this tells about the overview of glaucoma and the primary open angle glaucoma
valve surgery and cyclodestruction surgery are not listed, however they are important
5. Group of disorders
characterized by a progressive optic
neuropathy
resulting in a characteristic appearance
of optic disc
and a specific pattern of irreversible
visual field defects
that are associated frequently but not
invariably with raised intraocular
pressure.
6. A. CONGENITAL/
DEVELOPMENTAL
Primary congenital
glaucoma
Developmental glaucoma
B. PRIMARY ADULT
GLAUCOMA
Primary open angle
glaucoma [POAG]
Primary angle closure
glaucoma [PACG]
Primary mixed mechanism
glaucoma
C. SECONDARY
GLAUCOMA
7.
8. Global prevalence
2% > 40y
10% > 80y
Global 8%
India 12.8%
Glaucoma blindness
Ethnic POAG PACG
Indian 1 1
Urban
Chinese
1 2
Mongolian 1 3
European,
African,
Hispanic
5 1
Glaucoma blindness
9. GLAUCOMATOUS OCULAR DAMAGE
progressive optic neuropathy due to death of retinal
ganglion cells (RGCs) optic disc appearance and
specific visual field defects
RETINAL GANGLION CELL (RGC) DEATH
blocks the transport of growth factors (neurotrophins)
from the brain to the RGCs.
apoptosis engulfed by neighbouring cells, without
[inflammatory response]
loss of retinal nerve fibres. optic disc changes and
specific visual field defects
12. Aka chronic simple glaucoma of adult onset
Characterised by:
Slowly progressive raised IOP [ >21mmHg on few occasions]
Open normal appearing anterior angle chamber
Optic disc cupping
Specific visual field defects
13. Not known exactly
PREDISPOSING AND
RISK FACTORS
Intraocular pressure
Hereditary [ Myocilin C ,
Optineurin, WD repeat
domain 36]
Age
Race
Myopes
Central corneal thickness
Diabetics
High blood pressure
Smoking
Thyrotoxicosis
Corticosteroid
responsiveness
14. Failure of aqueous outflow
pump mechanism due to
trabecular meshwork
stiffening and apposition of
Schlemm’s canal wall
Thick, sclerosed trabecular
meshwork with faulty collagen
tissue
Narrowing of intertrabecular
spaces
Deposition of amorphous
material in juxtacanalicular
space
Collapse of schelmm’s canal and
absence of giant vacuoles in the
cells lining it
Immunogenic mechanism
Increased gammaglobulin
and plasma cell on
immunochemistry
Positive ANA reaction in
some
15. 1% above 40y
1/3 of glaucoma
Ethnic POAG PACG
European,
African,
Hispanic
5 1
Mongolian 1 3
Urban
Chinese
1 2
Indian 1 1
17. Asymptomatic
Mild headache and eye ache
Scotoma [ defect in visual
field]
Increasing difficulty in
reading and close work
Delayed dark adaptation
Significant loss of vision ,
blindness
18. I. Anterior segment signs
II. Intraocular pressure changes
III. Optic disc changes
IV. Visual field defects
V. Ocular associations
20. Initial:
Diurnal variation test [ 3-4 h/24h]
fall on evening
5mmHg : suspicious
>8mmHg : glaucoma
Later :
Permanent rise
30-45mmHg
21. Best examination technique:
stereoscopic view with contact or non-contact lens on slit lamp
biomicroscopic examination
Recording and documentation :
serial hand drawings, photography, photogrammetry, confocal
scanning laser topography [ CSLT], Heidelberg retinal
tomography [ HRT],coherence tomography [CT], nerve fibre
analyser [ NFA]
22. a. Early changes
Vertically oval cup
Cups symmetry between
eyes [>0.2]
Large cup [ >0.6]
Splinter hemorrhages
Pallor areas on disc
Retinal nerve fibre atrophy
[ red free light]
23.
