Glaucoma

1. GLAUCOMA
Aparna.A
I MSc. Nursing

2. What is glaucoma?
 Classified as a group of
diseases.
 Damages the optic
nerve.
 Can cause permanent
vision loss if left
untreated.

3. Magnitude
Second major cause of
blindness
Often asymptomatic in early
stage.
Damage is irreversible.
More prevalent among men
than women
Incidence increase with age

4. DEFINITION
It is a heterogeneous group of diseases in
which damage to the optic nerve(optic
neuropathy) is usually caused by raised
ocular pressure
IOP: Depends on the
balance between
production and
removal of
aqueous humour

5. NORMAL IOP = between 10 and 21mmHg
IOP > 21.7 is abnormal.

6. ANATOMY OF EYE

7. Eye Anatomy
 The optic nerve is a
bundle of nerve
fibers.
 It carries visual
information from the
retina to the brain.

8. Acqeous flow

9. Aqueous Humour Dynamics
 Produced by non-pigmented epithelia of pars
plicata
 Aqueous production rate - 2µL/min
 Facility of outflow – 0.22µL/min/mm of Hg

10. Fluid Circulation
 The eye has an
internal fluid
circulation system.
 Fluid is produced at
the base of the iris.

11. Fluid Circulation
 The fluid flows
through the pupil to
the front of the iris.

12. Fluid Circulation
 The fluid exits the
eye at the angle
between the iris and
the cornea where it
drains through a
spongy meshwork.

13. Angle of the Anterior Chamber of Eye
 The aqueous humor outflow
occurs by two routes
 Trabecular: Trabeculum is the
site for pressure dependent
aqueous outflow functioning as a
one way valve that allows
aqueous to leave the eye but
does not allow the flow inside it.
 Uveoscleral: Pressure
independent outflow. The
aqueous passes across the
cilliary muscles into the
supracilliary and suprachoroidal
spaces and drain into the venous
circulation.

14.  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.

15. IOP
 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.

16. *Age
*Sex
*Race
*Heredity
*Diurnal & Seasonal variation
*Blood pressure
*Obesity
*Drugs
*Posture
*Exercise
Factor affect IOP
*Hormone
*Refractive error
*Eye movement
*Eyelid closure
*Inflammation
*Surgery

17. Cause of glaucoma
 Slow fluid drainage.
 Pressure builds up and
damages the optic
nerve.
 Optic nerve damage
can occur at different
pressure levels for
different people.

18. Higher risk people
 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

19. Pathophysiology

20. Theories of damage
1. Mechanical theory
• Compression of axons leads to axonal death
2. Vascular theory
• Ischemia causes axonal necrosis
Direct damage due to
pressure
Capillary Occlusion
Interference to
Axoplasmic flow

21. Stages
1. Initiating events: precipitating factors include
illness, emotional stress, congenital narrow angles,
long-term use of corticosteroids, and mydriatics (ie,
medications causing pupillary dilation).

22. Stages
2. Structural alterations
in the aqueous
outflow system: Tissue
and cellular changes
caused by factors that
affect aqueous humour
dynamics lead to
structural alterations.

23. 3. Functional
alterations:
conditions such
as increased
IOP or impaired
blood flow
create functional
changes
Stages

24. 4. Optic nerve damage:
Atrophy of the optic
nerve is characterized
by loss of nerve fibers
and blood supply, and
this stage inevitably
progresses to the fifth
stage.
Stages

25. 5. Visual loss:
progressive loss of
vision is characterized
by visual field defects.
Stages

26. Glaucomatous Damage
 Axonal necrosis leading to cupping
 Loss of supporting glial tissue
 Normally leads to disc pallor
Histology of Normal and Glaucomatous Optic nerve

27. Glaucomatous Damage

28. GLAUCOMA
Optic nerve signs of glaucoma progression
 Development of disk pallor
 Disc hemorrhage (60% will show progression of VF damage)
 Vessel displacement
 Increased visibility of lamina cribosa

29. Pallor and cupping
Cupping and pallor correspond
Pallor - maximal area of colour contrast
Cupping is greater than pallor
Cupping - bending of small blood vessels crossing disc

30. CLASSIFICATION
ACORDING TO AETIOLOGY
*Primary
*Secondary
ACCORDING TO APPERANCE OF THE ANGLE
MECHANISMS CAUSE IMPAIRED AQUEOUS
OUTFLOW
*Open angle glaucoma.
*Closed angle glaucoma.
*Combined mechanism glaucoma
*Developmental-
Congenital, manifest at birth
Infantile, present in first year of life.
Juvenile, present in late childhood.

