Glaucoma

1. Glaucoma Manasa Manapragada PGY-2

3. Case • 62 y/o Asian female admitted to EJCH for enteritis • During the hospital course, patient developed left eye pain • The eye pain was acute. • The patient was also complaining of blurry vision, nausea, and HA

4. Case • On physical exam: • Left pupil was dilated and fixed • Left conjunctiva was injected • Pain was present with EOM

5. What does the patient have????

6. Introduction • Blindness or low vision affects more than 3 million Americans 40 years and older • This number is projected to reach 5.5 million by 2020

7. Introduction • Glaucoma is the second most common cause of legal blindness in the US • The leading cause of blindness among blacks • One half of people are unaware that they have the disease

8. Types of glaucoma • Congenital • Open-angle glaucoma • Primary • Secondary • Closed-angle glaucoma • Normal (low) tension glaucoma

9. Pathophysiology • Glaucoma is an optic nerve disease • It is often associated with elevated intraocular pressure

10. Normal eye • Aqueous is produced by the ciliary body and it circulates in the anterior portion of the eye to help maintain a healthy eye pressure • Aqueous must drain through the trabecular meshwork to help maintain this eye pressure

12. Glaucoma • In open-angle glaucoma, there is impaired outflow through the trabecular meshwork leading to increased intraocular pressure. • The increased intraocular pressure causes optic nerve damage • In closed-angle glaucoma, there is occlusion of the anterior chamber angle impairing access of aqueous to the drainage system.

13. Primary open angle glaucoma • This is a progressive, bilateral, optic neuropathy • There is increased intraocular pressure (IOP>21 mm Hg) • Not caused by another systemic or local disease • It is the most common form of glaucoma (60-90%)

14. Risk factors • Elevated intraocular pressure • Increased cup:disc ratio • African American • 3-6 times more likely • Increasing age • Positive family history in first degree relatives • Increases prevalence by a factor of 7 • Inconsistent associated factors: • Myopia • Diabetes • HTN • CAD

15. Symptoms • Asymptomatic • After loss of >40% of optic nerve fibers, patients may notice a gradual loss of peripheral vision • Can lead to decreased central acuity • Difficulty functioning in dim light • Decreased contrast sensitivity • Glare disability • Decreased dark/light adaptation

16. Signs • Normal/decreased visual acuity • Increased intraocular pressure • Enlarged cup to disc ratio (>0.5) • Cup to disc ratio asymmetry between two eyes of 0.2 or more • Highly asymmetric cup in one eye • Optic nerve cupping • Visual field deficits • Optic disc hemorrhage

21. Diagnosis • Direct fundoscopic exam • Tonometry • Visual field testing

24. Treatment • Observation • IOP checks q 3-6 months • Visual field exam q 6-12 months • Annual optic nerve evaluation • Medical • Topical prostaglandin analogues are now first-line drugs given better safety profile • Topical beta blockers used to be first line treatment

25. Treatment • Topical prostaglandin analogues • Increase aqueous outflow • Latanoprost (Xalantan), travopost (Travatan), bimatoprost (Lumigan) • Dosed q day • Topical B-blockers • Decrease aqueous production • Timolol maleate (Timoptic), levobunolol (Betagan) • Can have systemic beta blockade effects • Dosed qday-BID

26. Treatment • Topical alpha adrenergic agonists • Decrease aqueous production • Ex: alphagan • Used as adjunctive therapy • Topical carbonic anhydrase inhibitors • Decrease aqueous production • Ex: Trusopt • Adjunctive therapy • Topical cholinergic medication • Increases outflow through trabecular meshwork • Ex: pilocarpine

27. Treatment • Goal of IOP is generally 20-40% below pretreatment pressure • Regular aerobic exercise can help lower IOP • If medical management fails, surgery is available • Laser • Trabeculoplasty • Sclerostomy • cyclophotocoagulation • Surgical • Trabeculectomy • Glaucoma drainage implant • Cycloablation

28. Screening • USPSTF found insufficient evidence to recommend for or against screening adults for glaucoma • AAO recommendations • Age >40, comprehensive eye exams q2-4 years • Age 55-64, q 1-3 years • Age >65, q 1-2 years, even in absence of symptoms • If African American • Baseline exam at 20 years of age with FU q 2-4 years until age 40 • Age 40-54, q1-3 years • Age 55-64, q 1-2 years

29. Acute Angle-Closure Glaucoma • This is an emergency!! • If not treated immediately, damage to the optic nerve and significant and permanent vision loss can occur within hours • Caused by the peripheral iris occluding the anterior chamber angle, blocking aqueous outflow.

