UNIVERSITY OF CEBU – BANILAD CAMPUS

COLLEGE OF NURSING

RESOURCE UNIT ON
CHRONIC GLAUCOMA
SUBMITTED BY:
BSN 4Y - GROUP 32
CASINILLO , CRAIG T. FAJARDO , BARTOLOME JR.
DAAN , DAWN MICHOR A. FORTUNA , EARL JOSEPH
DAVID , CALVIN KLEIN GADOR , EDITA
DEL CORRO , DARYL GENOLAGA , MARIA ANGELIE
DELA CRUZ , JUDE MATHEW JAKOSALEM , YVONNE
DELOS SANTOS , JASTINE JIMENEZ , RUSSELL LLOYD
ENRIQUEZ , POCHOLO JORDA , PRINCESS FATIMA
ESCABAS , MARITESS

SUBMITTED TO:

MS. MARIA ELIZABETH C. MENDOZA, R.N.

CLINICAL INSTRUCTOR
DAUGHTERS OF ST. CAMILLUS de LELLIS - Home for the Aged
GENERAL OBJECTIVES: After more or less 90 MINUTES of group discussion, the BSN 4-Y GROUP 32 students will be able to gain basic knowledge, develop
positive attitude and proper skills in caring for patients having CHRONIC GLAUCOMA.
SPECIFIC TIME
OBJECTIVES
CONTENT ALLOTMENT
METHODOLOGY RESOURCES EVALUATION

Specifically, the BSN

4Y GROUP 32 Lecture –
 Book
students will be able Discussion References:
to: ( please see
separate
attachment)
I. State the
 Online
INTRODUCTION 10 minutes refrences:
Glaucoma refers to a category of eye disorders often ( please see
associated with a dangerous buildup of internal eye pressure separate
(intraocular pressure or IOP), which can damage the eye's optic attachment)
nerve that transmits visual information to the brain.
 Cartolina
With untreated or uncontrolled glaucoma, you might eventually  Markers
notice decreased ability to see at the edges of your vision
(peripheral vision). Progressive eye damage could then lead to
blindness.

Glaucoma is the second most common cause of blindness

in the US. There are four major types of glaucoma:
 Open angle (chronic) glaucoma
 Angle closure (acute) glaucoma
 Congenital glaucoma
 Secondary glaucoma

All four types of glaucoma are characterized by increased

pressure within the eyeball, and therefore all can cause
progressive damage to the optic nerve. Open angle (chronic)
glaucoma is by far the most common type of glaucoma.
II.Define related
Terms:

5 minutes
III. Review the
ANATOMY and
PHYSIOLOGY of the
EYE
THE HUMAN EYE

15 minutes

Eye Anatomy

The cornea is a clear cap that covers the pupil and the colored
part of the eye, called the iris. The anterior chamber is a space
that lies between the cornea and the iris. Clear fluid, called
aqueous humor, circulates through the anterior chamber.

Other structures of the eye include:

 Bony orbit and extraocular muscles:
o The bone around the eye that protects it and the
muscles that move the eyeball in the socket
 Conjunctiva:
o The thin, clear membrane that covers the white
part of the eye, as well as the inside surface of the
eyelids
 Sclera:
o The strong, white, outer layer of the globe

 Cornea:
o The clear, firm cap that protects the pupil and the
iris
 Pupil:
o The opening that allows light to pass to the lens

 Iris:
o The colored part of the eye that controls the size
of the pupil
 Lens of the eye:
o The clear, soft disc that receives light through the
pupil and focuses images on the retina
 Ciliary body:
5 minutes
o Contains muscles that control the shape of the
lens.
 Vitreous:
 o The clear gel inside the globe that helps to
maintain the shape of the eye
 Choroid:
o The thin layer that contains blood vessels that
supply the parts of the eye
 Retina:
o The retina is to the eye what film is to a camera. It
is a thin membrane in the back of the eye that
contains the rod and cone cells for vision. After
receiving light, the retina sends messages to the
brain though the optic nerve. This information is
IV. processed into images by the brain.

a. Discuss what
is CHRONIC
GLAUCOMA.
What is chronic glaucoma?

