field
defect in glaucoma, ischemic neuropathy, papilledema, and toxic neuropathy. Arch Ophthalmol 1982; 100:135.
12. Retinal ganglion cell atrophy correlated with automated perimetry in human eyes with glaucoma. Am J
Ophthalmol 1982; 107:135.

44. Progression of Glaucomatous Field defect.
From early to advanced
glaucomatous field defect

46. Scotoma
• Relative scotoma
– An area of the visual field in which perception of light is
only diminished, or loss is restricted to light of certain
wavelengths.
• Negative scotoma
– Scotoma appearing as a blank spot in the visual field; the
patient is unaware of it, and it is detected only by
examination.
• Positive scotoma
– One which appears as a dark spot in the visual field.
• Absolute scotoma
– An area within the visual field in which perception of light
is entirely lost.

47. Diagnosis of Preperimetric Glaucoma
• Confocal scanning laser Topography (HRT) - 670 nm
wavelength light from a diode laser
• Scanning laser polarimetry (GDxVCC) utilizes the
birefringence of the retinal NFL, uses 780 nm diode laser
• Optical coherence tomography - utilizes infrared, low-
coherence superluminescent diode at a wavelength of 810 nm
• Frequency doubling perimetry - large M-type ganglion cells are
preferentially affected in early glaucoma. (The stimuli are 5° squares of black and white grating with
a low spatial frequency which undergo a counter-phase flicker at a high temporal frequency).
• Short-wave automated perimetry (SWAP) Used in Early
glaucoma. It is believed that patients with glaucoma develop a tritan-like (blue-green) deficiency.
SWAP is designed to isolate the short wavelength (blue) pathway. It uses large, blue stimuli which
are presented on the bright yellow background. Brunescing lens acts as a yellow filter.

48. GDx VCC (variable corneal compensation) A number
between 0 and 30 is considered normal, between 30
and 50 is borderline, and a value of 50–100 is
considered highly suspicious for glaucoma.
Heidelberg Retinal Tomograph of a glaucomatous
eye (red X’s in areas of NFL thinning, and yellow in
areas with borderline NFL thickness per MRA)

49. Glaucoma-protocol OCT showing optic nerve
head, peripapillary retinal nerve fibre layer and
ganglion cell complex analysis
Frequency-doubling test (FDT). Large
diameter axon (magnocellular) ganglion cells appear to
be preferentially lost in early glaucoma.

50. SWAP
SWAP utilizes the koniocellular
pathway
Near-normal and severely
damaged visual fields will both
have low PSD.

51. Provocative tests
• Water drinking test
– Following a baseline intraocular pressure (IOP) measurement, the subject quickly
consumes one liter of water and undergoes subsequent IOP measurements every 15
minutes for one hour.
– A rise in IOP of 6 to 8 mmHg or an increase from baseline of 30% or more at any time
during the hour was considered a positive test.
• Dark room test A test is considered positive if the IOP increases by 8 or more mmHg.
Patient is seated in a dark room for 1 hours to dilate the pupil and increase resistance at the
lens-iris channel.
• Prone position test – Patient is placed in the prone position for 1 hour without
sleeping to anteriorly displace the lens and increase pupillary block.
• Mydriatic test – They carry a significant risk of angle closure in patient without
patent iridotomy. Considered positive if the IOP increases by 8 or more mmHg.
Use
• In partially opened angles post-iridotomy, to determine whether further intervention (e.g.
iridoplasty) might be appropriate or not. To check functionality of iridotomy.
• Combining anterior chamber imaging (e.g. ultrasound biomicroscopy) with provocative
testing assists in detecting apposition and allows measurement of various parameters of the
angle, but their ability to predict future angle closure is not well established.
IOP normal, angle normal/suspicious, disc suspicious, doubtful investigation/iridotomy

52. Anterior Segment Imaging in Glaucoma
• Anterior Segment OCT
• UBM

53. RECEPTOR ACTIVATION WILL: TO LOWER IOP, AIM FOR:
IRIS, Circular Fibers mAchR : Constrict Pupil  Activity
IRIS, Radial Fibers 1 R : Dilate Pupil  Activity
CILIARY MUSCLES mAchR : Contract for Accomodation
2 R : Relax for Far Vision
 Activity
Activity
Autonomic NS Effect on the Eye

54. Drugs used in glaucoma
• Topical IOP lowering Drugs
– Beta blockers (Timolol, Levobunolol , and Betaxolol )
– Sympathomimetics (epinephrine and dipivefrin )
– Prostaglandin analogues (latanoprost , bimatoprost, travoprost and
taflumaprost )
– Alpha2-adrenergic agonists (Brimonidine, Apraclonidine)
– Miotics (pilocarpine)
– Carbonic anhydrase inhibitors (dorzolamide , brinzolamide )
– RKIs are Ripasudil (K-115) and Netarsudil (AR-13503). Netarsudil dimesylate
(Rhopressa 0.02%) is both an RKI and a norepinephrine transport inhibitor (Rho is a
group of small GTP-binding proteins. These proteins aid in regulation of cell structure, motility, division, and apoptosis)
• Systemic IOP lowering Drugs
– Carbonic Anhydrase Inhibitor
• Acetazolamide oral and IV
– Hyperosmotic Agents
• Mannitol- Intravenously can decrease the IOP 30 mm Hg or more within 30 minutes of administration. The
recommended intravenous dose is 0.5-1.5 g/kg body weight as a 15% or 20% solution, delivered at 3 to 5
mL/minute
• Glycerol- orally - 1 to 1.5 g/kg body weight of a 50% solution. Onset of pressure reduction is 10 to 30
minutes. Avoid in diabetics
• Isosorbide - as a 45% (45 g/100 mL) solution (Ismotic ). The recommended dose is 1 to 1.5 g/kg body
weight. Its effect is similar to glycerin’s but is safe for use in diabetics because it is not metabolized.
• Neuroprotective drugs- Memantine, Citicholine

55. Beta-blocker/sympathomimetics
• Nonselective beta blockers
– Timolol preparations: Timolol maleate 0.25 and 0.50%; Preservative free timolol 0.25 and
0.50%; Timolol maleate gel-forming solution 0.5%; Timolol hemihydrate 0.25 and 0.50%
– Levobunolol hydrochloride 0.25 and 0.50%
– Carteolol hydrochloride 1%
– Metipranolol hydrochloride 0.3%
• Selective beta-1 blocker
– Betaxolol hydrochloride suspension 0.25%, 0.5%.
• Decrease aqueous production, mediated by an effect on the ciliary epithelium.
• In approximately 10% of cases the response decreases with time (Tachyphylaxis),
• Beta-blockers can be used in esp.
1. Mono ocular glaucoma to avoid skin darkening and/or conjunctival hyperaemia
with prostaglandins,
2. Ocular inflammation,
3. Cystoid macular oedema, or
4. In patients with history of herpes simplex keratitis.
• Beta-blockers should not be instilled at bedtime as they may cause a profound
nocturnal hypotension, thus reducing optic disc perfusion and potentially causing
visual field deterioration;

56. Beta-blocker / sympathomimetics
• Side effects
– Ocular. include allergy and punctate keratitis. Granulomatous uveitis has been
reported with metipranolol.
– Systemic.
• Exacerbation of asthma
• Exclude Heart block, bradycardia, worsening of heart failure and hypotension.
• Cautious use in patients with peripheral vascular disease, including Raynaud
phenomenon.
• Less severe side effects include sleep disorders, reduced exercise tolerance,
hallucinations, confusion, depression, fatigue, headache, nausea, dizziness, decreased
libido and dyslipidaemia.
• Less-selective sympathomimetics like epinephrine and dipivefrin
• Increase aqueous outflow through trabecular meshwork and possibly through
uveoscleral outflow pathway, by a beta 2-agonist action.
• Maximal response may take several months. Cause a 22–28% decrease in IOP.
• Local SE was much lower with dipivefrin. Reversible CME
• Dipivefrin also causes a distinctive follicular conjunctivitis like GPC
• Systemic side effects that may result from systemic absorption of either
epinephrine or dipivefrin include pallor, perspiration, syncope, and elevation
of pulse and blood pressure.

57. Prostaglandin analogues
– The mechanism of action is unclear but the upregulation of matrix
turnover within the ciliary body, and perhaps the trabecular
meshwork, has been suggested. Relaxation of the ‘elastic tissue
elements’ in the interstitial spaces of the ciliary muscle has also been
suggested.
– Enhancement of uveoscleral aqueous outflow,
– Increased trabecular outflow facility.
– Excellent nocturnal and overall diurnal IOP control.
– Minimal drift in IOP control over time. Lowers IOP from 27% to 34%
typically preferred to a beta-blocker as firstline treatment.
Agents
• Latanoprost (0.005%)
• Travoprost (0.004%) is similar to latanoprost, though it may lower
IOP to a slightly greater extent, particularly in black patients.
• Bimatoprost have a greater IOP-lowering effect . A newer 0.01%
(versus the older 0.03%) preparation with less hyperaemia.
• Tafluprost (0.0015%) . Its IOP-lowering efficacy may be slightly less
than that of other PG agents, but well tolerated.
• Unoprostone 0.15% lower IOP ~3–4 mmHg

58. Prostaglandin analogues
Side effects
• Ocular
– Conjunctival hyperaemia is very common.
– Trichomegaly, Eyelash thickening,
hyperpigmentation and occasionally increase in
number.
– Irreversible iris hyperpigmentation occurs in
upto 1/4th of patients after 6 months.
– Reversible Hyperpigmentation of periocular skin.
– Preoperative use of PG agents  CME following
cataract surgery. Stop PG 1 week Preop and 4-6
week Postop.
– Periorbital fat loss especially with bimatoprost.
– Reactivation of herpetic keratitis.
– To be used with caution in inflamed eyes, though
Anterior uveitis is rare.
• Systemic side effects are few include
occasional headache, precipitation of
migraine in susceptible individuals, malaise,
myalgia, skin rash and mild upper respiratory
tract symptoms.

59. Alpha-2 agonists
• Alpha2-adrenergic agonists such as brimonidine work by a dual
mechanism, decreasing aqueous production and increasing uveoscleral
outflow.
– There is probably a neuro protective effect.
– They cross the BBB and used with great caution in young children, with
reported severe CNS depression and hypotension, so Contraindicated under 2
years.
– They may potentiate vascular insufficiency.
– Risk of hypertensive crisis with oral MAO inhibitor.
Agents
• Brimonidine 0.2%
– Allergic conjunctivitis common & onset may be delayed for up to 18 months.
– Granulomatous anterior uveitis rare.
– Systemic side effects include xerostomia and fatigue.
• Apraclonidine 1% (or 0.5%)
– Used to prevent or treat an acute rise in IOP post laser surgery.
– Loss of therapeutic effect over weeks to months and a high incidence of local
side effects.
– used with caution in patients with a history of angina, severe coronary
insufficiency, recent myocardial infarction, overt cardiac failure, hypertension,
including apoplexy, cerebrovascular disease, Parkinson's syndrome, chronic
renal failure, Raynaud's disease or thromboangiitis obliterans.

60. Miotics
• Miotics are cholinergic agonists – used mainly in the treatment of angle
closure glaucoma.
• Mechanism
– Contraction of the sphincter pupillae - pulls the peripheral iris away from the
trabeculum, opening the angle.
– Contraction of the ciliary muscle, which increases the facility of aqueous
outflow through the trabecular meshwork.
• Local side effects include miosis, browache, myopic shift and exacerbation
of the symptoms of cataract, rarely RRD.
• Visual field defects appear denser and larger.
• Systemic side effects - rare but include diaphoresis, salivation, nausea,
confusion, bradycardia, bronchospasm, gastrointestinal symptoms and
urinary frequency. J
• Contraindicated in uveitic or neovascular glaucoma.
• Agents
– Pilocarpine 0.5%, 1%, 2%, or 4% solution as four times daily.
– Pilocarpine gel 4% is instilled once daily at bedtime.
– Carbachol (0.75–3% solution given three times daily) is an alternative to
pilocarpine

61. Miotics
• Pilocarpine e/d- miosis occurs in 15–30 min, maximal
reduction of IOP occurs in 2–4 h, with a total duration of 4–
8 h.
• Pilocarpine gel may be particularly useful for patients with
pigment dispersion for consistent miosis.
• Indirectly acting miotics- has extended duration of action ,
which can be as long as 7–21 days with echothiophate (Phospholine
iodide) 0.125%.
• Strong miotics should be discontinued for several weeks
before intraocular surgery
– To prevent the possibility of severe fibrinous postoperative iritis,
– To minimize the inhibition of systemic pseudocholinesterases
that reverse anesthetic drugs such as succinylcholine

62. Carbonic anhydrase inhibitors
• Carbonic anhydrase inhibitors like dorzolamide, brinzolamide ,
acetazolamide lower secretion of aqueous humor by inhibiting carbonic
anhydrase in the ciliary body.
• Via the topical route are used three times daily as monotherapy or twice
daily as adjunctive treatment.
• Have a supplementary neuro-protective effect.
Agents
• Dorzolamide. 2%
• Brinzolamide 1% It is a suspension, and a white residue may be left on
the eyelids after instillation if excess is not wiped away.
• Acetazolamide is available as 250 mg tablets (250–1000 mg daily in
divided doses), sustained-release 250 mg capsules (250–500 mg daily)
and 500 mg powder vials for injection (single dose, typically used in acute
angle-closure glaucoma).
• Dichlorphenamide 50 mg tablets (50–100 mg two or three times daily).
• Methazolamide 50 mg tablets (50–100 mg two or three times daily);

63. Carbonic anhydrase inhibitors
Side effects.
– Stinging and a transient bitter taste; allergic
blepharoconjunctivitis, Less with brinzolamide.
– Corneal decompensation , but some benefit in the treatment of
CME
– Topical (and systemic) CAI are relatively contraindicated in
patients allergic to sulfonamide antibiotics.
– Idiosyncratic aplastic anaemia (bone marrow suppression)
(exceptionally rare but with 50% mortality).
– Other Side effect of CAIs
• Ocular - Choroidal effusion, particularly after cataract surgery. Angle
closure may result.
• Systemic. Paraesthesia , hypokalaemia , malaise and lowered mood,
gastrointestinal symptoms, renal stones, Stevens–Johnson syndrome
(very rare), dose-related bone marrow suppression,
• Concomitant treatment with a topical and systemic CAI
does not usually give an additive effect.

