GLAUCOMA

INTRODUCTION

Glaucoma can cause blindness if it is left untreated. And unfortunately, approximately 10% of people with
glaucoma who receive proper treatment still experience loss of vision, according to Glaucoma Research
Foundation. There is no cure yet for glaucoma and the loss of vision is irreversible. However, with medication
and/or surgery, it is possible to halt further loss of vision. This topic will aid for better understanding on how
glaucoma as one of the causes of leading cause of blindness.

EPIDEMIOLOGY

According to the International Agency of the Prevention for Blindness, glaucoma is the third leading cause of
blindness and a leading cause of irreversible blindness worldwide in 2015. Irreversible blindness is a lack of vision
that cannot be corrected with contact lenses and glasses, unless surgical treatment is performed.

In the Philippines, the 2017 estimated number of persons who are bilaterally blind is 332,150 of which 33% or
around 109,609 is due to cataract, 25% (83,037) due to errors of refraction (EOR) and 14% (46,501) due to
glaucoma. The rest are due to other eye conditions like, retinopathy and maculopathy.

ETIOLOGY

Intraocular pressure (IOP) is the fluid pressure of the eye. It is a measurement involving the magnitude
of the force exerted by the aqueous humor on the internal surface area of the anterior eye.
Increased intraocular pressure (IOP), a traditional diagnostic criterion for glaucoma, is thought to play an important
role in the pathogenesis of glaucoma, but it is no longer a diagnostic criterion for glaucoma. Although IOP is a poor
predictor of which patients will have visual field loss, the risk of visual field loss increases with increasing IOP. IOP is
not constant; it changes with pulse, blood pressure, forced expiration or coughing, neck compression, and posture.

Many drugs can increase IOP. The potential to induce or worsen glaucoma depends on the type of glaucoma and
on whether it is adequately controlled.

Drugs That May Induce or Potentiate Increased Intraocular Pressure

Open-angle glaucoma Closed-angle glaucoma

Ophthalmic corticosteroids (high risk) Topical anticholinergics
Systemic corticosteroids Topical sympathomimetics
Nasal/inhaled corticosteroids Systemic anticholinergics
Fenoldopam Heterocyclic antidepressants
Ophthalmic anticholinergics Low-potency phenothiazines
Succinylcholine Antihistamines
Cimetidine (low risk) Ipratropium
Vasodilators (low risk) Benzodiazepines (low risk)
Theophylline (low risk)
Vasodilators (low risk)
Systemic sympathomimetics (low risk)
Central nervous system stimulants (low risk)

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 Selective serotonin reuptake inhibitors
Imipramine
Venlafaxine
Topiramate
Tetracyclines (low risk)
Carbonic anhydrase inhibitors (low risk)
Monoamine oxidase inhibitors (low risk)
Topical cholinergics (low risk)

PATHOPHYSIOLOGY

Glaucoma is a group of eye disorder which is usually interrelated with the increased pressure in the eye also known
as intraocular pressure (IOP). These intraocular pressure damages the nerve, and when left untreated leading to
blindness.

The Aqueous humor, dynamics, intraocular pressure (IOP),

and glaucoma.

Typically, all of the chambers of the eye are filled with fluid
called aqueous humor. The aqueous humor is a transparent
watery fluid secreted by the ciliary epithelium. These chambers
are composed by:

• The anterior chamber is an aqueous humor-filled

spaces between the cornea and iris.
• The posterior chamber which is the narrow spaces
between the iris and the lens.
• The vitreous chamber which is the space between the
lens and the back of the eye.

Additionally, ciliary epithelium provides structural Figure 1. Anatomy of the Eye

support to keep the shape of the eye. The fluid
secreted into the posterior chamber flows through
the narrow space between the lens and the back of
the iris, through the anterior chamber. From the
anterior chamber, the fluid flows out of the eye
through the spongy tissue that acts to drain which is
called the trabecular meshwork. Then, this
meshwork allows the fluid to go down into the
circular channel called the canal of Schlemm; and
finally, into the aqueous veins. The aqueous veins are
part of the episcleral venous system, the veins
around the sclera of the eye.

In glaucoma, the drainage system which includes the

episcleral venous system, aqueous veins, canal of Figure 2. Anterior chamber of the eye and aqueous humor flow.
Schlemm, and trabecular meshwork, are
completely blocked. As a result, the fluid can’t easily drain-out which leads to increased pressure in the space of

Prepared by: Camille N. Libranda CPM-501

the anterior chamber causing intraocular hypertension. Intraocular hypertension or high intraocular pressure is
defined as pressure >21 mmHg. These high pressure affects all the structures of the eye, including the optic nerve.

The optic nerve, is the nerve in the eye that carries visual information from the eyes to the brain. When the optic
nerve gets damaged over the time, visual loss can occur.

