Secondary Open Angle & Angle Closure Glaucomas

1. Diagnosis & Management Considerations Optometry 8570 September 22, 2008 Secondary Open Angle & Angle Closure Glaucomas

2. Review Primary Open Angle Glaucoma • Diagnosis of exclusion: The clinician has ruled out angle closure, pupillary block, and any substance mechanically blocking the outflow of aqueous through the TM. • Not associated with systemic disease. • By far the most common type of glaucoma. • Third most common cause of blindness in the U.S. • 6-8.5% more prevalent in African Americans.

3. Secondary Open Angle Glaucoma • Caused by pigment, exfoliation material, or RBCs blocking TM. • May also result from change in structure and function of TM due to trauma or inflammation. • All must be ruled out in cases of suspected POAG.

4. Pigment Dispersion Syndrome (PDS) • Occurs when posterior iris rubs against lens zonules or ciliary processes, mechanically damaging the pigment epithelium of the iris, releasing pigment. • Proposed mechanism of IOP increase: • Phagocytosis of pigment by trabecular endothelium damages cells of TM (through cellular toxicity?), causing them to drop off the trabecular lamellae. The damaged trabeculae collapse, obstructing aqueous outflow.

5. Signs and Risk Factors • Kruckenberg spindle • Increased TM pigment • Iris transillumination defects. • Large fluctuations in IOP may occur, especially due to exercise or pupillary dilation. • More frequent in caucasians

6. PDS photos Ultrasound Biomicroscopy

7. PDS photos Transilluminated Iris

8. PDS photos

9. Treatment Considerations • Watch for “reverse pupil block”. • Traditional glaucoma medications. • ALT works well • A condition that will sometimes “burn itself out”.

10. Exfoliation Syndrome (Pseudoexfoliation Syndrome) • Characterized by grayish-white, dandruff-like material, and/or a gray membrane with frayed or curled edges, on the anterior lens capsule. • Source of amyloid-like, fibrillo-granular material thought to be the various basement membranes of the eye, including the lens capsule. • Material also present in the posterior chamber, conjunctiva, and orbit.

11. Risk Factors for PES • Usually older (70 y.o.). • Females more than males but males more likely to get the glaucoma. • Scandinavian ancestry.

12. Exfoliation Syndrome (cont.) • Syndrome may represent abnormal BM production at multiple sites by aging epithelial cells • Elevated IOP likely due to direct blockage of TM by exfoliative material, and dysfunction of trabecular endothelium • Tx: Same as for POAG

13. PEX photos

14. PEX photos

15. Traumatic Glaucoma(Contusion Glaucoma) • May develop soon after injury (trauma itself), or 20 or more years later (Angle Recession or damage). • High IOP due to damage to angle structures or recessed angle.

16. Signs of Traumatic Glaucoma • Uneven iris insertion with area of torn or absent iris processes; a posteriorly recessed iris revealing a widened ciliary band. • Other eye normal (examination of fellow eye critical to Dx). • Absence of a recessed iris does not rule out a traumatic glaucoma.

17. Treatment Considerations for Traumatic Glaucoma • Tx: Same as for POAG, but widely variable response may occur. • Miotics do not work well, and may increase IOP due to reduced uveoscleral outflow. • ALT is rarely effective. • Annual follow-up important for both eyes; high incidence of delayed open angle glaucoma and high steroid-response IOP in the uninvolved eye, as well as the injured eye.

18. Traumatic Glaucoma (cont.) • Can manifest as “Red Cell Glaucoma”. • Hyphema results in stained corned and RBC’s blocking the TM. • The bigger the hyphema the more likely the glaucoma

19. Angle Recession

20. Angle Recession

21. Hyphema

22. Inflammatory Glaucoma(Uveitic Glaucoma) • Signs: Usually unilateral high IOP, significant aqueous white cells and flare, PAS, miotic pupil, inflammatory precipitates on posterior cornea or in TM, ciliary flush, conjunctival injection • High IOP due to inflammatory cells in TM and/or PAS • Must r/o narrow-angle glaucoma, which also results in anterior chamber inflammation • May occur in association with any kind of uveitis, including keratouveitis (HSV, fungal infections)

23. Inflammatory Glaucoma (cont.) • Tx: Pred acetate 1% q 1-6 hours, cycloplegic, B-blocker, Alphagan • Avoid Pilocarpine and Xalatan • Must determine etiology of uveitis • Consider steroid-response glaucoma when patient unresponsive to Tx • Use extreme caution with steroids when infection seems likely

