GLAUCOMA

INTRODUCTION
• Glaucoma is a group of ocular conditions
characterized by abnormal pressure within the
eyeball resulting to optic nerve damage.
• The optic nerve damage is related to the IOP
caused by congestion of aqueous humor in the eye.
• There is a range of pressures that have been
considered “normal” but that may be associated
with vision loss in some patients.
• Glaucoma is one of the leading causes of
irreversible blindness in the world.
 CONT’D
• The damage is silent, progressive, and
irreversible until the end stages, when loss of
peripheral vision occurs, followed by
reductions in central vision and eventually
blindness.
• Once glaucoma occurs, the patient will always
• have it and must follow treatment to maintain
stable intraocular eye pressures.
 CONT’D
• Glaucoma is more prevalent among people
older than 40 years of age, and the incidence
increases with age.
• It is also more prevalent among men than
women and in the African American and Asian
populations.
• Those in high-risk groups should have yearly
eye examinations for glaucoma detection.
 DEFINITION

• Glaucoma is an optic neuropathy associated

with characteristic structural damage to the
optic nerve and associated visual dysfunction
which is seen clinically as enlargement of the
disc cuff and loss of field vision.
 FORMATION AND DRAINAGE OF AQUEOUS
HUMOR
• Aqueous humor is a thin fluid present in front of retina which
fills the space between lens and cornea.
• This space is divided into anterior and posterior chambers by
iris.
• Both chambers communicate with each other through the
pupil
• Aqueous humor 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 Schlemm and the episcleral veins.
 CONT’D
• About 10% of the aqueous fluid leaves through the ciliary
body into the suprachoroidal space and then drains into the
venous circulation of the ciliary body, choroid, and sclera.
• 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 humor produced tends to decrease
with age, in systemic diseases such as diabetes, and in ocular
inflammatory conditions.
 CONT’D
• IOP is determined by;
 the rate of aqueous production,
 the resistance encountered by the aqueous
humor as it flows out of the passages, and
 the venous pressure of the episcleral veins
that drain into the anterior ciliary vein.
 CONT’D
• When aqueous fluid production and drainage
are in balance, the IOP is between 10 and 21
mmHg.
• 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.
 CONT’D
• 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.
 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.
 CONT’D
• 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.
 CONT’D
• The two common clinical forms of glaucoma
encountered in adults are open-angle and
angle-closure glaucoma.
 RISK FACTORS

1. Genetics: positive family history is a risk factor

for glaucoma, the relative risk of having POAG
is increased 2-4 fold from individuals who have
sibling with glaucoma.
• Glaucoma particularly POAG is associated with
mutation in several genes (including
MYOC,ASB10,WDR36,NTF4,and TBK1 genes)
2. Drugs: such as steroids(steroid induced
glaucoma)
 CONT’D
3. Disease conditions that severely affect blood
flow to the eye such as:
 Diabetic retinopathy and central retinal vein
occlusion.
 Hypertension.
3. Myopia (3%) of the cases.
4. Aging (>40yrs)
5. Race (African black)
 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 ischemic 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 ischemic types.
• Typically, most cases are a combination of both.
• Regardless of the cause of damage, glaucomatous changes typically
evolve through clearly discernible stages:
 CONT’D
1. Initiating events: precipitating factors include
illness, emotional stress, congenital narrow
angles, long-term use of corticosteroids, and
mydriatics (ie, medications causing pupillary
dilation). These events lead to the second stage.
2. Structural alterations in the aqueous outflow
system: tissue and cellular changes caused by
factors that affect aqueous humor dynamics lead
to structural alterations and to the third stage.
 CONT’D
3. Functional alterations: conditions such as
increased IOP or impaired blood flow create
functional changes that lead to the fourth stage.
4. Optic nerve damage: atrophy of the optic nerve
is characterized by loss of nerve fibers and blood
supply, and this fourth stage inevitably
progresses to the fifth stage.
5. Visual loss: progressive loss of vision is
characterized by visual field defects.
 TYPES OF GLAUCOMA

Open-Angle Glaucomas
• Usually bilateral, but one eye may be more severely
affected than the other.
• In all three types of open-angle glaucoma, the anterior
chamber angle is open and appears normal.
• Chronic open-angle glaucoma (COAG): Optic nerve
damage, visual field defects, IOP >21 mm Hg. May have
fluctuating IOPs.
• Usually no symptoms but possible ocular pain,
headache, and halos.
 CONT’D
Normal tension glaucoma: IOP ≤ 21 mm Hg.
Optic nerve damage, visual field defects.
• IOP ≤ 21 mm Hg. Optic nerve damage,
Ocular hypertension: Elevated IOP.
• Possible ocular pain or headache.
PRIMARY OPEN ANGLE GLAUCOMA(POAG)

• This refers to slow clogging of the drainage

canals resulting in increased intra ocular
pressure which cause progressive optic nerve
damage.
• It is characterized by gradual loss of peripheral
vision but eventually the entire vision will be
lost if left untreated.
• It is the most common type of glaucoma
accounting for 90%of all cases of glaucoma.
 CONT’D
• The onset is slow and painless and loss of
vision is gradual life long and irreversible.
• It has a wide and open angle between the iris
and cornea.
• POAG develops bilaterally
 PATHOPHYSIOLOGY

• The underline cause of POAG remains

unknown.
• The major risk factor and focus of treatment is
increased intra ocular pressure(IOP).
• IOP is the function of production liquid
aqueous humor by ciliary process of the eye
and its drainage through trabecular
meshwork.
 CONT’D
• In POAG, flow is reduced through the trabecular
meshwork due to degeneration and obstruction of
the meshwork whose original function is to absorb
aqueous humor.
• This leads to increase resistance and chronic painless
build up pressure in the eye.
• The mechanism is as a result of direct effect of
pressure on the nerve leading to apoptosis and optic
nerve atrophy as well as compression of arteries
supplying to the eye.
 TREATMENT

• Decrease IOP 20% to 50%.

