Glaucoma

Glaucoma and IOP elevation are not synonymous.

Glaucoma is characterized by damage to the optic nerve that results in visual field loss regardless of the IOP level.

Many patients with elevated IOP show no evidence of optic nerve damage or visual field loss. This condition is known as "ocular hypertension." Much debate exists as to when glaucoma therapy should be initiated in patients with mild ocular hypertension alone.

Glaucoma may manifest as

• Optic disc changes – cupping resulting from reduced width of the neuroretinal rim or notch-like nerve-head deficit with associated nerve fibre layer irregularities – detectable loss and thinning
• Visual field losses
• Usually both of the above, but the disc changes often precede the field loss.

There are two main types of glaucoma:

• Open angle – most commonly primary open-angle glaucoma
• Closed angle.

Management:

Screening: RACGP does not recommend routine screening of glaucoma with tonometer or visual field testing. However, high risk patients should be referred for further assessment every 12 months.

• a family history of glaucoma
• age ≥60 years
• high myopia >8 diopters
• diabetes
  
• history of long term steroid use

The aim of treatment of open-angle glaucoma is to normalise IOP and thus stabilise disease. Clinical trials indicate that the lower the IOP, the greater the likelihood of achieving stable disease.

Pharmacological Method -

When a topical medication is chosen as first-line therapy in a patient with primary open-angle glaucoma, a stepped approach is used. Thus, a single topical agent is given up to its maximum dosage, as tolerated, before another agent is added or a different agent is tried.

A prostaglandin derivative, or ß-blocker are most commonly chosen, and should be used at the lowest possible concentration, and as infrequently as possible while achieving the desired outcome.

ß-blockers

Non-selective ß-blocker - timolol 0.25% or 0.5% lowers IOP by reducing aqueous secretion.

Selective ß₁-adrenegic-blocking agent betaxolol is nearly as effective as timolol, but has the advantage of having little effect on the cardiopulmonary system.

Combining a topical and systemic ß-blocker can increase the risk of ß-blocker-related side effects. For patients taking an antihypertensive medication the possibility of low nocturnal blood pressure should be considered. Nocturnal hypotension has been linked to progression of glaucoma.

Prostaglandin derivatives

The synthetic prostaglandins – latanoprost, travoprost, bimatoprost – lower IOP by increasing aqueous outflow through the uveo-scleral pathway.

They commonly cause hyperaemia and can increase the length of eyelashes and can increase periorbital skin pigmentation.

α ₂-adrenergic agents

These agents – aproclonidine, brimonidine – stimulate α 2-receptors in the ciliary epithelium to reduce the formation of aqueous humour, and enhancing uveoscleral outflow. In long term treatment aproclonidine tends to diminish in efficacy over time and both agents have a relatively high incidence of local allergy.

Carbonic anhydrase inhibitors

Both topical – dorzolamide, brinzolamide and oral – acetezolamide – carbonic anhydrase inhibitors are used in the treatment of glaucoma, where they decrease the formation of aqueous humour, presumably by slowing the formation of bicarbonate ions resulting in reductions in sodium and fluid transport.

Miotics

Miotics – pilocarpine, carbachol – were the traditional agents used to treat glaucoma. They act by stimulating cholinergic receptors, reducing IOP by contraction of the ciliary muscle causing pressure on the trabecular meshwork and a consequent increase in the outflow.

Surgical Therapy:

• Laser therapies
• Selective laser trabeculoplasty
• Peripheral laser iridotomy
• Filtration surgery

It is essential for the best outcomes that all patients be followed-up on a regular basis. After initiation of therapy patients should be seen at 2–4 week intervals until control of IOP is achieved.

Once IOP has been controlled patients should be reviewed every 3–6 months.