_Glaucoma Talk pacEYES.pptx

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GLAUCOMA

Gary K Phelps MD

June 2012

Materials and illustrations used in this presentation were obtained from and used with the permission of:

• American Academy of Ophthalmology • Duane’s Ophthalmology

• Photographs by GK Phelps

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Glaucoma

Definition

Glaucoma is an acquired optic neuropathy characterized by:

1) excavation (cupping) of the optic nerve head with

thinning of the neuroretinal rim

2) with associated visual function (field defect) loss

•

Intraocular pressure is a primary risk factor

(5)

Epidemiology

•

The overall lifetime risk in the general population

is ~4%

•

Glaucoma is second only to cataract as cause of

blindness worldwide

•

Glaucoma is the leading cause of

irreversible

(6)

The Players

Optic Nerve

Visual Fields

(7)

Optic Nerve

•

A bundle of ~ 1,200,000 axons

heading from the retinal

ganglion cells to the lateral

geniculate nucleus

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There is an anatomic vertical

(8)

What Happens in Glaucoma?

•

Bundles of axons die

•

Corresponding

segments of the nerve

fiber layer disappear

•

Superior temporal and

(9)

Disc Appearance

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The optic disc atrophies

corresponding to the

nerve bundle loss

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This the superior and

inferior margins are

(10)

(11)

(12)

(13)

(14)

(15)

(16)

Visual Consequences

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As the nerve fibers

disappear, the areas of

the retina they supply are

disconnected

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This causes a

(17)

Arcuate Scotoma

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The area of retina

previously served by

the damaged axons is

no longer connected

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Thus a visual field

(18)

Paracentral Scotoma

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If a smaller number of

fibers are interrupted a

smaller area of retina is

disconnected

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A corresponding smaller

(19)

Intraocular Pressure ( IOP )

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The eye is an inflated sphere

•

There is no normal IOP

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Majority between 10 and 22 mm Hg

(20)

IOP Determinants

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Rate of aqueous production

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Resistance to outflow across

the trabecular meshwork

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Resistance to outflow across

the scleral spur and ciliary body

•

Episcleral venous pressure

(21)

Two Major Variants of Glaucoma

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Open Angle Glaucomas

•

Angle Closure Glaucomas

(22)

Open or Closed: how to tell?

(23)

•

Guess from the history?

(24)

•

Guess by how deep the anterior chamber looks?

(25)

•

Guess from the history?

•

Guess from the clinical picture?

(26)

•

Guess from the clinical picture?

(27)

Gonioscopy

(28)

Oddities of optics

• _{We cannot see directly into the chamber}

angle

• _{Light rays from the chamber angle are}

internally reflected so cannot get out

• _{A lens on the surface of the cornea}

eliminates the air interface so the light rays can get out of the eye

• _{Mirrors allow the image to be more easily}

(29)

Goniolenses

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Many types / variants

•

Clinical goniolenses have

(30)

Gonioscopy

(31)

Gonioscopy

In open angle syndromes Schwalbe’s line and the

trabecular meshwork are visible in the chamber angle

(32)

To Treat or Not to Treat

• _{Once a diagnosis of glaucoma has been made, the foremost decision in}

treatment of glaucoma is not how, but whether or not to treat

• _{This decision is relatively easy in the angle closure syndromes but much}

(33)

To Treat or Not to Treat

• _{The Ocular Hypertension Treatment Study (OHTS) and the European Glaucoma}

Prevention Study (EGPS) both verified that lowering IOP reduces the risk of progression of damage

• _{They also defined the high risk characteristics for progression to glaucoma and for}

progression of existing glaucoma:

• Higher IOP • Older age

• Larger vertical cup–disc diameter

• Greater pattern standard deviation on automated perimetry • Reduced central corneal thickness (CCT)

(34)

General Guidelines of

Treatment

(35)

General Guidelines of

Treatment

• _{The goals of glaucoma treatment are:}

(36)

Treatment

• Prevent further damage to the nerve fiber layer • Prevent or alleviate pain

(37)