33. Congenital
 Features
 Buphthalmos
corneal diameter 12 mm < 1 yr
 characterized by dysgenesis of the angle of the anterior
chamber, raised IOP, corneal opacities and
enlargement of the globe
 Optic disc cupping

35. Etiology:
 10% show autosomal recessive inheritance with
variable penetration
 Chromosomal abnormalities at 1p6 and 2p21
 The disease is caused by the maldevelopment of the
angle of the anterior chamber (angle dysgenesis).
 The characteristic gonioscopic appearance of an eye
with congenital glaucoma is marked by the presence
of open angle, Barkan’s membrane, abnormally high
insertion of the iris, poorly developed and posteriorly
placed sclera spur and collapsed Schlemm’s canal.

36. MANAGEMENT OF CONGENITAL
GLAUCOMA
GONIOTOMY TRABECULOTOMY

37. GLAUCOMA CLASSIFICATION
PRIMARY VERSUS SECONDRY
*PRIMARY
No detectable ocular or systemic abnormality.
Often bilateral.
Often familial
*SECONDARY
Predisposing ocular or systemic abnormality.
Often unilateral.
Often sporadic

38. Primary Glaucoma
Is the iris:
Covering the
Trabecular meshwork
NOT covering the
Trabecular meshwork
OPEN angle glaucoma CLOSED angle glaucoma
With high
pressure
With normal
pressure

39. Signs & symptoms
1. “Silent thief of sight”
2. Frequent change of
presbyopic glasses
Open Angle Glaucoma
Risk Factors
Age
Race
Family History
Diabetes
Myopia
Hypertension
Smoking

40. Primary OPEN angle
glaucoma
 It is the most common type of
glaucoma
 It is the 2nd cause of blindness in the
India
 It is also called chronic open angle
glaucoma.
 It causes SLOW damage to the optic
nerve, causing gradual loss of vision.

41. Definition of POAG
 POAG is defined as a chronic progressive optic
neuropathy associated with elevated IOP and visual
field defects

42. Primary Open Angle
Glaucoma (POAG)
 POAG is the most common form of glaucoma
 It occurs when the fluid drainage is poor and fluid
builds up in the eye and the internal eye pressure
goes up.
 This increased pressure can cause damage to the
optic nerve and vision loss.
 The exact mechanism of damage is still unknown.

43. Risk Factors for POAG
 High Intraocular (Eye) Pressure
 Over the age of 40
 Family history of glaucoma
 African or Caribbean descent
 Thin cornea
 High myopia (Nearsightedness)
 Diabetes
 High blood pressure

44. Primary OPEN angle glaucoma
 Pathogenesis:
Resistance of drainage of aqueous through the
Trabecular meshwok, due to:
 Thickening of Trabecular lamellae (reduces pore
size).
 Reduction in number of lining Trabecular cells.
 Increased extracellular material in the Trabecular
meshwork spaces.

45. Interference with
aqueous outflow
degenerative
changes in the
trabeculum,
schlemm’s canal and
exit channels
vascular insufficiency
optic nerve damage
(cupping).

46. Normal -tension Glaucoma
 IOP<21
 Mostly elderly people
 Vasospastic disease – Migraine, Raynaud’s
phenomena, Autoimmune disease

47. Ocular Hypertension
 Some people can have high eye pressure but the
optic nerve does not get damaged.
 This condition is called ocular hypertension.
 These patients must be closely followed because
of the risk of developing glaucoma.

48. Occular Hypertension
 It is defined as one who has an elevated IOP in the
absence of identifiable optic neuropathy and visual
field defects.
 It is benign rise of IOP usually found in about 6-10%
of population above 40yrs of age and is more
common than open angle glaucoma.

