Glaucoma

definition ,classification,symptoms and treatment

1. Glaucoma

2. What is glaucoma?
• Optic neuropathy that is the leading cause of
irreversible blindness in the world
• Major types are open angle and closed angle
• Differences among various types of glaucoma
complicate the nomenclature
• Glaucoma is commonly associated with elevated
intraocular pressure (IOP), but the disease can occur in
the context of normal IOP (normal iop-10-22mm Hg)
• Our understanding and treatment of the disease is very
focused on IOP

3. Types of glaucoma
I. Primary:
A. Congenital
B. Hereditary
C. Adult (common types)
1. Narrow angle
2. Open angle
II. Secondary
A. Inflammatory
B. Traumatic

4. Congenital Glaucoma
Onset: antenatally to 2 years old
SymptomsSymptoms
IrritabilityIrritability
PhotophobiaPhotophobia
EpiphoraEpiphora
Poor visionPoor vision
Signs
Elevated IOP
Buphthalmos
Haab’s striae
Corneal clouding
Glaucomatous cupping
Field loss

5. Congenital Glaucoma
Buphthalmos and cloudy corneasBuphthalmos and cloudy corneas

6. From www.ahaf.org

7. Open Angle Glaucoma
From http://www.merckfrosst.ca/e/health/glaucoma/glaucoma/classify/home.html
• 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
Chronic simple glaucoma (CSG)
and primary open angle glaucoma (POAG)
Risk Factors
IOP Diabetes
Age Myopia
Race Gender
Family history Cardiovascular
Central corneal disease
thickness Hormones

9. Open Angle Glaucoma
Onset: 50+ years of ageOnset: 50+ years of age
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

10. Closed Angle Glaucoma
• Apposition of iris and
trabecular meshwork
• Parasympatholytics
(pupillary dilation) can
precipitate attack
• Increase risk with age,
increase in volume of lens
• Acute onset, patient
complains of nausea, headache
(rather than eye ache),
malaise, general distress
• Requires immediate
treatment

11. Closed Angle Glaucoma
Onset: 50+ years of ageOnset: 50+ years of age
SymptomsSymptoms
Severe eye/headacheSevere eye/headache
painpain
Blurred visionBlurred vision
Red eyeRed eye
Nausea and vomitingNausea and vomiting
Halos around lightsHalos around lights
Intermittent eye acheIntermittent eye ache
at nightat night
SignsSigns
Red, teary eyeRed, teary eye
Corneal edemaCorneal edema
Closed angleClosed angle
Mid-dilated, fixedMid-dilated, fixed
pupilpupil
Iris atrophyIris atrophy

12. BOTTOM LINE: ­IOP from ¯Aqueous Flow,
3 Sites
1. Obstructed Trabecular Mesh
Open Angle: Age-related, genetic
Closed Angle: Anatomic,
exacerbated by:
2. Pupillary Block
Dilation of pupil® iris flattens,
¯ flow via pupil, iris forward
¯iris-cornea angle
3. Swelling of Ciliary Body
1
2
3
Modified from: Wood et al. NEJM 339:1298 (1998)

13. TREATMENT RATIONALE
LOWER IOP BY:
(1)Decreasing Production of Aqueous Humor
(2)Increasing Outflow of Aqueous Humor

14. DRUGS THAT DECREASE AQUEOUS PRODUCTION
I.Beta-Blockers [levobunolol, timolol, carteolol, betaxolol]
-Mechanism: Act on ciliary body to ¯ production of aqueous humor
-Administration: Topical drops to avoid systemic effects
-Side Effects: Cardiovascular (bradycardia, asystole, syncope), bronchoconstriction
(avoid with b1-selective betaxolol)
I.Alpha-2 Adrenergic Agonists [apraclonidine, brimonidine]
-Mechanism: ¯ production of aqueous humor
-Administration: Topical drops
-Side Effects: Lethargy, fatigue, dry mouth [apraclonidine is a derivative of clonidine
(antihypertensive) which cannot cross BBB to cause systemic hypotension]
I.Carbonic Anhydrase Inhibitors [acetazolamide,dorzolamide]
-Mechanism: Blocks CAII enzyme production of bicarbonate ions (transported to
posterior chamber, carrying osmotic water flow), thus ¯ production of
aqueous humor
-Administration: Oral, topical
-Side Effects: malaise, kidney stones, possible (rare) aplastic anemia

15. DRUGS THAT INCREASE AQUEOUS OUTFLOW
I.Nonspecific Adrenergic Agonists [epinephrine, dipivefrin]
-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
I.Parasympathomimetics (pilocarpine, carbachol)
-Mechanism: ­ contractile force of ciliary body muscle, ­ outflow via
-Administration: Topical drops or gel, (slow-release plastic insert)
-Side Effects: Headache, induced miopia. Few systemic SE for direct-acting agonists
vs. AchE inhibitors (diarrhea, cramps)
I.Prostaglandins [latanoprost]
-Mechanism: May ­ uveoscleral outflow
-Administration: Topical drops
-Side Effects: Iris color change

16. Rx GLAUCOMA: ADDITIONAL CONSIDERATIONS
1.No single medication can be used in all patients
2.Compliance
-Critical: Rx often requires several agents,
multiple times a day, everyday
- Role of slow-release drug delivery devices (Langer)
3.Non-pharmacologic ways to lower IOP:
- Laser (argon laser trabeculoplasty)
- ­ aqueous outflow, loses effectiveness over time
-Surgical (trabeculectomy)
-Creates alternative path for aqueous outflow
-Only definitive therapy for closed angle
4.Effectiveness of Rx measured by ability to lower IOP, but other
factors may be (more) important:
- Neuroprotection/increased blood flow to optic nerve

17. GLAUCOMA: 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: Beta blockers
Alpha-2 agonists
Carbonic anhydrase inhibitors
- ­ aqueous outflow: (Adrenergic agonists, nonspecific)
Parasympathomimetics
Prostaglandins
• Treatment slows progression

18. THANK YOU ALL FOR LISTENING!THANK YOU ALL FOR LISTENING!