Treatment

• Prevent further damage to the nerve fiber layer • Prevent or alleviate pain

• _{Approaches to achieve these goals are:}

• Reduce risk factors

• _{Treat any condition causing or aggravating the glaucoma}

• _{Lower IOP}

• _{Protect the nerve fiber layer from the risk factors present}

(38)

General Guidelines of

Treatment

• _{All glaucoma treatments have medical risks and both fiscal and social}

costs. Simply making the diagnosis can greatly alter a patients sense of well being and attitude towards life

• _{The risk of functional (real life) disability varies depending upon risk}

factors

• _{The threat posed by those risk factors then has to be weighed against the}

individual patient’s insight into their disease, expectations of treatment, overall health status, life expectancy, and likely compliance with a

treatment protocol

(39)

(40)

• _{Slowly progressive}

• _Painless

• _{“Sneak Thief of Sight”}

• _{Caused by an obstruction to}

aqueous outflow by an unknown mechanism

(41)

1ºOAG Risk Factors

• _{Intraocular pressure}

• _{IOP increasing over time}

• _{IOP fluctuating throughout the day}

• _{Family history of glaucoma}

• _{Increased vertical cup to disc ratio}

• _{Increasing age}

• _{Central Corneal Thickness}

• _{Thinner corneas at higher risk}

(42)

1ºOAG Treatment

• _{All treatments are designed to lower the intraocular pressure}

• _{We dwell on the intraocular pressure because we:}

• _{Can’t change our age}

• _{Can’t change the thickness of our cornea}

• _{Can’t change our race}

• _{Can’t change our family history}

(43)

Medications

(44)

Prostaglandin analogs

Latanoprost 0.005% (Xalatan®) Travoprost 0.004% (Travatan® Z)

Bimatoprost 0.01% & 0.03% (Lumigan®)

Unoprostone isopropyl 0.125% (Rescula®)

• _{Prostaglandin analogs work by increasing uveoscleral outflow.}

• _{They reduce IOP by 25%–32%.}

• _{Because they reach peak effect in 10–14 hours, once a day dosage at bedtime is}

recommended to both maximize efficacy and decrease patient symptoms related to vascular dilation

• _{They have a fairly low side effect profile}

(45)

β-adrenergic antagonists

Betaxolol 0.25% & 0.5% (Betoptic® S) Levobunolol 0.25% & 0.5% (Betagan®) Metipranolol 0.3% (OptiPranolol®)

Timolol maleate 0.25 & 0.5% (Timoptic® &Timoptic-XE® gel) Timolol hemihydrate 0.25% & 0.5% (Betimol®)

• Topical β-adrenergic antagonists lower IOP by reducing aqueous secretion by inhibition of cyclic adenosine monophosphate (cAMP) in ciliary epithelium

• IOP reduction is in the range of 20%–30%

• The effect of β-blockers occurs within 1 hour of instillation and can be present for up to 4 weeks after discontinuation

(46)

β-adrenergic antagonists

• _{Side effects are primarily due to systemic absorption and include:}

• Bronchospasm • Bradycardia

• Increased heart block • Lowered blood pressure

• _{Although selective β1 antagonist, betaxolol, is somewhat less effective than the}

nonselective β-adrenergic antagonists in lowering IOP, it may be a safer alternative in patients with asthma or cardiac arrhythmias

(47)

Parasympathomimetic (miotic) agents

Pilocarpine 0.2 – 10.0%

Carbachol (Miostat)1%

• _{Miotics increase aqueous outflow by contraction of the ciliary muscle which pulls}

the scleral spur which in turn tightens the trabecular meshwork

• _{Miotic agents can reduce IOP by 15%–25%.}

• _{As miotics require Q6H dosage and have a high side effect profile they are very}

poorly tolerated and are infrequently used anymore. Their only saving grace is that they are extremely cheap.

• _{Their use is limited largely to in office miosis prior to laser procedures or for short}

term prophylaxis for pupillary block glaucoma.