24. b. Advanced changes
Marked cupping [ 0.7-0.9]
Thinning of neuroretinal rim ( crescentic shadow)
[ISNT rule]
Nasal shift of retinal vessels [ Bayonetting sign]
Retinal arterioles pulsation
Lamellar dot sign
29. Initially observed in Bjerrum area
[ 10-25 degree from fixation]
1) Isopter contracture
2) Baring of blind spot
3) Small wing- shaped paracentral
scotoma
4) Seidel’s scotoma
5) Bjerrum’s scotoma /Arcuate
6) Ring/ Double arcuate scotoma
7) Roenne’s central nasal step
8) Peripheral field defects
9) Advanced glaucomatous field
defects [ tubular vision,
temporal island]
30.
31. Diagnosis
Tested twice
In conjunction with clinical
feature
Progression
Comparing individual
single field printouts
Overview printout
Progression analysis
software
Visual field index
32. High myopia
Fuch’s endothelial dystrophy
Retinitis pigmentosa,
Central retinal vein occlusion
Primary retinal detachment.
33. 1) Tonometry. Applanation tonometry
2) Central corneal thickness [ corrected
readings in < 545 and > 600 microns]
3) Diurnal variation test [ early cases ]
4) Gonioscopy [ rule out other forms of
glaucoma]
5) Documentation of optic disc changes
34. 1) Slit-lamp examination [rule out
causes of secondary open angle
glaucoma]
2) Perimetry to detect the visual
field defects.
3) Nerve fibre layer analyzer
(NFLA) detect glaucomatous
damage to retinal nerve fibre
before visual changes
4) Provocative tests [border-line
case]
Water drinking test, bulbar
pressure test, prescoline test,
caffeine test
35. Depend upon level of IOP,
glaucomatous cupping of
the optic disc and the
visual field changes :
Primary open angle
glaucoma (POAG)
IOP >21 mm of Hg +
definite glaucomatous optic
disc cupping + visual field
changes
Ocular hypertension
IOP >21 mm of Hg but no
optic disc or visual field
changes
Normal or low tension
glaucoma (NTG) (LTG)
IOP < 21 mm of Hg +
glaucomatous optic disc
cupping + /-visual field
changes
36. Aim : to lower
intraocular pressure
to a level where
(further) visual loss
does not occur
Baseline data :
visual acuity, slit-
lamp examination of
anterior segment,
tonometry ,optic disc
evaluation, gonioscopy
and visual field
charting.
American Academy of
Ophthalmology (AAO)
grading
Degree Description
Mild Characteristic optic-nerve
abnormalities are consistent
with glaucoma but with normal
visual field.
Moderate Visual-field abnormalities in one
hemi field and not within 5
degrees of fixation.
Severe Visual-field abnormalities in
both hemifields and within 5
degrees of fixation
38. BASIC PRINCIPLES
1. Identification of target
pressure.
<16 to 18 mmHg mild to
maderate damage.
12-14 mmHg severe
damage.
2. Single drug therapy.
topical antiglaucoma
drugs
3. Combination therapy
4. Monitoring of therapy
disc changes, field changes
, tonometry
39. Class Used in Mechanism of
action
Prostaglandin analogues
• Latanoprost 0.005
• Travoprost 0.004
• Bimatoprost 0.003
• Unoprostone 0.15
• First choice
• Good adjunctive drug
• Incease uveo-
scleral outflow
Topical beta-blockers
• Timolol maleate ( 0.25,
0.5% )
• Betaxolol (0.25% )
• Levobunolol (0.25, 0.5%)
• Carteolol (1%)
First choice in poor
• initial therapy, not in
bronchial asthma /heart
blocks.
• Cardiopulmonary problems.
• Once a day use
• hyperlipidemias
/atherosclerotic
cardiovascular disease.
• Reduces
aqueous
secretion [beta -
receptors in the
ciliary
processes].
40. Class Used in Mechanism of action
Adrenergic drugs.
Epinephrine
hydrochloride (0.5, 1, 2%)
Dipivefrine hydrochloride
(0.1%)
• Combination therapy:
failure of filtration
[glaucoma surgery,
• allergy]
increasing aqueous
outflow by stimulating
beta
recepters in the aqueous
outflow system
Brimonidine (0.2%) • second drug of choice ,
combination therapy
• [allergy and
tachyphylaxis]
lowers IOP by
decreasing aqueous
production
Dorzolamide
(2%: 2-3 times/day)
• second line of drug
adjunct drug.
decreasing aqueous
secretion by altering ion
transport along ciliary
epithelium
Pilocarpine
(1, 2, 4%: 3-4 times/day).
