efinition

Is a condition marked by high intraocular pressure (IOP) that damages the optic nerve.

TYPES:

Chronic open-angle glaucoma

Results from the gradual deterioration of the trabecular network that, as in the acute form, blocks
drainage of aqueous humor and causes IOP to increase.

If untreated, may result in degeneration of the optic nerve and visual field loss.

It is the most common form of glaucoma, and its incidence increases with age.

Genetics and conditions, such as diabetes and hypertension, also play a role.

glaucoma

Acute closed-angle (or narrow-angle) glaucoma

Results when the angle between the iris and the cornea becomes narrowed, restricting or blocking the
drainage of aqueous humor through the trabecular network and the canal of Schlemn. This causes IOP
to increase suddenly.

It may result from trauma, stress, or any process that pushes the iris forward against the inside of the
cornea when there is already an anatomically shallow anterior or chamber.

It is an acute, painful condition that can cause permanent eye damage within several hours.

Risk Factors

Congenital

Inherited

Trauma

Pathophysiology

In chronic open-angle glaucoma

Obstruction to outflow of aqueous humor through the trabecular meshwork into Schlemm’s canal leads
to increased IOP. It usually is bilateral. Increased IOP eventually destroys optic nerve function causing
blindness.

In acute closed-angle glaucoma

Results in increased IOP because of obstructed outflow of aqueous humor. However, acute closed-angle
glaucoma typically involves sudden, complete, unilateral closure with pupil dilation stimulated by a dark
environment, emotional stress, or mydriatic drugs.

Assessment/Clinical Manifestations/Signs and Symptoms

Chronic open-angle glaucoma

No early symptoms

Insidious visual impairment, blurring

Diminished accommodation

Gradual loss of peripheral vision (tunnel vision)

Mildly aching eyes

Halos around lights later with elevated IOP

effectofglaucoma

Acute closed-angle glaucoma

Transitory attacks of diminished visual acuity

Colored halos around lights

Reddened eye with excruciating pain

Headache

Nausea and vomiting

Laboratory and diagnostic study findings

Tonometry detects elevated IOP (>10 to 20 mmHg)

Slit-lamp examination reveals abnormalities in the anterior vitreous humor.

Medical Management
Objective of treatment is to prevent optic nerve damage by lowering the IOP to a level consistent with
retaining vision. Treatment is almost always lifelong. Treatment also focuses on achieving the greatest
benefit at the least risk, cost and inconvenience to the patient.

Pharmacologic therapy is the initial and principal treatment for glaucoma. Acute angle-closure glaucoma
is treated with medication (including miotics) to reduce IOP before laser or incisional iridectomy.
Commonly used agents include:

Beta-adrenergic blockers/antagonists are the most widely used hypotensive agents. They are effective in
many types of glaucoma.

Cholinergic agents (topical) are miotics (cause papillary constriction) and are used in short-term
management of glaucoma with papillary block.

Alpha-2-adrenergic agonists(topical) reduce IOP by increasing aqueous humor outflow.

Carbonic anhydrase inhibitors (systemic) and prostaglandins lower IOP by reducing aqueous humor
formation.

Osmotic diuretics reduce IOP by increasing the osmolality of the plasma to draw water from the eye into
the vascular circulation.

Surgical Management

Ophthalmic laser surgery is indicated as the primary treatment for glaucoma or is required when
medication therapy is poorly tolerated or ineffective in lowering IOP.

Conventional surgery procedures are performed when laser techniques are unsuccessful or when
patient is not a good candidate for laser surgery (eg. Patient cannot sit still or follow instructions)

Filtering procedures: an opening or a fistula in the trabecular meshwork (trabeculectomy) is made to

allow drainage implant or shunt surgery may be performed.

Nursing Diagnosis

Anxiety related to possible vision loss

Disturbed sensory perception related to visual impairment

Ineffective health maintenance related to knowledge deficit

Risk for injury related to impaired vision

Self-care deficit related to impaired vision

Nursing Management

Provide information regarding management of glaucoma

Discuss preoperative and postoperative teaching for immediate surgical opening of the eye chamber.

Prepare to administer carbonic anhydrase inhibitors IV or IM, to restrict production of aqueous humor.

Prepare to administer osmotic agents.

Discuss and prepare the client for surgical or laser peripheral iridectomy after the acute episode is
relieved.

Provide information about laser trabeculoplasty, if medication therapy proves ineffective.

