Glaucoma is an optic neuropathy characterized by cupping of the optic disc and loss of visual field. It is usually associated with increased intraocular pressure (IOP). If left untreated, glaucoma can lead to irreversible blindness. There are several types of glaucoma including open-angle glaucoma, angle-closure glaucoma, congenital glaucoma, and secondary glaucoma caused by injuries, infections, tumors or inflammation. Treatment options include medications, laser treatment, or surgery to lower IOP and prevent further vision loss. The goal is early detection and treatment to preserve sight.

1. GLAUCOMA
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2. • Glaucoma is an optic neuropathy characterized by
cupping of the optic disc and the loss of visual
field.
• Associated to ↑ intraocular pressure (IOP)
• ↓ visual field sensitivity and eventually leads to
blindness in the affected eye

3. • Worldwide, glaucoma is the leading cause of
irreversible blindness
• Almost 60 millions people have Glaucoma.
In fact, as many as 6 millions individuals are
blind in both eyes from this disease

5. Pathophysiology
increased intraocular pressure (usually > 24 mmHg)
 Overproduction of HA with normal
Drainage
 block of fluid flow from posterior to
anterior chamber
 reduced flow through the trabecular
meshwork
Ischemic of Optical
nerve
Push Optical Nerve
Diffuse ganglional cell
atrophy
Effect to the Vision

8. Risk Factors
• Age
• Family History
• Drug consumption (steroid)
• Trauma
• Severe Hypermethrophya
• Other systemic disease (ex ; DM, Hypertension)

9. Sign and symptom
Symptoms may include:
• Blurred vision
• Severe eye pain
• Headache
• Rainbow haloes around lights
• Nausea and vomiting
• Elevated intraocular pressure
• Visual field loss
• Optic disk changes
• Enlargement of the eye.

10. Diagnosis
• Measuring intra ocular pressure (tonometry);
• Inspecting the drainage angle of your eye (gonioscopy);
• Evaluating any optic nerve damage (ophthalmoscopy);
• Testing the visual field of each eye (perimetry).

11. Classification
1. Open Angle Glaucoma
2. Angle closure glaucoma
3. Congenital Glaucoma
4. Secondary glaucoma
Glaucoma can be divided roughly into two main
categories, "open angle" and "closed angle“ glaucoma.

12. Types of glaukcoma
Types Cause Symptoms Comment
Chronic Open Angle
Glaucoma
Gradual blockage of
drainage channel
Pressure builds slowly
Gradual loss of side
vision
Affects side vision first
This type of glaucoma
progresses very slowly
and
is a lifelong condition.
Acute Closed
Angle Glaucoma
Total blockage of
drainage channel
Sudden increase
in pressure
Nausea
Blurred vision
Severe pain
Halos around lights
This condition
constitutes a
medical emergency, as
permanent blindness
occurs rapidly without
immediate treatment.
Secondary Glaucoma Injury, infection, tumors,
drugs, or inflammation
cause scar tissue which
blocks the drainage
channel
Gradual loss of side
vision
Affects side vision first
This form of glaucoma
may progress slowly, as
in cases of chronic
glaucoma.
Congenital
Glaucoma
Fluid drainage system
abnormal at birth
Enlarged eyes
Cloudy cornea
Light sensitivity
Excessive tearing
This condition must be
treated soon after birth if
vision is to be saved.
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13. Examination Methods

14. Oblique Illumination of the Anterior Chamber

15. Slit-Lamp Examination

16. Gonioscopy
• Gonioscopy can differentiate the following conditions:
– Open angle: open angle glaucoma.
– Occluded angle: angle closure glaucoma.
– Angle access is narrowed: configuration with imminent risk
angle of an acute closure glaucoma.
– Angle is occluded: secondary angle closure glaucoma, for
example due to neovascularization in rubeosis iridis.
– Angle open but with inflammatory cellular deposits,
erythrocytes, or pigment in the trabecular meshwork: secondary
open angle glaucoma.

19. Measuring Intraocular Pressure

20. Applanation Tonometry

23. Optic Disk Ophthalmoscopy

24. Visual Field Testing
visual field testing can be grouped into several
important categories:
• Confrontational
• Amsler grid
• Static perimetry
• Kinetic perimetry
• Frequency doubling analysis

25. Treatment
• Principe: reducing IOP by decreasing aqueous
production or increasing aqueous outflow
• Currently, the effectiveness of a medication in
the treatment of glaucoma is measured by its
ability to lower IOP
• Medical, surgical or laser

26. Medical Treatment
• Suppression of Aqueous Production
Topical beta-adrenergic blocking agents, Apraclonidine,
Brimonidine, Dorzolamide hydrochloride and brinzolamide,
Carbonic anhydrase inhibitors—acetazolamide
• Facilitation of Aqueous Outflow
The prostaglandin analogs—bimatoprost 0.003%, latanoprost
0.005%, and travoprost 0.004% solutions,
Parasympathomimetic agents  Pilocarpine, Epinephrine,
Dipivefrin
• Reduction of Vitreous Volume
Hyperosmotic agents, Oral glycerin (glycerol)
• Miotics, Mydriatics, and Cycloplegics