24. Keratic Precipitates

25. Uveitis Spondyloarthropathies • Ankylosing spondylitis • Lower back arthritis • 90% association with HLA-B27 • 30% will develop glaucoma • Reiter Syndrome • urethritis, conjunctivitis, uveitis • 70% are positive HLA-B27 • 20% develop uveitis • Psoriatic arthritis • affects about 7% of patients with psoriasis

26. Angle Closure Glaucoma (ACG) • With pupillary block: • Primary angle closure (suspect, acute, chronic) • Secondary angle closure (posterior synechiae to lens, vitreous, or IOL; ectopia lentis, miotic-induced, spherophakia, phakomorphic, others)

27. ACG • Without pupillary block: • Primary angle closure (plateau iris configuration, plateau iris syndrome) • Secondary angle closure with anterior pulling mechanism (NVG, ICE syndrome, epithelial downgrowth, PAS) • Secondary angle closure with posterior pushing mechanism (aqueous misdirection and related causes)

28. Acute ACG • Responsible for 10% of all glaucomas • 2-8% of population have angles narrow enough to close • Very rare in African Americans, usually in chronic form when it occurs • High rate in Eskimos and southeast Asians • 3.5-6.0% higher risk if first degree relative has primary ACG • Rare under age 40, usually occurs in 60s & 70s

29. Acute ACG • Females have a higher risk of angle closure by a 2:1-4:1 ratio • Higher risk in hyperopic eyes • Signs of prior attack: PAS, posterior synechiae, glaukomflecken, iris atrophy, pigment anterior to Schwalbe’s line • Highest risk when dilated pupil returning to normal; greatest iris-lens contact when pupil is mid-dilated (3.5-4.0 mm) • Failure to Dx ACG can result in dense PAS and permanent high IOP

30. Acute ACG • Signs: Acutely increased IOP, closed angle in involved eye, corneal microcystic edema, shallow angle in fellow eye, mid-dilated pupil, A/C cells, glaukomflecken, pain, lacrimation, nausea; may need glycerin to clear cornea for adequate exam • Must determine whether or not pupillary block exists (may only be realized when a patent LPI fails to lowerIOP) • Careful history important to Dx; prior attacks? (episodes of blurred vision, transient vision loss, haloes around lights, pain, nausea, red eye) FHx?

31. AC Angle Grading System • Becker-Shaffer method is most widely used method of estimating relative width of angle • Grade Post.-most structure visible • 4 CB • 3 SS • 2 Ant. ½-1/3 TM • 1 Ant.-most TM, Schwalbe’s line • 0 No structures visible

32. Treatment of Acute ACG • Must lower IOP medically before definitive Tx with LPI • AOA Guidelines: • 500 mg oral Diamox • One drop Timolol 0.5% • One drop Pilo 2.0% • One drop Iopidine 1% • Check IOP q 15-30 minutes; if attack not broken in 1 hour, add oral hyperosmotics (Isosorbide or Osmoglyn) and repeat all topicals • If attack not broken in 2 hours, laser gonioplasty indicated; after 4-6 hours, emergency LPI or iridectomy

33. Treatment of Acute ACG • Once IOP has been lowered (under 20), patient should be maintained on Pilo 2% QID OU, B-blocker BID, and PF 1% QID in affected eye, until LPI performed in 2-7 days • Careful post-LPI monitoring vital, to r/o pressure spikes and other mechanisms that may cause high IOP (angle crowding, inflammation, etc.)

34. Plateau Iris • Flat central iris, with peripheral iris taking a sharp posterior turn before insertion into CB • Configuration: Mild degrees of pupillary block may cause angle closure glaucoma in these patients, due to angle anatomy; cured by LPI due to relief of pupillary block • Syndrome: Peripheral iris bunches up in angle, obstructing outflow without any element of pupillary block; LPI of no therapeutic value, Tx options include iridoplasty (gonioplasty)

35. Neovascular Glaucoma (NVG) • High IOP results from fibrovascular membrane growth over TM (not from actual vessels); the fibrovascular membrane eventually contracts, causing PAS formation and angle closure • Etiology of neo is ischemia from any number of causes (DR, CRVO, CRAO, ocular ischemic syndrome, others)

36. NVG (cont.) • Tx: Reduce pain & inflammation with PF 1% q 1-6 hours, and atropine 1% TID • B-blocker, Alphagan, topical or systemic CAI may be used as needed to lower IOP • Avoid Pilo • PRP is done if retinal ischemia is considered to be the source of neo • Goniophotocoagulation may delay or prevent angle closure during the time that PRP takes effect