64. Osmotic agents
• Mechanism- create an osmotic gradient so that water is ‘drawn out’ from
the vitreous into the blood  lower IOP .
• Use - For a short-term reduction in IOP is required that cannot be achieved
by other means, such as in resistant acute angle-closure glaucoma or
when the IOP is very high prior to intraocular surgery.
• They are of limited value in inflammatory glaucoma, in which the integrity
of the blood–aqueous barrier is compromised.
• Side effects include cardiovascular overload (caution in patients with
cardiac or renal disease), urinary retention (especially elderly men),
headache, backache, nausea and confusion.
Agents
• Mannitol is given intravenously (1 g/kg body weight or 5 ml/kg body
weight of a 20% solution in water) over 30–60 minutes; peak action occurs
within 30 minutes.
• Glycerol is an oral agent (1 g/kg body weight or 2 ml/kg body weight of a
50% solution). Peak action occurs within 1 hour. Avoid in diabetic patient.
• Isosorbide is a metabolically inert oral agent with a minty taste; the dose
is the same as for glycerol. Safer for diabetic patients.

65. Glaucoma treatment in pregnancy
• All glaucoma medications should be avoided during the first trimester of
pregnancy, if possible; systemic carbonic anhydrase inhibitors and
prostaglandin analogs should be avoided absolutely.
• There are no glaucoma medications that fall into category A.
• Brimonidine is a category B drug, but it has been shown to cross the
placenta and could potentially cause apnea in neonates if used through
parturition.
• Beta blockers, CAIs, prostaglandin analogs, and parasympathomimetics
are classified as category C.
• Category A: safety established using human studies
• Category B: presumed safety based on animal studies
• Category C: uncertain safety; no human studies; animal studies show
adverse effect
• Category D: unsafe; evidence of risk that in certain clinical circumstances
may be justifiable

66. Glaucoma treatment in pregnancy
• If pregnancy is established and treatment is necessary, laser
trabeculoplasty (LTP) is probably the best initial therapy.
• If medications cannot be stopped then the use of beta blockers,
(cholinergics, topical CAIs, and alpha agonists can be continued).
• Filtering surgery (avoid antimetabolite) can be considered if glaucoma is
progressive and an adequate IOP cannot be obtained with LTP or with the
medications mentioned above.
• Treatment in nursing mother
– Topical CAIs, prostaglandins, and miotics are reasonable choices during
lactation.
– Beta blockers are concentrated in breast milk and should be avoided while
nursing
– Alpha agonists should be avoided since their excretion into human breast milk
is unknown.
– Systemic CAIs should be used with caution or avoided all together to be safe.
– If surgery is planned, breast milk should be stored in order to have milk
unaffected by anesthetic agents.

67. Prevention
• Regular life long screening for Early detection of glaucoma is only
preventive tool.
• Early diagnosis and treatment is the best way to prevent vision loss from
glaucoma.
• Increasing awareness about high risk in population.
Preventive Measures advocated at individual level include –
• Regular eye care – Regular eye examinations are recommended once in
every 2/3 years after the age of 40 and every year after the age of 60.
Frequent screening for Individuals with risk factors for glaucoma.
• Treatment and follow up – Required lifelong even if no symptoms.
• Control of systemic diseases –
• Develop a healthy lifestyle – to prevent and control systemic illnesses.
• Protective eye wear – For those using power tools and high speed sports.
• Cautious use of steroids – e.g. Allergic conjunctivitis. Avoid or use for a
short period with regular IOP checks.
With regular treatment and follow up, most patients can preserve a good
quality of vision throughout their lifetime.

68. Ocular hypertension
• Ocular hypertension (OHT) is a term reserved for eyes
1. In which the IOP lies above the normal population range,
2. Open angle
3. The optic nerve and visual field show no signs of
glaucomatous damage, and
4. There is no ocular co-morbidity. E.g. Pseudoexfoliation
and pigment dispersion syndrome are excluded.
• Single/intermittent/persistent
• The percentage of people with an IOP > 22 mmHg in the absence of glaucoma
range from 1% to 4% in most population-based studies
• 4–10% of the population over the age of 40 years have OHT
K
(IOP >21 mmHg
without detectable glaucomatous damage)

69. Risk factors for conversion of OHT to POAG
• Ocular risk factors
– Height of IOP
– Large vertical cup/disc ratio, C/D ratio asymmetry>0.2
– CCT
• Systemic risk factors
– Increasing age
– Race, African-American race was associated with a higher glaucoma
risk.
– Pattern standard deviation (PSD). A greater PSD result represented a
significant risk.
– Gender. Males were more likely to convert.
– Heart disease significant risk factor.
• Factors, not found to be significant in the OHTS.
– Myopia,
– Diabetes..
– Family history of glaucoma was not found to be a risk factor for
conversion.
• Factors not examined in the OHTS but may be important include
RNFL defects and specific peripapillary atrophic changes

71. Management of OHT
• When to Treat as OHT Study
– IOP>35mmHg
– Associated high risk factor
Management
• In the OHTS, untreated patients with ocular hypertension had a 9.5% cumulative
risk of developing POAG after 5 years;
• Treatment (which aimed to reduce IOP by 20% or more and to reach 24 mmHg or
less) reduced this to 4.4%.
• In general, only higher risk cases treated, though patient preference may be a
decisive factor.
• Age, and so life expectancy, is a key point to consider.
• OHT increases the risk of retinal venous occlusion, an additional point to start
treatment.
• Treatment options same as for POAG,
– A less aggressive pressure-lowering approach is frequently taken, e.g. alternate day
prostaglandin dosing
– Low intensity selective laser trabeculoplasty ;
– Filtration surgery is occasionally indicated.
– Cataract surgery commonly results in a significant IOP reduction.
• Careful monitoring is reasonable in many circumstances: with baseline visual
fields and RNFL/disc imaging .

72. POAG
Dr. Rajeev Kumar
 sl. 8

73. IOP > 21 mmHg
Glaucomatous disc damage
Open angle of normal appearance
Visual field loss
Absence of signs of
secondary glaucoma or a
non glaucomatous
cause for the optic
neuropathy.
IF IOP <21  NTG
Definition

74. Risk Factors
1. IOP. The higher the IOP, the greater the chance of glaucoma.
– IOP > 21 mm Hg
• Circardian variation in IOP > 8 mm Hg
• Asymmetry of IOP > 5 mm Hg
2. Age - most cases present after age 65 years
3. Race - more common, earlier onset and more severe in blacks
4. Family history of POAG
– Level of IOP, outflow facility and disc size are inherited
– Risk is increased by 2 times if parent has POAG
– Risk is increased by 4 times if sibling has POAG
5. Myopia

75. Risk Factors
6. ONH changes
1. CD Ratio > 0.5
2. Asymmetry between two ONH > 0.2
3. Narrowing, Notching, Pallor of Neuroretinal rim, Disc hemorrage Blood
vessel abnormality
7. Contraceptive pill. Long-term use of the OCP
8. Vascular disease. Systemic hypertension, cardiovascular disease,
diabetes and vasospastic conditions such as migraine have all been
implicated. Poor ocular perfusion may be a risk factor for glaucoma
progression.
9. Translaminar pressure gradient. Difference in the levels of IOP and
orbital CSF pressure may increase the likelihood of the development and
progression of glaucomatous damage, perhaps due to associated
deformation of the lamina cribrosa.
10. Optic disc area. Large discs associated with laminar deformation.
11. Ocular perfusion pressure = Mean arterial BP - IOP,
– linked to increased risk for the development and progression of glaucoma.¹
1.Curr Opin Ophthalmol. 2009 Mar; 20(2): 73–78.

76. History
• Visual symptoms - usually be absent, unless damage is advanced.
• Generally asymptomatic or Non specific complain such as Headache and frequent change of
presbyopic glasses
• Inferior scotoma
• Difficulty in dark adaptation
• Previous ophthalmic history.
– Refractive status (myopia -- POAG), and (hypermetropia -- PACG).
– Causes of secondary glaucoma such as ocular trauma or inflammation; previous eye surgery, including
refractive surgery, may affect IOP readings.
• Family history
– POAG or OHT.
– Other ocular disease in family members.
• Past medical history.
– Asthma, heart failure or block, peripheral vascular disease: contraindicates the use of beta-blockers.
– Head injury, intracranial pathology including stroke: may cause optic atrophy or visual field defects.
– Vasospasm: migraine and Raynaud phenomenon.
– Diabetes, systemic hypertension and cardiovascular disease may increase the risk of POAG.
– OCP use for several years may increase risk of glaucoma.
• Current medication
– Steroids including skin cream and inhalants.
– Oral beta-blockers may lower IOP.
• Social history including smoking and alcohol intake, especially if toxic/nutritional optic
neuropathy is suspected.
• Allergies to drugs, e.g. sulfonamides.

77. Examination
• Visual acuity is normal except in advanced glaucoma.
• Pupils. Exclude RAPD; if initially absent but develops
later  substantial progression.
• Colour vision assessment in optic neuropathy other
than glaucoma.
• Slit lamp examination. Exclude features of secondary
glaucomas such as pigmentary and pseudoexfoliative.
• Tonometry , pachymetry.
• Gonioscopy.
• Optic disc examination. Red-free light for RNFL
defects.

78. Diagnostic Gonioscopy in Glaucoma with Open Angle

79. a. Normal (c:d ratio 0.2)
b. Concentric enlargement
(c:d ratio 0.5)
c. Inferior expansion with
retinal nerve fibre loss
e. Advanced cupping with nasal
displacement of vessels
f. Total cupping with loss of
all retinal nerve fibres
d. Superior expansion with
retinal nerve fibre loss
Progression of glaucomatous cupping

80. Normal Slit defects
Wedge defects Total atrophy
Progression of nerve fibre damage

81. • All neural disc tissue is destroyed
• Disc is white and deeply excavated
• Atrophy of all retinal nerve fibres
• Striations are absent
• Blood vessels appear dark and sharply defined
End-stage damage

82. Investigation
• Pachymetry for CCT.
• Perimetry should usually be performed prior to
clinical examination.
• Imaging of the optic disc, peripapillary RNFL
and/or ganglion cell complex,
– Red-free photography,
– Stereo disc photography,
– OCT,
– Confocal scanning laser ophthalmoscopy and/or
– Scanning laser polarimetry.

83. Management
Purpose of treatment
– The primary aim of treatment is to prevent functional impairment of
vision within the patient’s lifetime by slowing the rate of ganglion cell
loss closer to that of the normal population.
– Control of IOP
– To protect the Nerve fiber layer damage from oxidative radicals
– To increase the blood flow to optic nerve head
Patient instruction
• An explanation should be offered concerning the nature of the
disease.
• The timing of medication use should be specified, and the patient
educated in the technique of eye drop instillation.
• Lacrimal sac occlusion by applying fingertip pressure at the medial
canthus or to close the eyes for about 3 minutes after instillation.
• Common or severe potential adverse effects should be explained

84. Treatment goals
• Target pressure.
– A range of IOP low enough to limit progression of visual field loss to a
rate that will preserve the patients’ visual function and individual
patterns of daily living.
– This is identified taking into account the severity of existing damage
(vertical C/D ratio and a greater mean deviation on visual fields), the
level of IOP, CCT, the rapidity with which damage occurred if known,
and the age and general health of the patient, life expectancy.
– 20–25% reduction may produce a more physiologically normal
pressure that will prevent further optic nerve damage.
– With moderate damage exhibiting consistently reproducible field
defects in both hemifields, a larger percentage of IOP reduction in the
range of 25–30% or more is usually required,
– With severe damage, the target IOP range needs to be ‘subnormal’,
ordinarily less than 15 mmHg.

