Medical Management

of Glaucoma
BY: DR. SADYAJA SMITA
TREATMENT OF GLAUCOMA

 PRINCIPLES OF TREATING GLAUCOMA

 TO PREVENT GLAUCOMA ASSOCIATED VISION LOSS
 TO PRESERVE THE QUALITY OF LIFE
 COST CONTAINMENT

HIGH IOP IS THE ONLY MODIFIABLE RISK

FACTOR
 WHO TO TREAT?
 DECISION TO TREAT VARIES INDIVIDUALLY.

 TARGET IOP- RANGE OF IOP, WITH AN UPPER LIMIT THAT IS UNLIKELY TO RESULT
IN FURTHER DAMAGE TO THE OPTIC NERVE.
 AT THIS PRESSURE THE RATE OF GANGLION CELL LOSS EQUALS THE AGE RELATED
LOSS.
 NEEDS TO BE REASSESSED AND CHANGED AS DICTATED BY IOP FLUCTUATIONS,
OPTIC NERVE CHANGES AND VISUAL FIELD PROGRESSION.

 OTHER FACTORS SHOULD ALSO BE TAKEN INTO CONSIDERATION:

 Structural & functional damage
 Age (Life expectancy).
 Baseline IOP
 Additional risk factors; family history, Myopia, Nocturnal hypotension etc.
 Rate of progression
 ANTI-GLAUCOMA DRUGS

 PROSTAGLANDIN ANALOGS
 BETA-BLOCKERS
 ALPHA-ADRENERGIC AGENTS
 CHOLINERGIC AGENTS
 CARBONIC ANHYDRASE INHIBITORS
 HYPEROSMOTIC AGENTS
PROSTAGLANDINS ANALOGS
 First line of therapy
 MOA- PGAs are prodrugs which are hydrolyzed by esterase enzyme into biologically active acid
forms - It increases synthesis of matrix metalloproteinases - Removes extraocular matrix which is
blocking the uveoscleral pathway

 Cause maximum reduction of IOP. ( DECREASE IOP BY 25-35%)

 Prostaglandins have 9 types of receptors throughout the body.
 2 types in the eyes: PGFP and PGE are located on the schlemm canal and trabecular meshwork.

 CLASSIFICATION:
 PROSTANOIDS: Latanoprost, Latanoprostene bunod, Travoprost, Tafluprost
 PROSTAMIDES: Bimatoprost
 DOCOSANOIDS: Unoprostone isopropyl

 Dosage once a day preferably at night.

ADVERSE EFFECTS
CONJUCTIVAL HYPEREMIA- maximum around day 15 and starts
CONTRAINDIC

decreasing after day 30.
BIMATOPROST 0.03%> TRAVOPROST>LATANOPROST



HYPERPIGMENTATION of lids and periorbital skin
LATANOPROST>BIMATOPROST ATION
 M/C in people with dark skin
 Only affect the epidermis, which is periodically renewed so
disappears after cessation of drugs  Inflammatory conditions like active uveitis,
 TRICHOMEGALY and HYPERTRICHIASIS neovascular glaucoma
 MIGRAINE
 PROSTAGLANDINS ASSOCIATED ORBITOPATHY
 Activation of latent herpes (m/c latanoprost)
 Periorbital fat atrophy  Avoid in unilateral glaucoma(for cosmetic
 Upper lid ptosis reasons)
 Deepening of upper lid sulcus
 Involution of dermatochalasis
 Cystoid macular edema
 Mild enophthalmos  Choroidal effusion with latanoprost
 Inferior scleral show
 Preoperative use of PGAs increase incidence of cystoid macular edema
following cataract surgery.
 BETA-BLOCKERS
 Lower IOP by 20-30%
 MOA- inhibit cAMP in ciliary epithelium thus decreases aqueous production.
 Non selective beta blockers:
 Timolol maleate – most commonly used beta blocker
 Levobunolol
 Carteolol- have intrinsic sympathomimetic activity so, more selective for eyes.
 Metipranolol- linked with granulomatous anterior uveitis
 Selective beta blockers:
 Betaxolol- also have calcium channel blocking effect so optic nerve blood flow increase
 Dosage- twice a day
 Should not be used at bedtime because it causes hypotension thus reduces optic disc
perfusion and may cause visual disturbances
 Tachyphylaxis is seen in 10% of cases
ADVERSE EFFECT CONTRAINDICATION
 OCULAR :
 Cardiogenic shock

 Allergy, dry eye, punctate keratitis

 Overt cardiac failure

 SYSTEMIC:
 Second and third degree AV block not
controlled with pacemakers
 CVS- bradycardia, heart failure,
worsening of PVD, postural hypotension
 Sinus bradycardia, sick sinus syndrome,
sino-atrial block
 PULMONARY: worsening of COPD,
asthma
 Reactive airway disease including asthma

 GIT: nausea, vomiting, diarrhea

 COPD

 CNS- fatigue, depression, sleep

 Diabetes
disturbances  Timolol is actively secreted in breast milk
 Loss of libido in concentrated form, so avoided in
lactating women.
 Should be used with caution in geriatric
population due to systemic side effects.
 ALPHA AGONIST
 Decreases IOP by 20-30%
 MOA:
 Decreases AH production by inhibiting Camp and by preventing norepinephrine
release at presynaptic terminals.
 Increases uveoscleral outflow.

