Glaucoma CME - ND - SV - 22feb2021

RECENT ADVANCES IN
GLAUCOMA MANAGEMENT-
MEDICAL AND SURGICAL
DR NILANJANA DEB, DNB, FRCS(ED), PhD

SENIOR CONSULTANT, GLAUCOMA AND RETINA
SMARTVISION EYE HOSPITAL, HYDERABAD
WHAT IS GLAUCOMA
 Group of diseases characterized by progressive loss
of retinal ganglion cells (optic nerve fibres)
 High IOP is the strongest known risk factor, but not
the only factor
 Normal IOP range: 10-22mm Hg
 Diagnostic criteria:
 Intraocular pressure
 Visual fields
 Disc changes
BURDEN OF DISEASE
BURDEN OF DISEASE
2nd leading cause for global blindness (12.3% of
total cases)
Worldwide, 64 million cases in 2010, estimated to
increase to 76 million in 2020, 111 million in 2040
3rd leading cause of blindness in India (12.8% of
total blindness-11.9 million cases in 2010 )
Females have higher risk of ACG( 4:1) and
OHT(2:1)
Prevalence ↑ with age (2% at 40yrs, 5-9% at 65 yrs)
http://www.glaucomaindia.com ,
http://www.glaucoma.org/glaucoma/glaucoma-facts-and-stats.php
TYPES OF GLAUCOMA
TYPES OF GLAUCOMA
Primary Open Angle Glaucoma (POAG):
Patency of trabecular meshwork affected
Primary Angle Closure Glaucoma (PACG):
Narrow iridiocorneal angle- TM obstruction
Types of Glaucoma
VARIANTS OF GLAUCOMA
 Ocular hypertension: Elevated IOP without disc
changes
 Normal tension glaucoma: Optic disc changes
despite normal IOP
 Other types- secondary, congenital, juvenile,
drug-induced
DRUG INDUCED GLAUCOMA
DRUG INDUCED GLAUCOMA
 Steroids- open angle type
o ↑ GAG, collagen, elastin, fibronectin, ↓ TM Outflow
o Stop/ switch steroids, IOP normalises after 3-4 wks
o If not, give topical anti-glaucoma drugs/ Diamox
o Oral steroids safer than topical steroids
 Neurotropic drugs- induce angle closure

o TCA, SSRI, MAOI, anti Parkinsonian, anticholinergics,
H1 & H2 blockers, antispasmodics, sulpha antibiotics
o Rx- stop drug, IV mannitol in resistant cases
o Avoid Diamox – it can precipitate angle closure!
SYMPTOMS OF GLAUCOMA
 POAG may be totally asymptomatic
Late stages may present with reduced side-vision
 PACG – c/o pain, redness, watering , photophobia
 Congenital- child with buphthalmos, watering
 History of refractive errors, positive family history, trauma,
drug use, systemic diseases ( DM, BP, lipids, Thyroid,
Arthritis, Sleep Apnoea etc)
SIGNS
 ↑ in IOP >21mmHg
(IOP normal in NTG)
 Optic disc cupping
 Visual field changes
BUT…
 IOP not helpful diagnostically until it reaches approx 40mmHg

 Retinal nerve fiber layer loss precedes visual field loss in
glaucoma
 Disc damage in early glaucoma difficult to identify
ROLE OF OCT
PREPERIMETRIC GLAUCOMA
TREATMENT OPTIONS
Control of IOP is the only modifiable risk

factor
IOP control can be achieved by-
Ocular hypotensive drugs
Lasers/ultrasound
Surgery (Filtration/drainage device/ MIGS)
OCULAR HYPOTENSIVE AGENTS
 PG Analogues- Latanoprost, Travoprost, Bimatoprost

 β blockers- Timolol, Betaxolol
 α agonist – Brimonidine
 CA Inhibitors- Dorzolamide, Brinzolamide
Acetazolamide
 Miotics- Pilocarpine
 Hyperosmolar agents- Oral Glycerine, I.V. Mannitol
Glaucoma drugs
ROLE OF NEWER DRUGS
• Neural damage irreversible – hence need for

neuroprotective agents
• Patients with systemic comorbidities – not much

options left other than surgery
• Drug allergy- Need for preservative free drugs
• Long-term drug delivery systems- improved QOL

Drug Delivery Systems
BENEFITS
• Reduce dosing frequency- improve adherence
• Ensure proper application- reduce side effects
• Adequate drug delivery to target site - higher
bioavailability
• Long term safety not known CONCERNS

• Interaction and stability of drug in carrier system
unknown
• Amount of drug that maybe delivered limited
• Complicated technology , expensive
NEWER GLAUCOMA DRUGS
SLOW RELEASE BIMATOPROST
• Fornix ring
• Intracameral implant
TRAVOPROST SR Sytems
SLOW RELEASE TRAVOPROST
Punctal plug
Intracameral
implant
CONTINUOUS IOP MONITORING
SENSIMED Triggerfish®
1. Sensor
2. Contact lens
3. Data Cable
4. Portable recorder
Capsular Tension Ring

