Management of Glaucomas

Professor K N Jha,MS.

Learning Aim

• Approaching a case of glaucoma

• Treatment aims in glaucoma

• Medical therapy of glaucoma

• Surgical and LASER therapy of glaucoma

• Complications of glaucoma surgery

Management of Glaucomas

• Early diagnosis and therapy

• Life long therapy and follow-up

• Patient counseling

• Baseline parameters: IOP , field , fundus

Goal of Glaucoma Therapy

• To preserve visual function by reducing IOP.

• The treatment should have:

-minimum side effect.

-cause least disruption in patient’s life.

- should take into consideration the cost.

Risk benefit ratio need to be factored in case of

new medications.

Target pressure

• It is a range of IOP with an upper limit that is

unlikely to lead to further damage.

• Initial reduction: 20% from baseline.

• Target pressure need constant reassessment

dictated by IOP fluctuation , ONH changes,

and/or visual field progression.

Target pressure

• Target pressure goal depending on -initial IOP-severity of damage-life expectancy-associated risk factors like , family history.

Medical or, surgical treatment?• Pupillary block glaucoma Surgery/Laser• Infantile glaucoma Medical therapy is

secondary.

• POAG -Initially medical -Surgery, if medical

therapy fails or, it is not tolerated.

• Treatment of secondary glaucoma is comparable to

the primary glaucoma that it closely resembles.

Therapy of Glaucomas• Medical

• Surgical Internal drainage ( iridectomy)External subscleral drainage ( Trabeculectomy)Cyclodestructive procedure (

cyclocryopexy/DLCP)• Laser

Argon laser trabeculaoplasty(ALT)GonioplastyLaser peripheral iridotomy

Medical agents: Mechanism of action

- aqueous humor secretion

- outflow of humor through

- pupil- TM- uveoscleral path

Medical agents

-beta-adrenergic antagonists e.g. Timolol 0.5 %

-Parasympathomimetics(miotics):cholinergic and

anticholinesterase agents e.g. pilocarpine 2 %- 4 %

-CAI e.g. Acetazolamide (oral) parenteral, topical ( dorzolamide )

-Adrenergic agonists( non-selective and selective alpha₂ agonists)

e.g. brimonidine.

-Prostaglandin analogues and hypotensive lipids e.g. latanoprost

-Combination medications

- Hyperosmotic agents ( Injection Mannitol 20 % I.V. )

beta-adrenergic antagonists

-Lower IOP by inhibiting cAMP production in the ciliary epithelium,

thereby reduce IOP by reducing aqueous secretion.

-Effect starts within 1 hour and can be present for up to 4 weeks after discontinuation.

-Decrease IOP by 20-30%

-Timolol 0.5 %, Betoxolol 0.5 % b.i.d.

-Twice a day dosing, can be combined with other agents.

-Side effects: systemic and local.

Parasympathomimetic agents

-Direct-acting cholinergic affects motor endplate in the

same way as acetylcholine at postganglionic

parasympathetic junction, as well as other autonomic,

somatic and central synapses. e.g. Pilocarpine

-Indirect-acting anticholinesterase agents inhibit

acetylcholinesterase e.g. echothiophate iodide. May

precipitate angle closure.

Parasympathomimetic Agents (miotics)

Mechanism of action of IOP reduction:

-They reduce IOP by causing contraction of longitudinal

ciliary muscle, which exerts pull on the scleral spur to

tightens the trabecular meshwork, thus increasing the

outflow aqueous humor.

- Miosis (pupillary constriction) that pulls away the

peripheral iris away from the trabecular meshwork has IOP

lowering effect in ACG.

Parasympathomimetics

• Reduce IOP by 15-25 %• Uses: Prophylaxis for angle closure

glaucoma(ACG), in eyes with failed glaucoma surgery.

Pilocarpine

• Direct-acting parasympathomimetic

• Primarily used in PACG pending iridectomy.

• Strength and dose:1-2% drop q.i.d.

• Side effects: ocular , systemic.

Side effects of pilocarpine

• Systemic: stimulates of lacrimal and salivary secretions.

• Ocular:- disrupts blood retinal barrier- Brow ache, ciliary spasm, and induced myopia.- Retinal detachment- impaired vision in dim illumination- Lenticular opacities.-Punctual stenosis

Carbonic anhydrase inhibitor (CAI)

• Decreases aqueous humor production by

-direct antagonist activity on ciliary epithelial

carbonic anhydrase.

