Glaucoma

Dr Ben Wild

Overview

For fully functioning vision, light must be focused by the cornea and lens onto the retina. The retina senses this light and transmits signals via ganglion cells to the optic nerve. From the optic nerve the signals are then transmitted to the visual cortex in the brain for interpretation.

View of a healthy retinal fundus (back of the eye) with a healthy optic nerve (yellow circle).

Glaucoma is a set of progressive conditions whereby the ganglion cells that form the optic nerve start to die resulting in blind spots. This may be due to extended periods of elevated eye pressure, short periods of extremely elevated eye pressure, poor blood supply to the nerve or even auto-immune conditions. It affects 2-3% of people 40 years of age and older.

View of a retinal fundus showing optic nerve damage related to glaucoma (yellow circle).

Firstly, the eye is inflated with fluid called the aqueous humor. This fluid nourishes various structures of the inner eye and helps remove waste products. This fluid enters the eye via the ciliary body and exits the eye through a sieve-like structure called the trabecular meshwork. Simply put, elevated eye pressure is due to this sieve becoming blocked or clogged up and the fluid building up in the eye causing higher eye pressure. Without any damage to the eye, this is called ocular hypertension. Ocular hypertension can become glaucoma depending on various risk factors detailed below. Normal eye pressures range from 11mmHg to 21mmHg, anything over 21mmHg is deemed elevated.

Primary open angle glaucoma (POAG) is most often bilateral, defined as eye pressures above 21mmHg, visible optic nerve damage and measurable blind spots, without any visible blocking of the trabecular meshwork. Clogging of this meshwork is assumed.

Normal tension glaucoma (NTG) is also often bilateral, eye pressures under 21mmHg, visible optic nerve damage and measurable blind spots. This is often due to lack of oxygen supply to the optic nerve, abnormal eye structure, or possibly, auto-immune causes.

Primary angle closure glaucoma (PACG) refers to a condition where the trabecular meshwork gets completely blocked by the iris (the colored part of the eye) and makes up 50% of glaucoma cases worldwide. It can be from a thick iris that bunches up into the trabecular meshwork or an iris that bulges forward and blocks the trabecular meshwork. A third type occurs when the lens of the eye grows so much that it pushes the iris forward and blocks the trabecular meshwork. This can be stimulated by dilating drops, emotional stress, dark rooms, certain medications (motion sickness, inhalers, cold remedies, sulfa drugs).

Secondary types of glaucoma (glaucoma caused by other ailments) include pseudoexfoliation syndrome, pigment dispersion syndrome, neovascular glaucoma, inflammatory glaucoma, trauma, tumours, irregular corneal endothelial cells (iridocorneal endothelial syndrome) and many more.

Glaucoma can also be congenital (born with), infantile (acquired under 3 years old) or juvenile (acquired between 3 and 16 years old).

Signs and Symptoms

Signs

Ocular hypertension	No signs.
POAG	High eye pressure, optic nerve damage.
NTG	Optic nerve damage, bleeding around the nerve.
PACG	Blocked trabecular meshwork, elevated eye pressure, possible redness, corneal swelling, white blood cells floating in the eye, collections of white blood cells in the trabecular meshwork, white spots on the lens.

Symptoms

Ocular hypertension	No symptoms.
POAG and NTG	No visual symptoms until advanced (large blind spots).
PACG	Varies between no visual symptoms to intermittent blurry vision to very blurry vision, no pain to intense pain, headache.

Causes and Risk Factors

Causes

Ocular hypertension and POAG	Abnormal trabecular meshwork.
NTG	Insufficient oxygen to optic nerve, auto-antibodies (auto-immune condition), poor eye structure.
PACG	Iris blocking trabecular meshwork.

Risk Factors

Ocular hypertension	Age, thickness of cornea, African descent, male, vascular disease (diabetes, high blood pressure, etc.), myopia (nearsightedness), family history.
POAG	Age, African descent, family history, vascular disease (diabetes, high blood pressure, etc.), myopia (nearsightedness), long term use of contraceptives (birth control), large optic nerves, poor blood circulation, use of corticosteroids. NTG: age (older than POAG), female, Japanese and Caucasian descent, thin
NTG	Age (older than POAG), female, Japanese and Caucasian descent, thin corneas, vaso-dysregulation (prone to migraines, Raynauds, etc.), hypotension, sleep apnea, auto-antibodies, poor blood circulation, myopia, thyroid dysfunction.
PACG	Age (around 60), female, Far Eastern and Indian descent, hyperopia (farsightedness), small eye.

Prevention and Treatment

Prevention

Regularly scheduled eye exam can detect subtle changes to the optic nerve before blind spots develop. Glaucoma/pressure lowering drops in ocular hypertension can prevent future glaucoma. Laser iridotomies or iridoplasties can prevent PACG is people with trabecular meshworks that look almost blocked. There are no known preventatives for POAG or NTG other that healthy living and avoiding systemic medical issues.

Treatments

Ocular hypertension	Monitoring.
POAG + NTG	· Prostoglandin, B-blocker, alpha-agonist, carbonic anhydrase inhibitor, or dual acting glaucoma drops. · Laser trabeculoplasty to unclog trabecular meshwork. · Trabeculectomy to funnel aqueous humor outside the eye where it can be absorbed by the blood vessels outside the eye (POAG only).
PACG	· Miotic eye drop for acute attack (shrinks pupil). · Laser peripheral iridotomy to create a new passage for aqueous humor. · Laser iridoplasty to scar the iris and pull it towards the pupil to open the trabecular meshwork. · Trabeculoplasty. · Cataract surgery to open up trabecular meshwork.

Prognosis

How soon glaucoma is detected is the biggest variable when it comes to prognosis. If caught early, primary glaucoma is very manageable with either drops or surgery. Early in POAG or NTG refers to within a few years of the onset of optic nerve damage whereas with PACG early refers to within hours to days. Ideally, individuals at high risk of PACG undergo preventative treatments before glaucoma starts. Secondary causes of glaucoma are much more difficult to manage and even on treatment will likely lead to progressing blind spots.