Glaucoma

Glaucoma is a group of ocular conditions characterised by

optic nerve damage. The degree of harm to the optic nerve
is variable (Shaarawy et al., 201 5). The optic nerve damage is
related to the IOP caused by congestion of aqueous humour
in the eye. A range of IOPs are considered 'normal; but these
may also be associated with vision loss in some patients.
Glaucoma is one of the leading causes of irreversible blindness
in the world. Glaucoma is rare in people younger than
35 years, is more prevalent among people older than 35
years, and the incidence increases with age. Unfortunately,
many people who have glaucoma are unaware they have the
disease, as vision deficits are a late sign of the disease (Royal
Australian and New Zealand College of Ophthalmologists
[RANZCO), 2015). In both Australia and New Zealand, it is

CHART 53-5 RISK FACTORS

G laucoma
• Family history of glaucoma
• Exposure to strong sunlight
• Older age
• Diabetes
• Cardiovascular disease
• Migraine syndromes
• Nearsightedness (myopia)
• Eye trauma
• Prolonged use of topical or systemic corticosteroids
estimated that 50% of people with glaucoma are undiagnosed
(CERA, cited in Glaucoma Australia, 2014a; Glaucoma
New Zealand, n.d.). One in 10 Australians older than 80 years
will develop glaucoma (Glaucoma Australia, 2014a). In New
Zealand, approximately 2% of the population older than 40
and 10% older than 70 years have glaucoma (Glaucoma New
Zealand, n.d.). Risk factors for glaucoma are outlined in Chart
53-5. There is no cure for glaucoma, but the disease can be
controlled (5haarawy et al., 2015).

Physiology
Aqueous humour flows between the iris and the lens, nourishing
the cornea and lens. Most (90%) of the fluid then
flows out of the anterior chamber, draining through the
spongy trabecular meshwork into the canal of 5chlemm and
the episcleral veins. About 10% of the aqueous fluid exits
through the ciliary body into the suprachoroidal space and
then drains into the venous circulation of the ciliary body,
choroid and sclera (Jaeger & Tasman, 201 0). Unimpeded
outflow of aqueous fluid depends on an intact drainage
system and an open angle (about 45 degrees) between the
iris and the cornea. A narrower angle places the iris closer to
the trabecular meshwork, diminishing the angle. The
amount of aqueous humour produced tends to decrease
with age, in systemic diseases such as diabetes, and in
ocular inflammatory conditions.
IOP is determined by the rate of aqueous production, the
resistance encountered by the aqueous humour as it flows out
of the passages, and the venous pressure of the episcleral
veins that drain into the anterior ciliary vein. When aqueous
fluid production and drainage are in balance, the IOP is
between 10 and 21 mm Hg. When aqueous fluid is inhibited
from flowing out, pressure builds up within the eye. Fluctuations
in IOP occur with time of day, exertion, diet and medications.
It tends to increase with blinking, tight lid squeezing,
and upward gazing. Systemic conditions such as hypertension
and intraocular conditions such as uveitis and retinal detachment
have been associated with elevated IOP. Exposure to
cold weather, alcohol, a fat-free diet, heroin and marijuana
have been found to lower IOP. People with thin corneas may
have falsely low IOP and glaucoma may not be detected (Glaucoma
Australia, 2014b).

Pathophysiology
There are two accepted theories regarding how increased IOP
damages the optic nerve in glaucoma. The direct mechanical
theory suggests that high IOP damages the retinal layer as it
passes through the optic nerve head. The indirect ischaemic
theory suggests that high IOP compresses the microcirculation
in the optic nerve head, resulting in cell injury and death.
Some glaucomas appear as exclusively mechanical, and some
are exclusively ischaemic types. Typically, most cases are a
combination of both.

