The document provides an overview of glaucoma, its definitions, incidence, risk factors, pathophysiology, classifications, clinical manifestations, diagnosis, and management strategies. Glaucoma is a leading cause of irreversible blindness, characterized by increased intraocular pressure and subsequent optic nerve damage, with various types including open-angle and angle-closure glaucoma. Effective management involves early detection, medication, laser, and surgical interventions to prevent vision loss and maintain patient quality of life.

1. MEDICAL SURGICAL NURSING- II
UNIT – II
NURSING MANAGEMENT OF PATIENTS WITH
DISORDERS OF EYE
TOPIC : GLAUCOMA
PRESENTED BY
Mrs. SOUMYA SUBRAMANI, M.Sc.(N)
LECTURER, MSN DEPARTMENT
CON- SRIPMS, COIMBATORE.

2. Objectives
At the end of the session, the students are able to,
• define the Glaucoma
• know the incidence of Glaucoma
• identify the risk factors of Glaucoma
• classify the types of Glaucoma
• explain the etio pathophysiology of Glaucoma
• discuss the clinical manifestation, diagnostic evaluation and
management of Glaucoma

3. 1
Glaucoma

4. Introduction
Glaucoma: the “silent thief of sight”
Glaucoma is a leading cause of preventable sight loss.
Vision can often be preserved with early identification, good
adherence to treatment and long-term monitoring.

5. Meaning :
• Glaucoma is asymptomatic but causes irreversible vision loss.
One of the most common ophthalmic conditions in the world, it
is also the leading cause of irreversible blindness (World Health
Organization, 2010).
• Glaucoma occurs as a result of increased intraocular pressure
(IOP) caused by a malformation or malfunction of the eyes
drainage system. Normal IOP is 12 – 22 mm Hg.

6. Meaning :
• The increased pressure causes compression of the retina and
the optic nerve, and causes progressive , PERMANENT loss of
eyesight if left untreated.
• Glaucoma is an umbrella term for a large group of disorders
characterized by diverse clinical and pathological features. The
common characteristics are:
Optic nerve damage
Visual field loss and
Irreversible blindness.

7. DEFINITION OF GLAUCOMA

8. Incidence
• Glaucoma will affect almost 80 million people
by 2020, and 111.8 million people by 2040, affecting more people
residing in Asia and Africa.
• The estimated prevalence of glaucoma is approximately 5-7% in the black
population, and 3-5% in the white population.
• There are approximately 11.2 million persons aged 40 years and older with
glaucoma in India.
• Primary open angle Glaucoma is estimated to affect 6.48 million persons.

9. Risk factors for the development of Glaucoma :
A number of risk factors are known to be associated with
glaucoma,
and include the following:
• Pre-existing raised IOP.
• Age: incidence increases with age, most commonly presenting
after the age of 65 and rarely before the age of 40 years
• Family history: one of the strongest risk factors, risk is stronger
in siblings than offspring.
• A family history of glaucoma, especially seen in patients
diagnosed with juvenile open-angle glaucoma.

10. Risk factors of Glaucoma
• A genetic basis for glaucoma has been suggested but it is felt this
is only likely to be true in a few cases
• Other co-morbid conditions, including diabetes mellitus,
hypertension, Migraine syndrome, Cardiovascular disease, Myopia
and hyperthyroidism
• Pre-existing ocular conditions, including eye tumors, retinal
detachment or lens dislocation. Ocular surgery may also trigger
glaucoma.
• The use of chronic or long-term corticosteroid therapy. This may
include topical corticosteroids and other such dosage forms.

11. Review of Physiology
• The aqueous humor is a transparent nutrient rich fluid that
nourishes the cornea, is secreted by the ciliary body in the
posterior chamber .It flows through the pupil into the anterior
chamber
• Aqueous humor drains through the trabecular mesh work into
the canal of Schlemm.
• Balance between the production and absorption and free flow
of aqueous humor are critical to maintenance of IOP

12. Review of Physiology

13. PATHOPHYSIOLOGY
• A proper balance between the rate of aqueous production (referred
to as inflow) and the rate of aqueous reabsorption (referred to as
outflow) is essential to maintain the IOP within normal limits.
• The place where the outflow occurs is called the angle because it
is the angle where the iris meets the cornea.
• When the rate of inflow is greater than the rate of outflow, IOP can
rise above the normal limits. If IOP remains elevated, permanent
vision loss may occur.