Sensor
Microfluidic IOL Implant®

LASERS IN GLAUCOMA
Yag iridotomy
Relieves pupillary block &
equalizes pressure gradient
between AC & PC in angle
closure eyes
Argon laser trabeculoplasty

Targets trabecular meshwork
& allows aqueous to leave
eye more efficiently in open
angle glaucoma
LASERS IN GLAUCOMA
LASERS IN GLAUCOMA
Selective laser trabeculoplasty(SLT)

Pigmented TM cells are
selectively targeted in a process
called photo-thermolysis sparing
surrounding nonpigmented TM
cells. Less tissue damage
compared to ALT
Micropulse laser trabeculoplasty (MLT)
More precise than

ALT and SLT
Less tissue damage
ULTRASOUND CILIARYPLASTY ( UCP)
Using High Intensity Focused Ultrasound (HIFU)
EyeOP1 device
Disposable sterile probe Mobile System Set-up Selection of probe size Probe sits in a suction
(3 available) cone
Cone centering and Administration in six

fixation with vacuum Coupling with liquid programmed steps
• Computer assisted noninvasive glaucoma procedure

• Targeted treatment preserving anatomic structures
• Treatment takes only 3 minutes
Control console
SURGERY IN GLAUCOMA
Trabeculectomy
REFRACTORY
SURGERY INGLAUCOMA
GLAUCOMA
Aqueous drainage device
- For eyes with good visual potential
- Ahmed Glaucoma Valve (Valved)
- Baerveldt, AADI (nonvalved)
-Success rate- 79%
REFRACTORY GLAUCOMA
REFRACTORYGLAUCOMA
Cyclo-destructive procedures
 Cryotherapy
 Diathermy
 Transscleral Diode CPC
Newer gentle lasers

 Endocyclophotocoagulation
 Micropulse cyclophotocoagulation
MINIMALLY INVASIVE
GLAUCOMA SURGERY (MIGS)
 Implanting a tiny device to allow fluid to drain from the

eye, reducing internal pressure.
 Safer than more aggressive surgeries such as
trabeculectomy or tube shunt
 Comparable efficacy as traditional procedures
 Lower risk of complications and no additional recovery
time.
 Indicated in mild-moderate open angle glaucoma
TYPES OF MIGS
• Trabecular Meshwork Bypass- iStent, Hydrus

 Suprachoroidal stents- Cypass, StarFlo, iStent Supra
 Subconjunctival implants- Xen Gel, Innfocus
MIGS Contra Indications OF MIGS
CONTRAINDICATIONS
 Angle closure and Secondary glaucoma

 Moderate to advanced disease, very high IOP
 Age < 18 yrs
 H/o Previous glaucoma Sx, refractive Sx
 One-eyed patients
GENE THERAPY
Target Gene Target protein/ mechanism Cellular
tissue changes
Trabecular DN Rho Inhibiting Rho Disruption of
meshwork
C3 Inactivating Rho by rebosylation cellular
adhesions in
DNRK Inhibiting Rho kinase cultured cells
Caldesmon Inhibiting actin-myosin activating
myosin MgGene
ATPase
Ciliary PG synthase ↑MMPase expression Degrade ECM
meshwork
Retina ErK Mediate neuroprotective activity of ↑RtmGC survival

extracellular factors
MeK1 Upstream activity of Erk
CNTF neuroprotection
TNF Alpha Inhibit CNTF
BRICK-4 Inhibit caspases

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RECENT ADVANCES IN

DR NILANJANA DEB, DNB, FRCS(ED), PhD

 Neurotropic drugs- induce angle closure

 IOP not helpful diagnostically until it reaches approx 40mmHg

Control of IOP is the only modifiable risk

 PG Analogues- Latanoprost, Travoprost, Bimatoprost

• Neural damage irreversible – hence need for

• Patients with systemic comorbidities – not much

• Drug allergy- Need for preservative free drugs

• Long-term drug delivery systems- improved QOL

• Long term safety not known CONCERNS

Capsular Tension Ring

Microfluidic IOL Implant®

Argon laser trabeculoplasty

Selective laser trabeculoplasty(SLT)

Micropulse laser trabeculoplasty (MLT)

More precise than

Cone centering and Administration in six

• Computer assisted noninvasive glaucoma procedure

Newer gentle lasers

 Implanting a tiny device to allow fluid to drain from the

• Trabecular Meshwork Bypass- iStent, Hydrus

 Angle closure and Secondary glaucoma

Retina ErK Mediate neuroprotective activity of ↑RtmGC survival

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