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Glaucoma

Glaucoma. Kelli Shaon, O.D. 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).

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Glaucoma

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  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)

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