Glaucoma

Glaucoma is a group of ocular conditions characterized by optic nerve

damage.
 The optic nerve damage is related to the IOP caused by congestion of
aqueous humor in the eye.
 Some glaucomas appear as exclusively mechanical, and some are
exclusively ischemic types.
 Most cases are a combination of both

Incidences
 Glaucoma is one of the leading causes of irreversible blindness in the
world
 Glaucoma is more prevalent among people older than 40 years of age
and increases with age
 Glaucoma is more prevalent among men than women and in the African
American and Asian populations

Risk Factors for Glaucoma

 Family history of glaucoma
 African American race
 Older age
 Diabetes
 Cardiovascular disease
 Migraine syndromes
 Nearsightedness (myopia)
 Eye trauma
 Prolonged use of topical or systemic corticosteroids

Aqueous Humor and Intraocular Pressure

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
 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.
The amount of aqueous humor produced tends to decrease with age, in
systemic diseases such as diabetes, and in ocular inflammatory
conditions.

Intraocular Pressure (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.
 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

 It tends to lower with exposure to cold weather, alcohol, a fat-free

diet, heroin, and marijuana

Pathophysiology
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.
Stages of glaucomatous changes

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.
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
Classification of Glaucoma

Types of Glaucoma Clinical Manifestations Treatment

Open-Angle Glaucomas
1. Chronic open-angle  Optic nerve damage  Decrease IOP 20% - 50%.
glaucoma (COAG) Additional topical and oral
 Visual field defects agents added as necessary

 IOP >21 mm Hg  If medical treatment is

 May have fluctuating IOPs unsuccessful, laser
trabeculoplasty (LT) can
 Usually no symptoms but provide a 20% drop in
possible ocular pain, intraocular pressure
headache, and halos.
 Glaucoma filtering surgery if
continued optic nerve
damage despite medication
therapy and LT

2. Normal tension  IOP ≤21 mm Hg  Treatment similar to COAG

glaucoma
 Optic nerve damage
 Lower the IOP by at least
 Visual field defects 30%.
3. Ocular hypertension  IOP > 21 mm Hg
 Lower IOP by at least 20%.
 Possible ocular pain or
headache
Angle-Closure (Pupillary Obstruction in aqueous humor
Block) Glaucomas 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.
1. Acute angle-closure  Rapidly progressive visual
glaucoma (AACG) 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 semidilated position,
and unreactive to light and
accommodation
Subacute angle-closure  Transient blurring of vision
glaucoma  Halos around lights
 Temporal headaches
and/or ocular pain
 Pupil may be semi-dilated.
Chronic angle-closure  Progression of
glaucoma glaucomatous cupping
 Significant visual field loss
 IOP may be normal or
elevated
 Ocular pain
 Headache.
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
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
 Can lead to acute or chronic
angle-closure glaucoma if
untreated
 Management similar to that
for COAG: includes laser
iridotomy and medications
 adjusting eyes in low lighting, loss of peripheral vision, aching or
discomfort around the eyes, and headache.

Assessment and Diagnostic Findings

Four major types of examinations used in glaucoma evaluation,

diagnosis, and management:
1. Tonometry to measure the IOP
2. Ophthalmoscopy to inspect the optic nerve
3. Gonioscopy to examine the filtration angle of the anterior chamber
4. Perimetry to assess the visual fields

The changes in the optic nerve significant for the diagnosis of

glaucoma:
 Pallor (caused by a lack of blood supply that results from cellular
destruction)
 Cupping of the optic nerve disc (characterized by exaggerated
bending of the blood vessels as they cross the optic disc, resulting
in an enlarged optic cup that appears more basin-like compared
with a normal cup)
 The progression of cupping in glaucoma is caused by the gradual
loss of retinal nerve fibers accompanied by the loss of blood supply,
resulting in increased pallor of the optic disc.