85. Treatment goals
• Proportional reduction. An alternative strategy is to aim for a
reduction in IOP by a certain percentage – often 30% – and then
monitor, aiming for a further reduction if progression occurs.
• Response to progression..
– If damage progresses despite a target pressure, the target IOP is set to
a lower level;
– Each 1 mmHg reduction in IOP leads to a 10% reduction in the rate of
nerve fibre loss.
– If further damage is sustained despite apparently good IOP control,
surgery may be appropriate.
• Commencing medical therapy
– Initial treatment is usually with one type of medication, typically a
prostaglandin analogue or beta-blocker.
– Better to start the drug with the fewest potential side effects

86. Treatment Options

87. Therapeutical Algorithm in Glaucoma
Topical Therapy
4-8 wks
3-6 months
4-8 wks
4-8 wks

88. Assessing a Trial Medication Period
Efficacy
IOP reduction during initial medication
appropriate 1-6 week trial
Follow up for diurnal and inter-visit
variability
Safety
Ocular side effects
Systemic side effects
Acquiescence of primary care physician
Compliance
Technique of applying drops
Use of medication schedule
Rate of defaulting
Affordability
Degree of understanding of disease
process

89. Surgical Procedures
Procedures that facilitate outflow of aqueous humor
– Laser trabeculoplasty
– Argon laser trabeculoplasty (ALT)
– Selective laser trabeculoplasty (SLT).
– Iridotomy / Iridectomy
– Filtering procedures: penetrating and non-penetrating
Cyclodestructive procedure
– Cyclo-cryo
– Trans scleral Laser cyclophoto therapy
– Endo cyclo photocoagulation
Prognosis
– The great majority of POAG pt will not become blind in their lifetime,
– Incidence of blindness varies depending on factors such as the presence of
advanced damage at diagnosis, non-compliance with treatment and ethnic
origin (e.g. the prognosis is better for white than black patients).
– In a white population the lifetime chance of blindness in both eyes POAG is 5–
10%; the prognosis significantly improved with newer treatment strategies.
– The average period from diagnosis to death hasbeenestimated ataround15 yrs.

90. Follow Up
• Perimetry. If IOP control is good and glaucomatous damage
mild or moderate with no substantial threat to central
vision, every 6–12 months.
• Gonioscopy should be performed annually
• Optic disc examination should be performed at each visit,
as a disc haemorrhage may indicate ongoing damage
• Serial imaging.
• Causes of treatment failure
– Inappropriate target pressure. If the IOP is maintained in the
upper part of the statistically normal range, progressive field
loss is relatively common.
– Poor compliance with therapy occurs in at least 25% of patients.
– Wide fluctuations in IOP .
– Alternative cause -Impaired optic nerve perfusion, compressive
lesion.

91. Laser Trabeculoplasty
• Laser trabeculoplasty (LTP) involves the delivery of laser to the TM
with the aim of enhancing aqueous outflow .
• Selective laser trabeculoplasty (SLT). A 532 nm frequency-doubled,
Q-switched Nd:YAG laser is used to selectively target melanin
pigment in TM cells, leaving non-pigmented structures unscathed.
– It is probably similar in efficacy to medical monotherapy and argon laser trabeculoplasty .
– The mechanism includes stimulation of TM cell division, macrophage
recruitment and extracellular matrix recruitment.
– IOP reductions of 10–40% expected after 6 months in responsive
patients.
– The prior use of topical glaucoma medication does not seem to affect
results.
– Energy delivered to the TM is much lower than with argon laser,
– Extensive treatment may causes damage to corneal endothelial cells,
rarely of endothelial decompensation.
– HSV keratitis and macular edema reactivation can occur.

92. Laser Trabeculoplasty
• Argon laser trabeculoplasty (ALT - λ=454.5-528.7 nm) is a long-
established procedure;
– Mechanisms are similar as of SLT (i.e. stimulation of TM cell division,
macrophage recruitment and extracellular matrix recruitment), and there may
also be a mechanical opening of the trabecular spaces.
– Repeat treatment is of limited value.
– Complications include
• PAS, acute elevation of IOP, CME and anterior uveitis; ALT may have an adverse effect on
the outcome of subsequent filtration surgery.
• Micropulse laser trabeculoplasty (MLT) – 532nm
– Unlike SLT and ALT, a smaller area is targeted for subthreshold therapeutic
effect on the pigmented cells without the burning effect of the TM or damage
to adjacent tissues.
– Results comparable to other LTP forms
– Used in Macular edema of DR, RVO, CSR
• Titanium-Sapphire Laser Trabeculoplasty The Ti:sapphire laser (Ti:Al2O3)
is a tunable laser which emits red and near-infrared light in the range from
650 to 1180 nm.
– Ti:sapphire lasers operate most efficiently at wavelengths near 800 nm. They
can work in a pulsed as well as a continuous regime.

93. Indication of Laser Trabeculoplasty
• Type of glaucoma.
– In POAG, PXS and PDS, and also in OHT.
– Steroid-induced glaucoma has been treated with SLT.
– During pregnancy
• Primary therapy. Favourable safety profile, as a primary alternative
to topical medication.
• Adjunctive treatment to avoid polypharmacy.
• Intolerance of topical medication including allergy.
• Failure of compliance with medical therapy.
• Failure of medical therapy, as a less aggressive treatment measure
than surgery.

94. Technique of Laser Trabeculoplasty
• LTP is performed under topical anaesthesia.
• A drop of apraclonidine or brimonidine is instilled 30–60 minutes pre-procedure and
post-procedure.
• Instil a drop of pilocarpine if the angle is not wide. A goniolens is inserted.
• ALT: initial settings 50 μm spot size, 0.1 s, and 700 mW power (range of 400–1200
mW, dependent on angle pigmentation).
– The aiming beam is focused at the junction of the pigmented and nonpigmented TM
– A light blanching or the appearance of a minute gas bubble is aimed.
– Fifty burns are applied over 180° of the angle. Treating the other 180° if the initial response is
unsatisfactory.
– Topical fluorometholone or prednisolone 0.5% four times daily for one week is prescribed post-
laser.
• SLT: initial settings 400 μm spot size, 0.3 ns, and 0.8mJpower (range of 0.3-1.0mJ,
dependent on angle pigmentation).
– The aiming beam is centred on the pigmented TM and then fired, an optimal reaction consisting
of a few tiny (champagne) bubbles.
– The total energy used for SLT is considerably less than for ALT, significant inflammation less likely.
• Micropulse laser trabeculoplasty (MLT)
– 300 μm spot size diameter, 1 W power, 300ms duration with 15% duty cycle, 10 confluent laser
shots per clock hour. Applied 360°.
– No postlaser medications required after MLT
• Check IOP 30–60 minutes after the laser.
• Medical glaucoma therapy is generally continued.
• Follow-up 1–2 weeks,

95. Filtering procedures
• Non-penetrating (This circumvents large IOP fluctuations
during the early post-operative period that can occur with
trabeculectomy)
• Deep sclerectomy, with the Aquaflow
collagen wick (intrascleral implant).
• Viscocanalostomy
– Canaloplasty - cannulation of the entire circumference
of the Schlemm canal with a microcatheter
• MIGS
• Penetrating
• Trabeculotomy
• Trabeculectomy
• Glaucoma drainage devices.
– Non-restrictive (Molteno and Baerveldt
implants) and
– Flow-restrictive (Ahmed Glaucoma Valve)
– Pars Plana Clip which can be used with any
drainage device or Hoffman elbow, which
is mounted on a Baerveldt implant.

96. Indications for Trabeculectomy
1. As primary therapy in advanced disease or high IOP
unlikely to resolve with routine therapy.
2. Cases not suitable for other form of treatment,
compliance related issue or appropriate medical
treatment not available
Unsuitable for trabeculoplasty
• Poor patient co-operation
• Inability to adequately visualize trabeculum
3. Failed medical therapy and laser trabeculoplasty
• In condition when clinically significant disease progression can’t
be checked with medication and laser therapy i.e. target IOP
not achieved.
4. Patient preference

97. a. Conjunctival incision
b. Conjunctival undermining
d. Outline of superficial flap
(3 × 3–4 mm) rectangular
e. Dissection of superficial flap
of 50% thickness
f. Paracentesis
c. Clearing of limbus
f
d
b
a
c
e
Manual block removal
If a blade and scissors are used
it is difficult to cut sclerostomy
much smaller than 3 X 1.5 mm.
Punch sclerostomy
A punch sclerostomy is the
method of choice. A
sclerostomy measuring 0.5–
2mmX0.5–1.5 mm is
adequate and provides
optimum outflow control
Trabeculectomy (1)

98. a. Cutting of deep block -
anterior incision
b. Posterior incision
d. Peripheral iridectomy
e. Suturing of flap and
reconstitution of
anterior chamber
f. Suturing of conjunctiva
c. Excision of deep block
f
d
b
a
c
e
Trabeculectomy (2)

99. Postoperative Management In Trabeculectomy
• Topical Steroids- Prednisolone acetate 1% 2 hourly for the
first 2 weeks with subsequent dosing adjusted according to
bleb morphology. Most patients receive a reducing dose of
topical steroids for ~8 weeks postoperatively.
• Topical Antibiotics for ~4 weeks postoperatively.
• Topical Mydriatic/Cycloplegic Agents Atropine 1% is to
prevent postoperative AC shallowing AC and the risk of
malignant glaucoma, especially in eyes with short axial
lengths or chronic angle closure.
• Topical NonSteroidal Antiinflammatory Drugs (efficacy is
not proven).
• Oral or Intravenous Steroids started preop In severe uveitic
glaucoma.

100. Antimetabolites in filtration surgery
• 5-fluorouracil (50 mg/ml solution soaked sponges for 5 minutes prior to
creation of the scleral trapdoor, or postop subconjunctival injection of 0.1 ml
of 25 mg/ml or 50 mg/ml solution)
• Mitomycin C { 0.2 mg/ml for 2 minutes, though a higher concentration(e.g. 0.4
mg/ml)} may be used for particularly high-risk patients;
• Indications
– Presence of risk factors for surgical failure and used with caution In patients with very thin
conjunctiva or sclera or in high myopes.
– In uncomplicated glaucoma the use of low-dose antimetabolites may improve long-term
control of IOP.
• High-risk factors include
1. Previous failed trabeculectomy or filtering device, and
2. Neovascular glaucoma,
3. Certain secondary glaucomas (e.g. inflammatory, post-traumatic angle recession and
iridocorneal endothelial syndrome).
4. Aphakic glaucoma
• Intermediate- and lower-risk factors include
– Combined glaucoma filtration surgery/cataract extraction
– Previous conjunctival surgery, e.g., squint surgery/detachment surgery/trabeculotomy
– Patients on topical medication (particularly sympathomimetics) for over 3 years,
– Age under 40.
– Black ethnicity,

101. • Thin and polycystic
Type 1
• Good filtration
• Relatively avascular
• Microcysts present
• Good filtration
• Flat, thin and diffuse
Type 2
• Engorged surface vessels
• No microcysts
• No filtration
•
Type 3
• Engorged surface vessels
• No filtration
• Localized, firm cyst
Encapsulated
Non‐functioning flattened blebs
Diffuse filtering bleb
The cystic bleb is composed of a large
hyporeflective area filled with multiple fluid
collections of varying size and intensity.
Non‐functioning encapsulated blebs
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1857643/#ref1
Filtration blebs

102. Treatment Options for Failed Trabeculectomy
1. Digital massage
2. Laser suture lysis
3. Topical steroids
4. Subconjunctival injection of 5-FU
5. Re-operation
6. Re-commence medical therapy

103. Cause IOP Bleb Seidel test
Wound leak Low Poor Positive
Overfiltration Low Good Negative
Malignant
glaucoma
High Poor Negative
Post Trabeculectomy Shallow anterior chamber

104. Blebitis
Predisposition
• Thin-walled, cystic bleb
• Use of adjunctive antimetabolites
• Bleb trauma
• Subacute onset
• Milky bleb
• No hypopyon
• Good prognosis
• Acute onset
• Hypopyon
• Guarded prognosis
Endophthalmitis
Late bleb infection

105. Complication of GDD
• The early postoperative complications are similar to other filtration procedures including flat
chambers, hypotony, and suprachoroidal hemorrhage.
• Hypotony
• Valve Malfunction
• Hyphema
• Scleral Perforation
• Tube-Related Problems
– If the tube is placed too anteriorly, it will cause decompensation of the corneal endothelium.
– If the tube is placed too posteriorly, it will cause inflammation by rubbing on the iris and may also result in
cataract formation if it touches the anterior lens capsule.
– Tube block from blood, vitreous, fibrin, or iris incarceration in the early postoperative period can occur.
– Tube retraction and anterior migration are more commonly seen in children. As the eye grows, the tube may
retract or touch the corneal endothelium. Retracted tubes can be lengthened with tube extenders or,
alternatively, can be placed in the pars plana. Anterior migration of the tube can be fixed by shortening its
length and a more posterior reinsertion.
• Tube Erosion and Endophthalmitis
• Migration or Expulsion of the Plate
• Corneal Decompensation
• Overhanging Bleb
• Strabismus
• Hypertensive Phase
Hypertensive phase is characterized by elevated IOP, typically in 30- to 50- mm Hg range, occurring
anywhere between 1 and 6 weeks postoperatively.

106. Angle Closure Glaucoma
Dr. Rajeev Kumar
 sl. 8

107. Introduction to Angle Closure
• The term ‘angle closure’ refers to occlusion of the
trabecular meshwork by the peripheral iris
(iridotrabecular contact – ITC), obstructing aqueous
outflow.
• Angle closure can be primary, when it occurs in an
anatomically predisposed eye, or secondary to another
ocular or systemic factor.
• PACG may be responsible for up to half of all cases of
glaucoma globally, with a particularly high prevalence
in individuals of Far Eastern descent.
• PACG is associated with greater rapidity of progression
and visual morbidity than POAG.

108. • Convex iris-lens
diaphragm
• Shallow anterior
chamber on torch light
• Narrow entrance to
chamber angle
Anatomical predispositions

109. ClassificationJ
• The first classification divides these glaucomas by the type
of mechanism of closure; primary versus secondaryangle
closure.
• A second classification divides these glaucomas by the
location of the mechanism causing the closure; anteriorACG
(NVG,ICE,sarcoidosis)versus posteriorACG, with the iris as the
reference point.
• The third classification involves the timing and the course
of the closure process; acute, intermittent (subacute), and
chronicangleclosure.
• Finally, an important fourth classification involves the
nature of the trabecular meshwork coverage; appositional
angleclosure versus synechialangleclosure.

