Glaucoma

1. Glaucoma Kelli Shaon, O.D.

2. Glaucoma • Progressive optic neuropathy that is characterized by cupping of the optic nerve, loss of NFL, and VF defects • Elevated IOP can be associated, but NOT always • Theories of etiology: Mechanical vs. Ischemia vs. pre-programmend Cellular suicide (apoptosis)

3. Glaucoma • Various studies say GLC is 2nd or 3rd leading cause of blindness in the US • Estimated that 1-3 million Americans have glaucoma • Only 1/2 of the people who have glaucoma are aware that they have the disease • Glaucoma is the most common cause of blindness among African Americans • POAG 4-5x higher in African-Americans than in whites

4. Risk Factors for Glaucoma • IOP (24 mm Hg = 6x risk) • C/D & disc asymmetry • Thinner corneas (not only because of increased IOP) • Increasing Age • (+) Family history – (3x higher risk if sibling has GLC) • Race – (AA**, Hispanic) • High myopia (~up to -5.00D) • Vascular disease (ie. DM) • Vasospastic disease (Raynaud’s, Migraine, & sleep apnea) • H/O of Trauma – angle recession • Long term steroid use (steroid responders)

5. Ocular Hypertension • IOP = 21 mm Hg or more • No optic nerve changes • No VF loss • ~10-30% will develop glaucoma after 20 years

6. Ocular Hypertension Treatment Study (OHTS) • In case of Ocular HTN, treatment delayed or prevented onset of POAG • 4.4% rate of developing POAG in treated group vs. 9.5% in observation group • CCT measurement became important • Identified higher risk groups • Older individuals • Higher IOP • Larger C/D ratio • Thinner corneas

7. Classifications of Glaucoma • Open angle • Primary • High tension • “Normal Tension” • Secondary • Closed angle • Primary • w/ pupil block • w/o pupil block • Secondary

8. POAG • Most common form of GLC • Associated with elevated IOP*** • What is elevated? Based on the individual nerve • Cupping – vertical elongation • Rim notching or thinning • NFL defects • Peripapillary defects (in area of notching or rim thinning) • Angles open via gonioscopy • VF loss defects

9. Normal Tension Glaucoma (NTG) • Will have similar findings as in POAG, just will find IOP in normal/low ranges • Often find wider range of diurnal variation in IOP • May want to take IOP measurements & follow-up visits at different times of day • More likely to find disc splinter hemorrhages (Drance heme) • Thought to be associated w/ vasospastic disease

10. Collaborative Normal Tension Glaucoma Study Group • Trial that determined the effectiveness of lowering IOP in NTG suspects • 35% of untreated eyes showed progression (by optic nerve changes or VF loss) • 12% of treated eyes showed progression • Conclusion: IOP does play a role in the process of NTG • Dilemma: (1) It didn’t prove who is at more risk for progression (2) While 35% showed progression, 65% did NOT progress – Do you treat all patients, when only 35% will progress?

11. Glaucoma Work-up/Management • IOP measurement – every 3-4m (or sooner if changing Tx) • Gonioscopy – every year • Pachymetry – only can bill 1x for pachymetry • Thinner than average – IOP is falsely LOW • Thicker than average – IOP falsely HIGH • DFE to closely assess the nerve & cup – at minimum every year ( ↑ w/ severe GLC) • Disc photos – q1-2 years or sooner if changes • VF q6-12 months (or more frequent PRN)

12. Glaucoma Management • Goal: delay the progression of the disease, long enough to preserve vision during their remaining life • Do not increase morbidity by giving them medications that will decrease their quality of life – ie. side effects, $$ • Need to know about compliance to medications – ASK questions & pay attention to your findings

13. Glaucoma Management • Ocular hypotensive agents: • PG analogs • B-blockers • Alpha-agonist • CAI • Combination drops - Cosopt • ALT/SLT • Filtering surgery