Teach the client about specific safety precautions.

Instruct the client to avoid mydriatics such as atropine, which may precipitate acute glaucoma in a client
with closed-angle glaucoma.

Instruct the client to carry prescribed medications at all times.

Instruct the client to carry a medical identification card or wear a bracelet stating his type of glaucoma
and need for medication.

Instruct the client to take extra precautions at night (e.g. use of handrails, provide extra lighting to
compensate for impaired pupil dilation from miotic use).

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.

31. 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

32. 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.

33. MANAGEMENT OF CONGENITAL GLAUCOMA GONIOTOMY TRABECULOTOMY

34. 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

35. 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

36. 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

37. 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.
38. Definition of POAG POAG is defined as a chronic progressive optic neuropathy associated with
elevated IOP and visual field defects

39. 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.

40. 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

41. 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.

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

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

44. 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.

45. 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.

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

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

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

49. 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.

50. 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).
51. 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

52. 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

53. 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.

54. 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.

55. 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.

56. 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

57. 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.

58. 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.
59. Treatment of Absolute primary angle closure glaucoma cyclodestructive surgeries to reduce IOP
and enucleation in case of painful eyes

60. 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

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

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

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

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

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

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

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

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

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

70. How is glaucoma detected?

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

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

73. 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.

74. 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
75. 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

76. 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

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

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

79. Optic Nerve

80. Field Test

81. Humphery Field Trace

82. Normal Disc

83. Cupped Disc

84. Glaucoma treatment Medications Surgery ◦ Laser ◦ Conventional

85. MANAGEMENT OF CONGENITAL GLAUCOMA GONIOTOMY TRABECULOTOMY

86. Treatment

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

88. 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

89. 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.

90. Treatment Laser Trabeculoplasty Sclerostomy Cycloablation

91. 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

92. Treatment Surgical Goniotomy for congenital Trabeculotomy for congenital glaucoma's
Trabeculectomy for adult glaucoma's Implants for difficult non responsive
93. 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

94. 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

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

96. 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.

97. NURSING MANAGEMENT

98. 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.

99. 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.

100. 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.

101. 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

102. 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.

103. 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.
104. 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

105. Evaluation: Expected Outcomes Verbalizes understanding of glaucoma as a chronic disease;

demonstrates proper instillation of ophthalmic medication.

106. 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.

107. 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.

108. 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.

109. 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.

110. 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.

111. 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.

112. 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.

113. 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.

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

115. 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.

116. 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.

117. 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

118. 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.

119. 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

laucoma occurs when an imbalance in production and drainage of fluid in the eye (aqueous humor)
increases eye pressure to unhealthy levels.

Normally the aqueous fluid, which nourishes the eye, is produced by the ciliary body behind the iris (in
the posterior chamber) and flows through the pupil to the front of the eye (anterior chamber), where it
exits into drainage canals between the iris and cornea (the “angle”). When functioning properly, the
system works like a faucet (ciliary body) and sink (drainage canals).

Balance between fluid production and drainage—between an open faucet and a properly draining
sink—keeps the fluid flowing freely and prevents pressure in the eye from building up.

7 Mechanism

In glaucoma, the drainage canals become clogged, blocked, or covered. Fluid cannot leave the eye even
though new fluid is being produced in the posterior chamber.

In other words, the sink “backs up” while the faucet is still running. Because there is nowhere in the eye
for the fluid to go, pressure in the eye increases.

When the pressure becomes higher than the optic nerve can tolerate, damage to the optic nerve occurs.
This damage is called glaucoma. Sometimes eye pressure increases within the range of normal but is
nonetheless too high for the optic nerve to tolerate (called low tension glaucoma).

9 Classification

Open-angle glaucoma

Closed-angle glaucoma

10 Etiology In most people, the cause of glaucoma is not known,

Although both open-angle and closed-angle glaucomas tend to run in families. In others, damage to the
eye caused by infection, tumour, inflammation, large cataracts or surgery for cataracts, or other
conditions keeps the fluid from draining freely and leads to increased eye pressure and optic nerve
damage (secondary glaucoma).

11 Open-angle glaucoma: is more common

the drainage canals in the eyes become clogged gradually over months or years.

Pressure in the eye rises slowly because fluid is produced at a normal rate but drains sluggishly.

12 Symptoms Open-Angle Glaucoma:

painless and causes no early symptoms.