• adjunctive therapy
• second choice (poor
patient)
• [accommodation and
miosis spasm in young ]
mechanically
increasing aqueous
outflow
41. Combination of two drugs
One decreases aqueous production (timolol /betablocker,
/brimonidine / dorzolamide)
Another drug increase aqueous outflow (latanoprost /
brimonidine / pilocarpine)
42. Oral carbonic anhydrase inhibitors
Acetozalamide, methazolamide
Not recommended for long-term use , may be added to control
IOP for short term
Hyperosmotic agents
mannitol 1-2 mg/kg initially for patient with > 30mmHg IOP
43. Done using argon laser ,
diode laser or selective
laser trabeculoplasty
uncontrolled IOP despite
maximal tolerated medical
therapy
primary therapy in non-
compliance to medical
therapy
Technique and role of ALT
/ DLT
additive effect to medical
therapy.
Lower 8-10 mmHg / 12-16
mmHg
Treatment regime
50 spots on anterior half of
the trabecularmeshwork
over 180°.
Complications
transient acute rise of IOP,
(pretreatment with
pilocarpine /acetazolamide)
Transient inflammation
(topical steroids for 3-4
days)
haemorrhage, uveitis,
peripheral anterior
synechiae and reduced
accommodation.
44.
45. Selective laser trabeculoplasty (SLT)
Targets selctively pigmented trabecular meshwork (TM)
cells without causing thermal/ collateral damage to non-
pigmented cell
No scar / damage to TM
Can be used in patients treated with ALT
46. INDICATIONS
1. Uncontrolled glaucoma despite maximal medical therapy
and laser trabeculoplasty.
2. Non-compliance of medical therapy and nonavailability of
ALT.
3. Failure with medical therapy and unsuitable for ALT either
due to lack of cooperation or inability to visualize the
trabeculum.
4. Eyes with advanced disease i.e., having very high IOP,
advanced cupping and advanced field loss should be treated
with filtration surgery as primary line of management.
47. Trabeculectomy ( congenital/developmental glaucoma)
Filtration operations
provide a new channel for aqueous outflow and control the IOP
(below 21 mm of Hg).
A.External filteration surgery
1. Free-filtering operations (Full thickness fistula).
Elliot's sclero-corneal trephining, punch sclerectomy, Scheie's
thermosclerostomy and iridencleisis.
2. Guarded filtering surgery (Partial thickness fistula e.g.,
trabeculectomy).
3. Non-penetrating filtration surgery e.g., deep sclerectomy and
viscocanalostomy.
B.Internal filteration surgery
48. Carain in 1980
most frequently performed
partial thickness filtering
surgery
Indications
1. Primary angle-closure
glaucoma with peripheral
anterior synechial involving
more than 270 degree angle.
2. Primary open-angle
glaucoma not controlled with
medical treatment.
3. Congenital and
developmental glaucomas
where trabeculotomy and
goniotomy fail.
4. Secondary glaucomas where
medical therapy is not
effective.
Mechnanisms of
filtration
1. fistula created around
margin of scleral flap,
through which aqueous
flows from anterior
chamber into
subconjunctival space.
2. If the tissue is
dissected posterior to the
scleral spur, a
cyclodialysis produced
leading to increased
uveoscleral outflow.
49. Surgical technique
1. initial steps of anaesthesia,
draping, exposure of eyeball
and fixation with superior
rectus suture are similar to
cataract operation
2. Conjunctival flap
A fornix-based or limbal-based
conjunctival flap is fashioned
and the underlying sclera is
exposed. The Tenon’s capsule is
cleared away using a Tooke’s
knife,and haemostasis is
achieved with cautery.
3. Scleral flap .
A partial thickness limbal-based
scleral flap of 5 mm × 5 mm size
is reflected down towards the
cornea.
4. Excision of trabecular tissue
narrow strip (4 mm × 2 mm) of
the exposed deeper sclera near
the cornea containing the canal
of Schlemm and trabecular
meshwork is excised.