There are 2 major types of glaucoma:

 The Open-angle glaucoma. This is the most common type of glaucoma in which the angle between the iris
and cornea is open. In this type, the draining system gets clogged over time. So, there’s a gradual increase
of pressure in the optic nerve. This increased pressure initially result in the atrophy of the outer rim of the
nerve, resulting in the loss of peripheral vision. As that pressure increases, even more though, there’s a
continuous damage of the optic nerve eventually causing loss of central vision as well.
Patients may exhibit pressures in the 20 to 30 mm Hg (2.7 to 4.0 kPa) range for years before any disease
progression is noticed in the optic disk or visual fields. That is why OAG is often referred to as the “sneak
thief of sight”.
Increased intraocular pressure (IOP) was historically considered to be the sole cause of optic nerve
damages or optic neuropathy. Additional contributing factors include increased susceptibility of the optic
nerve to ischemia, reduced or dysregulated blood flow, excitotoxicity, autoimmune reactions, and other
abnormal physiologic processes.

 The Closed-angle glaucoma. This glaucoma is also known as narrow-angle glaucoma, and this is because
of the angle between the iris and cornea being too small. So, the passage way of the aqueous humor is
narrow, making the lens pushed against the iris. A rapid physical blockage of the trabecular meshwork
may occur, resulting in increased IOP causing severe abrupt onset of pain, eye redness, blurry vision,
headaches, nausea visual haloes.

There are general classifications of glaucoma:

 Primary glaucoma - glaucoma that has no known cause.

A. Open angle
B. Angle closure
1. With pupillary block
2. Without pupillary block
 Secondary glaucoma - has many causes including exfoliation syndrome, pigmentary glaucoma, systemic
diseases, trauma, surgery, lens changes, ocular inflammatory diseases, and drugs
A. Open angle
1. Pretrabecular - normal meshwork is covered and prevents outflow of aqueous humor
2. Trabecular - meshwork is altered or material accumulates in the intertrabecular spaces
3. Post-trabecular - episcleral venous blood pressure is increased
B. Angle closure -
1. Without pupillary block
2. With pupillary block
 Congenital glaucoma - This type of glaucoma occurs in babies when there is incorrect or incomplete
development of the eye's drainage canals during the prenatal period. This is a rare condition that may be
inherited. When uncomplicated, microsurgery can often correct the structural defects. Other cases are
treated with medication and surgery.
 Normal-Tension Glaucoma (NTG)
Also called low-tension or normal-pressure glaucoma. In normal-tension glaucoma the optic nerve is
damaged even though the eye pressure is not very high. We still don't know why some people’s optic
nerves are damaged even though they have almost normal pressure levels.

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SIGNS AND SYMPTOMS

Open-angle glaucoma

Open-angle glaucoma is slowly progressive and is usually asymptomatic until the onset of substantial visual field
loss. Central visual acuity is maintained, even in late stages.

There is no signs and symptoms until substantial visual field loss occurs.

Closed-angle glaucoma

In closed-angle glaucoma, patients typically experience intermittent prodromal symptoms (e.g., blurred or hazy
vision with halos around lights and occasionally, headache). Acute episodes produce symptoms associated with a
cloudy, edematous cornea; ocular pain; nausea, vomiting, and abdominal pain; and diaphoresis.

Some of the noticeably signs of closed-angle glaucoma include hyperemic conjunctiva, cloudy cornea, shallow
anterior chamber, and occasionally an edematous and hyperemic optic disk; IOP is generally elevated markedly (40
to 90 mm Hg [5.3 to 12.0 kPa]) when symptoms are present.

RISK FACTORS

 High eye pressure

 Family history of glaucoma
 Age 40 and older for African Americans
 Age 60 and older for the general population, especially Mexican Americans
 Thin cornea
 Suspicious optic nerve appearance with increased cupping (size of cup, the space at the center of optic
nerve, is larger than normal)
 High myopia (very severe nearsightedness)
 Diabetes.
 Eye surgery or injury.
 High blood pressure.

DIAGNOSIS

The diagnosis of open-angle glaucoma is confirmed by the presence of characteristic optic disk changes and visual
field loss, with or without increased IOP. Normal tension glaucoma refers to disk changes, visual field loss, and IOP
of less than 21 mm Hg. Ocular hypertension refers to IOP of more than 21 mm Hg without disk changes or visual
field loss.

For glaucoma, the presence of the angle is usually visualized by:

 Gonioscopy is using a goniolens together with a slit lamp or operating microscope to view the iridocorneal
angle, or the anatomical angle formed between the eye's cornea and iris. 
 Tonometry is used to asses intraocular pressure. Tonometry is the procedure eye care professionals
perform to determine the intraocular pressure, the fluid pressure inside the eye. It is an important test in
the evaluation of patients at risk from glaucoma. Most tonometers are calibrated to measure pressure in
millimeters of mercury.

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  Visual field testing can be done. This is a subjective measure of central and peripheral vision, or
“side vision,” and is used by your doctor to diagnose, determine the severity of, and monitor the
glaucoma. During an eye exam, visual field testing is performed one eye at a time, with the opposite eye
completely covered to avoid errors. In all testing, the patient must look straight ahead at all times in order
accurately map the peripheral visual field. When peripheral vision is loss, it is often an early and subtle
sign of glaucoma.
 Simply looking for the optic nerve damage through imaging and direct observation. In particular, the
pressure can make the outer rim of the nerve thin producing a “cupping”.