 Non selective alpha agonist: Epinephrine, Dipivefrine (not used now)

 Selective alpha agonist: Apraclonidine, Brimonidine
 Dosage- TID as monotherapy and BD as FDC with timolol

 Brimonidine is a neuroprotective agent.

ADVERSE EFFECTS CONTRAINDICATION

 OCULAR:  CHILDRENS under age of 2 years and

 Allergy below 20 kg in weight because it is a
lipophilic drug and crosses blood-brain
 Follicular conjunctivitis barrier and may cause serious CNS
 Periocular contact dermatitis depression and sleep apnea
 Blepharoconjuctivitis
 VKC like symptoms in children
 SYSTEMIC:
 Xerostomia- dry eye, dry mouth
 Headache, dizziness
 Hypotension
CARBONIC ANHYDRASE INHIBITOR

 Decreases IOP by 18-22%

 MOA: it inhibits enzyme carbonic anhydrase II in ciliary process

and thus, Reduces aqueous humour production
 Carbonic anhydrase enzyme convert CO2 into bicarbonate ions.

 Only antiglaucoma drugs which can be used topically, orally and

intravenously.
SYSTEMIC CAI TOPICAL CAI
 Used for short term treatment especially in  AGENTS:
patients with acute glaucoma.
 Dorzolamide- has acidic ph[5.4], given TID,
 AGENTS: Less tolerable
 Acetazolamide  Brinzolamide- natural ph[7.2], given BD
 Methazolamide  ADVERSE EFFECTS:
 ADVERSE EFFECTS:  Corneal erosions and corneal edema and
 OCULAR- choroidal effusion particularly after precipitations of corneal endothelial
cataract surgery dysfunction
 SYSTEMIC:  Allergic blepharoconjuctivitis
 Paraesthesia  Burning sensation of eye ( dorzolamide>
 Hypokalemia brinzolamide)
 Depression  Punctate keratitis
 Git symptoms  Blurred vision
 Renal stones  CONTRAINDICATION FOR CAI:
 Idiosyncratic aplastic anemia  sulfa drugs allergy
 Steven johnson syndrome  pregnancy
 MIOTICS- PILOCARPINE
 Parasympathomimetic muscarinic agonist agent  ADVERSE EFFECTS:
 Decreases IOP by 10-20%  Miosis
 MOA in PACG:
 Visual disturbances
 Causes miosis of pupil by contraction of iris sphincter muscle
 Constricts the pupil pulling the peripheral iris away from the  Brow ache due to ciliary spasm
trabecular meshwork
 Increase AC flare
 MOA in PAOG:
 Retinal detachment
 Pulls scleral spur posteriorly and internally because of that produces
alteration in ciliary body mediated configuration of the outflow  Anterior subcapsular cataract
apparatus.(relaxation of TM and widening of sclemm’s canal thus
enhances the outflow)
 Punctal stenosis

 INDICATIONS:
 Angle closure disease
 CONTRAINDICATIONS:
 Plateau iris  Peripheral retinal pathology
 Pigmentary glaucoma  Central media opacity
 Pseudo exfoliation glaucoma
 Young pt- it increases miopic effect
 Psuedophakic or aphakic glaucoma
 Adie pupil
 Inflammatory condition
 HYPEROSMOTIC AGENTS
 MOA: draws the water out from vitreous to  INDICATIONS:
blood by creating an osmotic gradient.  Acute angle closure glaucoma
 USES- when short term reduction of acute  LIG
elevation of IOP is required.
 Aqueous misdirection
 AGENTS:
 Secondary glaucomas
 Mannitol -20% sol, given intravenously at a  Pre-operative reduction of IOP
dose of 1g/kg of body weight
 CONTRAINDICATION:
 Glycerol – 50% sol, given orally
 Well established anuria
 Produce git symptoms so given with lemon
juice  Severe dehydration

 Glycerol is metabolized to glucose so careful

 Frank or impending acute pulmonary edema
monitoring with insulin cover may be required  Diabetic ketoacidosis
when given to diabetic patient  Congestive heart failure
 Renal failure
 IOP lowering Systemic Safety

 PGs (LP=BP=TP) > PGs (LP=BP=TP) >

 Timolol > Miotics >
 Miotics > Dorzolamide >
 Brimonidine > Brimonidine >
 Dorzolamide Timolol

Local Tolerance Convenience

Timolol > Prostaglandins *

Brimonidine >
Latanorpost > Beta-blockers * *
Dorzolamide >
Briminidine * * *
Travaprost >
Bimatoprost > Dorzolamide * * *
Miotics
Miotics * * * *