The anterior chamber is a space filled with fluid, the aqueous humour; it is bounded in front by the

cornea, behind by the iris and the part of the anterior surface of the lens which is exposed in the
pupil. Its peripheral recess is known as the angle of the anterior chamber, bounded posteriorly by the
root of the iris and the ciliary body and anteriorly by the corneosclera (Fig. 1.6). In the inner layers of
the sclera at this part, there is a circular venous sinus, sometimes broken up into more than one
lumen, called the canal of Schlemm, which is of great importance for the drainage of the aqueous
humour. At the periphery of the angle between the canal of Schlemm and the recess of the anterior
chamber, there lies a loosely constructed meshwork of tissues, the trabecular meshwork. This has a
triangular shape, the apex arising from the termination of Descemet’s membrane and the subjacent
fibres of the corneal stroma and its base merging into the tissues of the ciliary body and the root of
the iris. It is made up of circumferentially disposed flattened bands, each perforated by numerous
oval stomata through which tortuous passages exist between the anterior chamber and Schlemm’s
canal. The extracellular spaces contain both a coarse framework (collagen and elastic components)
and a fine framework (mucopolysaccharides) of extracellular materials, which form the probable site
of greatest resistance to the flow of aqueous
Primary Open Angle Glaucoma
DEFINITION:
Primary open angle glaucoma (POAG) is defined as a chronic progressive optic neuropathy with
characteristic morphological changes in the optic nerve head and retinal nerve fiber layer, in the
absence of underlying ocular disease or congenital anomalies

Key Features

• Loss of trabecular meshwork endothelial cells

• Fusion and sclerosis of trabecular beams

• Formation of electron dense plaques in trabecular meshwork

• Altered myocilin gene expression

The broad clinical profile of primary open angle glaucoma (POAG) is as follows:

1. Adult patient.

2. Open anterior chamber angles on gonioscopy .

3. Evidence of optic nerve damage as characterized by:

a. Diffuse thinning, focal narrowing, or notching of the optic disk rim, especially at the inferior or
superior poles.

b. Documented progression of cupping of the optic disk.

c. Diffuse or localized abnormalities of the peripapillary retinal nerve fiber layer, especially at the
inferior or superior poles.

d. Disk rim or peripapillary retinal nerve fiber layer hemorrhages.

e. Optic disk neural rim asymmetry of the two eyes consistent with loss of neural tissue.

4. Reproducible visual field defects corresponding to optic disk damage

Primary Open Angle Glaucoma Suspect
The clinical findings that define a glaucoma suspect are:

1. Open anterior chamber angles by gonioscopy.

2. Appearance of the optic disk or retinal nerve fiber layer that is suspicious for glaucomatous
damage.

3. A visual field suspicious for glaucomatous damage.

4. Consistently elevated intraocular pressure (IOP) associated with normal appearance of the optic
disk and retinal nerve fiber layer and with normal visual field test results (Ocular Hypertension).

Juvenile Open Angle Glaucoma

This is considered an early onset variety of POAG.

The typical patient profile would be as follows:

• Onset 10 to 35 years of life1

• Family history may be present

• Peak IOP >21 mm Hg

• Open angles on gonioscopy with multiple iris processes may be seen

• Optic nerve head typically shows diffuse damage to the optic rim, but any type of glaucomatous
optic neuropathy described above is possible

• Visual field defects corresponding to optic disk damage as listed above.

Mechanism of Glaucoma

A current theory is that JOAG is the result of the abnormal development of structures or the
migration of the neural crest cells. Anomalous migration of neural crest cells may contribute to the
abnormal development of the anterior chamber angle, thus leading to the obstruction of the
aqueous outflow by one or more developmental defects at various levels of the trabecular meshwork
and Schlemm's canal.

Management:

medical treatment may be initially effective but surgical treatment is generally required to control
the progress of glaucoma. Medical therapy is used preoperatively or sometimes postoperatively, if
repeated surgical interventions fail. Goniotomy and trabeculotomy are generally successful as they
possibly reduce the aqueous outflow resistance. If multiple incisional procedures fail, then
trabeculectomy can be tried. If all fails, then cyclodestructive procedures may be performed.

Diagnosis:
Diagnosing POAG requires
 evaluation of IOP;
 the anterior chamber angle by gonioscopy;
 optic disc and related structures, such as the retinal nerve fiber and ganglion cell layer;
 and visual field.
Treatment:

Treatment needs to be individualized because the IOP level needed to control disease varies
widely among individuals. The real guide for long-term clinical management is not IOP but
the course taken by the optic neuropathy. It is standard practice to sequentially examine the
visual field and optic disc to ascertain progression.

Groups of Drugs Used in Antiglaucoma Therapy

1. Beta Blockers Selective Betaxolol Non-selective Timolol, Levobunalol, Metipranolol,
Carteolol
2. Prostaglandin PG Analogs Latanoprost, Bimatoprost, Unoprostone, Travoprost
3. Cholinergic Agonist/Miotics Pilocarpine, Echothiophate iodide
4. Adrenergic Agonists Non-selective Ephedrine, Dipivefrin Selective alpha agonists
Brimonidine, Apraclonidine
5. Carbonic Anhydrase Inhibitors Systemic Acetazolamide, Methazolamide, Brinzolamide
Topical Dorzolamide, Brinzolamide 6. Hyperosmotic Agents Parenteral Mannitol Oral
Glycerol, Isosorbide
Class Concentration Mode of action Ocular side effects Systemic side effects
β adrenergic  Bronchospasm,
blocking agents:  Burning  Bradycardia,
Non-selective: Decreased  Stinging  arrhythmias,
Timolol maleate 0.25% aqueous  Punctate  heart failure,
Carteolol 0.5% production keratitis  ankle edema,
Levobunolol 0.5% By inhibiting cyclic  Corneal  nocturnal
Metipranolol 0.5% AMP anaesthesia hypotension,
Selective:  Dry eye  depression,
Betaxolol 0.5%  Allergic  fatigue,
conjunctivitis  lethargy,
 memory loss
Prostaglandin
analog 0.005% Increasing the  Conjunctival  Flu like
Latanoprost 0.004% Aqueous outflow hyperemia syndrome,
Travoprost 0.03%  Burning and  upper
Bimatoprost 0.15% stinging, respiratory
Unoprostone foreign body symptoms,
sensation,  myalgias and
blurred headache
vision and
itching
 Irreversible
increase in
iris
pigmentation
 Increased
pigmentation
of the
periocular
skin
Carbonic  By
Anhydrase decreasing
Inhibitors: HCO3 ion
Systemic: in the
Acetazolamide posterior
Methazolamide chamber
Dichlorphenamide leading to
Topical decrease
Dorzolamide in aqueous
Brizolamide humor
productio
n
 Metabolic
acidosis