Chapter 1. GLAUCOMA lecture three3 .ppt

Ophthalmology lecture

1. GLAUCOMA
Dr.hasan deedat

2. WHAT IS GLAUCOMA?
A disease of progressive optic neuropathy with
loss of retinal neurons and their axons (nerve
fiber layer) resulting in blindness if left
untreated.
Glaucoma is commonly associated with elevated
intraocular pressure (IOP)
Major types are open angle and closed angle

3. Intraocular pressure is not the only factor responsible
for glaucoma!
The disease can occur in the context of normal IOP
50% of people with glaucoma do not know it!
The normal range of IOP is : 10.5-21 mm Hg
30-50% of open angle glaucoma patients have IOP
<22 mmHg
Diurnal fluctuation normally < 6 mmHg
Women have slightly higher pressures

4. From www.ahaf.org

5. Types of glaucoma
I. Primary:
A. Congenital pediatrics
B. Adult (common types)
1. Narrow(closed)angle
e.g Acute Angle Closure Glaucoma
• 2. Open angle
II. Secondary
Traumatic E.g. post surgical

7. OPEN ANGLE GLAUCOMA
•Obstruction at the level of the
trabecular meshwork
• Progressive loss of visual field
over time from periphery to
center
• Presence of hollowed out optic
disc (‘cupping’) due to retinal
ganglion cell death
• Open anterior chamber angle
• Majority of patients have IOP >
21 mmHg,
•Asymptomatic

8. OPEN ANGLE GLAUCOMA
Onset: 50+ years of ageOnset: 50+ years of age
The hallmark of glaucoma is elevated IOPThe hallmark of glaucoma is elevated IOP
SymptomsSymptoms
Usually noneUsually none
May have loss of central May have loss of central
and peripheral visionand peripheral vision
latelate
SignsSigns
Elevated IOPElevated IOP
Visual field lossVisual field loss
Glaucomatous disk changesGlaucomatous disk changes

9. CLOSED ANGLE
GLAUCOMA
•Apposition of iris and
trabecular meshwork
•Pupillary dilation can
precipitate attack.
•Increase risk with age
•Acute onset
• patient complains painful red
eye.
•Requires immediate treatment

10. CLOSED ANGLE GLAUCOMA
Onset: 50+ years of ageOnset: 50+ years of age
SymptomsSymptoms
Severe eye painSevere eye pain
Headache Headache
Blurred visionBlurred vision
Red eyeRed eye
Nausea and vomitingNausea and vomiting
Halos around lightsHalos around lights

SignsSigns
Red, teary eyeRed, teary eye
Corneal edemaCorneal edema
Closed angleClosed angle
Mid-dilated, fixed pupilMid-dilated, fixed pupil

11. CLOSED ANGLE GLAUCOMA
Mid-dilated, fixed pupilMid-dilated, fixed pupil

12. GlaucomaGlaucoma
NormalNormal

13. CONGENITAL GLAUCOMA
Onset: antenatally to 2 years
old
Corneal clouding
glaucomatous
cupping

14. CONGENİTAL GLAUCOMA
Congenital glaucoma is a rare form of glaucoma
Affected infants may be born with a high intraocular
pressure or may develop an increased IOP within the
“first weeks of life".
Both eyes are usually involved, but to varying severity
Boys are affected slightly more frequently than girls.

15. THE CAUSE
A hereditary factor is occasionally present.
The IOP elevation is caused by the failure of the
anterior chamber angle and the trabecular
meshwork to develop appropriately during
intrauterine development.
In these infants, the aqueous humor does not
properly drain, but since the production of aqueous
humor is nevertheless normal,
The intraocular pressure is high

16. CONSEQUENCES OF AN
INCREASED IOP
Depending on the IOP level, glaucomatous
damage is inevitable after weeks, months or
even years.
This basically occurs via the same mechanisms
as in the adult.
In addition to optic nerve damage, the globe
(eyeball) enlarges because the sclera in the eye
of a baby is distensible. 

17. Enlargement of the globe (buphthalmos) is a result of
elevated intraocular pressure.
The anatomic landmarks are displaced.