DESIRED OUTCOME

The goal of drug therapy in patients with glaucoma is to preserve visual function by reducing the IOP to a level at
which no further optic nerve damage occurs.

PHARMACOLOGIC TREATMENT

The balance between the inflow and outflow of aqueous humor determines IOP. Inflow is increased by β
-adrenergic agents and decreased by α 2-, α -, and β -adrenergic blockers; dopamine blockers; carbonic anhydrase
inhibitors (CAIs); and adenylate cyclase stimulators. Outflow is increased by cholinergic agents, which contract the
ciliary muscle and open the trabecular meshwork, and by prostaglandin analogs and β - and α 2-adrenergic
agonists, which affect uveoscleral outflow.

Open-angle glaucoma

Treatment is indicated for ocular hypertension if the patient has a significant risk factor such as:

 IOP greater than 25 mm Hg

 Vertical cup-disk ratio greater than 0.5
 Central corneal thickness less than 555 micrometers.
 Family history of glaucoma
 Black race
 Severe myopia
 Presence of only one eye.

Treatment is indicated for all patients with elevated IOP and characteristic optic disk changes or visual field
defects.

Drug therapy is the most common initial treatment and is initiated in a stepwise manner, starting with a single well
tolerated topical agent (Figure 3).

• Historically, β -blockers (e.g., timolol) were the treatment of choice and continue to be used if there are
no contraindications to potential β blockade caused by systemic absorption. β -Blockers have the
advantage of low cost owing to generic formulations.

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Figure 3. Topical Agents used for treatment of open-angle glaucoma.

• Prostaglandin analogs (e.g., latanoprost, bimatoprost and travoprost) are used as first line treatment. It
has the advantage of strong potency, unique mechanism suitable for combination therapy, good safety
profile, and once-a-day dosing. Brimonidine has the theoretical advantage of neuroprotection, which has
not yet been demonstrated in humans. Topical CAIs are also suitable for first-line therapy.
• Pilocarpine and dipivefrin, a prodrug of epinephrine, are used as third-line therapies because of adverse
events or reduced efficacy as compared with newer agents.
• Carbachol, topical cholinesterase inhibitors, and oral CAIs (e.g., acetazolamide) are used as last-resort
options after failure of less toxic options.

Antiproliferative agents such as fluorouracil and mitomycin C are used to modify the healing process and maintain
patency.

Closed-angle glaucoma

• Drug therapy of an acute attack typically consists of an osmotic agent and secretory inhibitor (e.g., β
-blocker, α 2 agonist, latanoprost, or CAI), with or without pilocarpine.
• Osmotic agents are used because they rapidly decrease IOP. Examples include glycerin, 1 to 2 g/kg orally,
and mannitol, 1 to 2 g/kg IV.
• Although traditionally the drug of choice, pilocarpine use is controversial as initial therapy. Once IOP is
controlled, pilocarpine should be given every 6 hours until iridectomy is performed.
• Topical corticosteroids can be used to reduce ocular inflammation and synechiae.

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 • Epinephrine should be used with caution because it can precipitate acute closed-angle glaucoma,
especially when used with a β -blocker.

NON-PHARMACOLOGIC TREATMENT

 Trabeculoplasty. This is a laser treatment for glaucoma. It is done on an argon laser equipped slit lamp,
using a Goldmann gonioscope lens mirror. Specifically, argon laser is used to improve drainage through
the eye's trabecular meshwork, from which the aqueous humour drains. The optimal timing of laser or
surgical trabeculectomy is controversial, ranging from initial therapy to after failure of third- or fourth-line
drug therapy.
• Iridotomy. Acute closed-angle glaucoma with high IOP requires rapid reduction of IOP. Iridectomy is the
definitive treatment, which produces a hole in the iris that permits aqueous flow to move directly from
the posterior to the anterior chamber.
• Implants. This is a type of medical shunt used to help lower your eye pressure. The shunt consists of two
parts: a small tube and a plate. The small tube is inserted into your eye to let the fluid drain out. The plate
is attached to the tube. It is placed beneath the skin of the eye to form a small pool, where the fluid will
drain, called a bleb. This allows the fluid to drain out of your eye through your shunt instead of draining
through your eye’s natural drain. In glaucoma, the eye’s natural drain does not work very well. This
surgery helps bypass the natural drain and lower the eye pressure.

REFERENCES

DiPiro, Joseph T. Pharmacotherapy: a Pathophysiologic Approach. 8th ed., McGraw-Hill Medical, 2011.

Wells, B. G., Schwinghammer, T. L., DiPiro, J. T., & DiPiro, C. V. (2017).  Pharmacotherapy handbook (7th ed.). New
York: McGraw-Hill Education.

Bainter, P. S. (2019, October 17). Visual Field Test: Learn How the Procedure Is Performed. Retrieved from
https://www.medicinenet.com/visual_field_test/article.htm

Glaucoma: Prevention & Risk Factors. (2019, September 16). Retrieved from
https://www.brightfocus.org/glaucoma/prevention-and-risk-factors

https://www.glaucoma.org/glaucoma/types-of-glaucoma.php

Prepared by: Camille N. Libranda CPM-501