GLAUCOMA

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A&P
• Intraocular pressure is a function of production of liquid
aqueous humor by the ciliary body of the eye and its drainage
through the trabecular meshwork.
• Aqueous humor flows from the ciliary bodies into the posterior
chamber, bounded posteriorly by the lens and the zonule of
Zinn and anteriorly by the iris.
• It then flows through the pupil of the iris into the anterior
chamber, bounded posteriorly by the iris and anteriorly by the
cornea.

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A&P

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The aqueous outflow system.

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A&P
• From here the trabecular meshwork drains
aqueous humor via Schlemm's canal into scleral
plexuses and general blood circulation.
• In open angle glaucoma there is reduced flow
through the trabecular meshwork;
• in angle closure glaucoma, the iris is pushed
forward against the trabecular meshwork,
blocking fluid from escaping.
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Affected parts of the eye

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DEFINITION
• Glaucoma is a disorder in which the pressure in the eyeball
increases, damaging the optic nerve and causing a loss of vision
(Berkow et al, 1997).
• Glaucoma comprises a group of ocular disorders characterized
by increased intraocular pressure (IOP), optic nerve atrophy
and visual field loss (Black et al, 2001)

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AETIOLOGY/PREDISPOSING
FACTORS
• Usually, glaucoma has no known cause; however, the following
are some of the predisposing factors
• Old age related to thickening of the lens which narrows the
angle.
• Congenital due to abnormal development of the ocular
drainage system.
• Uveitis results in deposits of inflammatory debris that obstruct
the trabecular meshwork thereby decreasing fluid outflow or
iritis

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AETIOLOGY/PREDISPOSING
FACTORS
• Race - Open angle glaucoma is 8-10 times more prevalent
amongst black Americans than their white American due to
granules present in their eyes which cause ‘ageing’ of the
trabecular meshwork, in the angle of the anterior chamber,
through which the aqueous fluid escapes.
• Pupil dilation due to drugs e.g. atropine
• Thrombosis of the central vein of the eye leading to Venous
stasis

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AETIOLOGY/PREDISPOSING
FACTORS
• DM- diabetic retinothy causes damage to the blood vessels of
the retina resulting in neo-vasculation and if these new blood
vessel grows on the iris it leads to blockage of the fluid flow
thereby raising eye pressure

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AETIOLOGY/PREDISPOSING
FACTORS
• The following conditions can cause secondary glaucoma;
• Trauma: these include penetrating injuries to the globe,
contusions of the eyeball, partially or complete dislocation of the
lens or hypheama (blood in the anterior chamber)

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AETIOLOGY/PREDISPOSING
FACTORS
• Intraocular tumours- Trabecular block due to clogging by
tumour cells or direct invasion by tumour seedlings.
• Angle closure due to forward displacement of iris-lens
diaphragm by increasing tumour mass.

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AETIOLOGY/PREDISPOSING
FACTORS
• Complications from intraocular surgery especially cataract
surgery. in which trabecular meshwork is clogged by the lens
particles floating in the aqueous humour.
• It may occur due to lens particles left after accidental
• or planned extracapsular cataract extraction or
• following traumatic rupture of the lens.

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AETIOLOGY/PREDISPOSING
FACTORS
• Steroids - Under normal circumstances the endothelial cells
lining the trabecular meshwork act as phagocytes and
phagocytose the debris from the aqueous humour.
• Corticosteroids are known to suppress the phagocytic activity of
endothelial cells leading to collection of debris in the trabecular
meshwork and decreasing the aqueous outflow.

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AETIOLOGY/PREDISPOSING
FACTORS
• Drugs that causes pupil dilation (mydriatics) can cause the iris
to dilate and flatten resulting in angle closure

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PATHOPHYSIOLOGY
• Glaucoma is a condition in which the intraocular pressure is
increased above normal (10 – 21mmhg).
• The intraocular pressure is determined by the rate of aqueous
humor production in the ciliary body and the resistance to the
outflow of aqueous humor from the eye.

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PATHOPHYSIOLOGY
• Normally, aqueous humor enters and leaves the anterior
chamber so that intraocular pressure is maintained between 12
and 21 mm Hg.
• Increased intraocular pressure can be caused by a number of
changes that affect the flow of aqueous humor in the anterior
chamber of the eye.
• It may result from hyper-production of aqueous humor or
obstruction of outflow, though the exact cause is often unknown
(Black et al 2001).