Classification of glaucoma
There are several types of glaucoma. Whether glaucoma is
known as open-angle or angle-closure glaucoma depends
on which mechanisms cause impaired aqueous outflow.
Glaucoma can be primary or secondary, depending on
whether associated factors contribute to the rise in IOP.
Although glaucoma classification is changing as knowledge
increases, current clinical forms of glaucoma are open-angle
glaucomas, angle-closure glaucomas (also called pupillary
block}, congenital glaucomas, and glaucomas associated
with other conditions, such as developmental anomalies,
corticosteroid use, and other ocular conditions. The two
common clinical forms of glaucoma encountered in adults
are open-angle and angle-closure glaucoma. Table 53-4
explains the general characteristics of the different types of
open-angle and angle-closure glaucomas.
Clinical manifestation
Glaucoma is often called the 'silent thief of sight' because
most patients are unaware they have the disease until they
have experienced visual changes and vision loss. Patients
may not seek healthcare until they experience blurred vision
or 'halos' around lights, difficulty focusing, difficulty adjusting
eyes in low lighting, loss of peripheral vision, aching or discomfort
around the eyes, and headache.

Assessment and diagnostic findings

The purpose of a glaucoma investigation is to establish the
diagnostic category, assess the optic nerve damage, and formulate
a treatment plan. The patient's ocular and medical
history must be detailed to investigate the history of predisposing
factors. There are four major types of examinations
used in glaucoma evaluation, diagnosis and management:
tonometry to measure the IOP; slit-lamp biomicroscopy to
inspect the optic nerve; gonioscopy to examine the filtration
angle of the anterior chamber; and perimetry to assess the
visual fields.
As the optic nerve damage increases, visual perception in
the area is lost. The localised areas of visual loss (i.e. scotomas)
represent loss of retinal sensitivity and are measured and
mapped by perimetry. The results are mapped on a graph. In
patients with glaucoma, the graph has a distinct pattern that establishing
the diagnosis.

Medical management
The aim of all glaucoma treatment is prevention of optic
nerve damage through medical therapy, laser or non-laser
surgery, or a combination of these approaches. Lifelong
therapy is almost always necessary because glaucoma cannot
be cured. Although treatment cannot reverse optic nerve
damage, further damage can be controlled. The treatment
goal is to maintain an IOP within a range unlikely to cause
further damage. The initial target for IOP among patients with
elevated IOP and those with low-tension glaucoma with
progressive visual field loss is typically set at 30% lower than
the current pressure. The patient is monitored for changes in
the appearance of the optic nerve. If there is evidence of
progressive damage, the target IOP is again lowered until the
optic nerve shows stability.
Pharmacological therapy
Medical management of glaucoma relies on systemic and
topical ocular medications that lower IOP. Periodic follow-up
examinations are essential to monitor IOP, appearance of the
optic nerve, visual fields and side effects of medications. In
considering a therapeutic regimen, the ophthalmologist aims
for the greatest effectiveness with the least side effects,
inconvenience and cost. Therapy takes into account the
patient's health and stage of glaucoma. Comfort, affordability,
convenience, lifestyle and personality are factors to consider
in the patient's compliance with the medical regimen.
The patient is usually started on the lowest dose of topical
medication and then advanced to increased concentrations
until the desired IOP level is reached and maintained. Newer topical medications, such as
prostaglandins, are preferred
because of their efficacy, minimal dosing (can be used once
each day). One eye is treated first, with the other eye used as
a control in determining the efficacy of the medication; once
efficacy has been established, treatment of the fellow eye is
started. If the IOP is elevated in both eyes, both are treated.
When results are not satisfactory, a new medication is substituted.
The main markers of the efficacy of the medication in
glaucoma control are lowering of the IOP to the target pressure,
appearance of the optic nerve head, and the visual
field.
an action similar to beta-blockers and carbonic anhydrase
inhibitors. The newest group is the prostaglandins, which
increase aqueous outflow and uveoscleral outflow. They can
be used daily and do not affect pupil size.
Surgical management
Several types of ocular medications are used to treat glaucoma
(see Table 53-5), including miotics (i.e. cause papillary
constriction), adrenergic agonists (i.e. sympathomimetic
agents), beta-blockers, alphai-agonists (i.e. adrenergic agents),
carbonic anhydrase inhibitors and prostaglandins. Cholinergics
(i.e. miotics) increase the outflow of the aqueous humour
by affecting ciliary muscle contraction and pupil constriction,
allowing flow through a larger opening between the iris and
the trabecular meshwork. Adrenergic agonists increase aqueous
outflow but primarily decrease aqueous production with
If medications are poorly tolerated or ineffective in controlling
pressure in glaucoma, surgery or laser treatment may
become necessary to form a new drainage canal in the eye. A
number of surgical interventions can be performed to treat
glaucoma. These include laser trabeculoplasty for glaucoma;
laser iridotomy for pupillary block glaucoma; filtering procedures
for chronic glaucoma; drainage implants/shunts when
other procedures have been ineffective; and trabectome
when trabeculoplasty and medications have been unsuccessful.
Each should be looked at specifically if the nurse has a
patient undergoing any of them in conjunction with hospital
policies and procedures. Fortunately, serious complications
are uncommon in modern glaucoma surgery and surgery
may be the best alternative if optic nerve damage is occurring
(RANZCO, 201 S; Shaarawy et al., 2015).
Nursing management
Educating patients about self-care
The medical and surgical management of glaucoma slows
the progression of glaucoma but does not cure it. The lifelong
therapeutic regimen mandates patient education. The nature
of the disease and the importance of strict adherence to the
medication regimen must be explained to help ensure compliance.
A thorough patient interview is essential to determine
systemic conditions, current systemic and ocular
medications, family history and problems with compliance to
glaucoma medications. Then the medication program can be
discussed, particularly the interactions of glaucoma-control
medications with other medications. For example, the diuretic
effect of acetazolamide has an additive effect on the
diuretic effects of other antihypertensive medications and
can result in hypokalaemia.
The effects of glaucoma-control medications on vision must
also be explained. Miotics and sympathomimetics result in altered
focus; therefore, patients need to be cautious in navigating their
surroundings. Information about instilling ocular medication and
preventing systemic absorption with punctal occlusion is
described in the section on ophthalmic medications.
Nurses in all settings encounter patients with glaucoma.
Even patients with long-standing disease and those with
glaucoma as a secondary diagnosis should be assessed for
knowledge level and compliance with the therapeutic regimen.
Chart 53-6 contains points to review with glaucoma
patients.

