Glaucoma

Glaucoma is often referred to as the “silent thief of sight” and for good reason. It’s one of the leading causes of irreversible blindness worldwide, and yet many people don’t know they have it until it's too late. Understanding what glaucoma is, what causes it, and how it can be treated is essential for protecting your vision, especially as you age.

What Is Glaucoma?

Glaucoma is not a single disease but a group of eye conditions that damage the optic nerve causes damage at the optic nerve head and retinal nerve fiber layer (RNFL). This damage is often, but not always, associated with abnormally high intraocular pressure (IOP) - Normal IOP is around 10-22. Over time, this pressure can lead to permanent vision loss.

Because glaucoma often develops slowly and without symptoms, regular eye exams are crucial for early detection and prevention of further damage.

What Causes Glaucoma?

The most common risk factor for glaucoma is elevated intraocular pressure. Your eye continuously produces a fluid called aqueous humor, which normally drains out through a mesh-like channel. When this channel becomes blocked or isn’t functioning properly, fluid builds up, increasing pressure in the eye.

However, not all types of glaucoma are caused by high eye pressure. Other risk factors include:

• Age (especially over 60)
• Family history of glaucoma
• Diabeties
• Myopia
• Decreased perfusion pressure (BP - IOP)
• Retinal disease
• Severe eye injury
• Use of corticosteroid medications over time
• Thin central corneal thickness
• Vertical cupping of the optic nerve

The ISNT Rule

The neuroretinal rim is the rim around the optic cup. The thickness from thickest to thinnest is: Inferior, Superior, Nasal, and Temporal. The temporal is the thinnest because most of the retinal ganglion nerves from the fovea travel to the superior or inferior portions.

Cup to Disk Ratio

In advanced glaucoma, the optic disc appears noticeably abnormal. Normally, the disc has a small central depression, or “cup,” occupying less than one-third of its total diameter. As glaucoma progresses, the retinal ganglion cell layer gradually degenerates. With fewer ganglion cell axons passing through the optic disc, the cup enlarges. A cup-to-disc ratio greater than 0.5, or a significant difference between the two eyes, is a sign of ganglion cell loss due to glaucoma.

Types of Glaucoma

There are several forms of glaucoma, but here are the most common types:

1. Primary Open-Angle Glaucoma (POAG)

This is the most common form and develops slowly. The drainage angle formed by the cornea and iris remains open, but the trabecular meshwork is partially blocked, causing a gradual increase in eye pressure. It often has no symptoms until significant vision loss has occurred. The prolonged increase in pressure causes the ganglion nerves in the retina to atrophy. The exact mechanism by which this happens is not fully understood. The ganglion cell death occurs primarily through apoptosis rather than necrosis.

Some theories regarding the causes of glaucomatous optic neuropathy:

1. Damage to retinal nerve fibres at the optic nerve head may occur directly, particularly as the fibres traverse the lamina cribrosa. Increasing evidence points to the role of mechanical deformability in this region as a contributing factor.

Pathogenesis of Glaucoma via Lamina Cribrosa Damage

The lamina cribrosa is a sieve-like structure in the posterior sclera where retinal ganglion cell (RGC) axons and central retinal vessels exit the eye. It is supported by connective tissue beams and has pores through which axons and blood vessels supplying the optic nerve head pass. This preserves a pressure

mLpenguinmLpenguin

1. Ischaemic injury may also play a part, possibly resulting from compression of the blood vessels that supply the optic nerve head. This mechanism could be linked to ocular perfusion pressure, which is recognised as a potential risk factor for glaucoma.
   
2. Both processes may converge on shared pathways of damage, including disruption of axoplasmic transport, impaired delivery of nutrients, accumulation of metabolic waste, loss of neurotrophic support, oxidative stress, and activation of immune-mediated injury.

2. Angle-Closure Glaucoma

Also known as closed-angle or narrow-angle glaucoma, this occurs when the iris bulges forward and blocks the drainage angle. This can happen suddenly (acute angle-closure glaucoma) or gradually. Acute cases are a medical emergency and may cause severe eye pain, nausea, blurred vision, and halos around lights.

1. Relative pupillary block

• Failure of normal aqueous flow through the pupil → pressure builds in the posterior chamber → iris bows forward and blocks the trabecular meshwork.
• Large lens vault increases risk.