The anterior chamber is deep
All segments of the outer eye, but especially the
cornea and sclera, expand.
Principally at the corneoscleral junction
Clinical appearance

18. However, certain layers of the cornea are not very
elastic, and stretching may result in small tears(Haabs
striae) that cause a certain degree of corneal
opacification.
Haabs striaeHaabs striae

19. Corneal epithelial edema caused by elevated
intraocular pressure and failure of the corneal
endothelial pump mechanism.
Clinical triad
Epiphora(overflow of tears onto the face)
 photophobia and
blepharospasm

20. If the IOP is lowered, this opacity is partially
reversible.
As a result of the optic nerve damage and/or corneal
opacity, children with congenital glaucoma may be
permanently visually impaired.

21. DİAGNOSİS OF
CONGENİTAL GLAUCO MA
Clinical clues
Enlarged eyes; tearing, and photophobia
(avoidance of light).
Often, babies also rub their eyes.
If CG is suggested, a thorough examination
under general anesthesia is necessary.
to avoid blepharospasm (spasmodic closure of
the eyes). to prevent a transient rise in the IOP.
Besides measuring the IOP, anesthesia allows a
thorough investigation of all segments of the
eye and, in particular, the optic disc.

22. BOTTOM LINE: IOP from Aqueous Flow, 3
Sites
1. Obstructed Trabecular
Mesh
Open Angle: Age-related,
genetic
Closed Angle: Anatomic
2. Pupillary Block
Dilation of pupil iris
flattens,  flow via
pupil, iris forward iris-
cornea angle
3. Swelling of Ciliary Body
1
2
3

23. TREATMENT
LOWER IOP BY:
(1)Decreasing Production of Aqueous Humor
(2)Increasing Outflow of Aqueous Humor
Focus on Pharmacologic Rx: First-line

24. DRUGS THAT DECREASE AQUEOUS PRODUCTION
1. Beta-Blockers e.g timolol
-Mechanism: Act on ciliary body to  production of aqueous humor
-Administration: Topical drops to avoid systemic effects
-Side Effects: Cardiovascular (bradycardia, asystole, syncope),
bronchoconstriction and depression
2. Alpha-2 Adrenergic Agonists [apraclonidine, brimonidine]
-Mechanism:  production of aqueous humor
-Administration: Topical drops
-Side Effects: Lethargy, fatigue, dry mouth
3. Carbonic Anhydrase Inhibitors [acetazolamide, dorzolamide]
-Mechanism: Blocks CAII enzyme production of bicarbonate ions thus
 production of aqueous humor
-Administration: Oral, topical
-Side Effects: malaise, kidney stones

25. DRUGS THAT INCREASE AQUEOUS OUTFLOW
I.Nonspecific Adrenergic Agonists [eg.epinephrine)
-Mechanism:  uveoscleral outflow of aqueous humor
-Administration: Topical drops
-Side Effects: Can precipitate acute attack in patients with narrow iris-corneal angle,
headaches, cardiovascular arrhythmia, tachycardia
II.Parasympathomimetics [e.g.pilocarpine]
-Mechanism:  contractile force of ciliary body muscle,  outflow via TM
-Administration: Topical drops or gel, (slow-release plastic insert)
-Side Effects: Headache, induced miopia.?
III.Prostaglandins [latanoprost]
-Mechanism: May  uveoscleral outflow by relaxing ciliary body muscle
-Administration: Topical drops -Side Effects: Iris color change

26. Rx GLAUCOMA: ADDITIONAL
CONSIDERATIONS
1.No single medication can be used in all patients
2.Compliance is Critical: Rx often requires several agents,
multiple times a day, everyday
3.Non-pharmacologic ways to lower IOP:
-Laser –  aqueous outflow
-Surgical (trabeculectomy)
-Creates alternative path for aqueous outflow
-Only definitive therapy for closed angle
4.Effectiveness of Rx measured by ability to lower IOP,

27. Key Points
• Glaucoma: -Visual loss from optic neuropathy
-Open angle chronic, Closed angle acute
-Final common pathway:  IOP (usually)
• Drug Rx: -All directed towardsIOP either via:
-  aqueous production:
1.Beta blocker
2. Alpha-2 agonists
3.Carbonic anhydrase inhibitors
-  aqueous outflow:
1. Anonspecific adrenergic agonists,
2. Parasympathomimetics
3. Prostaglandins
• Treatment slows progression