110. Classification
• Latent – asymptomatic
– IOP may remain normal
– May progress to subacute, acute or chronic angle closure
• Subacute - intermittent angle closure
– May develop acute or chronic angle closure
• Acute
– Congestive - Sudden onset of IOP elevation resulting from total angle
closure, accompanied by symptoms of severe, usually unilateral, ocular
pain, red eye, blurred vision, haloes, headache (ipsilateral frontal), nausea,
and vomiting.
– Postcongestive - follows acute attack
• Chronic - ‘creeping ’ angle closure
– Follows intermittent angle closure - Chronic IOP elevation due to the
presence of peripheral anterior synechiae (PAS) that permanently close
the anterior chamber angle. Symptoms are usually absent
• Absolute No PL following acute attack

111. Staging of Primary angle closure
PrimaryAngle-ClosureSuspect(PACS){occludable angle}:
An eye in which 180−270° of the angle has appositional closure between
the peripheral iris and posterior trabecular meshwork is present or
considered possible,
In the absence of elevated IOP, PAS, disc, or VF changes.
The risk of PACG at 5 years may be around 30%.
PrimaryAngleClosure(PAC):
PACS with raised IOP and/or primary PAS,
without disc or VF (GON)
Ischaemic and non-ischaemic depending on presence of glaucomfleckens and
iris changes as evidence of prior IOP elevation.
PrimaryAngleClosureGlaucoma(PACG):
PAC with glaucomatous optic neuropathy and corresponding VF loss

112. Mechanism of ACG
• The mechanisms involved in angle closure can be categorized according to the
anatomical level (anterior to posterior) at which causative forces act. In many
patients more than one level is contributory.
Relative pupillary block (accounts for at least 90% of primary ACG.)
• Failure of physiological aqueous flow through the pupil leads to a pressure
differential between the anterior and posterior chambers, with resultant anterior
bowing of the iris  ITC
• Usually relieved by iridotomy. Control of IOP may not occur if there are
substantial PAS or an additional mechanism of angle closure is in effect.
• The lens vault quantifies the portion of the lens located anterior to the anterior
chamber angle;. A large lens vault is independently associated with angle closure.
Non-pupillary block
• Thought to be important in many Far Eastern patients (thicker peripheral iris ).
• Associated with a deeper anterior chamber (AC) than pure pupillary block.
• Patients with non-pupillary block, particularly those with plateau iris, tend to be
younger than those with pure pupillary block.
• If angle closure is not fully relieved by iridotomy. The term ‘mixed mechanism’ has
been suggested to describe glaucoma in which both significant pupillary block and
non-pupillary block iris-induced mechanisms coexist.
• Specific anatomical causative factors include plateau iris (anteriorly
positioned/rotated ciliary processes , a ‘thick peripheral iris roll’ .

113. Mechanism of ACG
• Plateau iris configuration (PIC) is characterized by a flat or only
slightly convex central iris plane, often in association with normal
or only slightly shallow central anterior chamber depth.
– The angle recess is typically very narrow, with a sharp backward iris
angulation over anteriorly positioned and/or orientated ciliary
processes.
– A characteristic ‘double hump’ sign is seen on indentation
gonioscopy,
• Plateau iris syndrome describesthepersistenceof gonioscopic angle
closure despite a patent iridotomy in plateau iris;
– Provocative test can demonstrate the angle closure.
– Complete form in which occlusion of the functional TM is present and
the IOP is elevated, and
– An incomplete form with occlusion to a lesser extent and normal IOP.
– Reversal of PIC ACG
• Chronic miotic therapy / laser iridoplasty.

114. Mechanism of ACG
• Lens-induced angle-closure. As Secondary Angle closure .
– Includes only those cases in which a sudden change in lens volume
and/or position leads to an acute or subacute IOP rise.
– Phacomorphic glaucoma or anterior lens subluxation.
– Virtually all pupillary block can be said to have a phacomorphic
element that increases with age as the lens enlarges.
• Retrolenticular
– Malignant glaucoma (‘ciliolenticular block’ ).
– Posterior segment causes of secondary angle closure .
• ‘Combined mechanism’ - the combination of angle-closure and
open-angle elements.
– Reduced aqueous outflow in angle closure - caused by the following
mechanisms in varying degree:
• Appositional obstruction by the iris.
• Degeneration of the TM itself due to chronic or intermittent contact with the
iris or damage sustained due to elevated IOP.
• Permanent occlusion of the TM by PAS.

115. Risk factors for ACG
• Age.
– The average age of relative pupillary block is about 60 years at
presentation.
– Non-pupillary block forms of PAC tend to occur at a younger age.
• Gender. Females > males.
• Race. Particularly prevalent in Far Eastern (thicker peripheral iris)
and Indian Asians.
• Family history. An increased prevalence of angle closure in family
members.
• Refraction. Eyes with ‘pure’ pupillary block are typically
hypermetropic, although this is not as clear-cut with non-pupillary
block, which can occur in myopic eyes.
– Up to one in six patients with hypermetropia of > 1 dioptre are PAC
suspects, so routine gonioscopy indicated in all hypermetropes.
• Axial length. Short eyes tend to have a shallow AC ;
nanophthalmos eyes with a proportionally large lens and are at
particular risk.

116. Clinical features: Symptoms
• Most patients with intermittent or chronic angle closure
(elevated IOP) are asymptomatic.
• Presentation can be with
– Intermittent mild symptoms of blurring (‘smoke-filled room’)
and haloes (‘rainbow around lights’) due to corneal epithelial
oedema, or
– Acutely with markedly decreased vision, redness and
ocular/periocular pain and headache;
– Abdominal pain and other gastrointestinal symptoms may occur.
• Precipitating factors include
– Watching television in a darkened room, adoption of a
semiprone position (e.g. reading), acute emotional stress,
– Pharmacological mydriasis or rarely miosis and
– Systemic medication: parasympathetic antagonists or
sympathetic agonists including inhalers, motion sickness
patches and cold/flu remedies (mydriatic effect), topiramate
(ciliary body effusion).

117. Clinical features: Signs
• Chronic presentation
– VA is normal unless damage is advanced.
– Shallow AC .
– ↑IOP - persistent or intermittent.
– ‘Creeping’ angle closure is characterized by a gradual band-like
anterior advance of the apparent insertion of the iris.
– Intermittent ITC  discrete PAS with pyramidal (‘saw-tooth’)
appearance on gonioscopy.
– Optic nerve signs depend on the severity of damage.
• Acute primary angle closure (APAC)
– VA is usually 6/60 to HM.
– The IOP is usually very high (50–100 mmHg).
– Conjunctival hyperaemia with violaceous circumcorneal injection.
– Corneal epithelial oedema .
– The AC is shallow, and aqueous flare is usually present.
– An unreactive mid-dilated vertically oval pupil is classic .
– Fellow eye with an occludable angle; if not search secondary cause.

118. Clinical features: Signs
• Resolved APAC
– Early: low IOP (ciliary body shutdown and effect of intensive
treatment), folds in Descemet membrane if IOP has reduced
rapidly, optic nerve head congestion, choroidal folds.
– Late: iris atrophy with a spiral-like configuration, glaukomflecken
, and irregular pupil; the optic nerve may be normal or pallor
and/or cupping .
– The greater (i) the duration of an attack of APAC and (ii) the
extent of post-APAC PAS,
• the lower the likelihood of IOP control with medical treatment alone.
• Subacute angle closure = intermittent episodes of
spontaneously resolving mild/moderate APAC.
 chronic course/or severe/unresolving episode of APAC.

119. • Severe corneal oedema
• Dilated, unreactive,
vertically oval pupil
• Ciliary injection
• Complete angle closure
(Shaffer grade 0)
• Shallow anterior
chamber
The optic nerve head blood supply interrupted by
the high IOP, and the retinal artery may pulsate,
signifying that the IOP has exceeded retinal
diastolic pressure and should be lowered as quickly
as possible.
Permanent damage to the nerve can perhaps occur
within 24–48 h.
The other eye has ~50% chance of an acute attack
developing within 5 years.
Signs of Acute congestive angle-closure glaucoma

120. Investigation
• Anterior segment OCT , UBM or Scheimpflug
photography
• Anterior chamber depth measurement- 1 to 2 CCT
severely narrow AC
• Biometry if lens extraction is considered.
• Posterior segment ultrasonography in atypical cases to
exclude causes of secondary angle closure.
• Provocative testing. - for partially opened angles post-
iridotomy, and to determine whether further
intervention, e.g. Iridoplasty, required or not .

121. Differential diagnosis of acute IOP elevation
• Lens-induced angle closure due to a swollen or subluxated lens.
• Malignant glaucoma, especially if recent intraocular surgery.
• Neovascular glaucoma – post DM, CRVO.
• Hypertensive uveitis, e.g. iridocyclitis with trabeculitis (particularly
herpetic including cytomegalovirus), glaucomatocyclitic crisis
(Posner–Schlossman syndrome).
• Scleritis with or without angle closure.
• Pigment dispersion.
• Pseudoexfoliation.
• Orbital/retro-orbital lesions including orbital inflammation,
retrobulbar haemorrhage and carotid-cavernous fistula.
• Ghost cell glaucoma with a history of vitreous hemorrhage, trauma
to the anterior hyaloids face, an open angle, and pathognomonic
khaki-colored cells in the anterior chamber and on the trabecular
meshwork;

122. Treatment
• PACS (prophylactic+symptomatic)
– Laser/surgical iridotomy.
– Observation , laser iridoplasty, and/ long-term pilocarpine
prophylaxis 1% BD;
– Provocative testing.
– If symptomatic cataract is present, lens extraction usually
definitively opens the angle.
• PAC and PACG
– Management is as for PACS, with a lower threshold for further
intervention, particularly if IOP remains elevated.
– Medical treatment as for POAG for elevated IOP.
– Urgency and intensity of treatment, and frequency of review is
individualized, taking into account IOP, extent of angle closure
and glaucomatous damage.

123. APAC Attack Management
K
Initial treatment (Decrease AH Production, Reopen angle, Reduce the
Inflammation)
– Supine position.
– IV Acetazolamide 500 mg - if IOP >50 mmHg, and orally (not slow-release) if
IOP is <50 mmHg.
– A single dose of each of apraclonidine 0.5%, Timolol 0.5%, and prednisolone
1% or dexamethasone 0.1% to the affected eye, at the interval of 5 minutes.
– Pilocarpine 2–4% one drop to the affected eye, repeated after half an hour;
one drop of 1% into the fellow eye.
– Analgesia and an antiemetic as per requirement.
Resistant cases
– Central corneal indentation with a squint hook or indentation goniolens ,
(Topical 50% glycerol for Epithelial oedema ).
– Further Pilocarpine 2–4%, Timolol 0.5%, Apraclonidine 1% and Topical steroid.
– Mannitol 20% 1–2 g/kg intravenously over 1 hour, oral glycerol 50% 1 g/kg, or
oral isosorbide 1–1.5 g/kg, (check contraindications).
– Surgical options (Break the Pupillary block and reopen the angle): Early
bilateral laser iridotomy or iridoplasty , peripheral iridectomy, lens extraction,
goniosynechialysis, trabeculectomy and cyclodiode; (Paracentesis carries
significant risks).

124. APAC Attack Management
K
Subsequent medical treatment
– Pilocarpine 2% four times daily to the affected eye and PI
to the fellow eye.
– Prednisolone 1% / dexamethasone 0.1% four times daily X
1 week.
– Timolol 0.5% twice daily, apraclonidine 1% three times
daily and
– Oral acetazolamide 250 mg four times daily for short term.
– Surgery (Trabeculectomy) if needed.
– The greater (i) the duration of an attack of APAC and (ii)
the extent of PAS,
• the lower the likelihood of IOP control with medical treatment
alone.

125. Laser iridotomy
• Principally used in the treatment of primary angle closure, secondary angle closure
with pupillary block, sometimes in pigment dispersion syndrome.
Technique
• Preparation-A topical anaesthetic agent + Apraclonidine or brimonidine + topical
pilocarpine 2%.
• A special iridotomy contact lens (e.g. Abraham , Volk MagPlus) is inserted.
– A 66D magnifying lens for viewing the patient's iris. The power density of the laser beam at the iris is increased 2.5x
compared with a flat lens. A 50 micron spot size setting yields a 31 micron spot on the iris. Reduce the power density
at the cornea and retina by 2.8x.
• Target an iris crypt under the upper eyelid between 11 and 1 o’clock.
• Power settings of 4–5 mJ; 1-3 pulse shots. The optimal size -150 to 500 μm .
• Pre-treatment with thermal (argon or diode) laser is often required in thick dark
irides.
• Successful penetration is characterized by a gush of pigment debris.
• Avoid Over-treatment .
Post-procedure
• A second drop of apraclonidine is instilled and oral acetazolamide given.
• A potent topical steroid (e.g. dexamethasone 0.1%) Four times daily for 1 week.
• The IOP should be checked 1–2 hours after the procedure. Routine review is usually
at 1 or 2 weeks.