49. Symptoms of Primary Open
Angle Glaucoma
 POAG develops gradually and painlessly and
has no initial symptoms
Vision is normal in
the early stages

50. Symptoms of Primary Open
Angle Glaucoma
 If untreated, peripheral or side vision is slowly
lost
Tunnel vision

51. Symptoms of Primary Open
Angle Glaucoma
 Eventually, all vision may be lost

52. Angle Closure Glaucoma
 This type of glaucoma is
an emergency situation.
 It occurs when the iris
itself blocks the drainage
angle and results in a
sudden increase in
pressure.
 Symptoms include severe
eye pain, nausea, eye
redness and very blurred
vision.
 Immediate treatment is
required.

53. Primary Angle Closure Glaucoma(PACG)
 Risk factors include
 race (varies in different race),
 age (increases with age),
 gender (2-4 times frequently in females),
 family history (first degree relatives)
 personality (anxious).

54. PRIMARY ANGLE CLOSURE
GLAUCOMAS
PRIMARY ANGLE-
CLOSURE
GLAUCOMA
ANATOMIC FEATURES:
• SMALL CORNEAL
DIAMETER
• SHALLOW ANTERIOR
CHAMBER
• THICKER LENS
• SMALL RADIUS OF THE
ANTERIOR LENS
CURVATURE
• ANTERIOR LENS POSITION
• SHORT AXIAL LENGTH
• HYPEROPIC EYES

55. PRIMARY ANGLE CLOSURE
GLAUCOMAS STAGES
A. PRIMARY ANGLE-CLOSURE
GLAUCOMA SUSPECT
B. SUBACUTE ANGLE-CLOSURE
GLAUCOMA
C. ACUTE ANGLE-CLOSURE
GLAUCOMA
D. CHRONIC ANGLE-CLOSURE
GLAUCOMA
E. ABSOLUTE GLAUCOMA

56. CLINICAL COURSE
 Primary angle closure glaucoma suspect
 Small hyperopic eyes with small anterior chamber
associated with an occludable angle are usually prone to
develop primary angle closure glaucoma
 The patient is usually symptom free.
 Treatment is laser iridotomy.

57. CLINICAL COURSE….
 Subacute or intermittent primary angle closure
glaucoma
 Transient attacks of unilateral head ache, blurring of
vision, coloured halos, associated with sudden and sharp
rise of IOP in an eye with a shallow anterior chamber and
an occludable angle characterize the subacute primary
angle closure glaucoma.
 The attack is precipitated by several factors like dim
illumination, emotional stress and drugs.
 The attack is usually subsides without any medication,
probably by spontaneous resolution of the pupillary block
due to miosis during sleep.

58. CLINICAL COURSE….
 Acute primary angle closure glaucoma
 An acute congestive attack is characterized by a sudden
neuralgic pain, profound diminution of vision, intense
cilliary congestion, corneal edema, very shallow anterior
chamber, complete closure of the angle of anterior
chamber, vertically dilated non reacting pupil and
markedly raised IOP.
 An acute congestive attack occurs always with the
closure of the angle by peripheral anterior synechiae and
edematous and congested root of the iris and ciliary
processes. The changes in the iris are secondary to the
vascular strangulation which results from the raised IOP.

59. CLINICAL COURSE….
 Chronic primary angle closure glaucoma
 It develops either after recurrent attacks of subacute or
acute primary angle closure glaucoma or when the angle
closes gradually and IOP rises slowly.
 A gradual asymptomatic angle closure is known as
creeping angle closure glaucoma

60. CLINICAL COURSE….
 Absolute primary angle closure glaucoma
 The terminal stage of primary angle closure glaucoma is
marked by the complete loss of vision and stony hard
eye.
 Etiology is untreated acute primary angle closure
glaucoma or chronic primary angle closure glaucoma
which ends up in absolute glaucoma.

61. Features of Absolute primary angle closure
glaucoma
 The eyes are painful and blind.
 A chronic congestion is seen in circumcorneal region and
often the anterior ciliary vessels are dilated.
 The cornea is edematous and has bullous or filamentary
keratopathy; it is hazy and insensitive.
 The anterior chamber is shallow.
 The iris may show atropic patches.
 The pupil is dilated and does not react to light and
accommodation.
 Ectropion of uveal pigment is frequent at the papillary
boarder.
 IOP is very high and the eyeball is stony hard.
 The optic nerve head is deeply cupped.

