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Drug Treatment of Glaucoma

Glaucoma is from Greek word “Glaukoma” meaning clouded or blue green hue.

Glaucoma is a group of diseases characterized by progressive form of optic nerve damage

It is associated with raised intraocular pressure, rise should be more than 21 mmHg.

Etiology –exact cause is not known, however there are usually many risk factors.

Chief therapeutic measure is to reduce intraocular pressure either by decreasing formation of aqueous humor or increasing outflow.

Production and Drainage of Aqueous Humor

Produced by ciliary body behind iris, then flows through pupil and drains at angle between iris and cornea (drainage angle).

Within drainage angle, a porous tissue, the trabecular meshwork from where goes into canal of Schlemn, then drains into the veins under conjunctiva.

Most of the aqueous humor leaves the eye through this conventional pathway.

Rest drains through the non-conventional pathway or uveoscleral pathway i.e. leaves through ciliary body.


Normal Intraocular Pressure

10-20 mm Hg


According to:


    1. Primary
    2. Secondary


  1.             Open angle
  2.             Closed angle


  1.             Congenital or infantile
  2.             Adult type
Glaucoma based on Morphology
Angle closure glaucoma


Occurs in individuals having narrow iridiocorneal angle or shallow anterior chamber.

Intraocular Pressure

Remains normal until an attack is precipitated by mydriasis.

Intraocular pressure rises very rapidly to high values and  becomes emergent condition. Failure to lower this IOP can result in loss of sight.

Risk factors

There are many risk factors:

  1. Old age
  2. Physiological enlargement of lens
  3. Hyper opia –far sightedness
  4. Prolonged uveitis
  5. Diabetes mellitus
  6. Drugs causing pupillary dilatation –sympathomimetics, anticholinergics, antihistamines, TCA, quinine and quinidine


  • Severe throbbing pain in eye along with blurring of vision.
  • Dilated pupil not responding to light
  • Cornea discoloured or steamy.
  • Redness of eye.
  • May be accompanied by abdominal discomfort, nausea, vomiting


Made on basis of symptoms and tonometry.


Definitive treatment is surgery or laser iridotomy.

Vigorous medical therapy is employed to decrease intraocular pressure.

Drugs used are:

  1. Acetazolamide 500 mg I/V followed by 250 mg.
  2. Mannitol I/V à decongests eye, once I/V given
  3. Pilocarpine, drug is instilled after every 10 minutes for 1st one hour, then 4 times daily.
  4. Topical beta blockers like Timolol are instilled after every 12 hours.
  5. Apraclonidine
  6. Latanoprost
  7. PGF2 alpha analog

Once intraocular is decreased then surgery or laser iridotomy is done, hole is made in iris which facilitates flow of aqueous humor.

Open Angle Glaucoma

More common/dangerous than closed angle because of no signs/symptoms usually.


Due to changes in trabecular meshwork that occurs with advancing age

Genetic Predisposition

Genetically predisposed condition due to mutations in myocilin, genes are present on chromosome 1, which encodes myocilin glycoproteins present in meshwork.

Optic nerve/optic disc damage, increase in cup disc ratio, if more than .2-.3 then suspicion of glaucoma is made.


Usually no complains of hallows around light, central vision remains intact till last and there is loss of peripheral vision.


Made on visual field examinations, on tonometry and optic disc examination.

Drug Treatment of Glaucoma

Beta-adrenergic Antagonists

Are one of the 1st line drugs. However, nowadays, PGF2 alpha analogs have replaced them.

Beta-1 nonselective

—  Timolol  maleate (0.25, 0.5%) bid

—  Timolol Hemihydrates (5-12 mg/ml) bid

—  Levobunolol HCL (0.25, 0.5%) bid

—  Metopranolol  (0.3%) bid

—  Carteolol HCL (1.0%) bid

Beta-1 selective

—  Betaxolol HCL (0.25, 0.5%) bid

Mechanism of Action

These block beta receptors in ciliary epithelium and decrease aqueous humor production by inhibiting adenylyl cyclase, so decrease intraocular pressure.

Have secondary effect, i.e. decrease intra ocular blood flow.


There are a few advantages over meiotics:

  1. No change in pupil size
  2. No headache or pain
  3. No fluctuations in IOP
  4. Convenient to be used, given once daily or twice daily.