CHART 53-6 PATIENT EDUCATION

Managing glaucoma
• Know your IOP measurement and the desired range.
• Be informed about the extent of your vision loss and optic
nerve damage.
• Keep a record of your eye pressure measurements and visual
field test results to monitor your own progress.
• Review all your medications (including over-the-counter and
herbal medications) with your ophthalmologist, and mention
any side effects each time you visit.
• Ask about potential side effects and drug interactions of your
eye medications.
• Ask whether generic or less costly forms of your eye
medications are available.
• Review the dosing schedule with your ophthalmologist and
inform him or her if you have trouble complying with the
schedule.
• Participate in the decision-making process. Let your doctor
know what dosing schedule works for you and other
preferences regarding your eye care.
• Have the nurse observe you instilling eye medication to
determine whether you are administering it properly.
• Be aware that glaucoma medications can cause adverse
effects if used inappropriately. Eye drops are to be
administered as prescribed, not when eyes feel irritated.
• Ask your ophthalmologist to send a report to your general
practitioner after each appointment.
• Keep all follow-up appointments.
Continuing care
For patients with severe glaucoma and impaired function,
referral to services that assist the patient in performing customary
activities may be needed. The loss of peripheral
vision impairs mobility the most. These patients need to be
referred to low-vision and rehabilitation services. Patients
who meet the criteria for legal blindness should be offered
referrals to agencies that assist in obtaining federal
assistance.
Reassurance and emotional support are important aspects
of care. A lifelong disease involving a possible loss of sight has
psychological, physical, social and vocational ramifications.
The family must be integrated into the plan of care, and
because the disease has a familial tendency, family members
should be encouraged to undergo regular examinations at
least once every 2 years to detect glaucoma early (Glaucoma
Australia, 2014a).