Medical Management
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 the stability of the optic nerve. If there is
evidence of progressive damage, the target IOP is again lowered until
the optic nerve shows stability
PHARMACOLOGIC THERAPY
Pharmacological therapy takes into account the patient’s health and stage
of glaucoma.
Beta-blockers are the preferred initial topical medications.
The main markers of the efficacy of the medication in glaucoma control
  Lowering of the IOP to the target pressure
 Appearance of the optic nerve head
 Appearance of the visual field
Medication Action Side Effects Nursing
Implications
Cholinergics  Increases  Periorbital pain  Caution patients
(miotics) aqueous fluid  Blurry vision about diminished
 Pilocarpine outflow by  Difficulty seeing vision in dimly lit
contracting the in the dark area
 Carbachol ciliary muscle

 Causes miosis
(constriction
of the pupil)

 Causes the
opening of
trabecular
meshwork
Adrenergic agonists  Reduces  Eye redness  Teach patients
 Dipivefrin production of and burning punctal occlusion
 Epinephrine aqueous  Palpitations to limit systemic
humor  Elevated blood effects
 Increases pressure
outflow  Tremor
 Headaches
 Anxiety
Beta-blockers  Decreases  Bradycardia  Contraindicated
 Betaxolol aqueous  Exacerbation of in patients with
 Timolol humor pulmonary asthma, copd,
production disease second- or third-
 Hypotension degree heart
block,
bradycardia, or
cardiac failure

 Teach patients
punctal occlusion
to limit systemic
effects
Alpha-adrenergic  Decreases  Eye redness  Teach patients
agonists aqueous  Dry mouth punctal occlusion
 Praclonidine humor  Dry nasal to limit systemic
production passages effects
 Brimonidine
Carbonic anhydrase  Decreases Oral medications  Do not
inhibitors aqueous (acetazolamide administer to
humor and patients with
 Acetazolamide production methazolamide) sulfa allergies
 Methazolamide associated with
serious side  Monitor
 Dorzolamide
effects, including electrolyte levels
anaphylactic
reactions,
electrolyte loss,
depression,
lethargy,
gastrointestinal
upset, impotence,
and weight loss;
topical form
(dorzolamide)
side effects include
topical allergy
Prostaglandin  Increases  Darkening of  Instruct patients
analogs uveoscleral the iris tob report any
 Latanoprost outflow  Conjunctival side effects
redness
 Possible rash

Surgical management
In laser trabeculoplasty for glaucoma, laser burns are applied to the inner
surface of the trabecular meshwork to open the intratrabecular spaces and
widen the canal of Schlemm, thereby promoting outflow of aqueous humor
and decreasing IOP
 Contraindicated when the trabecular meshwork cannot be fully
visualized because of narrow angles.
 A serious complication of this procedure is a transient rise in IOP
(usually 2 hours after surgery) that may become persistent
In laser iridotomy for pupillary block glaucoma, an opening is made in the
iris to eliminate the pupillary block.
 Contraindicated in patients with corneal edema, which interferes with
laser targeting and strength.
 Potential complications are burns to the cornea, lens, or retina;
transient elevated IOP; closure of the iridotomy; uveitis; and blurring.
 Pilocarpine is usually prescribed to prevent closure of the
iridotomy
Filtering procedures for chronic glaucoma are used to create an opening
or fistula in the trabecular meshwork to drain aqueous humor from the
anterior chamber to the subconjunctival space into a bleb, thereby bypassing
the usual drainage structures.
 This allows the aqueous humor to flow and exit by different routes

Trabeculectomy is the standard filtering technique used to remove part of

the trabecular meshwork.
 Complications include hemorrhage, an extremely low (hypotony) or
elevated IOP, uveitis, cataracts, bleb failure, bleb leak, and
endophthalmitis
 Scarring is inhibited by using antifibrosis agents such as the
antimetabolites fluorouracil (Efudex) and mitomycin (Mutamycin).
 Fluorouracil can be administered intraoperatively and by
subconjunctival injection during followup
 Mitomycin is much more potent and is administered only
intraoperatively.

Drainage implants or shunts are open tubes implanted in the anterior

chamber to shunt aqueous humor to an attached plate in the conjunctival
space.
 A fibrous capsule develops around the episcleral plate and filters the
aqueous humor, thereby regulating the outflow and controlling IOP.