Glaucoma

From Ganfyd

Excess pressure in the eye impairing function of the optic nerve, characterized by optic atrophy and vision loss. A major cause of blindness, sometimes avoidable.

Introduction

Glaucoma, although long used as a term for untreatable blindness was first recognised as due to increased pressure in the eye by Richard Banister in 1622.

There are two main presentations both tending to present after 5th decade.

• Acute closure glaucoma
  • Care as most patients with this do not have classic acute attacks, but rather present with a chronic disorder
  • Diagnose by examining the anterior chamber angle (gonioscopy)
• Primary open-angle glaucoma
  • Classic slow progression

These are different conditions with the first disproportionately contributing to the visual loss load.

Secondary glaucoma occurs with diabetic retinopathy, after retinal vessel occlusion and with carotid stenosis. Drugs can cause it as after exposure to steroids. Only eye monitoring can detect this.

Intra-ocular pressure (IOP)

Not all glaucoma is associated with an absolute rise in IOP, but all is associated with sufficient rise to impair function of the optic nerve, and by implication the perfusion of the nerve and eye by the retinal arteries. In open-angle glaucoma IOP is no longer considered a defining criteria. However it is extremely important as the only common risk factor open to modification^[1]. The Advanced Glaucoma Intervention Study (AGIS)^[2] contributed to better understanding that IOPs below 18 mm Hg relate to minimal disease progression. It also suggested that IOP variability was related to glaucoma progression but this was not confirmed in the Early Manifest Glaucoma Trial (EMGT) where mean IOP was predictive^[3].

Measurement

IOP is measured using a class of instruments called tonometers. A force applied to the globe of the eye deforms the surface. Measuring the displacement and knowing the force allows estimation of the internal pressure distending the globe. The force may be applied statically by contact with a solid object - Schwartz tonometry - or inertially with a puff of air. All methods have significant limitations as far as a gold standard or absolute pressure measurement goes, but trends in one eye, and extreme pressures can reasonably be relied upon.

Production

The pressure in the eye results from the balance of aqueous humour

• Production
• Absorption (or escape)

and from

• Perfusing blood pressure (minor)
• External pressure (usually minor except with trauma and with suxamethonium administration.)

Control

Physiological

Acute closure glaucoma is associated with eye size (although the five times increased incidence in those of Chinese extraction is not explained by this). Closure of the angle between the iris and the cornea obstructs the outflow of the aqueous humour. A channel less than 25 µm in adults is diagnostic.If closure happens for several weeks the resulting permanent adherence of the iris to the trabecular network leads to chronically raised IOP. Iridotomy will prevent this. However if it is too late treatment essentially becomes identical to that of open-angle glaucoma.

Open-angle glaucoma is now understood to not be a direct effect of IOP, but rather related to factors such as the stress generated in the sclera and optic nerve head chronically by the interaction between IOP and systemic blood pressure. The higher the IOP however, the higher the likelihood of damage. Genetic risk factors exist. For example mutations of CYP1B1 can produce severe glaucoma of childhood onset. And African race is associated with quicker progression. It is the retinal ganglion cells that are specifically affected and once function is lost recovery does not occur. Hence all treatment is preventative. Most glaucoma world wide is undiagnosed and as the only screening strategy involves eye examination even in developed countries 50% may be undiagnosed.

Generally lowering the IOP by about 30% (whatever it is when retinal damage has occurred) reduces the rate of visual field loss by 50%.

Therapeutic

Monitoring

This can be acceptable in some patients with raised IOP and no retinal damage. It is unacceptable once retinal damage has occurred.

Drugs

Various drugs reduce secretion of aqueous or alter the physical variables influencing its absorption. Most of these are usually administered as eye drops and reach much higher concentrations in the aqueous humour than systemically.

• Prostaglandin analogues
  • Bimatoprost
  • Latanoporost
  • Tafluprost
  • Travoprost
• β-adrenergic antagonists
  • Betaxolol
  • Carteolol
  • Levobunolol
  • Metipranolol
  • Timolol
• Sympathomimetics
  • Brimonidine
  • Dipivefrine
• Carbonic anhydrase inhibitors
  • Acetazolamide
  • Brinzolamide
  • Dorzolamide
• Miotics
  • Pilocarpine

Surgery

Acute closure glaucoma

• Iridectomy, nowdays with a laser, is the initial treatment and will often be curative^[1].

Open-angle glaucoma

Surgically opening a new channel for escape of aqueous using blades or a laser treatment to the trabecular network reduces the pressure. Laser treatment has a low rate of complications but is less effective than mechanical intervention.

The Molteno tube is an example of a device for implantation in severe complex cases.

Surgical trabeculectomy tends to work for at least 5 years and may be supplemented by antifibrotic drugs such as mitomycin and fluorouracil. It may worsen cataracts.

External links

Royal College of Ophthalmologists Guidelines for the Management of Open Angle Glaucoma and Ocular Hypertension 2004

PRODIGY Glaucoma (2002) guideline

References