The most important symptom is the development of blind spots, or patches of vision loss, over months
to years.

The blind spots slowly grow larger.

Peripheral vision is usually lost first.

Vision loss occurs so gradually that it is often not noticed until much of it is lost.

Because central vision is generally lost last, many people develop tunnel vision: they see straight ahead
perfectly but become blind in all other directions.

If glaucoma is left untreated, eventually even tunnel vision is lost, and a person becomes totally blind.

13 Closed-angle Glaucoma

is less common than open-angle glaucoma.

The drainage canals in the eyes become blocked or covered because the angle between the iris and
cornea is too narrow.

The blockage can occur suddenly or slowly. If the blockage occurs suddenly, pressure in the eye rises
rapidly. If the blockage occurs slowly, the pressure in the eye rises slowly like in open-angle glaucoma.

14 Symptoms Closed-Angle Glaucoma

If eye pressure rises rapidly in closed-angle glaucoma (acute closed-angle glaucoma), people typically
notice an abrupt onset of severe eye pain and headache, redness, blurred vision, rainbow-colored halos
around lights, and sudden loss of vision.

They may also have nausea and vomiting as a response to the increase in eye pressure.

Acute closed-angle glaucoma is considered a medical emergency, because people can lose their vision as
quickly as 2 to 3 hours after the appearance of symptoms if the condition is not treated.

People who have had open-angle or closed-angle glaucoma in one eye are likely to develop it in the
other.

15 Screening and Diagnosis

An early detection of the disease is extremely important.

All people at high risk of glaucoma should have a comprehensive eye examination every 1 to 2 years

There are four parts to a comprehensive eye examination for glaucoma

Monitoring eye pressure (20-22 mm Hg)

Ophthalmoscope and a slit lamp to look for changes in the optic nerve

Visual field (peripheral vision) testing allows a doctor to detect blind spots

Doctors may also use a special lens to examine the drainage channels in the eye

16 Treatment

The goal of glaucoma treatment is to prevent the onset of vision loss or stop its progression.

Treatment of glaucoma is lifelong. It involves decreasing eye pressure by increasing fluid drainage out of
the eyeball or by reducing the amount of fluid produced inside the eyeball.

Some people with high eye pressure who do not have signs of optic nerve damage (known as glaucoma
“suspects”) can be monitored closely without treatment.

17 Treatment

Eye drops and surgery are the main treatments for open-angle and closed-angle glaucomas.

Eye drops containing beta-blockers, prostaglandin-like compounds, alpha-adrenergic agonists, carbonic

anhydrase inhibitors, or cholinergic drugs are commonly used to treat glaucoma.

Laser surgery can be used to increase drainage

ntroduction <ul><li>Glaucoma refers to a group of diseases characterized by </li></ul><ul><ul><li>optic

neuropathy </li></ul></ul><ul><ul><li>specific pattern of visual field defect
</li></ul></ul><ul><ul><li>raised intraocular pressure </li></ul></ul><ul><li>Damage to optic nerve is
irreversible process </li></ul><ul><li>Normal IOP is 10-21mmHg </li></ul>

3. Aqueous production and drainage <ul><li>Secretion of aqueous humour </li></ul><ul><ul><li>ciliary

body (posterior chamber ) </li></ul></ul><ul><li>Route of Drainage </li></ul><ul><ul><li>primary
(90%): trabecular meshwork </li></ul></ul><ul><ul><li>uveal-scleral outflow (10%) </li></ul></ul>
4. Aqueous drainage Ciliary body Posterior chamber Anterior chamber Trabecular meshwork Schlemm’s
canal Collector channels Intrascleral Venous plexus Episcleral plexus Sub- ophthalmic vein Cavernous
sinus

5. Uveoscleral Ciliary body Suprachoroidal space Venous circulation of ciliary body, choroid and sclera

6. Classification <ul><li>Congenital and developmental glaucoma </li></ul><ul><ul><li>Primary

congenital glaucoma </li></ul></ul><ul><ul><li>Developmental glaucoma
</li></ul></ul><ul><ul><ul><li>With associated anomalies such as Rieger syndrome, peter’s anomaly,
aniridian, ectopia lentis, Sturge-Weber syndrome, nanophthalmos, congenital microcornea etc.,
</li></ul></ul></ul><ul><li>Primary glaucoma </li></ul><ul><ul><li>Primary open angle glaucoma
(POAG) </li></ul></ul><ul><ul><li>Primary angle closure glaucoma (PACG) </li></ul></ul>