14. Ocular hypotensive agents • PG analogs – ↑ Uv.scleral outflow (IOP ↓ 30%) • qHS dosage (easiest & best compliance; $$$ • SE: conjunctival hyperemia, stinging, iris pigment changes, increased lash growth, re-activation of ocular inflammation • Don’t use in patients with active uveits, HSV, & caution in aphakic patients • B-blockers - ↓ aq. Production (IOP ↓ 25%) • BID dose, unless Timoptic XE qAM • SE: wheezing, bradycardia, depression, impotence • Don’t use in asthma or CHF patients • Alpha-agonist - ↓ aq. Production (IOP ↓ 25-30%) • TID or BID dosage • Avoid in NTG glaucoma b/c of vasospstic properties • SE: stinging, hypotension, & rarely bradycardia (more likely w/ B-blocker) • CAI - ↓ aq. Production (IOP ↓ 15-20%) • Don’t use if SULFA allergy • TID dosage • SE: metallic taste, tingling/numbness in arms or feet

15. Secondary Open Angle Glaucoma • Pigment Dispersion Syndrome • Pseudoexfoliation Syndrome • Traumatic Glaucoma (angle recession) • Causes damage to the TM matrix ?? • Inflammatory Glaucoma • Inflammatory cells block the TM • Phacolytic Glaucoma • Ruptured lens – releases cellular particles that induces inflammation (macrophages) then block the TM

16. Pigment Dispersion Syndrome • Pigment is dislodged from posterior iris due to mechanical rubbing by the zonules • Only classified as GLC if optic nerve damage & VF loss • Signs/symptoms: • Krukenberg spindle • Transillumination defects of the iris • Dark “chocolate band” pigment on TM & back bowing iris seen during gonioscopy • Large fluctuations in IOP • Blurred vision after exercise or coming out of dark room (dilation of the pupil)

17. Pigment Dispersion Syndrome • Treatment: • ALT works well • LPI often used – to equalize pressure & allows the posterior bowing iris to move forward • Miotics can reduce pigment release by pulling the iris away from the zonules

18. Pseudoexfoliation Syndrome • Systemic condition found in the eye & other tissues in the body • Seen as whitish, flaky material seen on the edge of pupil anterior lens capsule, and anterior chamber • GLC is thought to be caused by blockage of the TM by the material

19. Angle recession

20. Angle Closure Glaucoma • Primary Angle Closure • With pupillary block • Acute or Chronic angle closure • W/O pupillary block • Plateau iris • Angle pulled close – NVG, ICE syndrome, or PAS (inflammation) • Secondary Angle closure • Aqueous misdirection ?? • Posterior synechiae of iris to lens (Uveitis) • Phacomorphic • Ectopia Lentis

21. Angle Closure • Common in shallow anterior chambers • Hyperopes>>Myopes • More common in Asian & Eskimo decent • Females>>Males • Signs: Significantly elevated IOP, corneal edema, mid-dilated pupil, AC cells, narrow angle in fellow eye • Symptoms: Pain, blurred vision or halos around lights, nausea

22. Angle Closure • Treatment: • (1) Oral Diamox – 500 mg (2x 250 tabs – not time released tabs) – (Dehydrates, pulls fluid from eye) • Questions to ask (CI) – Sulfa allergy? Kidney problems? Sickle cell disease? • (2) Beta-blocker (↓ aqueous production) • Questions to ask (CI)– Asthma? CHF or bradycardia? • (3) Alpha agonist – (prevents mydriasis) • Alphagan or Iopidine • (4) Pilocarpine 2% (↑ outflow) • Last medication: ***Wait until IOP <40mm Hg • Pulls iris out of angle • Prepares eye for LPI Paul Karpecki, O.D – 8/14/05 August Academe Lecture

23. Plateau iris • Plateau configuration of the iris with deeper central anterior chamber but shallow in periphery • Will NOT improve longterm with an LPI, due to iris configuation • Long-term miotic therapy is usually required

24. NVG • New vessels growth over the TM secondary to DM, CRVO, CRAO, or OIS • Avoid pilocarpine*** (Boards) • Treatment: Retinal PRP

25. Aqueous misdirection • AKA: Malignant glaucoma • Often occurs after an event (surgery, trauma) disturbs the equilibrium of an eye and the aqueous misdirection comes on within a matter of hours • Occurs when aqueous becomes directed back into the vitreous causing the aqueous to build up, pushing iris forward, closing the angle • Signs: Flat anterior chamber with elevated IOP despite patent LPI • Treatment: Surgical management

26. Aqueous misdirection

27. Posterior synechiae

28. Phacomorphic Glaucoma • Swollen, mature cataract pushes the iris forward closing the angle

29. Ectopia Lentis • Dislocated lens can pushes the iris forward (less common to cause complete block)