14. Pathophysiology
• Two theories explains how increased IOP damages the Optic nerve in
Glaucoma:
1. The Direct mechanical theory:
High IOP damages the retinal layer as it passes through the optic
nerve head.
2. The Indirect Ischemic theory:
High IOP compresses the microcirculation in the optic nerve head,
resulting in cell injury & death.

15. Pathophysiology:
Regardless of the cause of damage, glaucomatous changes typically
evolve through clearly discernible stages:
 Initiating Stage
Structural alteration in the aqueous outflow system.
Functional alterations
Optic nerve damage
Visual loss

16. Pathophysiology:
1.Initiating Stage:
Precipitating factors include illness, emotional stress, congenital
narrow angles, long term use of corticosteroids & mydriatics.These
events leads to the second stage.
2.Structural alteration in the aqueous outflow system:
Tissue & cellular changes caused by factors that affect aqueous
humor dynamics lead to structural alterations and to the third stage.

17. Pathophysiology:
3.Functional alterations:
Conditions such as increased or impaired blood flow create
functional changes that lead to the fourth stage.
4.Optic nerve damage:
Atrophy of the optic nerve is characterized by loss of nerve fibers
& blood supply and this fourth stage inevitably progresses to the fifth
stage.
5.Visual loss:
Progressive loss of vision is characterized by visual field defects.

18. CLASSIFICATION OF GLAUCOMA
Glaucoma can be classified into several different and unique
types:
• Open Angle Glaucoma (Wide angle Glaucoma)
• Angle – closure Glaucoma ( Narrow angle Glaucoma)
• Secondary Glaucoma
• Congenital Glaucoma

19. Open Angle Glaucoma is caused when the normal drainage system of the
eye becomes partially blocked, causing pressure to build within the eye.
Normal Eye
Open Angle Glaucoma
(Wide Angle Glaucoma)

20. Glaucoma usually affects the perimitery vision first, with sight
gradually being lost towards the center of the eye.
Vision loss with
Glaucoma
In OAG the outflow of aqueous humor is decreased in the trabecular
meshwork. The drainage channels become clogged, like a clogged
kitchen sink. Damage to the optic nerve can then result.

21. Glaucoma
Open Angle Glaucoma
Normal Eye
Pressure builds when the drainage system
is blocked. This increasing pressure
presses against the Optic Nerve and
causes a gradual loss of sight.
Total loss of
vision

22. CLASSIFICATION OF GLAUCOMA:
I. Open Angle Glaucoma: Usually Bilateral, But One Eye May Be More
Severely Affected Than The Other. In All Three Types Of Open –Angle
Glaucoma, The Anterior Chamber Angle Is Open And Appears Normal.
A. Chronic Open Angle Glaucoma
(COAG)
Optic Nerve Damage, Visual Field
Defects,IOP>21mmhg Usually No
Symptoms But Possible Ocular
Pain,headache And Halos
B. Normal Tension Glaucoma Optic Nerve Damage, Visual Field
Defects,IOP<21mmhg
C. Ocular Hypertension Elevated IOP, Possible Ocular Pain
Or Headache

23. CLASSIFICATION OF GLAUCOMA:
II. Angle Closure Glaucoma: Obstruction In Aqueous Humor Outflow Due To The Complete Or
Partial Closure Of The Angle From The Forward Shift Of The Peripheral Iris To The Trabecula. The Obstruction
Results In An Increased IOP.
A. Acute Angle Closure Glaucoma (AACG) Rapidly Progressive Visual Impairment ,Periocular
Pain,pain May Be Associated With Nausea,
Vomiting,bradycardia And Profuse Sweating.Reduced
Cental Visual Acuity,severly Elevated IOP,corneal
Edema.Pupil Is Vertically Oval,fixed In A Semi Dilated
Position And Unreactive To Light And Accommodation.
B. Subacute Angle Closure Glaucoma Transient Blurring Of Vision, Halos Around
Lights,temporal Headaches And/Or Ocular Pain:pupil
May Be Semi Dilated.
C. Chronic Angle Closure Glaucoma Visual Field Loss: IOP May Be Normal Or Elevated;
Ocular Pain And Headache.

