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GLAUCOMA (Class 7) : Faculty Name Institute Name

1) The document discusses the management of primary open-angle glaucoma (POAG), including lowering intraocular pressure (IOP), increasing aqueous outflow, and providing neuroprotection. 2) Treatment options include medical management using drugs like prostaglandin analogues, beta blockers, and carbonic anhydrase inhibitors to lower IOP, as well as laser trabeculoplasty procedures and surgical options like trabeculectomy. 3) Regular follow-up is important to monitor for disease progression using structural assessments of the optic disc and retinal nerve fiber layer, as well as functional visual field testing, with more frequent follow-ups needed for more advanced cases.

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Pranshu Prajyot 67
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49 views

GLAUCOMA (Class 7) : Faculty Name Institute Name

1) The document discusses the management of primary open-angle glaucoma (POAG), including lowering intraocular pressure (IOP), increasing aqueous outflow, and providing neuroprotection. 2) Treatment options include medical management using drugs like prostaglandin analogues, beta blockers, and carbonic anhydrase inhibitors to lower IOP, as well as laser trabeculoplasty procedures and surgical options like trabeculectomy. 3) Regular follow-up is important to monitor for disease progression using structural assessments of the optic disc and retinal nerve fiber layer, as well as functional visual field testing, with more frequent follow-ups needed for more advanced cases.

Uploaded by

Pranshu Prajyot 67
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as PPTX, PDF, TXT or read online on Scribd
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Subject Name (ophthalmology)

Topic Name –GLAUCOMA(class 7)

Faculty name --Dr Suprava Das (asst. professor)

Institute name --Siksha O Anusandhan


MANAGEMENT OF POAG

• LOWER IOP

• INCREASE OUTFLOW

• NEUROPROTECTION/
VASOPROTECTION
Principles of management
Initiation
Establishment
Establishment
of baseline
of diagnosis
therapy IOP
Target IOP

F
o
ll
o
w

u
p
Family of ocular diseases characterized by progressive
optic neuropathy and visual field loss

Raised IOP

Progres
Gradua
sive
l optic
retinal
disc
ganglio
cuppin
n cell
g
loss

Associated visual
field deficits
Establishment of diagnosis
• VA
• S/L examination
• Tonometry
• Gonioscopy
• Disc & RNFL evaluation
• Visual field testing
Grading of glaucomatous damage
Mild damage Moderate damage Severe damage
Minimal cupping Thinning of NRR Lost NRR
MD < -6 dB MD -6 dB to -12dB MD > -12dB
Paracentral scotoma Field abnormality in one Field abnormality in
hemifield not within 5 both hemifield and
degree of fixation within 5 degree of
fixation
• Severe damage
Base line IOP
• IOP is the only treatable risk factors
• One time IOP reading is misleading
• Diurnal variation provides information about peak IOP and
fluctuation

IOP

<30mm Hg >30mm Hg
Target pressure
The highest IOP in a given eye at which no
clinically apparent nerve damage occurs

Target IOP is the pressure estimated to slow or halt disease progression.

It is determined from the baseline IOP, stage of disease, estimated progression


rate and life expectancy.

When the target IOP is achieved the patient needs continued monitoring for
structural and functional changes
AAO Guidelines: Target IOP
Treatment plans
Medical management

Laser

Surgical
MEDICAL MANAGEMENT

Ideal drugs-directly
protect optic
nerve/reverses
damage

Most appropriate medication


Greatest chance of reaching
target iop
Best safety profiles
Minimal inconvenient
affordable

Start low and


slow
Minimal conc.
Minimal frequency
How to put drops????
Anti-glaucoma Drugs: Mechanism of action

Cholinergics

Prostamides 2-agonists
2-agonists
2-blockers
prostaglandins
CA inhibitors
PROSTAGLANDIN analogues

• Increase uveoscleral outflow


Used as first line drug for POAG

• Latanoprost (0.005%)
• Travoprost (0.004%)
• Bimatoprost (0.03%)

Side effects –conjunctival hypermia, uveitis ,CME, iris


pigmentation, eyelash growth due to increase
blood flow
Bimatoprost 0.03%
BETA BLOCKERS
(Timolol /Levobunolol /Betaxolol)
• Timolol(0.25,0.5%) and Levobunolol
Nonselective beta blocker- IOP
by blocking beta 2 receptor

Ocular side effects- not frequent


allergy and punctate keratitis

Systemic side effect- bradycardia, arrhythmias


bronchospasm and airway
obstruction
Adrenergic drugs
Brimonidine 0.2%

Alpha 2 agonist
MAO
• Reduces the secretion of aqueous
• Increases Uveoscleral outflow

• Ocular side effects ---


ocular allergy, conjuctival hyperemia, pigmentation

• drowsiness , depression
Carbonic anhydrase inhibitors

Carbonic anhydrase inhibitor

topical systemic

MOA –Inhibits carbonic anhydrase enzyme –reduces aqueous


formation

• Side effects- paresthesia,


GI upset
electrolyte imbalance
Pilocarpine(1, 2 or 4%)

Side effects - miosis, brow ache,


myopic shift

Side effects - miosis, brow ache,


myopic shift
Combination therapy
• When mono therapy is not effective

• Two drugs of different MOA

Timolol /dorzolamide

Pilocarpine/ Latanoprost/
brimonidine
IOP REDUCTION

20% ●
Beta blocker is the first line drug

30-35% ●
PGA are first line

30% Cost problem/not achieved with PGA


●

●
Combi. Beta blocker+ brimonidine/dorzolamide
LASER TRABECULOPLASTY
• Done in patients with uncontrolled IOP despite maximal
tolerated medical therapy

• Avoidance of polypharmacy

• Avoidance surgery

• Poor patient compliance


ALT AND SLT
MOA
Collagen shrinkage on the inner aspect of TM

Opening the intratrabecular space

Increase the outflow facility

Decrease the IOP by 8-10mm

ALT - Over 180 degree around 50 spots are


applied on the anterior half of TM

SLT- selectively targets pigmented TM without


Collateral damage to nonpigmented part of TM
Surgical management
• Trabeculectomy
IOP is not controlled with maximum medical management
poor patient compliance
Bleb
Follow up
• Regular follow-up is necessary to detect progression .

• Progression in glaucoma is assessed by structure (optic disc and RNFL) and


function (visual field testing)

• Glaucoma ( early ) with IOP at target might be reviewed in 6 months

• Stable patients with moderate damage would be examined at 6-month


intervals

• For severe glaucoma in the better eye, the interval could be 3-4 months.
THANK YOU

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