126. Complications of Laser iridotomy
• Bleeding controlled with pressure on the globe with the
contact lensfor 30–60 s
• IOP elevation. Usually early and transient but occasionally
persistent.
• Iritis. Especially if excessive laser is applied or post-laser steroid
therapy is inadequate, or in darker irides (including those due to
prostaglandin derivative treatment).
• Corneal burns may occur if a contact lens is not used or if the AC is
shallow; these usually heal very rapidly without sequelae.
• Glare and/or diplopia due to a ‘second pupil’
effect
• Cataract. Localized lens opacities occasionally develop at the
treatment site; age-related cataract formation may be accelerated by
iridotomy.
• Peripheral Iridoplasty
– Argon laser peripheral iridoplasty involves placing
low power (250–400 mW) long duration (.5 s) and
large (500 mm) spot size burns on the peripheral
iris to contract the iris stroma near the angle.

127. • Folds in Descemet
membrane
• Stromal iris atrophy with
spiral-like configuration
• Posterior synechiae
• Fine pigment on iris
• Fixed dilated pupil
• Glaukomflecken
Signs of postcongestive angle-closure glaucoma
The optic nerve
may be normal
or pallor and/or
cupping .
Gonioscopic
changes

128. Chronic angle-closure glaucoma
• Cupping and field loss
similar to chronic OAG
• Variable amount of angle closure with PAS
• Easily missed unless routine gonioscopy performed
• Synechial closure for > 1 year –TM becomes
nonfunctional due to degeneration, fibrosis, and
Sclerosis, loss of intertrabecular space
Signs of past post congestive angle closure
Signs

129. Management of Chronic Angle Closure

130. Normal Tension Glaucoma
Dr. Rajeev Kumar

131. Introduction to NTG
• Normal tension glaucoma (NTG), also referred to as low tension or normal
pressure glaucoma, is usually regarded as a variant of POAG.
• It is characterized by:
1. IOP consistently < 21 mmHg,
2. An open anterior chamber angle,
3. Characteristic glaucomatous optic nerve damage,
4. Visual field loss, consistent in pattern with the optic nerve appearance.
5. No features of secondary glaucoma or a non-glaucomatous cause for
the optic neuropathy.
• The distinction between NTG and POAG is based on an epidemiologically
derived range of normal IOP.
• Up to two-thirds of Japanese patients and 30% of Caucasians with OAG
may have normal IOP at initial assessments.
POAG

132. Pathogenesis
• Various mechanisms have been postulated including
• Anomalies of local and systemic vascular function,
structural optic nerve anomalies and autoimmune
disease.
• NTG insomepatients hasbeenexplained byverylow CCT,
– Overall CCT in patients with NTG is lower than in POAG.
• A small proportion of NTG patients have been found to
have marked nocturnal IOP spikes,
– sometimes only detected on testing in the supine position.

133. Risk factors of NTG
• Age. Older than those with POAG, due to delayed diagnosis.
• Gender - higher prevalence in females.
• Race. more in Japanese origin than in European or North American
Caucasians.
• Family history. The prevalence of POAG is greaterinfamiliesofpatientswithNTG
• CCT is lower in patients with NTG than POAG.
• Abnormal vasoregulation, particularly migraine and Raynaud
phenomenon, more common in NTG.
• Systemic hypotension including nocturnal blood pressure dips of >20%,
• Obstructive sleep apnoea syndrome , via an effect on ocular perfusion.
• Autoantibody levels
• Translaminar pressure gradient. larger than in POAG.
• Ocular perfusion pressure may be relatively lower than in POAG.
• Myopia .
• Thyroid disease.

134. Clinical features of NTG
History
– Headache, Migraine and Raynaud phenomenon.
– Episodes of shock.
– Head or eye injury.
– Medication, e.g. systemic steroids, beta-blockers.
IOP is usually in the high teens, but may rarely be in the low teens.
Optic nerve head
– The optic nerve head may be larger on average in NTG than in POAG.
– The pattern of cupping is similar, but acquired optic disc pits and focal RNFLD
may be more common.
– Peripapillary atrophic changes may be more prevalent.
– Disc splinter haemorrhages (Steven Drance ) may be more frequent, and are
associated with progression. two-thirds of disc hemorrhages occur
inferotemporally.
– If Disc Pallor is disproportionate to cupping  think alternative diagnosis.
Visual field defects are essentially the same as in POAG .
– In > half of patients, field changes are non-progressive over a period of 5 years
or more without treatment.
– But because of delayed diagnosis, patients present with more advanced
damage than in POAG.

135. Other investigations in selected patient of NTG
– Assessment of systemic vascular risk factors.
– Blood pressure measurement - to calculate ocular perfusion
pressure; 24-hour ambulatory monitoring will exclude nocturnal
systemic hypotension in selected patients.
– Blood tests for other causes of non-glaucomatous optic
neuropathy such as vitamin B12, red cell folate, full blood count,
erythrocyte sedimentation rate/C-reactive protein, treponemal
serology including Lyme disease, serum angiotensin-converting
enzyme level, plasma protein electrophoresis and autoantibody
screen.
– Cranial MRI.
– Carotid Duplex imaging.
– Ocular blood flow assessment (e.g. laser flowmetry) may have
useful clinical potential.

136. Differential diagnosis of NTG
• Angle closure should always be ruled out by meticulous dark-room gonioscopy.
• Low CCT, Prior refractive surgery and corneal ectasia lead to falsely low IOP
readings.
• POAG with apparently normal IOP because of wide diurnal fluctuation. Do a
diurnal IOP charting.
• Previous episodes of raised IOP - due to ocular trauma, uveitis or steroid therapy.
• Masking by systemic /oral betablocker, started after glaucomatous damage has
been done.
• Spontaneously resolved pigmentary glaucoma. In some cases of POAG .
• Progressive RNFL defects not due to glaucoma e.g. in myopic degeneration and
optic disc drusen.
• Congenital disc anomalies simulating glaucomatous cupping, e.g. disc pits and
colobomas.
• Neurological lesions causing optic nerve or chiasmal compression can produce
visual field defects confusing as glaucomatous, and in suspicion do cranial MRI.
• Previous (AION) . NAAION often in a ‘crowded’ disc, so check fellow eye, prior
RVO.
• Previous acute optic nerve insult e.g. hypovolaemic/septicaemic shock, or head
injury.
• Miscellaneous optic neuropathies including inflammatory, infiltrative and drug-
induced.

137. Treatment of NTG
– Approximately 50% of untreated patients will not deteriorate at 5 years .
– Further lowering of IOP is effective in reducing progression in most patients.
– Progression should be demonstrated before commencing treatment, Exceptions - advanced
glaucomatous damage and young age.
– Regular assessment including perimetry 4–6 monthly.
• Medical treatment.
– The α-2 agonist brimonidine, Carbonic anhydrase inhibitors, particularly dorzolamide, may
improve ocular perfusion.
– Selective β1-blockade (e.g. betaxolol) - have a beneficial effect on optic nerve perfusion.
– Prostaglandin derivatives tend to have a greater ocular hypotensive effect.
• Laser trabeculoplasty, particularly SLT.
• Surgery may be considered if progression occurs despite IOP in the low teens;
– antimetabolite enhancement of trabeculectomy.
• Control of SI e.g. DM, HT & hyperlipidaemia is important to optimize optic nerve
perfusion.
• Systemic CCB , Nilvadipine (Nilvad).
• Antihypotensive measures.
– If significant nocturnal dips in BP are detected, reduce antihypertensive medication
(bedtime).
• Neuroprotective agents ; Citicholine, memantine . Ginkgo biloba (40 mg three
times daily) or an antiplatelet agent .

138. Secondary Glaucoma
Dr. Rajeev Kumar

139. Classification Of Secondary glaucoma
Secondary open-angle glaucoma (on the basis of the
site of aqueous outflow obstruction.)
• Pre-trabecular, (in which aqueous outflow is
obstructed by a membrane covering the
trabeculum) consist of:
– Fibrovascular tissue (neovascular glaucoma).
– Endothelial cellular membranous proliferation
(iridocorneal endothelial syndrome).
– Epithelial cellular membranous proliferation
(epithelial ingrowth).
• Trabecular, in which the obstruction occurs as a
result of ‘clogging up’ of the meshwork and
secondary degenerative changes.
– Pigment particles (pigmentary glaucoma).
– Pseudoexfoliative material (pseudoexfoliation
glaucoma).
– Red blood cells (red cell glaucoma).
– Degenerate red cells (ghost cell glaucoma).
– Macrophages and lens proteins (phacolytic
glaucoma).
– Proteins &Trabeculitis in (hypertensive uveitis).
– TM scarring (e.g. post-traumatic angle recession).
• • Post-trabecular - TM is normal but elevated
episcleral venous pressure.
– Carotid-cavernous fistula.
– Sturge–Weber syndrome.
– Obstruction of the superior vena cava.
Secondary Angle-closure
• With pupillary block
– Seclusio pupillae (360° posterior synechiae), usually
secondary to recurrent iridocyclitis.
– Subluxated lens.
– Phacomorphic glaucoma.
– Capsular block syndrome with 360° iris–capsule
adhesion in a pseudophakic eye.
– Aphakic pupillary block.
– Anterior chamber lens implant without a patent
iridotomy.
• Without pupillary block
– Secondary causes of PAS such as advanced
neovascular glaucoma and chronic anterior uveitis.
(anterior pull mechanism)
– Malignant glaucoma (cilio-lenticular block).
(posterior push mechanism)
– Cilio-choroidal effusion.
– Capsular block syndrome without iris–capsule
adhesion.
– Ciliary body/iris cyst or other ciliary body or
posterior segment tumour.
– Contraction of retrolenticular fibrovascular tissue
such as in proliferative vitreoretinopathy and
retinopathy of prematurity.
 sl.8

140. Pseudoexfoliation glaucoma
Introduction
• Pseudoexfoliation syndrome (PXF) is a systemic condition characterized by the
deposition of white dandruff-like material, called exfoliation material, within the
anterior segment of the eye and other organs such as the heart, lungs and kidneys.
• The deposition of this material in the trabecular meshwork can result in aqueous
outflow obstruction, raised intraocular pressure (IOP) and glaucoma.
• Pseudoexfoliative glaucoma is the most common form of secondary open angle
glaucoma.
• Rare before the age of 50, after this age its prevalence increases rapidly.
Prevalence is up to 5% in many older populations .
• More common in women.
• Approximately 20% of patients with newly diagnosed exfoliation have either
glaucoma (15–30%) or increased IOP.
• The cumulative risk of eyes with PXS requiring glaucoma treatment may be as high
as 60% at 5 years.
• True capsular exfoliation occurs due to chronic infrared exposure (‘glassblower’s
cataract’ ).

141. Pseudoexfoliation glaucoma
Pseudoexfoliative material Iris sphincter atrophy Gonioscopy
Central disc with
peripheral band
Heterogeneous (segmental)
Trabecular Hyperpigmentation
may extend anteriorly
(Sampaolesi line)
On retroillumination

142. Pathogenesis of PXF
• PXF is a grey-white fibrillary amyloid-like material;
• Abnormal ECM metabolism in ocular and other tissues.
• The material is deposited on various ocular structures including the
lens capsule , zonular fibres, iris, trabeculum and conjunctiva.
• PXF has been found in skin and visceral organs, leading to the
concept of PXS as the ocular manifestation of a systemic disorder;
– PXS is associated with an increased prevalence of vascular disorders,
hearing loss and Alzheimer disease.
• Plasma homocysteine tends to be higher than controls, and
inadequate dietary folate intake (folate reduces homocysteine) may
be a risk factor.
• Aetiopathogenesis is multifactorial.
• Likely mechanisms - trabecular obstruction by PXF and liberated
iris pigment, with secondary degenerative outflow dysfunction.
• Fellow eye - Conjunctival biopsy will usually reveal subclinical PXF.

143. Clinical features of Pseudoexfoliation glaucoma
• Diagnosis is usually incidental, though follows vision loss from advanced glaucoma more
commonly than POAG.
• Cornea. PXF may be deposited on the endothelium, and scattered pigment deposits are common;
a Krukenberg spindle may rarely form, similar to PDS.
• Anterior chamber. Mild aqueous flare is common.
• Iris. Granular PXF deposits, pupillary ruff loss and patchy transillumination defects at the
pupillary margin.
• Lens.
– The anterior lens capsule - a central disc and a radially indented peripheral layer of PXF material, separated
by a clear zone.
– Peripheral capsular deposition is often visible with pupillary dilatation. Deposits - flaky with scrolled edges.
– Cataract is more common than average.
– Phacodonesis due to zonular weakness , but spontaneous subluxation is rare.
• Anterior chamber angle. Regular annual gonioscopy .
– Patchy trabecular and Schwalbe line hyperpigmentation , especially inferiorly.
– A Sampaolesi line is an irregular band of pigment running on or anterior to the Schwalbe line.
– Dandruff-like PXF angle deposits may be seen.
– There is an increased risk of angle closure and of post-surgical malignant glaucoma (cilio-lenticular block),
due to zonular laxity.
• IOP. Usually unilateral IOP elevation at first with marked fluctuation.
• Investigation - similar to POAG.

144. Treatment of Pseudoexfoliation glaucoma
Treatment
• Medical treatment similar to POAG, but failure is more common.
• Laser trabeculoplasty is more effective than in POAG, with mean
IOP reduction around 30% following SLT.
• Phacoemulsification alone may significantly lower IOP, though it
may give better control combined with trabeculectomy.
– More complication due to poor mydriasis, increased capsule, zonule
and lens friability, and endothelial deficiency; also an increased risk of
a postoperative IOP spike, postoperative corneal oedema, capsular
opacification, capsulorhexis contraction (capsular phimosis) and late
IOL decentration or dislocation.
• Filtration surgery in PXG - similar success rate as POAG.
• Trabecular aspiration confer short-term benefit, and can be
performed at the same time as other intraocular procedures.