7. Classification <ul><li>Secondary glaucoma </li></ul><ul><ul><li>Phacomorphic glaucoma

</li></ul></ul><ul><ul><li>Phacolytic glaucoma </li></ul></ul><ul><ul><li>Glaucoma due to uveitis
</li></ul></ul><ul><ul><li>Pigmentary glaucoma </li></ul></ul><ul><ul><li>Neovascular glaucoma
</li></ul></ul><ul><ul><li>Glaucoma associated with intraocular tumours
</li></ul></ul><ul><ul><li>Steroid induced glaucoma </li></ul></ul><ul><li>Secondary glaucoma
</li></ul><ul><ul><li>Traumatic glaucoma </li></ul></ul><ul><ul><li>Ciliary block glaucoma
</li></ul></ul><ul><ul><li>Glaucoma associated with intraocular haemorrhage
</li></ul></ul><ul><ul><li>Glaucoma associated with iridocorneal endothelial syndrome
</li></ul></ul><ul><ul><li>Glaucoma due to pseudoexfoliation syndrome </li></ul></ul>

8. PRIMARY CONGENITAL GLAUCOMA <ul><li>DESCRIPTION </li></ul><ul><ul><li>A rare condition

</li></ul></ul><ul><ul><li>manifests without associated anomalies </li></ul></ul>Pathogenesis
<ul><li>Classification </li></ul><ul><ul><li>True congenital glaucoma (40%). IOP becomes elevated
intrauterine life and child is born with ocular enlargement. </li></ul></ul><ul><ul><li>Infantile
glaucoma (50%). It manifests prior to child’s third birthday. </li></ul></ul><ul><ul><li>Juvenile
glaucoma (10%). It manifests between 3-16 years. </li></ul></ul>Maldevelopment of the angle
structures Impaired aqueous outflow Raised IOP

10. Symptoms and signs <ul><li>Symptoms </li></ul><ul><ul><li>Photophobia, Lacrimation,

blepharospasm, enlarged eyeball, </li></ul></ul><ul><li>Signs </li></ul><ul><ul><li>Corneal edema,
corneal enlargement more than 13mm diameter. </li></ul></ul><ul><ul><li>Sclera become thin and
appers blue </li></ul></ul><ul><ul><li>Iris may show iridodonesis and atrophic patches in late stage
</li></ul></ul><ul><ul><li>Lens becomes flat or subluxated </li></ul></ul><ul><ul><li>Optic disc shows
increased cup/disc ratio and atrophy specially after third year. </li></ul></ul><ul><ul><li>IOP is
invariably high. </li></ul></ul>

11. NURSING ASSESSMENT Child may need examination under anesthesia <ul><li>History on
lacrimation, photophobia, and blepharospasm </li></ul><ul><li>Assess visual acuity and perform
refraction to find out loss of vision </li></ul><ul><li>Examine cornea for edema and opacity
</li></ul><ul><li>Measure IOP with hand held perkin’s applanation tonometer
</li></ul><ul><li>Measure corneal diameter by calipers. </li></ul><ul><li>Perform a dilated fundus
examination to evaluate the optic disc and retina </li></ul>

12. <ul><li>NURSING DIAGNOSIS </li></ul><ul><ul><li>Altered visual perception secondary to increased

intraocular pressure and manifested as Profound lacrimation, photophobia, corneal haze, and
buphthalmos </li></ul></ul><ul><ul><li>Loss of vision </li></ul></ul><ul><li>EXPECTED OUTCOME
</li></ul><ul><ul><li>Intraocular pressure will be controlled and bring down to normal.
</li></ul></ul><ul><ul><li>Lacrimation will be controlled. </li></ul></ul><ul><ul><li>Photophobia and
corneal haze will be eliminated </li></ul></ul><ul><ul><li>Prevent eye from loss of vision.
</li></ul></ul>

13. Intervention <ul><li>Counsel the child’s parents for urgent need of surgery </li></ul><ul><li>Prepare
them psychologically </li></ul><ul><li>Check the ophthalmologic order of management plan
</li></ul><ul><ul><li>Topical beta-blocker (timolol 0.25% to 0.50% b.i.d.)
</li></ul></ul><ul><ul><li>Goniotomy is the first choice of surgery (Clear cornea)
</li></ul></ul><ul><ul><li>Trabeculotomy </li></ul></ul><ul><ul><ul><li>corneal clouding prevents
visualization of the angle </li></ul></ul></ul><ul><ul><ul><li>Failed repeated goniotomy
</li></ul></ul></ul><ul><li>Monitor IOP, optic disc, and corneal diameter on regular follow up
</li></ul>