5. Peripheral iridectomy
performed at 12 O’clock
position with de Wecker’s
scissors.
6. Closure.
The scleral flap is replaced
and 10-0 nylon sutures are
applied. Then the
conjunctival flap is reposited
and sutured with two
interrupted sutures (in case
of fornix-based flap) or
continuous suture (in case of
limbal-based flap)
7. Subconjunctival
injections of dexamethasone
and gentamicin are given.
8. patching
Eye patched with sterile eye
pad
50.
51. Complications
Postoperative shallow
anterior chamber,
hyphaema,
iritis,
Cataract due to accidental
injury to the lens,
endophthalmitis
Antimetabolites
for wound modulation, when
any risk factors for the failure
of trabeculectomy present :
1. Previous failed filtration
surgery.
2. Glaucoma-in-aphakia.
3. Certain secondary glaucomas
e.g. inflammatory glaucoma,
post-traumatic angle recession
glaucoma, neovascular glaucoma
4.Patients treated with topical
antiglaucoma medications >
three years.
5. Chronic cicatrizing
conjunctival inflammation.
Agents.
5-fluorouracil (5-FU)
mitomycin-C (MMC)
Collagen implant
52. Sutureless trabeculectomy
1. initial steps
2. conjunctival flap
Sclero-corneal valvular
tunnel (4mmX 4mm )
Make 4mm partial
thickness scleral groove,
2.5mm away from superior
limbus. 4mm wide extends
1.5mm in corneausing a
crescent knife.
4. entry into anterior
chamber using 3.2 angled
keratome
5.Punching of post. Lip of
anterior chamber entry
site with Kelly’s punch
6. peripheral iridectomy at
12 o’clock position using
Wecker’s /Vanna’s scissors
7. closure
Anterior chamber filled
with BSS/air to close
sclero-tunnel incision.
53.
54. Non- penetrating filteration surgeries
anterior chamber not
entered. [reduce post-
operative endophthalmitis,
overfiltration and
hypotony]
disadvantage : less IOP
control
1. Deep sclerectomy.
partial thickness scleral
flap, a second deep partial
thickness scleral flap is
fashioned and excised
leaving very thin sclera,
trabeculum and
Descemet’s membrane
superficial scleral flap is
loosly approximated and
conjunctival incision
closed.
2. Viscocanalostomy.
similar to deep
sclerectomy, except that
after excising the deeper
scleral flap, high viscosity
viscoelastic substance is
injected into the
Schlemm's canal with a
special cannula.
55. Restore filteration through
Schlemm’s canal
To keep normal anatomy
and conjunctival bleb
free reducing risk of
endophthalmitis and
ocular hypotomy
1. canaloplasty ( dilatation
and circumferential
traction of canal)
2. trabectome ab interno
microcautery that ablates
TM and inner wall of
Schlemm’s canal
3.iStent titanium micro
device placed inside
Schelmm’s cannal
56.
57.
58.
59. OCULAR
HYPERTENSION
IOP >21 mm of Hg
but no optic disc/
visual field changes
Treated as POAG in
the presence of high
risk factors
GLAUCOMA SUSPECT
An adult having normal open
angle on gonioscopy and any
of:
Elevated IOP
Suspicious disc changes [
asymmetric cup-disc >0.2,
narrowing of neuroretinal
rim, disc hemmorrhage
Visual field consistent with
glaucomatous damage
60. High risk factors :
Ocular hypertension study
[ OHTS] & European
Glaucoma Prevention
Study [ EGPS]
IOP> 30mmHg
CCT > 550µm
Vertical cup :disc > 0.7
Increased age
Increased pattern
standard deviation (PSD)
on Humphrey visual field
test
Disc haemmorrhages
Other risk factors :
Family history
Fellow eye of unilateral
POAG
Ocular condition: myopia,
steroid responder , positive
diurnal variation
Systemic: DM , sleep
apnea, hypertension,
hypothyroidism,
migranous headaches and
vasospasm
61. Treatment
Patients with high-risk
factors
Same as POAG
Patients with no high risk
factors
annual examination of
optic disc, perimetry and
record of IOP
Treatment is not required
till glaucomatous damage
is documented.