37. Malignant Glaucoma(Aqueous Misdirection Synd.) • Signs: Shallow or flat AC, and high IOP, in the presence of a patent PI, and in the absence of choroidal detachment and iris bombe’ • Believed that aqueous is misdirected and accumulates within vitreous, displacing vitreous, ciliary processes, lens (or IOL or vitreous face) anteriorly, causing secondary angle closure; many potential causes, see Wills • Tx: LPI if not already done; other medical and surgical therapies

38. Glaucoma Surgery Basics • Wide variety of surgeries (both conventional and laser) are used to control IOP and prevent vision loss in patients with glaucoma • Because glaucoma mechanisms vary widely, and surgeon education and skill may vary, there is usually no single correct approach to surgical management of a particular type of glaucoma • The O.D. is usually wise to obtain consult from a glaucoma specialist, or OMD experienced in managing the condition in question (complications can be difficult to manage and devastating)

39. Filtration Surgery • Indicated for progressive VF and/or ONH damage associated with IOP that is too high for the health of the ONH despite maximal tolerated medical Tx • Laser trabeculoplasty is usually used as a intermediate measure between medical Tx and filtration surgery in many forms of open-angle glaucoma

40. Filtration Surgery (cont) • Trabeculectomy • The most commonly used filtration procedure • May be performed on almost any type of glaucoma in a patient of any age • Conjunctival and scleral flaps are made, extending from the limbus; sclerectomy and iridectomy performed to create avenue for aqueous to leave eye; scleral and conjunctival flaps closed; tightness of flaps adjusted (by suture manipulation) for optimal flow of aqueous from eye and bleb formation; antibiotics and steroids used to control infection and inflammation • Antifibrotic therapy (5-Fluorouracil and Mitomycin-C) decreases scarring and has greatly improved results in high-risk eyes

41. Cyclodestructive Procedures • Generally used only when previous surgical approaches have failed, when the eye has limited visual potential, and/or when no reasonable alternative exists • Procedures disrupt the ciliary epithelium, thereby reducing aqueous production and IOP • The vascular supply of the ciliary processes and the blood-aqueous barrier may also be disturbed

42. Cyclodestructive Procedures (cont) • Cyclocryotherapy • Performed under topical and retrobulbar anesthesia • Cryoprobe held firmly 2.5-3.0 mm posterior to the corneal limbus, overlying the pars plicata • 6-8 overlapping lesions are made over ½ of the ciliary body • Freezing the area to -60 to –80 C for 45-60 seconds creates an iceball that destroys the underlying tissue

43. Cyclodestructive Procedures (cont) • Transscleral YAG Laser Cyclophotocoagulation • YAG laser beam allows enables the infrared laser energy to penetrate the the scleral wall before producing its effect within the ciliary body • Better control of the location and amount of ciliary body treated makes this therapy an appealing alternative to cyclocryotherapy

44. Surgical Iridectomy • Most cases of angle-closure glaucoma and eyes with anatomically narrow angles are treated with laser iridotomy; however, an incisional surgical iridectomy may be necessary when: • Laser Tx fails to produce a patent iridotomy • A laser iridotomy closes repeatedly (inflamm.) • Media opacity exists • A/C is flat or exceedingly shallow • An acute attack of angle-closure glaucoma cannot be terminated by medical Tx, and corneal edema, shallow A/C, and thickened inflammed iris prevent successful laser iridotomy • Patient is uncooperative or unable to sit at a slit lamp

45. Posterior Tube Shunt Implants • “Filtration surgery” or “filter” • Silicon tube implant is placed into the A/C to shunt aqueous humor posteriorly into an area of encapsulation around an episcleral explant sutured to the globe 8-12 mm posterior to the limbus • Indicated when filtration surgery with antifibrotic agents has failed to control IOP, or in neovascular glaucoma and ICE syndromes • Rarely used as a primary glaucoma surgical procedure

46. Laser Iridoplasty • Argon laser iridoplasty can be used to terminate an acute attack of angle closure glaucoma when a patent iridotomy cannot be achieved • Performed to widen a narrow but open angle to facilitate ALT, and to widen a narrow angle following laser iridotomy in eyes with plateau iris, nanophthalmos, and primary angle-closure glaucoma • Burns applied to the peripheral iris to cause iris contraction and widening of the angle. The burns contract the iris stroma toward the site of the burn, eliminating iris contact with the TM