- By producing generalized acidosis, on

systemic administration.

Carbonic anhydrase inhibitor (CAI)

• Systemic CAI e.g. Acetazolamide ,

methazolamide are used in emergency

situations in AACG.

• Topical carbonic anhydrase inhibitor e.g.

acetazolamide , Dorzolamide drop for

treatment of chronic IOP elevation in OAG

Carbonic anhydrase inhibitor• Side effects:

-on systemic use: anorexia, abdominal discomfort, diarrhea, unpleasant taste in mouth. -Paresthesias of fingers or toes-Formation of renal stones.-Allergic reactions-Blood discrasias-Hypokalemia- on topical administration: punctate keratopathy, corneal decompensation.

Carbonic anhydrase inhibitor (CAI)

Preparations

Oral: -Acetazolamide(250 mg) t.i.d., or sustained

release tablet once a day.

-Methazolamide 20-50 mg t.i.d

Intravenous : Acetazolamide in emergency.

Topical : dorzolamide , brinzolamide t.i.d.

Nonselective Adrenergic Agonists

• Nonselective adrenergic agonists( e.g.

epinephrine and depivefrin) increase

conventional trabecular and uveoscleral

outflow.

Alpha₂-Adrenergic agonists

-Decreases IOP( by 26%) by decreasing aqueous

production and increasing uveoscleral outflow.

-Comparable in effect to non-selective beta blocker.

-Brimonidine 0.2% / 0.15 % is much more highly

selective for alpha₂ receptor. Dose: tid/bid.

-Alpraclonidine HCl used after laser procedure.

- Avoided in children and in patients on MAO inhibitors.

Hypotensive lipids

• Prostaglandin analogues: travoprost, latanoprost ( increases uveoscleral outflow)

• They are pro-drugs. • Reduce IOP by 25-32%. • Prostamide: Bimatoprost ( both us +

trabecular outflow)• Decosanoid: unoprostone isopropyl

Hypotensive lipids

Latanoprost( Xalatan),Bimatoprost (Lumigan), travoprost(

Travatan) are used once in 24 hours, at night.

Side effects:

-Darkening of iris and periocular skin.

- Conjunctival hyperemia, hypertrichosis, trichiasis,

distichiasis.

- Exacerbation of herpes keratitis , CME and uveitis.

Combined medications

• Improved efficacy , convenience, compliance,

and reduced cost.

• Examples: Timolol 0.5%+ dorzolamide 2% bid.

Hyperosmotic agent

• Used to control acute episodes of elevated IOP.

• They reduce IOP by increasing blood osmolarity and creating an osmotic gradient between blood and vitreous humor.

• Water is drawn from vitreous and IOP falls.

Hyperosmotic agent

• Common agent mannitol 20 % solution.• Dose : Mannitol1.5-2 gm/kg body weight• Side effects: may cause rapid increase in

cardiac preload and may precipitate CCF.• Contraindicated in patients with renal failure

or on dialysis.• Glycerol 1-2 ounce with fruit juice.

ACG

• Laser/surgical iridectomy• Chronic ACG: trabeculectomy

• Medical treatment is used for preparation for

laser surgery, to tide over sudden rise in IOP,

and prevent PAS formation

Open angle glaucoma

Medical treatment

-efficacy and compliance

- start with single drug

-agent is individualized

Laser ( ALT) initially ,as an alternative to drug

Surgery: Trabeculectomy

Drug therapy in OAG

First choice: hypotensive lipid( Bimatoprost) , beta-blocker (Timolol), alpha-2 agonist(Brimonidine) and topical CAI (Dorzolamide)

-Add 2ndagent if IOP is not controlled with one

-When individual requires 3 or more topical drop compliance and complications are considered

TRABECULECTOMY

Surgery for open angle glaucoma

Trabeculectomy

• Creates a fistula in the sclera for bulk flow of

aqueous humor from anterior chamber to the

sub-conjunctival and sub- Tenon’s space

where a ‘filtering bleb’ is created.

Complications of filtering surgery

• Early: infection , flat anterior chamber, uveitis

• Late: cataract, endophthalmitis , hypotony