A person with chronic glaucoma has worsening damage to the

optic nerve, resulting in loss of vision. The optic nerve is a 20 minutes
bundle of nerve fibers that carries information from the eye to
the brain. Blind spots develop when the nerve fibers become
damaged. Left untreated, chronic glaucoma can result in
blindness. Chronic glaucoma is very common and responds
b. DISCUSS THE Well to treatment.
INCIDENCE &
ETIOLOGY
Chronic Glaucoma Incidence

 About 2.2 million Americans suffer from chronic

glaucoma.
 Approximately 1:100 people over 40 years old are
affected but about half of them are unaware of this.
  The prevalence increases with age, affecting about 16%
of people aged over 70.
 Male:female = 1:1 (some studies suggest a slightly
higher prevalence in males).3
 Responsible for approximately 12% of all cases of blind
c. Identify the registration in the UK.
RISK
 This number is expected to rise to 3.4 million by 2020.
FACTORS

Risk factors

 Age - the incidence increases with age, most commonly

presenting after 65 years old (and rarely before 40 years
old).5
 Family history - there is a clear inherited component in
many individuals (IOP, aqueous outflow facilities and
disc size are inherited characteristics). However, it is
thought that there is incomplete penetrance and variable
expressivity of the genes involved. There are also
several factors thought to contribute to the inheritance
and therefore the risk to relatives is currently only an
estimate: 4% to children and 10% to siblings of an
affected individual.
 Race - it is 3 to 4 times more common in Afro-Caribbean
people in whom it tends to present earlier and is more
severe.
 Other factors - myopia (short-sightedness) and retinal
disease (e.g. central retinal vein occlusion, retinal
detachment and retinitis pigmentosa) can predispose
individuals to POAG. It is postulated that diabetes4 and
d. Enumerate the
systemic hypertension4 (and possibly also systolic
SIGNS AND
hypotension) may also contribute to risk.
SYMPTOMS

The difficulty with this condition is that in the vast majority

 of cases, patients do not notice anything at all. Indeed, it is
estimated that up to 50% of cases in the western world go
undetected.Suspicion arises during the course of a routine
optician check where abnormal discs, IOPs or visual fields may
be noted.

Signs and Symptoms include:

 Initially none
 Gradual loss of peripheral vision (vision eventually
becomes "tunneled")
 Examination:
1. Cupping of an optic disk (scooped-out
appearance); or asymmetry of disks comparing
one eye to the other
2. Visual field defects
3. Central visual field testing
Tonometry shows increased intraocular pressure.
IV. Explain the
PATHOPHYSIOLOGY
of CHRONIC
GLAUCOMA
 10 minutes

V. Discuss the
various DIAGNOSTIC
PROCEDURES

As glaucoma becomes much more common over the age of 40

you should have eye tests at least every two years and ask for
all three glaucoma tests. This has been shown to be much more
effective in detecting glaucoma than just having one or two of
the tests. These tests are:

 Raised IOP - IOP is a little like blood pressure in that

there is not an absolute correct value but a normally
distributed range of values (from 10-21 mmHg) with
some normal individuals having IOPs outside these
ranges. Furthermore, there are physiological diurnal
fluctuations of up to 5 mmHg in about 30% of the
population, this variation being exaggerated in patients
with POAG.2 In addition to this, the IOP has to be
measured in the context of corneal thickness as the latter
affects IOP readings. A slightly thick cornea may give
rise to an erroneously high reading and there is a 10%
inter-examiner variation.1 So all these factors, combined
with others such as changes with season, respiration and
aerobic exercise,3 make this measure a useful guide
rather than an absolute standard if the readings are
sitting on the borderline of normality.5
 Optic disc changes - this is a key assessment in these
patients as it is a direct marker of disease progression.
Optic disc damage is assessed by looking at the vertical
ratio of the pale centre (cup) to the overall size of the
disc. A small cup and a thick neuroretinal rim (the darker
bit surrounding the cup) may give a ratio of 0.3 or less
 (normal). A small number of people have a cup:disc ratio
up to 0.7 but anything beyond that is definitely
pathological. These measurements are made by
observation and comparisons to charts. There are also
imaging techniques available to carry out objective
measurements.
 Visual fields - these can be assessed using a couple of
15 minutes
different perimetry machines which objectively document
what the patient perceives in the periphery of their vision.
These can also assess the degree of false positive errors
(the patient clicks away when they can't see much) so
adding weight to the assessment. These assessments
require the co-operation of the patient and can also be
affected by fatigue, spectacle frames, miosis and media
opacities.3 Where this is not possible, the assessor will
have to rely on IOPs and cup:disc ratios alone.
 Gonioscopy - this will be carried out in the
ophthalmology clinic to ensure that the iridocorneal
angles are open, so confirming the diagnosis of this
particular form of glaucoma. This test is performed on the
first visit only and, from the patient's perspective, it is not
painful but may feel strange and some patients find it
hard to tolerate, as the direct contact of the gonio lens
against the (anaesthetised) cornea induces
blepharospasm (squeezing the eye shut) in some.
 Other aspects - the corneal thickness will also be
assessed (pachymetry) on the first patient visit, as a
thicker than usual cornea will give an erroneously high
IOP reading (and vice versa). Visual acuities and any
comorbid factors will be assessed in each patient.