62. Treatment of Absolute primary angle closure
glaucoma
 cyclodestructive surgeries to reduce IOP and enucleation in
case of painful eyes

63. Secondary Glaucoma
 Glaucoma can develop as a complication from other
conditions including:
 Eye injuries
 Uveitis (internal eye inflammation)
 Pigment dispersion
 Diabetes (Neovascular glaucoma)
 Steroid use

64. Pseudoexfoliation Glaucoma
 Elderly white women
 Fibrillar material deposited on trabecular
meshwork
 Moth-eaten iris transillumination defects
 Pigment on trabecular meshwork

65. STEROID INDUCED GLAUCOMA
 Risk Factors
 POAG
 Diabetes
 Myopia
 Stronger the steroid more the elevation

66. Malignant Glaucoma
 Aqueous misdirected posteriorly behind vitreous
 Vitreous moves forward, collapses iris & lens into
AC
 Typically after intraocular surgery particularly
cataract & glaucoma

67. Lens related Glaucoma
Intumescence
Dislocation and Subluxation
Phacolytic
Lens particle

68. Symptoms
 At first, there are none.
 As glaucoma
progresses, side vision
fails.
 Field of vision narrows
as glaucoma worsens.

69. What does vision with glaucoma
look like?
Normal Vision Vision with Glaucoma

70. Glaucoma detection
 Regular eye examinations by an optometrist or
ophthalmologist are vital to detecting glaucoma.
 A number of tests are performed.

71. Glaucoma can be detected through a comprehensive dilated eye exam.

72. STEPWISE DIAGNOSIS
 IOP with Applanation tonometry with Corneal Pachymetry
 Good S/L examination & Stereoscopic Dialated
Ophtalmoscopic examination
 Gonioscopy
 Formal visual-field testing(WWP)
 Imaging

73. How is glaucoma detected?

74. Glaucoma Tests:
History
 A patient’s medical history, family history and
background are important to determine the
presence of risk factors.

75. Glaucoma Tests:
Visual Acuity
 A refraction is done to determine best corrected
vision.
 This shows central vision function.

76. Glaucoma Tests:
Slit Lamp & Gonioscopy
 A special microscope called a slit lamp is used to
examine the structures of the eye.
 A gonioscopy lens may be used to view the
drainage angle.

77. Glaucoma Tests:
Tonometry
 Eye pressure is measured with an instrument called
a tonometer.
 Three types that are commonly used are:
 Goldmann (Perkins)
 Non-contact (air puff)
 Tonopen

78. Tonometers
Goldmann
Contact applanation
Perkins
Portable contact applanation
Pulsair 2000 (Keeler)Air-puff
Schiotz
Portable non-contact applanationNon-contact indentation
Contact indentation
Tono-Pen
portable contact applanation

79. Glaucoma Tests:
Ophthalmoscopy
 Eye drops may be placed in the eyes to dilate the
pupils.
 Special magnifying lenses are used to examine the
retina and optic nerve for damage.
Normal Optic
Nerve
Suspicious Optic
Nerve

80. Glaucoma Tests:
Ophthalmoscopy
 Advances are being made in digital imaging of the
retina.

81. Glaucoma Tests:
Visual Field Test
 Peripheral (side) vision is tested with a
perimeter.
The patient responds to flashes of
light in different locations

82. Optic Nerve

83. Field Test

84. Humphery Field Trace

85. Normal Disc

86. Cupped Disc

88. Glaucoma treatment
 Medications
 Surgery
◦ Laser
◦ Conventional

89. MANAGEMENT OF CONGENITAL
GLAUCOMA
GONIOTOMY TRABECULOTOMY

90. Treatment

91. Treatment
 Medical
 Beta blockers (Timolol)
 Carbonic anhydraze inhibitors
Azopt and Trusopt
 Sympathomimetics
Propine and Apraclonidine
 Parasympathomimetics (pilocarpine)
 Prostaglandin Derivatives (Xalatan)

92. Glaucoma Medications
 Medications are usually the
first type of treatment used
 Eyedrops or pills are used to
either decrease the fluid
production or to increase the
fluid drainage

93. Glaucoma Medications
 There are several different types of medication
available.
 The right choice will depend on what other
medications are being taken, other medical
conditions and the effectiveness in decreasing the
eye pressure.
 Often, combinations of eyedrops are used.