62. NORMAL TENSION
GLAUCOMA
IOP< 21 mm of Hg with typical glaucomatous disc changes
w/wo visual field defects a
angle of anterior chamber is open on gonioscopy , no
secondary cause for glaucomatous disc changes.
16% of all cases of POAG ,
> 40 years is 0.2%.
63. Etiopathogenesis
chronic low vascular
perfusion, which makes
the optic nerve head
susceptible to normal IOP.
supported by following :
Raynauld phenomenon i.e.,
peripheral vascular spasm
on cooling,
Migraine,
Nocturnal systemic
hypotension and
overtreated systemic
hypertension.
Reduced blood flow velocity
in the ophthalmic artery
Clinical features
IOP < 21mmHg
Optic disc changes
Significant thinning of
neuroretinal rim
Frequent disc splinter
hemmorrhages
Prevalent peripapillary
atrophic changes
Visual field defects :
Deeper, steeper, more
localised,
64. High pressure glaucoma
Early stages of POAG
Glaucoma with
intermittent rise in IOP
Previous episode of
glaucoma
Non-glaucomatous optic
neuropathy
Congenital optic disc
anomalies
Acquired optic
neuropathies
65. 1.Medical treatment
lower IOP by 30% [12-14 mm
of Hg]
Betaxolol ,drug of choice
[lowering IOP , increases
optic nerve blood flow]
Avoid other beta blockers
and adrenergic drugs
(nocturnal systemic
hypotension )
Neuroprotective effect –
brimonidine
Prostaglandin analogues,
e.g., latanoprost [greater
ocular hypotensive effect in
eyes with normal IOP]
2. Trabeculectomy
progressive field loss
3. Systemic calcium channel
blockers (e.g., nifedipine)
patients with peripheral
vasospasm.
4. Monitoring of systemic
blood pressure should
bedone for 24 hours. avoid
night dose of anti-
hypertensive.
Editor's Notes
This is a difficult topic. Be prepared.
Explain about production, path, outflow of aqueous humor
Trabecular and uveoscleral are the 2 outflow pathway
Known about:
Ocular hypertension
Normal or low tension glaucoma
The classification intermingled: in congenital and secondary , there can be open and close glaucoma too
Know about Schaferr grading and that angle
Neurotrophins stimulates regeneration of RGC
Visual field defect develops after the damage extends beyond the normal physiological overlap of functional zones.
Important to know these theories
I will only present about primary open angle glaucoma
No obvious cause of rise IOP
50-70, black, thin CCT, DBP<55, 6w steroids
Most pt present asymptomatic, the raised IOP are found out accidentally
Periodic eye examination after 50y, freq change sin presbyopic glasses,
Central corneal thickness
morning 20%, aftrnoo 25%, biphasic 55%
Study the normal optic disc first
Selective loss of neural rim in inf n sup poles,
Adv case: crescentic shadow ,Isnt rule ,, broken off at margin,, in high IOP,, in LC, slit shaped
Pathophysiology of disc changes :Mechanical [ raised IOP forces LC back n squeeze nerve]and vascular factor [ischemic atrophy]
Progression of optic disc changes
Mild constriction of c n p field, exclusion of blind spot from central field due to inward curve of outer boundry of 3o,
Grading based on Humphrey field analyzer. Difficult to understand
asymmetrical, bilateral, slowly progressive edema of the cornea in elderly patient
rare, genetic disorders that involve a breakdown and loss of cells in the retina
8
From the baseline evaluation data a ‘target pressure’ (below which glaucomatous damage is not likely to progress)
Selective alpha-2-adrenergic agonist
Contracts longitudinal muscle of ciliary body and opens spaces in trabecular meshwork
ncreasing outflow facility, possibly by producing collagen shrinkage on the inner aspect of the trabecular meshwork and opening the intratrabecular spaces
no longer performed [ full thickness fistula]
Mitomycin-C is onlyused at the time of surgery. A sponge soaked in 0.02%(2 mg in 10 ml) solution of mitomycin-C is placed atthe site of filtration between the scleral and Tenon’s
6mm diamtr n imm thick sutured over scleral flap
capsule for 2 minutes, followed by a thorough
irrigation with balanced salt solution.