2. Non-pupillary block

• Plateau iris configuration
  • Ciliary body processes are positioned more anteriorly or rotated forward.
  • This pushes the peripheral iris toward the trabecular meshwork, even when the central iris is flat.
  • Angle recess is extremely narrow, with a sharp backward bend of the iris over the ciliary processes.
  • Double hump sign on indentation gonioscopy:
    • Central hump → lens bulging behind the iris.
    • Peripheral hump → ciliary processes lifting the iris.
• Thick peripheral iris roll
  • The iris tissue near the angle is bulky, crowding the drainage area.
  • Thought to be especially relevant in Asian eyes.

3. Lens-induced

• Lens swelling (phacomorphic glaucoma) or forward movement (subluxation) narrows the angle.
• All pupillary block cases have some lens contribution, which increases with age as the lens thickens.

4. Retrolenticular causes

• Malignant glaucoma (ciliolenticular block).
• Other posterior segment causes of secondary angle closure.

5. Combined mechanism

• Coexistence of angle-closure and open-angle features.

During an acute glaucoma attack, the patient typically presents with a severely red, painful eye and may also experience nausea and vomiting. On examination, the affected pupil is usually sluggish and mid-dilated, and have a high IOP. The eye feels rock-hard to the touch, and the difference in firmness compared with the unaffected eye can be appreciated by palpation. A classic symptom patients report is seeing halos around lights, a result of corneal swelling caused by fluid being forced through the corneal endothelium into the stroma under high pressure. This corneal edema not only produces halos but also makes it difficult to visualize intraocular structures, complicating diagnosis and treatment.

Ocular Signs

• Markedly elevated IOP (often >40–50 mmHg).
• Corneal edema → gives a hazy or cloudy cornea.
• Mid-dilated, sluggish pupil (often oval in shape).
• Conjunctival injection (especially ciliary flush pattern: redness more intense around cornea).
• Shallow anterior chamber (best seen with slit lamp or penlight oblique illumination).
• Optic disc changes (cupping may appear later, not immediate).

Patient Symptoms (often accompany the signs)

• Severe ocular pain.
• Headache (often ipsilateral).
• Blurred vision and halos around lights (due to corneal edema).
• Nausea and vomiting (autonomic response to high IOP).

3. Normal-Tension Glaucoma

In this form, optic nerve damage occurs even though eye pressure remains within the normal range (<21mmHg). The exact cause isn’t fully understood, but it may be linked to reduced blood flow to the optic nerve. - Low central cornea thickness (CCT)

4. Secondary Glaucoma

This type results from another eye condition or trauma, such as inflammation, cataracts, diabetes, or the use of certain medications.

5. Congenital Glaucoma

A rare form present at birth due to abnormal development of the eye's drainage system. Symptoms may include cloudy eyes, excessive tearing, and light sensitivity.

How Is Glaucoma Treated?

While glaucoma damage cannot be reversed, treatment can slow or prevent further vision loss. The only proven method of achieving this is to reduce IOP to less than 18mmHg (According to the Advanced Glaucoma Intervention Study (AGIS)). Depending on the type and severity of glaucoma, treatment options may include:

1. Medications (Eye Drops)

Prescription eye drops are often the first line of treatment. They work by either decreasing fluid production or improving fluid drainage in the eye.

• Beta blockers (high side effect profile) (Timolol), Carbonic anhydrase inhibitors (Diamox), pilocarpine, alpha agonists, prostaglandin analogues

2. Oral Medications

In some cases, oral medications are used to reduce eye pressure when drops alone aren't effective.

3. Laser Treatment

• Laser trabeculoplasty: Often used for open-angle glaucoma, it helps fluid drain more effectively.
• Laser iridotomy: Commonly used for angle-closure glaucoma, it creates a small hole in the iris to improve fluid flow.
• Cyclophotocoagulation: Targets the ciliary body to reduce fluid production.

4. Surgical Procedures

If medications and laser treatments aren’t enough, surgical options include:

• Trabeculectomy: Creates a new drainage pathway for fluid.
• Glaucoma drainage implants: Small devices are inserted to help drain fluid.
• Minimally Invasive Glaucoma Surgery (MIGS): A newer category of procedures that are less risky and have faster recovery times.

Monitoring Glaucoma

Monitoring glaucoma is typically done by checking pressure, disk changes, and visual field.

Glaucoma pressure management