14. EVALUATION <ul><li>Outcome criteria </li></ul><ul><ul><li>Cornea should be transparent; and IOP

should be maintained with in normal range </li></ul></ul>

15. PRIMARY OPEN ANGLE GLAUCOMA <ul><li>Usually bilateral with asymmetry in onset.
</li></ul><ul><li>Slow progressive rise in IOP (above 21mmHg), </li></ul><ul><li>Glaucomatous optic
nerve damage, </li></ul><ul><li>Visual field loss </li></ul>

16. Risk-factors <ul><li>Ocular risk Factors </li></ul><ul><li>. IOP </li></ul><ul><li>. Myopia

</li></ul><ul><li>. Increased cup/disc ratio </li></ul><ul><li>. Asymmetric cupping </li></ul><ul><li>.
Disc hemorrhage </li></ul>

17. Risk-factors <ul><li>Non ocular risk factors </li></ul><ul><li>. Age </li></ul><ul><li>. Race
</li></ul><ul><li>. Family history </li></ul><ul><li>. Diabetes and Systemic hypertension
</li></ul><ul><li>. Migraine and peripheral vasospasm </li></ul><ul><li>. Alcohol consumption
</li></ul><ul><li>. Cigarette smoking </li></ul>

18. PATHOGENESIS <ul><li>Elevated IOP in glaucoma results from increased resistance within the
aqueous drainage system </li></ul><ul><li>Retinal ganglion cell death
</li></ul><ul><ul><li>compromise of the microvasculature with resultant ischaemia in optic nerve head
</li></ul></ul><ul><ul><li>mechanical damage due to raised IOP </li></ul></ul>

19. Symptoms <ul><li>Commonly A symptomatic </li></ul><ul><li>Detected I ncidentally

</li></ul><ul><li>Mild headache, ocular pain </li></ul><ul><li>Minimal blurring of vision
</li></ul><ul><li>Frequent changes in presbyopic spectacles </li></ul><ul><li>Subjective visual field
defect occasionally </li></ul>

20. Signs on examination <ul><li>Minimal decrease in vision </li></ul><ul><li>Normal conjunctiva

</li></ul><ul><li>Normal Cornea </li></ul><ul><li>May be afferent pupillary defect
</li></ul><ul><li>Normal AC depth </li></ul><ul><li>Open angles on gonioscopy </li></ul><ul><li>Large
CDR </li></ul><ul><li>Raised or normal IOP </li></ul>

21. ASSESSMENT <ul><li>History: mild headache, eyeache, poor vision at night, color haloes
</li></ul><ul><li>Optic nerve: Cupping </li></ul><ul><li>Risk factors: family history, hypertension,
diabetes, age and race. </li></ul><ul><li>Record the IOP measurement: Diurnal variation of 8mm Hg
between the lowest and the highest values of IOP. </li></ul><ul><li>Central corneal thickness
</li></ul><ul><li>Visual field testing </li></ul>

22. <ul><li>NURSING DIAGNOSIS </li></ul><ul><ul><li>Progressive loss of vision

</li></ul></ul><ul><li>EXPECTED OUTCOME </li></ul><ul><ul><li>Stop progression of POAG and
damage to retinal ganglion cells. </li></ul></ul><ul><ul><li>Prevent permanent loss of vision.
</li></ul></ul>

25. Glaucomatous optic atrophy

27. Intervention <ul><li>Counseling: tests, retest, and examination </li></ul><ul><li>Instruct the patient
to avoid conditions that will increase IOP such as emotional stress, heavy exertion, wearing tight clothes
around neck. </li></ul><ul><li>Institute proper treatment advice </li></ul>

28. Medical treatment <ul><li>B-blocker: 1 st drug of choice for initial therapy

</li></ul><ul><li>Mechanism of action: </li></ul><ul><ul><li>Lowers IOP by reducing the aqueous
secretion by effect on beta -receptor in ciliary processes </li></ul></ul><ul><li>Preparation:
</li></ul><ul><ul><li>Timolol Maleate(0.25, 0.5%) BD- non selective
</li></ul></ul><ul><ul><li>Levobunolol (0.25,0.5%) BD- nonselective
</li></ul></ul><ul><ul><li>Betaxolol (0.25%) BD- cardioselective </li></ul></ul><ul><li>Contraindication
: bronchial asthma, chronic obstructive pulmonary disease, heart-block, congestive hearth failure,
depression. </li></ul>