20 minutes
VI. Discuss the
MEDICAL
MANAGEMENT for
CHRONIC
GLAUCOMA Treatment aims

 Treatment is not necessarily started immediately on

simple detection of an elevated IOP. Bearing in mind the
comments made above, the patient should be assessed
on several occasions; the diagnosis is significant and
treatment lifelong. Even apparent disc cupping will
considered in conjunction with visual fields and IOP. In
some patients, the disease is obvious and advanced, in
which case treatment should start promptly.
 Once a diagnosis and decision to treat have been made,
a target IOP is set according to the degree of damage:
this is the pressure below which further damage is
considered unlikely.3 This is usually in the region of a
30% drop of IOP. It is different between patients and may
be different in each eye.
 Regular monitoring via ophthalmology clinics to assess
IOP, the optic disc and the visual fields. Some areas
have schemes whereby trained opticians carry out all the
monitoring.
 Patient education is key as this is a largely asymptomatic
condition until it is very advanced. It is important that they
understand the irreversible nature of the disease and that
they feel involved in issues around taking drops
(including how to take them correctly and potential side-
effects), when and why one might move on to surgery,
educating their own family with regards to careful
screening and so on.

Medical therapy
This is the first line and only treatment for many patients. There
is no single drug that stands out above others as the optimal
treatment of glaucoma.It may take a few trials with different
agents before one is found that effectively lowers the IOP
without causing unwanted side-effects. Generally, drugs are
initiated one at a time but subsequent addition of further drugs
may be necessary if IOP remains unsatisfactorily high.
Treatment may be to one or both eyes. Traditionally, beta-
blockers were the preferred first option but since about the year
2000, prostaglandin analogues have been favoured as they are
as efficient with fewer side-effects.The drugs fall into the
following groups:
 Beta-blockers
o Action: reduce aqueous secretion by inhibiting
beta-adrenoceptors on ciliary body.
o Contra-indications: bradycardia, heart block,
uncontrolled heart failure, asthma and patients
with a history of chronic obstructive pulmonary
disease.
o Caution: depression, myasthenia gravis,
possibility of interactions with other medication
such as verapamil.
o Common ocular side-effects: irritation, erythema,
dry eyes, blepharoconjunctivitis and allergy
anaphylactic reaction possible.
o Common systemic side-effects: bronchospasm,
bradycardia, exacerbation of heart failure,
nightmares.
 Prostaglandin analogues
o Action: increase aqueous outflow via uveoscleral
route.
o Contra-indications: active uveitis, pregnancy and
breastfeeding.
o Caution: brittle or severe asthma, aphakia (patient
with no lens), pseudophakia (patient with artificial
lens such as the one put in following a cataract
extraction), do not take within 5 minutes of using
thiomersal-containing preparations.
 o Common ocular side-effects: change in eye
colour: brown pigmentation, thickening and
lengthening of eye lashes, more rarely: uveitis,
ocular pruritus, photophobia and keratitis.
o Systemic side-effects: rarely - hypotension,
bradycardia, brow ache.
 Sympathomimetics
o Action: reduce aqueous secretion and increase
outflow through trabecular meshwork.
o Contra-indications: angle closure glaucoma (due
to mydriatic effects), patients currently taking
monoamine oxidase inhibitors (possibility of
hypertensive crisis).
o Caution: hypertension, heart disease.
o Common ocular side-effects: mydriasis, dry eye,
severe smarting and redness of the eye.
o Common systemic side-effects: lethargy,
hypotension.
 Carbonic anhydrase inhibitors and systemic drugs
o Action: reduce aqueous secretion by ciliary body.
Weak diuresis in systemic use.
o Contra-indications: renal impairment, metabolite
imbalance, severe hepatic impairment,
sulphonamide sensitivity (acetazolamide),
breastfeeding.