24. Acute Angle Closure Glaucoma
• It is a medical emergency.
• when the normal drainage system of the eye becomes suddenly
blocked, causing pressure to build within the eye at a very rapid
rate.
• Complete blindness can occur in as little as 3 to 5 days!
Normal Eye Sudden blockage causes pressure
to build rapidly.
Glaucoma

25. DIFFERENCE BETWEEN THE TWO MAJOR TYPES
OF GLAUCOMA
Open-angle glaucoma
• Accounts for at least 90% of all
glaucoma cases
• It is caused by the slow clogging
of the drainage canals, resulting
in increased intraocular pressure
• There is a wide and open angle
between the iris and cornea
• It involves symptoms and
damage that are not readily
noticed
Angle-closure glaucoma
• Is a less common form of
glaucoma
• It develops very quickly
• There is a closed or narrow angle
between the iris and cornea
• It involves symptoms and
damage that are usually very
noticeable

26. • Congenital Glaucoma results as a condition from birth.
• Children are born with conditions such as an abnormal development of the Anterior
Chamber angles which prohibit the normal drainage of fluid from the eyes, which
then causes an increase in the pressure within the eye, and subsequent Retinal and
Optic Disc damage.
Congenital Glaucoma

27. Secondary Glaucoma is usually the result of a trauma to the
eye, although it can develop due to several causes:
• Abnormal deposits in the eye fluid
• Uveitis
• Lens Changes
• Drugs
• Haemorrhage
Secondary Glaucoma

28. Clinical Manifestations
• Glaucoma is often called the silent thief of sight
• Most patients are unaware that they have the disease until they have
experienced,
visual changes
vision loss
• The patient may not seek health care until they experiences blurred
vision or halos around lights, difficulty focusing, difficulty adjusting eyes
in low lighting, loss of peripheral vision, aching or discomfort around
the eyes and headache.

29. CONTI..
• Eventually the patient with untreated glaucoma
has “tunnel vision” in which only a small centre
field can be seen, and all peripheral vision is
absent. blurred vision

30. • History Collection
• Physical examination
• Visaual acuity measurement
• Opthalmoscopy- direct and indirect
Diagnosis

31. Diagnosis
Tonometry is often used as a diagnostic tool.
The Tonometer is gently pressed against the eyeball, and the resistance
(internal pressure) is measured.
In the patient with elevated pressures, the ophthalmologist
usually repeats the measurements over time to verify the elevation.
• open-angle glaucoma, IOP is usually between 22 and 32 mm Hg.
• acute angle-closure glaucoma- IOP may be over 50 mm Hg.

32. Diagnosis
• Gonioscopy can be used to determine if the angle where the
iris meets the cornea is open or closed.

33. Diagnosis
Visual field Perimetry is an essential method used to
determine if there is any loss of the visual field.

34. Diagnosis
Slit Lamp Examination
In open-angle glaucoma, slit lamp microscopy reveals a normal angle.
In angle-closure glaucoma the examiner may note a markedly narrow or flat anterior
chamber angle, an edematous cornea, a fixed and moderately dilated pupil, and ciliary
injection (hyperemia of the ciliary blood vessels produces a red color).

35. Stereo disc photography of the optic disc is
performed to determine if there is
abnormal cupping in the optic nerve head.
Subsequent exams or photos are compared
over time.
Diagnosis

36. Measurement of Retinal Nerve Fiber Layer thickness with the StratusOCT is
the most recent advancement in technology that aids in the diagnosis of
Glaucoma.
Diagnosis

37. MANAGEMENT :
The aim of all glaucoma treatment is prevention of optic nerve damage
through medical therapy, laser or nonlaser surgery or a combination of
these approaches.
• Medical management
• Surgical management
• Nursing management
Medications are available
in several forms.
Laser surgery can reduce
the need for medications
Filtration Surgery creates a new
drainage channel

38. Medical management
Medical management of glaucoma relies on systemic and topical ocular
medications that lower IOP.
• Alpha –adrenergic agonists-Decreases aqueous humor production
• Beta-blockers-Decreases aqueous humor production
• Carbonic anhydrase inhibitors-Decreases aqueous humor production
• Cholinergics (miotics)-increases aqueous fluid outflow by contracting the
ciliary muscle and causing miosis ( constriction of the pupil)
• Prostaglandin analogs-Increases uveoscleral outflow.