(48)

Adrenergic agonists

Apraclonidine HCI 0.5%, 1% (Iopidine®)

Brimonidine tartrate 0.1%, 0.15% (Alphagan® P)

• _{They decrease aqueous production and improve both trabecular and}

uveoscleral outflow

• _{IOP reduction is 25% at two hours but drops by half at 12 hours}

• _{Although approved for TID dosage, they are commonly used BID.}

• _{Apraclonidine (Iopidine) when administered preoperatively and}

postoperatively diminishes the acute IOP rise that follows laser procedures

(49)

Carbonic anhydrase inhibitors

Acetatolamide 65mg, 125mg 250 mg (Diamox®)

Brinzolamide ophthalmic suspension 1% (Azopt™) Dorzolamide HCI 2% (Trusopt®)

• _{CAIs decrease aqueous humor formation by direct antagonist activity on ciliary}

epithelial carbonic anhydrase

• _{Onset of action of oral CAI’s is within one hour with maximum effect in 2-4 hours}

• _{IV acetazolamide onset of action is within 2 minutes of administration with peak}

effect reached within15 minutes

• _{Acetazolamide duration of action is limited to 6 hours thus frequent dosing}

necessary

(50)

Carbonic anhydrase inhibitors

• _{CAIs are sulfa compounds thus are not used in patients with sulfa allergies}

• _{Fatigue, loss of appetite, tingling of lips and extremities, and a metallic taste are}

universal side

• _{Potassium loss (hypokalemia) risking cardiac events and acidic urine leading to}

calcium stones are common

• _{This constellation of side effects limits CIAs to short term usage}

(51)

Placing laser burns to the trabecular meshwork

ALT: small argon burns coagulate full thickness trabecular meshwork SLT: frequency doubled Nd:YAG laser selectively targets only the

pigmented cells preserving most of the trabecular structure

Achieves roughly the same IOP lowering effect as one topical medication

(52)

Cycloablation

Transscleral destruction of the ciliary body

Can be accomplished by cryopexy or diode laser

(53)

Filter ( Trabeculectomy )

Filters entail creating a surgical fistula through the coats of the eye Multiple variations described over the years

(54)

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• _{Many ophthalmic syndromes are}

associated with an open angle glaucoma

• Pigmentary dispersion • Pseudoexfoliation

• Steroid induced

• Photolytic (TM obstruction by absorbing lens material)

• Inflammatory based

• _Uveitis

• _{Phacoantigenic (sensitivity}

to retained lens material)

• Elevated episcleral venous pressure

(56)

• _{Initial treatment is directed at}

the underlying cause

• Cease steroids

• Suppress inflammation • Remove lens material

• _{After treating underlying the}

underlying disease, the

treatment becomes the same as for primary open angle glaucoma

(57)

Angle Closure “Glaucoma”

(58)

Acute Angle Closure

(Pupillary Block) Glaucoma

• _{Can be a relative or a complete}

blockage of flow through the pupil

• _{Acute onset}

• _{Blurred vision}

• _Halos

• _Pain

(59)

Treatment

• _Recognize!

• _{Treatment is to create new hole}

in the iris to bypass the pupillary blockage

• YAG or Argon laser iridotomy

(60)

Primary Angle Closure

• _{Slow sealing of angle without an}

acute pupillary block

• _{It is the most common form of}

glaucoma in the Asian population

• _{Slow gradual onset and}

(61)

Treatment

• _Recognize!

• _{Iridectomy will convert ~50% to}

an open angle and a lower IOP

• _{Laser iridoplasty will help if}

there is a steep angle to an otherwise open angle (plateau iris)

• _{If laser iris treatment fails, the}

(62)

Secondary Angle Closure

• _{A number of disorders can lead to a}

secondary angle closure without pupillary block

• Neovascular (rubeotic) • Iridocorneal Endothelial

Syndrome (ICE)

(63)

Treatment

• _{Initial treatment is directed at}

the underlying cause

• PRP for rubeosis

• Suppress any inflammation

• _{After treating underlying the}

underlying disease, the

(64)