145. Prognosis. Worse than POAG; the IOP is often
higher and exhibit marked fluctuation.
– Severe damage may be present at diagnosis, or
can develop rapidly.
– Monitor patients closely, and at intervals of no
more than 6 months.

146. Pigment Dispersion
Introduction
• Pigment dispersion syndrome (PDS) is characterized by the
liberation of pigment granules from iris pigment epithelium (IPE),
and their deposition throughout the anterior segment.
• More common in young myopic white men; Although PDS is rare in
black individuals, PG tends to be more severe than in whites.
• About a third of patients with PDS will have developed elevated IOP
or glaucoma after 15 years.
• AD inheritance with variable penetrance in at least some families
with additional factors such as gender, iris color and refractive error
play a role in the phenotypic expression of the disease;
• Secondary pigment dispersion can occur, causes including trauma,
intraocular tumour and rubbing of a malpositioned IOL on the IPE.
• Sugar and Barbour were the first to coin the term pigment dispersion
syndrome

147. Pigment Dispersion
Pathogenesis
• The pigment epithelium - abnormally susceptible to shedding in affected
individuals.
• In primary PDS/PG, pigment shedding is precipitated by rubbing of the
posterior pigment layer of the iris against the zonule.
• Reverse pupillary block – due to an increase in anterior chamber pressure
relative to the posterior chamber
• Pigment shedding decreases from middle age onwards due to decreased
iridozonular contact.
– Acute IOP elevation can occur due to direct trabecular obstruction by shed
melanin granules;
– Chronic IOP elevation caused by pigmentary obstruction of the intertrabecular
spaces and damage to the trabeculum secondary to denudation, collapse and
sclerosis.
– PG patients have an increased incidence of steroid responsiveness.
• Mechanical and developmental theory
– Histopathologic studies of the iris pigment epithelium demonstrated focal
atrophy, hypopigmentation, delay in melanogenesis, and hyperplasia of the
dilator muscle
– Developmental theory- strengthened by EOG studies suggesting that global
abnormalities of the RPE/Photoreceptor complex exist in patients with PDS

148. Pigment Dispersion
Prevention
• In young patients with iris concavity , a laser iridotomy probably-
equalize pressures in the anterior and posterior chambers and
pulling the iris away from the zonules.
• Older patients with glaucoma are less likely to benefit from
iridotomy due to permanent changes in the trabecular meshwork
architecture.
• Risk of conversion from PDS to PG is approximately 10% at 5 years
and 15% at 15 years.[1] So iridotomy is not advisable in all.
• The decision to perform a laser should be individualized depending
on the patient’s IOP and amount of pigment liberation.
1.Siddiqui Y, Ten Hulzen RD, Cameron JD, Hodge DO, Johnson DH. What is the risk of developing
pigmentary glaucoma from pigment dispersion syndrome? Am J Ophthalmol. 2003;135(6):794-799.

149. Diagnosis of Pigment Dispersion
• Presentation. PDS and PG are typically detected at a routine eye examination;
– Regular review of the myopic patients.
– Occasionally symptoms - glaucomatous visual loss, or from corneal oedema due to an acute
IOP rise particularly after physical exercise.
• Signs of PDS are usually bilateral; subtle and go undetected.
– Cornea. Krukenberg spindle .
– Anterior chamber (AC). The AC - deep. Melanin granules may be seen in the aqueous.
– Iris. Characteristic radial spoke-like transillumination defects are seen often in lighter irides.
• Melanin granules may be present on the surface of the iris, usually inferiorly .
• Partial loss of the pupillary ruff.
– Gonioscopy. The angle is wide as in the myopic patients
• Characteristic mid-peripheral iris concavity .
• The trabecular meshwork is homogeneously hyperpigmented,
• Pigment on or anterior to the Schwalbe line, forming a Sampaolesi line .
• Pigmentation of the angle typically reduces with increasing age.
– Lens. Pigment granules may be deposited on the anterior surface.
• Line (Scheie stripe) or a (Zentmayer) ring of pigment on the peripheral/equatorial surface around the
zonular insertions.
– IOP. This may be volatile and wider fluctuations of IOP than in POAG.
– Posterior segment.
• Peripheral retinal pigmentation , and lattice degeneration ; Higher incidence of retinal detachment.
• Glaucomatous optic neuropathy may be markedly asymmetrical;

150. Urets-Zavalia Syndrome (UZS) has been defined as a fixed and dilated pupil following penetrating keratoplasty (PKP) for
keratoconus in patients who receive mydriatics.
•Typically affects young myopic males
•Increased incidence of lattice degeneration
Krukenberg spindle and very
deep anterior chamber
Mid-peripheral iris
atrophy,
Trabecular hyperpigmentation
Fine pigment granules on
anterior iris surface
UBM
Pigmentary Glaucoma

151. Scheie stripe (also known as Zentmayer line).
pathognomonic for PDS
Collection on the anterior hyaloid face known as Eggert’s Line.
Mid-peripheral iris atrophy, These defects are
found in 86% of PDS pts at the time of diagnosis
The frequency of retinal detachments in
patients with PG ranges from 6–12% while in
the normal population it is 0.001%.
UBM studies have demonstrated the insertion
of the iris into the ciliary body is more
posterior in PDS eyes than in control eyes

152. Causes of Pigment Dispersion
• Normal acquired physiologic pigment liberation
• Pigment dispersion syndrome/Pigmentary glaucoma
• Exfoliation Syndrome
• Iris cyst formation
• Pigment liberation due to intraocular lens
• Diabetes mellitus
• Uveitis
• Pigmented tumors
• Trauma or prior intraocular surgery
• Rhegmatogenous retinal detachment (Shaeffer’s sign)/
(Schwartz syndrome- pigment dispersion in the anterior
segment with high IOP).

153. Treatment of Pigment Dispersion
• Lifestyle measures. Exercise involving jolting - associated with acute iris pigment
liberation, so better to avoid jogging and running up and down stairs.
• Medical treatment is similar to that of POAG. Miotics decrease iridozonular
contact in addition to facilitating aqueous outflow.
– Disadvantage of exacerbating myopia, and precipitating retinal detachment in short-sighted
eyes.
– Topical thymoxamine (Moxisylyte), a selective alpha-adrenergic antagonist, induces miosis
without causing spasm of accommodation, poorly tolerated as it causes irritation.
• Laser trabeculoplasty .
• Laser iridotomy has been proposed to retard pigment liberation by reversing iris
concavity and eliminating iridozonular contact. It may have utility especially in
patients under the age of 40 years.
• Filtration surgery is indicated more commonly than in POAG. Adjunctive
antimetabolites -particularly in younger patients .
– Post-surgical hypotony - common in young myopic eyes.
• Review patients with PDS regularly – at least annually in low-risk cases – for IOP
and/or glaucomatous damage.

154. Acute bilateral iris pigment loss with raised IOP
• Bilateral acute depigmentation of the iris (BADI) and bilateral acute
iris transillumination (BAIT) - distinct idiopathic clinical syndromes
involving pigment dispersal from the iris into the anterior chamber.
• More common in young to middle-aged women, occurring
spontaneously or following a flu-like illness and possibly after oral
antibiotic treatment, especially moxifloxacin.
– Proposed Primary process is uveitic, another mechanism is
phototoxicity following sensitization in predisposed individuals.
• Presentation - acute bilateral ocular redness and photophobia.
– Both may be associated with an IOP rise,
– IOP rise has been reported to be more severe and resistant in BAIT.
– Findings in the two differ in that pigment is lost from the iris stroma in
BADI and the iris pigment epithelium in BAIT, with marked iris
transillumination defects and irregular mydriasis in the latter.
• Differential diagnosis - viral anterior uveitis and pigment dispersion
syndrome.

155. Neovascular Glaucoma
Pathogenesis
• Neovascular glaucoma (NVG) is the result of aggressive
iris neovascularization (rubeosis iridis).
• The common aetiological factor is severe, diffuse and
chronic retinal ischaemia.
• Hypoxic retinal tissue produces angiogenic factors in an
attempt to revascularize hypoxic areas;
– VEGF - induce both retinal and anterior segment
neovascularisation,
– Over angle, NVA form an obstructing fibrovascular
membrane that contracts to close the angle
circumferentially leading to secondary synechial angle-
closure glaucoma without pupillary block very high IOP,
severe visual impairment, congested painful globe.

156. Causes of Neovascular Glaucoma
• Ischaemic CRVO - a third of cases.
– Up to 50% of eyes develop NVG following ischaemic CRVO.
– Extensive peripheral retinal capillary non-perfusion on FFA is a useful
predictor of subsequent NVG. ‘ischaemic’ (nonperfusion ) CRVO
defined as 10 or more disc areas of nonperfusion on FA.
– Glaucoma typically occurs 3 months after the occlusive event (‘100-
day glaucoma’) .
• Diabetes mellitus accounts for a slightly smaller proportion. The
risk of glaucoma is decreased by appropriate PRP , but may be
increased by cataract extraction. PPV in diabetics may precipitate
NVG (7% overall in a large study), especially if NVA is present
preoperatively.
• Retinal arterial vascular disease e.g. CRAO and ocular ischaemic
syndrome- less common causes.
• Carotid Arterial Occlusive Disease
• Miscellaneous causes include intraocular tumours, longstanding
retinal detachment (RD) and chronic intraocular inflammation.

157. • Caused by rubeosis iridis associated with chronic, diffuse retinal ischaemia
Ischaemic CRVO (most common) PDR (common)
CRAO (uncommon) Carotid obstructive
disease (uncommon)
Causes of neovascular glaucoma

158. Clinical features of NVG
Symptoms - asymptomatic to severe pain, decreased vision, redness and
photophobia.
Signs-
• Conjunctival congestion
• Cornea. leads to corneal oedema.
• IOP may be normal early in the disease process, but is frequently extremely high
later on. The anterior segment will often be congested .
• Anterior chamber. Flare, cells, hyphema and posterior synechiae , depending on
severity and stage.
• Pupillary margin. Subtle vessels at the pupillary margin are often an early sign.
Afferent pupillary defect - Diagnosis at this stage is likely to substantially improve
the prognosis.
• Iris - NVI / NVA
• Gonioscopy. NVA without other signs, particularly after CRVO. Synechial angle
closure
• Cataract due to underlying Ischaemia.
• Posterior segment. Signs as per aetiology and Glaucomatous optic neuropathy .

159. Signs of advanced neovascular glaucoma
•Ocular Investigations.
1. FA helpful in
confirming
aetiology and
delineating
ischaemia.
2. B-scan USG to
exclude RD when
the posterior
segment view is
impaired.
3. Anterior segment
OCT ,
4. UBM for angle
assessment.
1. Chandler PA, Grant WM: Lectures on
glaucoma. Philadelphia: Lea & Febiger;
1965:268.
Severely reduced visual
acuity, congestion and pain
NVA - a blood vessel crossing scleral
spur onto the TM, is abnormal1
Distortion of pupil,
ectropion uveae and
rubeosis iridis
Smooth, zippered-up line of iridocorneal
adhesion is pathognomonic

160. Treatment of NVG
• Find the Cause of the neovascularization  appropriate management of systemic
disease is one of key.
• Frequent review during high-risk periods is critical: the first few months following
an ischaemic CRVO, and the first few weeks following diabetic vitrectomy.
• Medical treatment of elevated IOP is as for POAG
– Beta blockers
– Topical atropine 1% to resist PAS formation, and topical steroids.
– But miotics, and prostaglandin derivatives should be avoided- as pro inflammatory.
– Topical apraclonidine and oral acetazolamide - temporary measures;.
• Panretinal photocoagulation (PRP) - induce regression of neovascularization.
– It will not reverse an established fibrovascular membrane.
• Goniophotocoagulation. Laser application directly to new vessels of angle,
– Better effect with intravitreal anti-VEGF injection .
– PDT to the iris and angle .
• Intraocular VEGF inhibitors, e.g. bevacizumab (Avastin®) at a dose of 1.25 mg in
0.05 ml, while waiting for PRP to take effect.
– Intracameral (AC) injection is an alternative to the intravitreal route.

161. Treatment of NVG
• Early PPV with endolaser
– Preoperative intravitreal anti-VEGF.
– in eyes with vitreous haemorrhage, especially in CRVO, Retinal detachment, Diabetic TRD
• Ciliary body ablative procedures. TS-DLCP/ Endoscopic cyclophotocoagulation or
Trans-scleral cryotherapy .
– Lowering of raised IOP generally improves comfort,-- clearing corneal oedema - an adequate
retinal view for PRP.
– in eyes with opaque media or for increasing peripheral retinal coverage
• Filtration surgery - If VA is HM or better.
– Active neovascularization and inflammation should be controlled preoperatively ( includes
preoperative anti-VEGF treatment).
– An GDD and Trabeculectomy with mini-shunt implantation, adjunctive mitomycin C and
postoperative subconjunctival 5-fluorouracil.
– Postoperative anti-inflammatory treatment should be aggressive and may include systemic
steroids.
• Blind painful eye
– Cyclo-ablation
– Retrobulbar alcohol injection
• Cause permanent ptosis and does not relieve congestion.
– Enucleation.