29. Medical treatment <ul><li>Carbonic anhydrase inhibitor </li></ul><ul><li>Preparation

</li></ul><ul><ul><li>Dorzolamide 2% t.i.d </li></ul></ul><ul><li>Inhibits enzyme carbonic anhydrase -
thus reduces aqueous humor formation </li></ul>

30. Medical treatment <ul><li>Prostaglandin Analogue </li></ul><ul><li>Preparation

</li></ul><ul><ul><li>Latanoprost(0.005%) </li></ul></ul><ul><ul><li>Tarvoprost 0.004%: superior
ocular hypotensive effect </li></ul></ul><ul><ul><li>Bimatoprost 0.3%: potentiate trabecular outflow
</li></ul></ul><ul><li>Increase the uveo - scleral outflow of Aqueous and decrease episcleral venous
pressure </li></ul>
31. Medical treatment <ul><li>Miotics (pilocarpine1, 2, 4% q.i.d.) </li></ul><ul><ul><li>It mechanically
increases aqueous outflow contracting ciliary muscles. </li></ul></ul><ul><li>Sympathomimetics
(dipivefrin 0.1% bid, epinephrine 0.5% to 25 bid,) </li></ul><ul><ul><li>They reduce IOP by increasing
aqueous outflow. </li></ul></ul>

32. Medical treatment <ul><li>Systemic carbonic anhydrase inhibitors ( methazolamide 25 to 50mg

orally bid to tid, acetazolamide 125mg to 250mg po bid to qid or acetazolamide 500mg po bid)
</li></ul><ul><ul><li>Contraindication: sulpha allergy and history of renal stones.
</li></ul></ul><ul><ul><li>Side effects: fatigue, nausea, confusion, and paresthesia, aplastic anemia.
</li></ul></ul>

33. Intervention <ul><li>Make sure patient is instructed application of medication or therapy

appropriately. </li></ul><ul><li>Advise patient to visit on follow up on appropriate time usually 3 to 6
weeks. </li></ul><ul><li>Patient with carbonic anhydrase inhibitors, alpha agonist or miotics should be
quickly reviewed after 3 days. </li></ul><ul><li>When damage is severe or IOP is high, patient has to be
reexamined with in 3 days regularly. </li></ul><ul><li>Once IOP is reduced to desired level, patient is
followed up in 3 to 6 months. </li></ul>

34. Surgical <ul><li>Argon Laser Trabeculoplasty </li></ul><ul><ul><li>Next therapeutic option if

medical treatment fails </li></ul></ul><ul><ul><li>Reduces IOP in 70-80% of patients
</li></ul></ul><ul><ul><li>Reduction of IOP about 30% </li></ul></ul><ul><li>Trabeculectomy
</li></ul><ul><ul><li>Creating an opening or fistula at the limbus which allows aqueous to drain from
AC directly or indirectly to the sub-conjunctival space, is then removed by one or more routes
</li></ul></ul>

35. EVALUATION <ul><li>Outcome criteria: </li></ul><ul><ul><li>IOP is controlled to desired level so

that POAG is controlled and retinal ganglion cells damage is prevented.
</li></ul></ul><ul><ul><li>Vision is restored. </li></ul></ul>

36. Definition: ACG <ul><li>It is defined as an optic neuropathy which occurs as a result of high
intraocular pressure due to narrow or closed angles </li></ul>

37. Primary Angle Closure Glaucoma <ul><li>Risk Factors: </li></ul><ul><ul><li>Age: after 40 yrs
</li></ul></ul><ul><ul><li>Gender: Female:Male::4:1 </li></ul></ul><ul><ul><li>Race
</li></ul></ul><ul><ul><ul><li>prevalence higher in South-East Asians, Chinese & Eskimos
</li></ul></ul></ul><ul><ul><li>Family history </li></ul></ul><ul><ul><ul><li>first-degree relatives are
at increased risk (≈ 3.5 times) </li></ul></ul></ul><ul><ul><li>Hypermetropes </li></ul></ul>