27. Surgical and laser treatment
• Peripheral Iridotomy, Iridectomy, and
Iridoplasty
• Laser Trabeculoplasty
• Glaucoma Drainage Surgery
– Trabeculectomy
– Viscocanalostomy and deep sclerectomy with
collagen implant
– Goniotomy
• Cyclodestructive Procedures

28. OPEN ANGLE GLAUKOMA

29. OPEN ANGLE GLAUCOMA
• Primary open-angle glaucoma (POAG), the most
common form of glaucoma, accounts for 60–
70% of all glaucomas and 90–95% of primary
glaucomas.
• POAG is a bilateral,
chronic progressive condition
that typically appears in
individuals over 60
years of age
PRIMARY OPEN ANGLE GLAUCOMA

31. Groups at risk
• Age : from the 40-49 age group into those
aged over 80.
• ocular hypertension
• myopia

32. Signs
• the optic disc changes.
The cup to disc ratio
increases. Asymmetry
of disc cupping

33. Diagnostic considerations
• Measurement of intraocular pressure 
Elevated intraocular pressure is an alarming
sign
• Twenty-four-hour pressure curve 
Fluctuations in intraocular pressure of over 5–
6 mmHg may occur over a 24-hour period.
• Gonioscopy
• Ophthalmoscopy

34. treatment
• The goal is to maintain IOP less than 21 mmHg
and continued visual field loss should be minimal.
• Various treatment modalities include medical
treatment, laser therapy,and surgery.
• Patients will initially start with topical ocular drug
therapy
• Prognosis : If discovered early and treated
adequately, the prognosis for POAG is excellent

35. ACUTE ANGLE CLOSURE
GLAUCOMA

36. Acute angle closure glaucoma
History
• The attack comes on quite quickly
• the intraocular pressure rises rapidly
• Red eye
• There is pain in one eye, can be extremely severe
• impaired vision and haloes around lights
• may have had similar attacks in the past
• may be systemically unwell, with severe
headache, nausea, and vomiting

38. Risk factors
• increasing age
• female gender
• family history of glaucoma
• South-East Asian, Chinese, or Inuit ethnic
background.

39. Examination
• The eye is inflamed and tender
• The cornea is hazy and the pupil is semidilated
and fixed. Vision is impaired according to the
state of the cornea
• On gentle palpation the eye feels harder than
the other eye.
• The anterior chamber seems shallower than
usual, with the iris being close to the cornea

40. Management
• Urgent referral to hospital is required.
• intravenous acetazolamide 500 mg and
pilocarpine 4% should be instilled in the eye to
constrict the pupil
• (iridotomy) or surgically (iridectomy) to
restore normal aqueous flow
• The other eye should be treated
prophylactically in a similar way.

41. Aqueous Humor flow after iridectomy

42. Congenital Glaucoma
• Primary congenital glaucoma
• Together with other anomaly

43. Primary Congenital Glaucoma
• Present at birth; however, but its manifestations
may not be recognized until infancy or early
childhood
• Pathophysiology : Primary congenital glaucoma is
restricted to a developmental abnormality that
affects the trabecular meshwork
• Estimated to affect fewer than 0.05% of
ophthalmic patients
• The disease is bilateral in approximately 75% of
cases.

44. • Primary congenital glaucoma usually is diagnosed
at birth or shortly thereafter, and most cases are
diagnosed in the first year of life.
• Most cases oare sporadic in occurrence may be
transmitted through an autosomal recessive
pattern
• Male patients are found to have a higher
incidence of the disease, comprising
approximately 65% of cases.

45. Clinical
History
Triad of manifestations :
• Epiphora
• Photophobia
• Blepharospasm

46. Secondary glaucoma

47. Secondary glaucoma
• Inflammatory glaucoma
– Uveitis of all types
– Fuchs heterochromic iridocyclitis
• Phacogenic glaucoma
– Angle-closure glaucoma with mature
cataract
– Phacoanaphylactic glaucoma secondary to
rupture of lens capsule
– Phacolytic glaucoma due to phacotoxic
meshwork blockage
– Subluxation of lens
• Glaucoma secondary to intraocular
hemorrhage
– Hyphema
– Hemolytic glaucoma, also known as
erythroclastic glaucoma
– Neovascular glaucoma
• Traumatic glaucoma
– Angle recession glaucoma: Traumatic
recession on anterior chamber angle
– Postsurgical glaucoma
– Aphakic pupillary block
– Ciliary block glaucoma
• Drug-induced glaucoma
– Corticosteroid induced glaucoma
– Alpha-chymotrypsin glaucoma.
Postoperative ocular hypertension from
use of alpha chymotrypsin.
• Glaucoma of miscellaneous origin
– Associated with intraocular tumors
– Associated with retinal detachments
– Secondary to severe chemical burns of the
eye
– Associated with essential iris atrophy
– Toxic Glaucoma

48. Secondary glaucoma
is caused by:
• Drugs such as corticosteroids
• Eye diseases such as uveitis
• Systemic diseases
• Trauma
• Due to lens changes
• Post operative
• Raised episcleral venous pressure