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PATHOPHYSIOLOGY
• As the aqueous fluid build up in the eye, the
increased intraocular pressure inhibits blood
supply to the retina and the optic nerve, resulting
into visual impairment.
• Peripheral vision is lost first due gradual
narrowing of the visual field until the patient has
tunnel vision

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PATHOPHYSIOLOGY
• As the disease progresses, complete blindness
eventually occurs.
• Vision may be restored if glaucoma is treated
early; otherwise, vision loss is permanent (Linton
and Maebius, 2003).

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CLASSIFICATION
• Primary Glaucoma which may be
• Open angle glaucoma or
• Closed angle glaucoma
• Secondary glaucoma. results from another
cause such as drugs, injury, tumor, inflammation
• Congenital glaucoma. inherited condition
appearing in infants, incomplete development of
the drainage canals during the prenatal period
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Primary Open angle glaucoma
• It is also called chronic glaucoma
• It is a more common type than closed angle glaucoma.
• Fluid drains too slowly from the anterior chamber, resulting
into gradual increase in intraocular pressure (almost always in
both eyes), causing optic nerve damage and a progressive loss of
vision

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Primary Open Angle

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Open Angle Glaucoma

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Primary Open angle glaucoma
• it may not cause any symptom until irreversible damage has
occurred.
• Usually, the diagnosis is made by checking intraocular pressure,
therefore, every routine eye examination should include a test of
intraocular pressure.
• This condition tends to run in families and is most common in
people with diabetes.

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Clinical Manifestations
• Initially, increased intraocular pressure produces no symptoms.
• Later symptoms may include:
• Narrowing peripheral vision due to progressive loss of
peripheral visual field.
• headache – due increased intraocular pressure
• Dilated pupil -
• Lens becomes flat due to stretching of zonules.

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Clinical Manifestations
• Nausea and vomiting
• Vague visual disturbances such as seeing halos around electric
lights, or having difficulty in adapting to darkness.
• Cupped optic disc due to retinal ganglion cell death

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Clinical Manifestations
• It is important to note that open angle glaucoma may not cause
any symptoms until irreversible damage has developed.

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Primary Closed angle glaucoma.
• Closed angle glaucoma causes sudden attacks of
increased intraocular pressure, usually in one eye
(Linton and Maebius, 2003).
• In this condition, the space between the iris and
the cornea where the fluid filters out of the eye is
narrower than normal.
• There is a rapid increase in intraocular pressure,
rising as high as 50 mm Hg.
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Primary Closed angle glaucoma.
• If the pressure is not lowered promptly
permanent blindness can result.
• Therefore, closed angle glaucoma is considered a
medical emergency unlike open angle glaucoma.
•.

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Angle Closure Glaucoma

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Closed Angle Glaucoma

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Clinical Presentation

• Closed angle glaucoma causes;

• Sudden, acute pain.
• blurred vision
• halos around lights
• nausea and vomiting, and
• headache on the affected side

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Clinical Presentation
• Photophobia, is thought to be caused by irritation of corneal
nerves, which occurs as a result of the elevated IOP

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 Secondary glaucoma
• Secondary glaucoma results from ocular diseases
that cause a narrowed angle or an increase in
volume of fluids within the eye.
• These diseases/disorders indirectly disrupt the
activity of the structures involved in circulation
and reabsorption of aqueous humor.
• This can happen suddenly and without warning
(Ignatavicius and Workman, 2002).

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Congenital glaucoma
• This results from failure of normal development
within the angle of the anterior chamber resulting
in some blockage of aqueous fluid outflow.
• This blockage will vary according to the extent of
the abnormality.
• This type of glaucoma is present at birth.

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Clinical Presentation
• It is usually bilateral but one eye usually present with more
symptoms than the other.
• Buphthalmos (ox eye) this is an abnormally large eye this is
due to the increase of pressure in the eye as the child’s eye has
an ability to stretch.
• The cornea is edematous
• As the cornea stretches, it causes splits in the descemets
membrane.

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Clinical Presentation
• Photophobia, These are thought to be caused by irritation of
corneal nerves, which occurs as a result of the elevated IOP.

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Investigations
• Ophthalmoscopic examinations of the client
with glaucoma reveal cupping and atrophy of the
optic disk.
• The disk becomes wider and deeper and turns
white or gray.
• Visual field testing: To determine the extent of
peripheral field losses, visual fields are measured.

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Investigations
• A visual field examination maps the areas seen by
the eye while it fixates on a central point.
• In chronic open angle glaucoma, the visual field
initially show a small crescent-shaped defect that
gradually progresses to a larger field defect.
• While in acute closed angle glaucoma, the visual
fields can quickly decrease.