o Caution: elderly, hepatic impairment, history of
renal calculi, history of intra-ocular surgery,
pregnancy and breastfeeding. Extravasation at
infusion site of intravenous acetazolamide can
cause necrosis.
o Ocular side-effects: localised discomfort,
lacrimation, topical allergy, more rarely:
superficial punctate keratitis, uveitis, transient
myopia.
o Systemic side-effects: (particularly with systemic
administration), taste disturbance,
 nausea/vomiting, headache, dizziness, fatigue,
paraesthesia and sulphonamide-related side-
effects with acetazolamide.
 Miotics
o Action: open up the drainage channels in the
trabecular meshwork by ciliary muscle contraction.
o Contra-indications: situations where pupillary
constriction is undesirable (such as uveitis),
presence of retinal holes.
o Caution: darkly pigmented irides require higher
concentrations but overdosage must be avoided,
patients with retinal disease (especially previous
detachment), cardiac disease, hypertension,
asthma, peptic ulceration, urinary tract
obstruction and Parkinson's disease.
o Ocular side-effects: miosis: this can cause
blurred vision and patients should be warned of
this as it can affect driving and other skilled tasks,
especially in the presence of a cataract.
Accommodative spasm with brow ache (often
causing intolerance in patients over 40), localised
discomfort, pupillary block.
o Systemic side-effects: sweating, bradycardia,
gastrointestinal disturbance.
If the patient is on maximum tolerated medical therapy and
there is ongoing disease progression, laser and surgical
treatments will be considered.
Laser therapy2,5
 Argon laser trabeculoplasty - laser burns to the
trabecular meshwork in the iridocorneal angle enhance
aqueous outflow. It has the benefit of reducing (stopping)
the need for drops whilst not having the complications of
surgery. However, trials relating to its effectiveness are
old and compare it to drops that have been replaced by
newer, more efficacious drugs. Research has yet to be
done in this area as well as into the different responses
 of different patients (particularly of different ethnicities)
and a definitive treatment protocol has yet to be
established.9
 Diode laser trabeculoplasty - similar principle as
above, using a higher laser power.
 Nd:YAG laser iridotomy - a small hole is made in the
iris in patients with angle closure glaucoma, to enhance
aqueous outflow. Both eyes are treated to prevent
subsequent acute episodes in the fellow eye.
 Diode laser cycloablation - part of the secretory
component of the ciliary body is destroyed, so reducing
aqueous secretion. This is used in intractable end-stage
20 minutes
glaucoma.
Surgical therapy2,5
 Trabeculectomy - this procedure creates a fistula
between the anterior chamber of the eye and the sub-
Tenon space (immediately around the globe), so allowing
aqueous outflow. Adjunctive anti-metabolites such as 5-
fluorouracil and mitomycin C may be used to prevent
scarring over of the fistula.
 Artificial shunts in the form of plastic devices
connecting the anterior chamber to the sub-Tenon space
can be inserted but are associated with many post-
operative complications.
 New techniques and devices are being developed to
minimise the complications of laser and surgical
treatment. An example is canaloplasty whereby
Schlemm's canal is artificially widened with a temporary
tube and viscoelastic.10
VII. Discuss the
NURSING
MANAGEMANT
for CHRONIC
GLAUCOMA
15 minutes
BIBLIOGRAPHY

 BOOK REFERENCE:

 Seely, R. “Essentials of Anatomy and Physiology” 2007, 6th Edition. The McGraw-Hill Companies, Inc., 1221 Avenue of the Americas, New York, NY

10020

 Smeltzer, S, et al. “Textbook of Medical-Surgical Nursing”. Volume 1.2008.11th Edition. Lippincott William & Wilkins. Norristown Road, Suite 200, New

York

 ONLINE REFERENCE:

 http://www.freemd.com/chronic-glaucoma/

 http://www.patient.co.uk/doctor/Primary-Open-Angle-Glaucoma.htm

 http://www.rnib.org.uk/xpedio/groups/public/documents/PublicWebsite/public_rnib003655.hcsp

 http://www.allaboutvision.com/conditions/glaucoma.htm

 http://www.caridon.com/chronic-glaucoma.html