• Additional topical and oral agents added as
necessary.
• If medical treatment is unsuccessful, laser
trabeculoplasty (LT) can provide a 20% drop in
intraocular pressure.
• Glaucoma filtering surgery if continued optic
nerve damage despite medication therapy and
LT.
Angle-Closure (Pupillary Block) Glaucomas

• Obstruction in aqueous humor outflow due to

the complete or partial closure of the angle
from the forward shift of the peripheral iris to
the trabecula.
• The obstruction results in an increased IOP.
 Acute angle-closure glaucoma (AACG)

• AACG occurs in people who have an

anatomically narrowed angle at the junction
where the iris meets the cornea.
• When nearby eye structures such as the iris
protrude into the anterior chamber, the angle
is occluded, which blocks the flow of aqueous
fluid
 CONT’D
• Certain medications, regardless of their route,
are contraindicated in AACG and can result in
blindness if given to a patient with AACG.
• These medications include any
anticholinergics such as atropine and
antihistamines such as diphenhydramine
(Benadryl) or hydroxyzine (Vistaril) because
they are mydriatics.
 CONT’D
• Rapidly progressive visual impairment, periocular
pain, conjunctival hyperemia, and congestion.
• Pain may be associated with nausea, vomiting,
bradycardia, and profuse sweating.
• Reduced central visual acuity, severely elevated IOP,
corneal edema.
• Pupil is vertically oval, fixed in a semi-dilated position,
and unreactive to light and accommodation.
• Photophobia and tearing are also present
 CONT’D
• Subacute angle-closure glaucoma: Transient
blurring of vision, halos around lights;
temporal headaches and/or ocular pain; pupil
may be semi-dilated.
• Chronic angle-closure glaucoma: Progression
of glaucomatous cupping and significant visual
field loss; IOP may be normal or elevated;
ocular pain and headache.
 DIAGNOSIS
• 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,
 Tonometry to measure the IOP,
 ophthalmoscopy to inspect the optic nerve,
 gonioscopy to examine the filtration angle of the
anterior chamber, and
 Perimetry to assess the visual fields.
 CLINICAL MANIFESTATIONS

• Glaucoma is often called the silent thief of sight because

most patients are unaware that they have the disease until
they have experienced visual changes and vision loss.
• The patient may not seek health care until he or she
experiences 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.
 MANAGEMENT

• It is important to note that ; the only

identifiable factor in glaucoma is controlling the
IOP, therefore the goal of management is to
avoid glaucomatous nerve damage and
preserve visual field and total quality of life for
patients.
• The management include medical, surgical and
nursing.
 TREATMENT

• Ocular emergency; administration of hyperosmotics,

azetazolamide, and topical ocular hypotensive agents,
such as pilocarpine and beta-blockers (betaxolol).
• Possible laser incision in the iris (iridotomy) to release
blocked aqueous and reduce IOP.
• Other eye is also treated with pilocarpine eye drops
and/or surgical management to avoid a similar
spontaneous attack.
• Prophylactic peripheral laser iridotomy.
 MEDICAL MANAGEMENT

I. Prostaglandin analogs e.g. Latanoprost

M.O.A: Increases uveoscleral outflow
2. Beta-blockers e.g. Timolol, betaxolol
3. Adrenergic agonists e.g. ephinephrine, dipivefrin
M.O.A: Reduces production of aqueous humor and
increases outflow
4. Alpha-adrenergic agonists e.g. apraclonidine,
brimonidine
 CONT’D
5. Carbonic anhydrase inhibitors eg
Acetazolomide, methazolamide, dorzolamide.
6. Hyper osmotic diuretics e.g. Mannitol.
7. Cholinergics (miotics) e.g. pilocarpine, carbachol
• M.OA: Increase the outflow of the aqueous
humor by affecting ciliary muscle contraction and
pupil constriction, allowing flow through a larger
opening between the iris and the trabecular
meshwork.
 NURSING MANAGEMENT
 Counseling; visual loss due to glaucoma is
irreversible and the only treatment modality is to
control the pressure , preserve vision and prevent
the patient from becoming blind.
 Programmed individualized and family
counseling is important to relieve anxiety and
improve stress coping skills.
 Genetic counseling to individuals with family
history of glaucoma
 CONT’D
• Counsel on adherence to lifelong drug treatment,
surgery and visual outcomes after surgery and
complications that may arise.
• Health educate on regular medical check up .

REHABLITATION OF GLAUCOMA PATIENTS

 Use of low vision aids e.g. Hand held magnifier and
Telescope.
 Use of high powered lens.
 CONT’D
 Changing the environment of the patient
based on the colors he appreciate.
 Measures to prevent falling and trauma.
 Occupational therapy and social therapy.
 Enlightening the friend and family of the
patient about the condition
 NURSING DIAGNOSIS

• Pain related to increased intraocular pressure

• Disturbed sensory perception: visual related to
altered sensory reception
• Self-care deficit related to decreased vision
• Anxiety related to partial or total visual loss
• Risk for injury related to decreased vision
• Deficient knowledge related to medical regimen,
disease process due to no prior experience
THANKS FOR YOUR
ATTENTION