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Investigations
• Visual acuity: central vision may be normal in
early stages but is reduced or lost in advanced
cases.
• Slit lamp examination: Used to assess the
structures and depth of the anterior chamber
• Tonometry: This investigation will be done
using the Schiotz tonometer.
• It is done in order to determine the intra-ocular
pressure (IOP).
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Investigations
• Gonioscopy: This is a technique used to
examine the angle of the anterior chamber using a
specially designed contact lens with a small
mirror.
• Thus, the diagnosis of ‘open and closed angle
glaucoma.

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MANAGEMENT
• The management of glaucoma can either be
medical or surgical.
Medical management
• Medical therapy is given, even for a short period
of time.
• Drugs prescribed are intended to enhance
aqueous humor outflow, decrease its production,
or both.
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Treatment
• Miotics: They do this by constricting the pupil
(miotics) or by inhibiting the formation of
aqueous humor.
• the commonly used miotic is Pilocarpine 1, 2 or
4% eye drops , given 3-4 times daily.
• Miotics cause blurred vision for 1-2 hours after
use and adjustment to dark rooms is difficult
because of pupil constriction.
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Treatment
• Drugs that decrease the formation of aqueous
humor; these are beta-adrenergic-blocking
agents such as Timolol maleate eye drops
(Timoptol) 0.25 or 0.5% given twice a day.
• The other drugs that decrease the production of
aqueous humor are the carbonic anhydrase
inhibitors such as Diamox 250mg- 1gm given 3-
4 divided doses daily.
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Surgical management
• When drugs are not able to control glaucoma and
increased IOP persist, surgery is an alternative.
• The goal of surgery is to create openings so that
excess fluid can escape.
• The procedures done include:

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Surgical management
• Trabeculectomy, this is the surgical removal of the trabecular
meshwork so as to promote the drainage of the aqueous humor.
• Laser trabeculoplasty, this burns the trabecular meshwork,
scaring it and causing the meshwork fibers to tighten.
• This tightening of the fibers increases the size of the spaces
between the fibers, allowing the outflow of aqueous humor and
reduce the IOP.

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Technique of trabeculotomy.

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SPECIFIC NURSING CARE
• Nursing care will depend on the type of glaucoma the patient
has and the extent of visual loss.
• Control of pain: if the patient has closed angle glaucoma he
will be in pain.
• Give the prescribed drugs such as diclofenac 100mg TDS to
relieve pain.

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SPECIFIC NURSING CARE
• Drugs: give the prescribed drugs such as miotics,
to reduce the intraocular pressure.
• Observations: check IOP daily to monitor the
efficacy of the treatment you are giving and report
to the ophthalmologist of your findings.
• Monitor any deteriorating in visual field and
visual acuity.

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SPECIFIC NURSING CARE
• Psychological care: Counsel the patient for emotional
support and acceptance.
• Link the patient to organizations that can help e.g. Association
for the blind, if the patient has lost the sight.
• The family members will be counseled to continue regarding
him/her as one of the family circle with all the potential.

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SPECIFIC NURSING CARE
• Personal care: Male clients will be taught how to use an
electric shaver rather than a razor.
• Female clients will be encouraged to be using a hairstyle that is
easy to care for that will help in independent life.
• The family will be advised to have a nonskid surface in the
bathrooms and/or probably the whole house.

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SPECIFIC NURSING CARE
• Involve the adult or child in the daily interactions such as
playing with friends
• Give directions to places where things are put especially in the
home.
• Teach children the directions, feeling of things and
differentiating things through touch, smell, taste and hearing.

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SPECIFIC NURSING CARE
• Communication: Talk to the blind people in normal low tone
voice.
• People should introduce themselves on each contact to help the
blind distinguish the voices and know who is speaking to them.
• Explain whatever is being done on the blind to keep them
informed.

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SPECIFIC NURSING CARE
• Safety: It is best to leave furniture the way the client wants it
and not move it without informing him/her.
• Keep things in specific places to avoid bumping on them and to
promote knowing their usual places.
• Teach them to use a walking stick or lead them by having them
hold the hand of the aider.

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SPECIFIC NURSING CARE
Patient teaching:
• Teach the patient on the importance of adherence to the
prescribed treatment.
• Explain the condition to the patient and his family.
• Explain the side effects of the drugs to the patient.
• Explain the importance of keeping review dates.
• NB. Post – operative care as for cataract.

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COMPLICATIONS
• Blindness
• Painful blind eye (absolute glaucoma)

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END OF LECTURE

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