94. Treatment
 Laser
 Trabeculoplasty
 Sclerostomy
 Cycloablation

95. Laser Trabeculoplasty
 This laser treatment helps to increase the fluid
drainage
 The surgeon uses a laser to burn the spongy
meshwork that is located in the drainage angle

96. Treatment
 Surgical
 Goniotomy
for congenital
 Trabeculotomy
for congenital glaucoma's
 Trabeculectomy
for adult glaucoma's
 Implants
for difficult non responsive

100. Conventional Surgery
 With this treatment, the surgeon creates a new
opening in the eye for the fluid to drain out from
 If the new opening becomes plugged or
narrowed, further surgery may be required

101. Coping with Vision Loss
 Many patients with sight loss due to glaucoma can
benefit from low vision aids
 Optometrists can perform low vision assessments
and prescribe magnifying devices to enhance both
distance and reading vision

102. Coping with Vision Loss
 These aids will not restore sight to normal levels but
they allow people to maximize the amount of vision
remaining

103. Early Detection & Treatment
Regular eye health
examinations are important to
detect glaucoma early
so that treatment can be
started and vision loss can
be prevented.

104. NURSING MANAGEMENT

105. Acute angle closure glaucoma
 Nursing Assessment
 Establishing demographic data
 Family history of glaucoma or other eye problems
 OTC drugs
 History of allergy to drugs/ dye
 Evaluate patient for severe pain, nausea and
vomiting, signs of increased IOP.
 Assess visual symptoms.
 Establish history of onset of attack and previous
attacks.
 Assess patient's level of anxiety and knowledge
base.

106. Nursing Diagnoses
Acute Pain related to increased IOP
 Goal: Relieving Pain
 Nursing Interventions:
 Notify health care provider immediately of
patient's condition.
 Administer opioids and other medications
as directed.
 Medications that may cause nausea and
vomiting are avoided. Patient may be
medicated with antiemetic if nausea
occurs.

107. Acute Pain related to increased IOP
 Explain to patient that the goal of
treatment is to reduce IOP as quickly as
possible.
 Explain procedures to patient.
 Reassure patient that, with reduction in
IOP, pain and other signs and symptoms
should subside.

108. Acute Pain related to increased IOP
 Explain adverse effects of medications:
 Mannitol (Osmitrol) (I.V.) for transient blurred vision,
rhinitis, thirst, nausea, transient circulatory overload,
and headache
 Acetazolamide (Diamox) or methazolamide
(Neptazane) (oral) - drowsiness, anorexia,
paresthesia, stomach upset, tinnitus, fluid and
electrolyte imbalance, rare kidney or liver dysfunction
 Pilocarpine (Pilocar, Isopto carpine, Ocupress)
(topical) - burning and redness of eye, headache,
constricted pupil, poor vision in dim light, retinal
detachment, rare lens opacity

109. Fear related to pain and potential loss of
vision
 Goal: Relieving Fear
 Intervention:
 Provide reassurance and calm presence
to reduce anxiety and fear.
 Prepare patient for surgery, if necessary.

110. Fear related to pain and potential loss of
vision
 Describe procedure to patient; surgery
will likely be done on outpatient basis.
 Patch will be worn for several hours, and
sunglasses may help with photophobia.
 Vision will be blurred for first few days after
the procedure.
 Frequent initial follow-up will be necessary for
tonometry to make sure control of IOP.

111. Fear related to pain and potential loss of
vision
 Recommend the following:
 Continuous daily use of eye medications as prescribed
 Moderate use of the eyes
 Exercise in moderation to maintain general well-being
 Unrestricted fluid intake: alcohol and coffee may be
permitted unless they are noted to cause increased
IOP in the particular patient
 Maintenance of regular bowel habits to decrease
straining
 Wearing a medical identification tag indicating the
patient has glaucoma

112. Evaluation: Expected Outcomes
 Verbalizes understanding of glaucoma as a
chronic disease; demonstrates proper
instillation of ophthalmic medication.

113. Key points to patients:
 Know intraocular pressure (IOP)
measurement and the desired range.
 Be informed about the extent of vision loss
and optic nerve damage.
 Keep a record of eye pressure
measurements and visual field test results
to monitor progress.