  1. Dryness
  2. Redness of eye
  3. Blurring of vision
  4. Corneal hypo esthesia
  5. Allergic blepharoconjunctivitis


Systemic effects occur when beta blockers act through nasolacrimal duct.

  1. Severe bronchospasm in asthmatics
  2. Bradycardia
  3. Enhancement of heart blocks
  4. Congestive heart failure
Adrenergic agonists

Nonselective adrenergic agonists

—  Epinephrine  (0.25,0.5,1.0,2.0%) bid

—  Epinephrine HCL (1.0,2.0%) bid

—  Epinephryl borate (0.5, 1.0,2.0%) bid

—  Epinephrine bitartrate (2.0%) bid

—  Dipivefrin (0.1%)

Alpha2– selective adrenergic agonist

—  Apraclonidine  HCL (1.0%) (0.5%) pre and post laser tid

—  Brimonidine tartrate (0.2%)

Brimonidine has selective actions on alpha 2 receptors than apraclonidine, has lesser adverse effects than apraclonidine.

Mechanism of Action
  1. Initially produce vasoconstriction and decrease aqueous humor production,
  2. later on also increase outflow of aqueous humor

Dipivefrin is prodrug, activated while it transverses the cornea, has less systemic effects than epinephrine.



  1. Allergy
  2. Follicular conjunctivitis
  3. dermatoconjunctivitis


Mainly on cardiovascular system;

  1. Arrhythmias
  2. Tachycardia
  3. hypertension
Parasympathomimetic Drugs

Cholinergic agents

  • Pilocarpine HCL (0.25 -10.0%) bid to qid
  • Pilocarpine Nitrate (1.0,2.04.0%) bid to qid
  • Carbachol (0.75,1.5,2.25,3.0%) bid to qid



  • Echothiophate Iodide (0.03,0.06, 0.125, 0.25%) bid
  • Demecarium Bromide (0.125, 0.25%) bid
  • Physostigmine (0.25%) (0.25, 0.5%) bid
Mechanism of Action
  1. Act by contraction of ciliary muscles
  2. Cause opening and re-alignment of trabecular meshwork
  3. Facilitate drainage of aqueous humor
Adverse effects

Contact allergy is possible to pilocarpine. Since produce meiosis, interfere with visual acuity and should not be given for longer time since Echothiophate produces cataract formation if given for prolonged period because of degradation of proteins.

  • Latanoprost  (0.005%) bid
  • Bimatoprost
  • Travoprost
Mechanism of Action

Increase uveoscleral outflow of aqueous humor, exact mechanism is not known.

Said to be due to relaxation of ciliary muscles as well as remodeling of elements of ciliary muscles.

Side effects
  1. Thickening and darkening of eye lashes
  2. Darkening of iris
  3. Redness of eyelids
  4. Redness of eyes
  5. Blurring of vision
  6. Macular edema
Carbonic Anhydrase Inhibitors


Acetazolamide (125, 250 mg) bid to qid (500mg)

Acetazolamide  (500 mg)  6-8 hr


Dichlorphenamide (50mg) bid, tid

Methazolamide  (25, 50 mg) bid, tid       


Dorzolamide  (2.0%) tid

Brinzolamide (1.0%) tid

In health it is production of bicarbonates that drain sodium and then water follows by osmosis.

These carbonic anhydrase inhibitors inhibit production of bicarbonate inhibiting aqueous humor production.

Side effects

Systemic effects are common with drugs used parentally.

Dorzolamide has more topical adverse effects than Brinzolamide.

  1. Anorexia
  2. Hypokalemia
  3. Metabolic acidosis
  4. Renal stone formations
  5. Lethargy
  6. paresthesias
Hyperosmotic agents
  • Mannitol parenteral (5-25% solution) 2g/kg
Mechanism of Action

Osmotic agents are inert in humans. They increase blood plasma osmolarity and in this way drain water from eyes into plasma and decrease vitreous volume and intraocular pressure.

Side effects
  1. Headache
  2. Back ache
  3. Diuresis
  4. Ataxia

Sometimes cerebral hemorrhage.

Want a clearer concept, also see

Glaucoma Medications in Ophthalmology Section

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One comment

  1. Great Post.Thanks admin to share drug Treatment for Glaucoma.I like your way of writing a post.Keep blogging and best of luck.

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