39. DRUG THERAPY FOR GLAUCOMA

40. SURGICAL MANAGEMENT

41. Surgical Management
• Laser trabeculoplasty: Laser beams are applied to the inner surface of
the trabecular meshwork to open the intrabecular spaces & widen the
canal of schlemm thereby promoting outflow of aqueous humor and
decreased IOP.
• Laser Iridotomy: It is for pupillary block glaucoma an opening is made
in the Iris to eliminate the pupillary block.
• Cyclophotocoagulation: A laser destroy the parts of ciliary body which
produces aquous humor. It decreases the production of aquous humor
thus decrease IOP.

42. Surgical Management
• Filtration Surgery/ Trabeculectomy :
• Is indicated if medical management and laser therapy are not successful
• It is the standard filtering technique used to remove part of the trabecular meshwork.
• Surgical iridectomy:
• An iridectomy, also known as a surgical iridectomy or corectomy,
• Is the surgical removal of part of the iris.
• These procedures are most frequently performed in the treatment of closed-angle
glaucoma.

43. Nursing Diagnosis:
• Disturbed sensory perception ( visual ) related to damage to the
nerve fibers due to increased IOP as evidenced by Blurred vision.
• Acute pain related to an increased in IOP as evidenced by facial
expression.
• Risk for injury related to decrease in the visual field.
• Anxiety related to loss of vision, lack of knowledge as evidenced by
feeling nervous.
• Deficient knowledge related to Glaucoma as evidenced by asking
frequent questions.

44. Post operative care
• On the day of surgery allow the patient to lay on the supine postion with minimal
head movement.
• Administer prescribed Pain medications
• Do not remove the eye shield: Leave the patch and shield on until the next day
morning.
• Advice the patient to wear sunglasses or regular eyeglasses while up and about
during the first 2 weeks after surgery.
• Cover the operated eye while sleeping with the plastic shield for 2 weeks after
surgery.
• Advice patient to avoid sleeping on the operated eye. Can sleep on back or the
other side if possible.
• Remove the discharge from the eyelids after sleeping by gently wiping them with a
clean moist washcloth.
• Use medications according to directions.
• Always wash your hands before eye drops are instilled.
• Some drooping of the eyelid is not uncommon during the first few weeks following
surgery

45. Post operative care Education
• Daily Activities: Do not bend you head below your waist. The pressure in the
operated eye goes up if your head is placed below your waist.
• Do not lift anything heavy: Lifting heavy objects raises the pressure in the
operated eye. Try also to avoid excessive straining or cough. Avoid Showers
during the first two week after surgery to avoid getting water or soap in the
operated eye.
• Avoid straining or lifting anything more than 10 pounds for 3 weeks after
surgery. Light exercise is permissible.
• Sexual relations may be resumed 2 weeks after surgery.
• Increase activities progressively between 2 an4 weeks after surgery.
• Resume a full, normal life with usual activities after 4 weeks

46. Nursing Management: Patient education
• Educate the patients about the need for life long medication and regular
follow up to maintain the IOP in near normal ranges .
• Educate patient to keep a record of the eye pressure measurement and
visual field test.
• Review all the patient medications.
• Explain about the potential side effects and drug interactions.
• Teaching Eye drop instillation and providing support may improve
treatment adherence
• Keep all follow-up appointments.
• People aged over 40 should be encouraged to have regular eye tests

48. Conclusion
• Glaucoma may have devastating consequences if left undetected
and untreated for too long.
• Reducing IOP is the mainstay of pharmacological intervention in
glaucoma.
• This may be achieved via one of two mechanisms, namely reducing the
formation of aqueous humor or promoting its drainage.
• Patients with glaucoma should be carefully assessed and monitored, and
a stepwise approach to their treatment followed.
• It is vital that the target IOP is reached to prevent any further
deterioration to a patient’s visual field loss.

49. References
• King A et al (2013) Glaucoma. The BMJ; 346: f3518. National Institute
for Health and Care Excellence (2009) Glaucoma: Diagnosis and
Management of Chronic Open Angle Glaucoma and Ocular
Hypertension.
• Wittenborn J, Rein D (2011) Cost-effectiveness of glaucoma
interventions in Barbados and Ghana. Optometry and Vision Science;
88: 1, 155-163
• Hinkle.J.L.,(2017), Brunner & Suddarth’s Textbook of Medical –
Surgical Nursing, Wolters Kluwer,1757-1762.