114. Key points to patients:
 Review all medications (including over-the-
counter and herbal medications) with
ophthalmologist, and mention any side
effects each visit.
 Ask about potential side effects and drug
interactions of eye medications.
 Ask whether generic or less costly forms of
eye medications are available.

115. Key points to patients:
 Review the dosing schedule with ophthalmologist
and inform him or her if you have trouble
complying with the schedule.
 Participate in the decision-making process. Let
the doctor know what dosing schedule works for
you and other preferences regarding eye care.
 Have the nurse observe instilling eye medication
to determine whether you are administering it
properly.

116. Key points to patients:
 Be aware that glaucoma medications can
cause adverse effects if used
inappropriately.
 Eyedrops are to be administered as
prescribed, not when eyes feel irritated.
 Ask your ophthalmologist to send a report
to primary care physician after each
appointment.
 Keep all follow-up appointments.

117. CONTINUING GLAUCOMA CARE AT HOME
 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.

118.  Reassurance and emotional support are
important aspects of care.
 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 examinations at
least once every 2 years to detect
glaucoma early.

119. Patient Education and Health Maintenance
 Instruct patient in use of medications.
 Do not rub the eyes
 Stress the importance of long-term
medication use to control this chronic
disease.
 Remind patient to keep follow-up
appointments.

120. Patient Education and Health Maintenance
 Instruct patient to seek immediate medical
attention if signs and symptoms of increased IOP
return, severe eye pain, photophobia, and
excessive lacrimation.
 Advise patient to notify all health care providers
of condition and medications and to avoid use of
medications that may increase IOP, such as
corticosteroids and anticholinergics (such as
antihistamines), unless the benefit outweighs the
risk.

121. Patient Education and Health Maintenance
 Evaluation: Expected Outcomes
 Pain is decreased
 Describes treatment regimen and verbalizes reduced
fear

122. Chronic open angle glaucoma
 Nursing Assessment
 Assess frequency, duration, and severity of visual
symptoms.
 Assess patient's knowledge of disease process and
anxiety about the diagnosis.
 Assess patient's motivation to participate in long-term
treatment.

123. Nursing Diagnoses
Deficient Knowledge about glaucoma
and surgical procedure
 Goal: Providing Information about Glaucoma
 Nursing Interventions :
 Review the normal anatomy and physiology of the
eye as well as the changes that occur in the drainage
of aqueous humour with glaucoma.
 Make sure that the patient understands that,
although he may be asymptomatic, IOP could still be
elevated, and damage to the eye could be occurring.
Therefore, ongoing use of medication and follow-up
are essential.

124.  Teach patient the action, dosage, and adverse
effects of all medications. Make sure adequate
administration of eyedrops by watching return
demonstration.
 Timolol (Timoptic) and betaxolol (Betoptic) and adverse
effects include headache, eye irritation, decreased corneal
sensitivity, blurred vision, bradycardia, palpitations,
bronchospasm, hypotension, and heart failure
 Pilocarpine (Pilocar, Isopto Carpine) - adverse effects include
eye irritation, blurring, and redness; headache; pupil
constriction; poor vision in dim light; possible hypertension
and tachycardia; and rare retinal detachment and lens
opacity
 Acetazolamide (Diamox) and methazolamide (Neptazane)-
adverse effects include drowsiness, anorexia, paresthesia,
stomach upset, tinnitus, fluid and electrolyte imbalance, and
rare kidney and liver dysfunction

125.  Discuss visual defects with patient and ways to
compensate. Vision loss is permanent, and
treatment is aimed at stopping the process.
 Inform patient that surgery is done on outpatient
basis and recovery is quick. Prolonged
restrictions are not required.
 After surgery, elevation of head 30 degrees will
promote aqueous humour drainage after a
trabeculectomy.
 Additional medications after surgery will include topical
steroids and cycloplegics to decrease inflammation and
to dilate the pupil.

126.  Patient Education and Health Maintenance
 Patient must remember that glaucoma cannot be
cured, but it can be controlled.
 Remind patient that periodic eye checkups are
essential because pressure changes may occur.
 Alert patient to avoid, if possible, circumstances
that may increase IOP:
 Upper respiratory infections
 Emotional upsets - worry, fear, anger
 Exertion, such as snow shoveling, pushing, heavy
lifting