Subtypes of Glaucomas

We now have the tools to review

some of the various specific

subtypes of the major forms of

(65)

Open Angle Glaucomas

• Primary Open-Angle Glaucoma

• Normal Tension Glaucoma

• Ocular Hypertension

• Juvenile Primary Open-Angle Glaucoma

• Pigmentary Dispersion Syndrome

• Exfoliation Syndrome

• Steroid-Induced Glaucoma

• Elevated Episcleral Venous Pressure Glaucoma

• Uveitis Associated with Joint diseases

– HLA-B27 Associated diseases

• Ankylosing spondylitis

• Reiter syndrome

• Psoriatic

– Juvenile rheumatoid arthritis

• Uveitis associated with infectious diseases

– Herpes simplex keratouveitis

– Herpes zooster keratouveitis

– Congenital rubella

– Leprosy

– Syphilis

– Cytomegalic inclusion retinitis

– Toxocariasis

– Meningococcal endopohthalmitis

– Mumps

– Nephropathia epidemica

– Onchocerciasis

– Toxoplasmosis

– Coccidioidomycosos

• Uvietis addciated with Other disorders

– Fuchs Heterochromic iridocyclitis

– Glaucomatocyclitic crisis

– Sarcoidosis

– Voght-Koyanagi-Harada syndrome

– Sympathetic opohthalmia Bechets disease

– Pars Planitis

– Phakolytic uveitis

(66)

Angle Closure Glaucomas

• Primary – Acute – Intermittent – Chronic • Secondary

– Ectopia lentis

– Phacomorphic

– Microspherophakia

– Captured IOL

– Captured vitreous face

– Central posterior synechiae

– Fuchs corneal dystrophy

• Iris displaced forward

– Plateau iris syndrome

– Aqueous misdirection

– Ciliary body swelling or rotation

– Tumor

– Iris cysts

– Suprachoroidal hemorrhage

– Retinal detachment (non-rhegmatogenous)

• Iris pulled forward

– Neovasculariztion

• Diabetic

• Vascular ischemic

– ICE syndromes

• Chandler syndrome

• Essential iris atropohy

• Iris-nevus syndrome

– Posterior polymorphous corneal dystrophy

– After flat anterior chamber

– Epithelial downgrowth

– Fibrous downgrowth

• Iris splitting

(67)

Glaucomas of Childhood

• Axenfield-Rieger Syndrome

• Iris Hypoplasia

• Peters Anomaly

• Aniridia

• Phakomatoses

– Sturge-Weber Syndrome

– Neuorfibromatosis

– Nevus of Ota

• Juvenile Primary Open-Angle glaucoma

• Aphakia

• Colobomata

• Cornea plana

• Ectopia lentis (simple)

• Ectopia lentis et pupillae

• Iris hypoplasia

• Lenticonus • Lentiglobus • Megalocornea • Microcornea • Microphthalmos • Microspherophakia

• Retinopathy of prematurity

• Sclerocornea

• Spherophakia

• Patau syndrome

• Edward syndrome

• Down syndrome

• Cockayne syndrome

• Cystinosis

• Fetal Alcohol syndrome

• zHallermann-Streiff syndrome

• Homocystinuria

• Lowe syndrome

• Marfan syndrome

• Michel syndrome

• Von Recklinhausen syndrome

• Oculodental dysplasia

• Nevus of Ota

• zPrader-Willi syndrome

• Refsum syndrome

• Rubenstein -Taybi syndrome

• Stickler syndrome

• Weill - Marchesani syndrome

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Good News

Winner gets a bottle of (cheap) Australian wine

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Pop Quiz !!!

1. Define Glaucoma

(72)

Tie Breaker

1. Define Glaucoma

2. What is the normal IOP?

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Etymology

•

From the Greek

Glaukos

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“gleaming, silvery”

•

Homer’s

glauk-opis Athene

was a “bright

eyed” or “gray-eyed” goddess

•

Greek for “owl” was

glauk

– from its bright,

staring eyes.

•

Before 1700 cataract and glaucoma were