38. <ul><li>Predisposing Factors </li></ul><ul><ul><li>Anterior shifting of iris

</li></ul></ul><ul><ul><ul><li>large lens size </li></ul></ul></ul><ul><ul><ul><li>narrow entrance to
the chamber angle </li></ul></ul></ul><ul><ul><li>Smaller axial length
</li></ul></ul><ul><ul><ul><li>Nanophthalmos & microphthalmos </li></ul></ul></ul>Primary Angle
Closure Glaucoma
39. <ul><li>Precipitating Factors </li></ul><ul><ul><li>Dim illumination
</li></ul></ul><ul><ul><li>Emotional Stress </li></ul></ul><ul><ul><li>Trauma/illness
</li></ul></ul><ul><ul><li>Intense concentration </li></ul></ul><ul><ul><li>Pharmacological pupil
dilatation </li></ul></ul>Primary Angle Closure Glaucoma

40. Pathogenesis of Attack: <ul><li>Mid dilatation of pupil (4-6 mm) </li></ul><ul><li>Maximum

pupillary block and relaxation </li></ul><ul><li>of peripheral iris allowing </li></ul><ul><li>forward
displacement of iris </li></ul><ul><li>Angle closure attack </li></ul>

41. Pupil Block: <ul><li>Increase in physiological </li></ul><ul><li>pupil block

</li></ul><ul><li>Dilatation of pupil renders peripheral </li></ul><ul><li>iris more flaccid
</li></ul><ul><li>Increased pressure in posterior </li></ul><ul><li>chamber causes iris bombe
</li></ul><ul><li>Angle obstructed by peripheral iris </li></ul><ul><li>and rise in IOP </li></ul>

42. Symptom <ul><li>presents at emergency unit </li></ul><ul><li>sudden onset of acute pain in eye /
head </li></ul><ul><li>diminution of vision </li></ul><ul><li>colour halos around the bulb
</li></ul><ul><li>lacrimation / lid oedema </li></ul><ul><li>anxiety and fatigue - nausea & vomiting
</li></ul>

43. Signs on Examination: <ul><li>Reduced visual acuity </li></ul><ul><li>Acute red eye

</li></ul><ul><li>hazy cornea </li></ul><ul><li>vertically oval & mid-dilated pupil
</li></ul><ul><li>closed angles on gonioscopy </li></ul><ul><li>high IOP over 60 or 70 mm Hg
</li></ul><ul><li>cellular reaction in anterior chamber </li></ul>

44. Management: <ul><li>Principle of therapy is to bring down the IOP as quicker as possible
</li></ul><ul><li>Admit the patient </li></ul><ul><li>Counsel the patient to make her anxiety free as far
as possible </li></ul><ul><li>Give IOP lowering drugs </li></ul><ul><li>Reduce inflammation
</li></ul><ul><li>LASER therapy </li></ul>

45. Medical Therapy: <ul><li>IV Acetazolamide (Inj Diamox, 500mg IV) followed by (250 mg tablet TID)
</li></ul><ul><li>Beta-blockers </li></ul><ul><li>Miotics </li></ul><ul><li>Steroid Eye drops </li></ul>

46. Medical Therapy: <ul><li>If IOP is still more than 50mmHg </li></ul><ul><li>Hyperosmotic agents:
</li></ul><ul><ul><li>Mannitol 20% </li></ul></ul><ul><ul><ul><li>1-2 gm/kg given I/V within 30-45
minutes </li></ul></ul></ul><ul><ul><li>Oral Glycerol 50%-----1-1.5 gm/kg </li></ul></ul><ul><li>Raise
serum osmotic pressure and withdraw fluid from the eye specially from vitreous
</li></ul><ul><li>Vitreous dehydration allows the lens to fall back deepening the AC </li></ul>

47. Fellow eye? <ul><li>Fellow eye should be treated with Pilocarpine eye drops 1drop QID
</li></ul><ul><li>To be followed by prophylactic LASER Peripheral Iridotomy </li></ul>

48. Nursing management of glaucoma <ul><li>Measures taken to relieve pain

</li></ul><ul><li>Reassure patient that pain and other signs and symptoms should subside with
reduction of IOP </li></ul><ul><li>Provide reassurance and calm to reduce anxiety and fear
</li></ul><ul><li>Provide preoperative care </li></ul><ul><li>Post operative care </li></ul>
49. THANK YOU !