162. Artificial filtering devices
- in very advanced cases
• Topical
•Atropine and steroids to decrease inflammation
•Beta-blockers
Panretinal photocoagulation
- in early cases
Cyclodestructive procedures
- to relieve pain
Retrobulbar alcohol injection
- to relieve pain
Treatment options of neovascular glaucoma

163. Lens Induced Glaucoma
• Secondary angle closure Glaucoma
– Phacomorphic
– Phacotopic
• Secondary open angle Glaucoma
– Phacolytic
– Phacoanaphylactic

164. Phacolytic glaucoma
Introduction
• Phacolytic glaucoma is a secondary open-angle glaucoma occurring in association
with a hypermature cataract. Trabecular obstruction is caused by high molecular-
weight lens proteins that leak through the intact capsule into the aqueous humour
leading to trabecular obstruction; macrophages containing lens proteins may also
contribute . Phacolytic glaucoma should not be confused with phacogenic
(previously phacoanaphylactic) uveitis, an autoimmune granulomatous reaction to
exposed lens proteins occurring with a compromised lens capsule.
Diagnosis.
• Presentation is with pain; vision is poor due to cataract.
• Slit lamp biomicroscopy shows corneal oedema, a hypermature cataract and a
deep anterior chamber. There may be large floating white particles in the AC,
consisting of lens protein and protein-containing macrophages , which may impart
a milky appearance to the aqueous if very dense , and can form a
pseudohypopyon .
• Gonioscopy, if a reasonable view can be obtained, shows an open angle with
lens-derived material and inflammatory cells that are most substantial inferiorly.
Treatment
• After IOP is controlled medically, proteinaceous material is washed out from the
anterior chamber and the cataract is removed. Care should be taken not to rupture
the zonule, which is likely to be more fragile than usual.

165. Pathogenesis Signs
• Deep anterior chamber
• Control IOP medically
• Remove cataract • Floating white particles
Treatment
Phacolytic glaucoma

166. Phacomorphic glaucoma
Pathogenesis
• Phacomorphic glaucoma is an acute secondary angle-closure glaucoma precipitated by an
intumescent cataractous lens.
– Equatorial age-related growth of the lens slackens the suspensory ligament and allows the lens to move
anteriorly. Associated anteroposterior growth leads to increased iridolenticular contact and potentiates
pupillary block and iris bombé.
Diagnosis
• Presentation is similar to acute PACG with a shallow AC and mid-dilated pupil; cataract is evident.
• Gonioscopy , Anterior segment OCT or UBM.
• The fellow eye may or may not be. Phacomorphic glaucoma is more likely in eyes with a shorter
axial length and shallower AC.
Treatment
• Medical treatment is initially similar to that of acute PACG.
• Miotics are omitted as they tend to increase iris–lens apposition and shift the lens anteriorly;
dilatation (Fig.) is sometimes helpful to break pupillary block but should be implemented with
caution.
• Systemic hyperosmotic agents .
• Laser iridotomy / Laser iridoplasty . May be considered for the fellow eye..
• Cataract extraction constitutes the definitive treatment, ideally once the IOP has been normalized
and the eye is quiet; the surgery can be difficult and carries a higher risk of complications.
• Patients should be followed for at least 2 years postoperatively, because 20% of cases may require
further glaucoma intervention for IOP control.

167. Corticosteroid induced glaucoma
• Topical, systemic or periocular corticosteroid administration
• Risk factors
– Genetic predisposition (high steroid responders)
– Patients with primary open angle glaucoma
– First degree relatives of POAG patients
– High myopia
– Diabetes mellitus
– Connective tissue disorders (especially rheumatoid arthritis)
– Eyes with traumatic angle recession and their fellow eyes
– Pigment dispersion syndrome
– Endogenous hypercortisolism
• Management
– Stop the use of steroid - 1/3rd case IOP return to normal.
– Removal of depot steroids
– Rest need treatment as for POAG.
– The constant level of steroid in these eyes may produce excellent surgical results in
trabeculectomy with minimal scarring
– Use of Anecortave acetate does not lead to increased IOP

168. Angle-closure with pupil block
• Caused by seclusio pupillae
•Anterior chamber is shallow
• Caused by progressive synechial angle closure
• Anterior chamber is deep
Angle-closure without pupil block
Inflammatory glaucomas

169. Posner–Schlossman syndrome (PSS)
• Recurrent attacks of unilateral acute raised IOP associated with mild anterior uveitis. , although
50% of patients have fellow eye at risk.
• Mechanism -? acute trabeculitis, and infection, possibly CMV or H. pylori;
• PSS typically affects young to middle-aged adults. M>F.
• The intervals between attacks vary, but usually become longer with time.
Diagnosis
• Presentation - mild discomfort, haloes around lights and slight blurring of vision in one eye, and
sometimes redness.
• Slit lamp biomicroscopy
– Conjunctival Injection – absent to minimal.
– Mild corneal epithelial oedema is frequent.
– few anterior chamber cells and one to several fine white central keratic precipitates.
• Mydriasis is common; posterior synechiae are not a feature. Mild heterochromia may be present
in 30–40% of the cases
• IOP is typically raised to over 40 mmHg, out of proportion to iritis severity, and untreated persists
for hours to weeks; precedes the inflammatory signs.
• Gonioscopy - open angle; PAS do not form.
• Glaucomatous optic neuropathy is relatively uncommon.
• D/d - PDS, viral anterior uveitis, POAG, especially the juvenile variant,
Treatment
• Topical steroids + Aqueous suppressants + Topical or oral non-steroidal antiinflammatory agents .
Antiviral treatment doubtful benefit .

170. Malignant Glaucoma
• It is caused by anterior rotation of the ciliary processes and iris root, leading
aqueous misdirection (ciliolenticular block) in which blockage of aqueous flow
occurs in the vicinity of the pars plicata of the ciliary body, so that aqueous is
forced backwards into the vitreous.
• Following iridectomy, filtering surgery , laser iridotomy, cataract surgery or
capsulotomy.
• Typical clinical findings: extremely shallow or flat anterior chamber with patent PI
+ High IOP + Negative Seidel test + (flat bleb in trab)
• D/d choroidal detachment, pupillary block, suprachoroidal detachment.
• Treatment
– Cycloplegics (atropine 1% and phenylephrine 10%) to dilate the ciliary ring + IV Mannitol to
shrink vitreous
– Medical therapy for raised IOP. If medical therapy fails  Nd:YAG laser anterior hyaloidotomy
through the iridectomy.
– In pseudophakic eyes, laser posterior capsulotomy to disrupt the anterior hyaloid face.
– PPV + lensectomy

171. Malignant Glaucoma
• Prevention-
– Identify Eyes with reduced axial length preoperatively. In
nanophthalmos, prophylactic sclerotomies may be required.
– The capsulorrhexis should be kept relatively small to prevent
lens implant/pupil capture if the AC shallows
– A rigid one piece implant may prevent a flat AC.
– In high-risk eyes with cataract, a combined GFS and cataract
procedure may debulk lens volume.
– Topical atropine at the end of GFS and postoperatively is useful
in preventing malignant glaucoma.
– Aqueous overdrainage must be avoided in the early
postoperative period by having a high scleral flap resistance –
scleral flap sutures are removed later when needed.

172. Traumatic glaucoma
Dr. Rajeev Kumar

173. Post-traumatic angle recession glaucoma
Blunt traumatic damage to
trabecular meshwork
Pathogenesis Signs
Irregular widening of ciliary body band

174. Hyphaema
• Although most traumatic hyphaemas are relatively small , innocuous and
– Transient, IOP elevation may result from trabecular obstruction by RBC or occasionally from
angle closure due to pupillary occlusion by a blood clot.
– Severe and prolonged elevation of IOP may cause corneal blood staining and damage the optic
nerve.
• Good vision is achieved in only about one in three eyes with total hyphaema.
• Secondary hyphaema (2-5d) is associated with a poorer visual outcome.
• Patients with sickle-cell haemoglobinopathy are at increased risk of complications.
– Grade I Less than one-third of the anterior chamber
– Grade II One-third to one-half of the anterior chamber
– Grade III One-half to nearly total
– Grade IV Total (‘eight ball’)
• Unlike clots in other parts of the body, hyphemas demonstrate no fibroblastic
activity or neovascularization.
• Dilated ophthalmoscopy is recommended at the time of presentation, but scleral
depression is generally reserved for the 1-month follow-up visit to avoid
precipitating rebleeding.

175. Treatment
• General
– A coagulation abnormality should be excluded.
– Any current anticoagulant medication should be discontinued after consulting a general
physician to assess the risk;
– NSAIDs should not be used for analgesia.
• Hospital admission may be required for a large hyphaema.
– Strict bed rest is probably unnecessary, but substantially limiting activity is prudent with sitting
or semi-upright posture 30 degree angle , including during sleep.
– A protective eye shield should be worn.
• Medical
– A beta-blocker and/or a topical or systemic CAI is administered, depending on the IOP;
• Alpha-agonists can be useful, but are avoided in small children and sickling disorders.
• CAI are avoided in sickle haemoglobinopathies if possible.
• Miotics should also be avoided as they may increase pupillary block and disrupt the blood–aqueous
barrier, and
• Prostaglandins may promote inflammation.
– Occasionally a hyperosmotic agent is needed,
– Topical steroids .
– Atropine for constant mydriasis
– Antifibrinolysis with systemic aminocaproic acid (ACA) or tranexamic acid or with topical ACA
in recurrent bleeding.

176. Treatment
• Laser photocoagulation of angle bleeding points via a gonioprism has
been described, though gonioscopy should be deferred for 5–6 days post-
injury.
• Surgical evacuation of blood is required in around 5%.
– IOP criteria for AC wash are: greater than 50 mmHg for 5 days, or greater than
35 mmHg for 7 days to avoid optic nerve damage
• To reduce the risk of permanent corneal staining and optic atrophy, and
• To prevent the occult development of PAS and chronic secondary glaucoma;
– In haemoglobinopathy patients (even moderate pressure elevation can lead to
optic atrophy), patients with prior glaucomatous optic neuropathy and in
young children with a risk of amblyopia.  Anterior chamber washout is
advised for IOP elevations >25mmHg for more than 24 h
– To prevent or minimize corneal blood staining, surgery should be performed at
the first sign of staining or in total or nearly total hyphema and with IOP
greater than 25 mmHg for 5 days.J-5097
– A bleeding point should be cauterized if possible. A glaucoma filtration
procedure may be needed.
• Rest on discharge and rebleed should prompt immediate review.

177. Angle recession glaucoma
• Angle recession involves rupture of the face of the ciliary body, the portion
between the iris root and the scleral spur, due to blunt trauma.
• Glaucoma only develops in < 10% after 10 years.
• The rise in IOP is secondary to associated trabecular damage; but the risk of
glaucoma is directly related to the extent of angle recession.
Diagnosis
• Presentation is with unilateral chronic glaucoma.
• Slit lamp examination -- signs of previous blunt trauma;
• Gonioscopy - irregular widening of the ciliary body face, fibrosis of cleft and the
hyperpigmentation of angle.
Treatment
• Long-term regular review of patients at risk is required.
• Medical treatment is as for other types of secondary open-angle glaucoma but is
frequently unsatisfactory; laser trabeculoplasty is likely to be of little benefit.
• Trabeculectomy with adjunctive antimetabolite.
• An artificial filtering shunt or cyclodiode - if trabeculectomy fails.

178. Classification of Iridocorneal Endothelial Syndrome
• Proliferation of abnormal corneal endothelial cells that can lead to varying degrees
of corneal edema, iris atrophy, and secondary angle-closure glaucoma.
• Typically affects young to middle aged women
• ICE syndrome is a group of disorders with three clinical variants:
1. Chandler syndrome
• most common of the three sub-types, representing approximately 50% of all cases
• The iris findings are less common, and a majority of patients have no iris changes at all,
• Iris atrophy in 40%
• Corneal changes predominate
2. Essential / Progressive iris atrophy
• The iris findings of this variant can be quite robust and progressive over time
• Iris atrophy in 100%
3. Iris naevus (Cogan-Reese) syndrome
• Unique feature - Anterior surface of iris has tan pedunculated nodules or diffuse pigmented lesions
• Iris atrophy in 50%
• Each can result in substantial visual impairment from glaucomatous optic
neuropathy and / or corneal edema.
• Clinically, the corneal endothelium has been described to have a "hammered silver"
or "beaten bronze" appearance in ICE syndrome patients
• Diagnosis: Work up and F/u
– Specular microscopy, IOP and Gonioscopy for PAS.
– with Stereo disc photographs and Visual Field Analysis , HRT or OCT.

