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Glaucoma PowerPoint PPT Presentation

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Glaucoma. Manasa Manapragada PGY-2. 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. Case . On physical exam:

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Glaucoma l.jpg


Manasa Manapragada


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  • 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

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  • On physical exam:

    • Left pupil was dilated and fixed

    • Left conjunctiva was injected

    • Pain was present with EOM

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What does the patient have????

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  • 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

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  • 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

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Types of glaucoma

  • Congenital

  • Open-angle glaucoma

    • Primary

    • Secondary

  • Closed-angle glaucoma

  • Normal (low) tension glaucoma

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  • Glaucoma is an optic nerve disease

  • It is often associated with elevated intraocular pressure

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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

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  • 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.

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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%)

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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

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  • 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

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  • 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

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  • Direct fundoscopic exam

  • Tonometry

  • Visual field testing

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  • 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

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  • 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

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  • 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

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  • 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

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  • 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

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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.

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  • Blurred vision

  • Eye redness

  • Frontal HA

  • Severe eye pain

  • Colored halos around lights

  • Nausea

  • Vomiting

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  • IOP>30

  • Mid-dilated pupil (4-6 mm)

  • Sluggish reaction of pupil to direct illumination

  • A shallow anterior chamber

  • Hazy cornea

  • Hyperemic conjunctiva

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  • 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

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  • 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

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  • 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.

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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

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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

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  • 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

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  • Treat increased IOP

  • Laser trabeculoplasty is usually not effective

  • May require trabeculectomy or glaucoma drainage implant to lower pressure adequately

  • Treat underlying problem

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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

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  • 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

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  • Topical glaucoma medications

  • FU ever 6 months with complete eye exam and visual fields

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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

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  • Due to developmental abnormality of the angle with faulty cleavage and abnormal insertion of ciliary muscle

  • 70% bilateral

  • 65% male

  • Multifactorial inheritance

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  • 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

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Other forms

  • Secondary

    • Due to inflammation, trauma, tumors

    • Can be steroid induced, lens inducted

  • Associated syndromes

    • Sturge-Weber syndrome

    • Neurofibromatosis

    • Marfan’s

    • Aniridia

    • Rubella

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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.

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