31. Symptoms • Blurred vision • Eye redness • Frontal HA • Severe eye pain • Colored halos around lights • Nausea • Vomiting

32. Signs • IOP>30 • Mid-dilated pupil (4-6 mm) • Sluggish reaction of pupil to direct illumination • A shallow anterior chamber • Hazy cornea • Hyperemic conjunctiva

33. Causes • An attack in predisposed persons can occur from dim lighting or use of certain medications: • Dilating drops • Anticholinergics • Antidepressants • Medications such as sulfa derivatives and Topomax can cause swelling of the ciliary body and secondary angle closure

34. Treatment • Send to ophthalmology • In the office can give: • 0.5% timolol maleate, 1% apraclonidine, and 2% pilocarpine one minute apart • Also give 500 mg tablet of acetazolamide • These will help decrease IOP • Eye drops should be repeated three times at 5 minute intervals

35. Treatment • Therapy is initiated to lower the IOP, reduce pain, and clear corneal edema • Definitive treatment is laser iridotomy • Surgical iridectomy can be performed if laser iridotomy is not successful.

36. Secondary Open-Angle Glaucoma • Due to local or systemic disorders • Etiology includes • Drug induced (ex: steroids) • Trauma • Tumors • Uveitis • Retinal disease • Pituitary tumors, Cushing’s syndrome, thyroid dz • Postoperative

37. Drug induced • Steroids • Most common cause • Correlates with potency and duration of use • 30% of population develop IOP after 4-6 weeks of topical steroid use • Viscoelastic agents • Used during ophthalmic surgery • Transiently obstructs the trabecular meshwork

38. Traumatic • Angle recession • If >2/3 of the angle involved, 10% of pts will develop glaucoma from scarring of angle structures • Chemical injury • Hemorrhage • RBCs or macrophages that have ingested RBCs obstruct the TM • Siderosis/chalcosis • Toxicity to angle structures from iron or copper intraocular foreign bodies

39. Treatment • Treat increased IOP • Laser trabeculoplasty is usually not effective • May require trabeculectomy or glaucoma drainage implant to lower pressure adequately • Treat underlying problem

40. Normal (Low) Tension Glaucoma • Similar optic nerve and visual field damage as primary open angle glaucoma but with normal IOP (<21 mm Hg). • Pts have a higher prevalence of vasospastic disorders including migraine, Raynaud’s, ischemic vascular disease, autoimmune disease, and coagulopathies. • Also associated with hx of poor perfusion to the optic nerve

41. Signs/Symptoms • Asymptomatic • May have decreased vision or constricted visual fields in late stages • Optic nerve cupping • Visual field defects • Normal IOP • Normal or decreased visual acuity

42. Treatment • Topical glaucoma medications • FU ever 6 months with complete eye exam and visual fields

43. Congenital Glaucoma • Onset of glaucoma from birth to 3 months of age • Incidence of 1 in 10,000 births • Three forms • 1/ 3 is Primary • 1/3 is Secondary • 1/3 associated with systemic syndromes or anomalies

44. Primary • Due to developmental abnormality of the angle with faulty cleavage and abnormal insertion of ciliary muscle • 70% bilateral • 65% male • Multifactorial inheritance

45. Syptoms: light sensitivity, tearing, and eventual opacification of the cornea • Signs: decreased visual acuity, myopia, amblyopia, increased IOP, corneal edema, corneal cloudiness, conjunctival injection • Treatment • Medical (temporary before surgery) with glaucoma eye drops • Surgical • Correct any refractive error • Patching or occlusion therapy for amblyopia

46. Other forms • Secondary • Due to inflammation, trauma, tumors • Can be steroid induced, lens inducted • Associated syndromes • Sturge-Weber syndrome • Neurofibromatosis • Marfan’s • Aniridia • Rubella

48. Works Cited • Friedman, Neil J. MD and Peter K. Kaiser, MD. The Massachusetts Eye and Ear Infirmary; Illustrated Maual of Ophthalmology. 3rd ed. Elsevier Inc, 2009. • Rosenberg, Eric A. MD, and Laura C. Sperazza, OD. “The Visually Impaired Patient.” American Family Physician 15 May 2008. • Distelhorst, James S. MD, and Grady M. Hughes, M.D. “Open-Angle Glaucoma.” American Family Physician 1 May 2003. • Pokhrel, Prabhat K. MD and Sanaz A. Loftus, MD. “Ocular Emergencies.” American Family Physician 15 Sept. 2007. • Simon, John W., MD and Pamela Kaw, MD. “Commonly Missed Diagnoses in the Childhood Eye Exam.” American Family Physician 15 Aug. 2001.