179. Chandler syndrome
Initially ‘hammered-silver’ endothelial
changes
Later oedema which may cause halos

180. Progressive iris atrophy
Progressive stromal iris atrophy
Broad-based PAS Displacement of pupil
towards PAS

181. Iris naevus (Cogan-Reese) syndrome
Diffuse iris naevus Pedunculated iris nodules

182. Surgical outcome in ICE
• Long-term surgical outcomes have been reported to be
slightly better with glaucoma drainage implants (survival of
71% at 1 year, 71% at 3 years, and 53% at 5 years)
versus trabeculectomy with antifibrotic agents (survival of
73% at 1 year, 44% at 3 years, and 29% at 5 years).[1]
• Maintaining long-term success can be challenging, as the
fistula can be obstructed with advancing abnormal corneal
endothelial cells may require multiple surgeries to maintain
stable IOP control.[1]
• Diode laser cyclophotocoagulation is reserved For
intractable cases (failed trabeculectomy or glaucoma
drainage device).
1. Doe EA, Budenz DL, Gedde SJ, Imami NR. Long-term surgical outcomes of patients with glaucoma secondary to the iridocorneal endothelial
syndrome. Ophthalmology. 2001 Oct;108(10):1789-95

183. Glaucoma associated with iridoschisis
• Rare, affects elderly, often bilateral
• Underlying, angle-closure glaucoma in about 90%
Shallow anterior chamber Iridoschisis - usually inferior

184. Congenital Glaucomas
1. Primary
2. Iridocorneal dysgenesis
– Axenfeld-Rieger anomaly
– Peters anomaly
– Aniridia
3. In phacomatoses
– Sturge-Weber syndrome
– Neurofibromatosis - 1

185. Primary infantile glaucoma occurs in ~1 in 10 000 births.
Bilateral in 65–80% of cases
65% boys
Most sporadic & ~10% are familial, usually transmitted as an
autosomal recessive trait, with penetrance varying from 40% to 100%
Flat iris insertion Concave iris insertion
Primary congenital glaucoma

186. Primary congenital glaucoma
– True congenital glaucoma (40%) in which IOP is elevated during intrauterine
life.
– Infantile glaucoma (55%) which manifests prior to age 3.
– Juvenile glaucoma, the least common, in which IOP rises between 3 and 16
years of age.
• PCG, by definition unassociated with other major ocular abnormalities,
– is thought to be caused by trabeculodysgenesis  impaired aqueous outflow .
– It is usually sporadic, but approximately 10% are AR with variable penetrance.
Several genes have been implicated, prominently CYP1B1.
– The prognosis is dependent on severity and age at onset/diagnosis; in true
congenital glaucoma, legal blindness is the outcome in at least 50% of eyes.
• Secondary infantile glaucoma - tumours such as retinoblastoma, persistent
fetal vasculature (persistent hyperplastic primary vitreous) and uveitis.

187. Primary congenital glaucoma
Diagnosis
• Presentation usually with
– Primary congenital glaucoma typically presents in the neonatal or
infantile period with the classic triad of epiphora, photophobia, and
blepharospasm.
– corneal haze, large (buphthalmos ) or asymmetrical eyes .
• Corneal haze -- raised IOP diffuse oedema or localized oedema
due to breaks in DM.
• Buphthalmos is due to stretching of sclera by elevated IOP prior to
the age of 3 years. Blue sclera. Complications include myopia and
lens subluxation.
• Haab striae are curvilinear healed breaks in Descemet membrane.
• Corneal scarring and vascularization .
• Optic disc cupping in infants may regress once IOP is normalized.
Most normal infants exhibit no apparent cup.

188. Primary congenital glaucoma
• Evaluation under general anaesthesia is generally required;
intravenous ketamine lowers IOP less than other agents.
– IOP measurement should be performed first. It is preferable where
possible for this to be measured in a conscious or sedated child; 10–12
mmHg is normal.
– Corneal diameter measurement; >12 mm prior to the age of one year
is highly suspicious.
– Anterior chamber examination with an operating microscope and/or
portable slit lamp.
– Optic disc examination; asymmetry or a cup/disc ratio of >0.3 is
suspicious.
– Refraction.
– Gonioscopy using a direct goniolens may be normal or reveal
trabeculodysgenesis, vaguely characterized by an anteriorly located
iris insertion and a hypoplastic appearing peripheral iris.

189. Clinical features of primary congenital glaucoma
• Depend on age of onset
• Bilateral in 75% but frequently asymmetrical
Breaks in Descemet membrane
Corneal oedema associated with
lacrimation and photophobia
Buphthalmos if IOP becomes
elevated prior to age 3 years.
Optic disc cupping
A newborn’s cornea is typically 9.5-10.5
mm in diameter and
Increases to 10.0-11.5 mm by age 1.
Any diameter above 12.5 mm suggests
an abnormality, especially if there is
asymmetry between the two eyes.

190. Management of primary congenital glaucoma
2. Goniotomy 3. Trabeculotomy
1. Measurement of IOP and
corneal diameters
4. Trabeculotomy Plus Trabeculectomy with Mitomicin C
5. Shunt Implant
6. Cycloablation using Diode, Microinvasive endo-photocoagulation, cryotherapy.
The success rate for angle surgery is approximately 80% after 1 or 2 procedures, while
the other procedures report a success rate of 33-80%.
7. Amblyopia and refractive error need to be monitored long term

191. • Bilateral but asymmetrical
• Glaucoma is uncommon
Posterior embryotoxon Attached strands of iris to posterior
embryotoxon
Axenfeld anomaly

192. • Autosomal dominant
•Bilateral but asymmetrical
•Glaucoma in 50%
Stromal hypoplasia and corectopia Ectropion uveae
Full-thickness iris atrophy Angle anomalies
Rieger anomaly

193. Rieger syndrome
Rieger anomaly Dental and facial anomalies

194. Axenfeld–Rieger syndrome
• Axenfeld–Rieger syndrome is the umbrella term for a spectrum of disorders featuring bilateral
developmental ocular anomalies: Axenfeld anomaly, Rieger anomaly and Rieger syndrome.
• It is caused by defective neural crest cell-related processes during fetal development;
• An abnormal endothelial cell membrane has been identified on anterior segment structures in some
patients.
• The key implication of the syndrome is a 50% risk of glaucoma.
• Associated variants in several different genes have been found, including PITX2, PAX6, FOXC1 and
RIEG2; that is, different genetic abnormalities can give a similar clinical picture.
• Two genetic forms of Rieger syndrome. Type I results from mutations on chromosome 4 and Type II
results from mutations on chromosome 13.
• Family history is common, with AD inheritance & variable expressivity but very high penetrance.
• Cases may be sporadic, no gender predilection.
Clinical features
• Axenfeld anomaly is characterized by posterior embryotoxon with attached strands of peripheral
iris,
• Rieger anomaly often manifests with an anterior segment appearance similar to that of ICE syndrome.
1. Posterior embryotoxon.
2. Iris stromal hypoplasia
3. Ectropion uveae
4. Corectopia and full-thickness iris defects

195. Axenfeld–Rieger syndrome
• Gonioscopy in mild cases shows the Axenfeld anomaly. In severe cases,
broad leaves of iris adhere to the cornea anterior to the Schwalbe line.
• Glaucoma develops in about 50%, usually during childhood or early
adulthood. Surgical management is often necessary.
• Rieger syndrome is characterized by the Rieger anomaly together with
extraocular malformations that are caused by defective neural crest cell
related tissue development:
– Dental anomalies: hypodontia (few teeth) and microdontia (small teeth).
– Facial anomalies: maxillary hypoplasia, broad nasal bridge, telecanthus and
hypertelorism.
– Other anomalies include redundant paraumbilical skin and hypospadias.
– Hearing loss, hydrocephalus, cardiac and renal anomalies and congenital hip dislocation
are rare.

196. Peters anomaly
• Usually sporadic
•Bilateral in 80%
•Glaucoma in 50%
Corneal opacity with iris adhesions
Peters type I
Corneal opacity with lenticular adhesions
Peters type II

197. Peters anomaly
• Peters anomaly is a rare but bilateral in more than half of cases.
• Neural crest cell migration defect during fetal development.
• Most cases are sporadic.
Clinical features
• Peters type I affects the cornea alone, type II shows both corneal and lens
abnormalities.
• Central corneal opacity of variable density
• Posterior corneal defect involving the posterior stroma, Descemet
membrane and endothelium with or without iridocorneal or
lenticulocorneal adhesions.
• Glaucoma occurs in about 50% due to associated angle anomaly. Onset is
usually in infancy but occasionally in childhood or later. The prognosis
tends to be worse than in primary congenital glaucoma.
• Systemic associations including craniofacial and central nervous system
anomalies . ‘Peters plus’ syndrome (AR) includes dwarfism and mental
retardation, plus disorders of the ear and cleft palate.

198. Systemic Implications of Aniridia
• AN-1 - 85%
– Autosomal dominant
– Isolated
• AN-2 (Miller syndrome) - 13%
– Deletion of short arm of chromosome 11
– Wilm tumour, genitourinary anomalies and mental
handicap
• AN-3 (Gillespie syndrome) - 2%
– Autosomal recessive
– Mental handicap and cerebellar ataxia

199. Aniridia
Genetics
• Aniridia (AN) is a rare bilateral condition that may have life threatening
associations.
– Result of abnormal neuroectodermal development secondary to a mutation in
the PAX6 gene.
– PAX6 is adjacent to gene WT1, mutation to which promote to Wilms tumour.
• >2/3rd - AD aniridia and has no systemic implications. Penetrance is
complete with variable expressivity.
• Rest - Sporadic, including WARG, previously known as Miller, syndrome
(Wilms tumour, Aniridia, mental Retardation, Genitourinary abnormalities),
includes about a third of patients.
– Children with sporadic aniridia have about a 30% chance of developing Wilms
tumour.
• Gillespie syndrome accounts for only about 1% of cases. Inheritance is AR
but is not caused by PAX6 mutations. Cerebellar ataxia and mental handicap
are features.
• Marinesco-Sjögren syndrome in which congenital cataract is present, as
well as cerebellar ataxia, intellectual disability, and aniridia

200. Aniridia
Diagnosis
– All patients with sporadic aniridia should have abdominal ultrasonography every 3 months
until 5 years of age, every 6 months until 10 years of age and annually until 16 years of age to
detect the development of Wilms tumour or until molecular genetic analysis confirms the
absence of a WT1 mutation.
• Presentation is typically at birth with nystagmus and photophobia. Notice of the
absence of irides or apparently large pupils.
• Aniridia is variable in severity, ranging from minimal to total absence
• Lids - meibomian gland dysfunction.
• Cornea
– Tear film instability, dry eye and epithelial defects are common.
– Limbal stem cell deficiency may result in ‘conjunctivalization’ of the peripheral cornea.
– Total corneal central stromal scarring and vascularization may occur in end-stage disease.
• Lens - cataract and subluxation (usually superiorly ).
• Fundus. Foveal and/or optic nerve hypoplasia and choroidal coloboma.
• Gonioscopy even in eyes with apparently total aniridia usually shows a
hypoplastic or rudimentary frill of iris tissue .
• Glaucoma (75%) presents in late childhood or adolescence due to secondary
synechial angle closure glaucoma .

201. Signs of aniridia
Subtotal absence
Synechial angle-closure
glaucoma in 75%
Occasional cataract and lens
subluxation
Partial absence

202. Treatment in Aniridia
• Treatment is difficult and the prognosis guarded.
Glaucoma
– Medical treatment is usually inadequate in the longer term.
– Goniotomy should be performed before the development of irreversible
angle closure.
– Trabeculectomy or combined trabeculectomy + an antimetabolite and/ a
mini-shunt.
– Glaucoma drainage devices may be effective.
– Diode laser cycloablation - if other modalities fail.
• Painted contact lenses may be used to create an artificial pupil and
improve both vision, nystagmus and cosmesis; or simple tinted lenses
• Lubricants - required for associated keratopathy.
• Cataract surgery is often required; A tinted artificial lens implant may
improve photophobia. Minimal Trauma to the corneal limbus to preserve
stem cell function.
• Prosthetic iris implantation - in pseudophakic aniridic eyes, but may
worsen glaucoma.
• Limbal stem cell transplantation with or without keratoplasty may be
required.
• Refractive errors, amblyopia and squint need proper management.

203. Glaucoma in Sturge-Weber syndrome
• Glaucoma in 30%
• Ipsilateral to facial haemangioma
• Buphthalmos in 60% of SWS with glaucoma
• Caused by raised episcleral venous
pressure associated with episcleral
haemangioma
• Angle anomaly may also be responsible
Glaucoma Causes

204. Sturge-Weber syndrome
• Sturge–Weber syndrome (encephalotrigeminal angiomatosis) is a
congenital, sporadic phacomatosis .
• Glaucoma ipsilateral to the facial haemangioma develops in about 30%,
and in 60% of these IOP elevation occurs before the age of 2 years and
may result in buphthalmos .
• In the remainder, glaucoma may develop at any time from infancy to
adulthood.
• The pathogenesis is uncertain; putative mechanisms include
trabeculodysgenesis in infants and raised episcleral venous pressure
Treatment
• Medical treatment alone may be adequate.
• Goniotomy may be successful in eyes with angle anomalies.
• Combined trabeculotomy–trabeculectomy gives good results in early-
onset cases, but carries a relatively high risk of choroidal effusion and
suprachoroidal haemorrhage.
 sl. 8

205. • Caused by angle anomaly
• Angle neurofibroma may also be
responsible
Associated ectropion uvea
Glaucoma Causes
• Inheritance is AD with irregular penetrance
and variable expressivity
• Glaucoma is relatively rare and, when present,
usually unilateral and congenital
• 50% of patients with glaucoma have an
ipsilateral plexiform neurofibroma of the upper
eyelid, or facial hemiatrophy
Glaucoma in neurofibromatosis - 1

206. Thank You
Source :
Kanski’s clinical ophthalmology
Kanski Tutorials,
https://eyewiki.aao.org/
Genetics for Ophthalmologists The molecular genetic basis of ophthalmic disorders_Black_2002
https://www.nhp.gov.in/disease/eye-ear/glaucoma
Atlas of GLAUCOMA second edition Edited by Neil T Choplin,
Jakobiec's Principles & Practice of Ophthalmology volume 2 3rd edition_Albert, Miller, Azar, Blodi_2008