Glaucoma

GLAUCOMAGLAUCOMA

GERARDO P. CINCO, M.D., DPBOGERARDO P. CINCO, M.D., DPBO

GlaucomaGlaucoma

• Refers to a group of diseases that have in common a characteristic optic neuropathy with associated visual field loss for which elevated intraocular pressure is one of the primary risk factor.

• 3 key words: IOP

Optic N

Visual field loss

Definitions:Definitions:

• Primary glaucoma- not associated with known ocular or systemic disorders- usually affects both eyes and may be inherited.

• Secondary glaucoma- associated with ocular or systemic disorders responsible for decreased aqueous outflow- often unilateral and familial occurrence is less common

• Ocular HPN - Normal optic disc and visual field associated with elevated IOP

• Glaucoma suspect- Suspicious optic disc and/or visual field with normal IOP

• Normal tension glaucoma - Optic N damage and visual field loss associated with normal IOP

What is Intraocular Pressure?What is Intraocular Pressure?

• IOP is the fluid pressure inside the eye.

Aqueous production and outflowAqueous production and outflow

• The aqueous humor is actively secreted by the non- pigmented ciliary epithelium.

• Two different exit routes

a. Trabecular route

b. Uveoscleral route

Two exits route of aqueousTwo exits route of aqueous

• I. Trabecular route

- most of the aqueous exits the eye through the trabecular meshwork into Schlemm canal and is then drained by the episcleral veins

- accounts for approximately 90% of aqueous outflow

- 3 zones of trabecular meshwork

1. uveal

2. corneoscleral

3. juxtacanalicular where the primary resistance to outflow occurs

Two exits route of aqueousTwo exits route of aqueous

• II. Uveoscleral route

- accounts for the remaining 10% of aqueous outflow

- from the anterior chamber it flows into the ciliary muscle and then into the supraciliary and suprachoroidal spaces. The fluid then exits the eye

through the intact sclera or along the nerves.

GlaucomaGlaucoma

• 3 factors determine the IOP

1. The rate of aqueous humor production by the ciliary

body.

2. Resistance to aqueous outflow across the trabecular

meshwork-Schlemm’s canal system.

3. The level of episcleral venous pressure

How to measure IOP? Or what method to How to measure IOP? Or what method to measure IOP?measure IOP?

• Tonometry is the objective measurement of IOP, based, most commonly, on the force required to flatten the cornea, or the degree of corneal indentation produced by a fixed force

• Tonometer – instrument to measure IOP• 2 methods

1. Schiotz tonometry2. Goldmann applanation tonometry

• 2 methods 1. Schiotz tonometer relies on the principle of indentation tonometry in which a plunger with a pre-set weight indents the cornea. The amount of indentation is measured on a scale and the reading is converted into millimeters of mercury on a specific table.- cheap and easy to use but less accurate because it is affected by the patient’s scleral rigidity

2 methods to determine IOP2 methods to determine IOP

2. Goldmann applanation tonometry is based on the Imbert-Fick principle, which states that for an ideal dry thin walled sphere, the pressure inside the sphere (P) equals the force necessary to flatten its surface (F) divided by the area of flattening (A) ( P= F/A). The IOP is proportional to the pressure applied to the globe and the thickness of the walls of the globe.

- Very accurate because it flattens a small area of the central cornea which has a diameter of 3.06mm

What is a normal IOP?What is a normal IOP?

• Normal IOP: 11-21mmhg

What is the effect of a high IOP on the What is the effect of a high IOP on the optic nerve?optic nerve?

• 2 theories

a. Ischemic theory

b. Direct mechanical theory

Optic NerveOptic Nerve

• 3 groups of nerve fiber bundle

1. Papilllomacular bundle – most resistant

2. Superior and inferior arcuate nerve fiber

bundle – most vulnerable

3. Nasal nerve fiber bundle

• 1.2 million nerve fibers

Examination and Clinical Evaluation of Examination and Clinical Evaluation of the Optic Nerve Headthe Optic Nerve Head

• Direct ophthalmoscope Indirect ophthalmoscope Slit lamp combined w a 70 or 90 diopter lens.• N optic disc: shape- round or slightly oval • neural rim has a uniform width• color ranges from orange to pink normal vertical cup:disc ratio is 0.3 or less• Myopes have larger eyes and larger discs and cups than

emmetropes and hyperopes. • Photograph is the best record of the optic disc. This

record allows the examiner to compare the present status of the patient to the baseline status

Examination and Clinical Evaluation of Examination and Clinical Evaluation of the Optic Nerve Headthe Optic Nerve Head

• Early changes of glaucomatous optic neuropathy– Generalized enlargement of the cup– Focal enlargement of the cup– Superficial splinter hemorrhage– Loss of nerve fiber layer– Asymmetry of cupping between the patient’s two eyes

What test to determine or measure the What test to determine or measure the visual function?visual function?

• Perimetry

- measurement of visual function in the

central field of vision

- most useful in the diagnosis of early glaucoma

and in documenting the control or the

progression of the disease

- the visual field defect is usually proportionate to

the severity of the optic N atrophy

Visual Field Visual Field

• Perimetry – the measurement of the visual field

- types of perimetry

1. kinetic perimetry - a target is moved from

a non seeing to a seeing area, and the

patient signals when it is perceived

2. Static perimetry - a stationary stimulus is

presented at various locations. The

intensity and duration of the stimulus can

be varied at each location to determine

the threshold.

Visual Field Visual Field

• Harry Moss Traquair describes Visual field as an island

hill of vision in a sea of darkness

Patterns of Glaucomatous Nerve LossPatterns of Glaucomatous Nerve Loss

• The pattern of nerve fibers in the retinal area served by the damaged nerve fiber bundle will correspond to the specific defect.

• The typical glaucomatous defects:

1. Paracentral scotoma

2. Arcuate or bjerrum scotoma

3. Nasal step

4. Temporal wedge

Glaucoma that is far advanced may leave merely a central island of vision.

GlaucomaGlaucoma

• Two types

a. open-angle

b. angle closure

GlaucomaGlaucoma

• Open angle glaucoma

- the aqueous humor has free access to

the trabecular meshwork• Angle closure glaucoma

- the peripheral iris is in contact with the

cornea or the trabecular meshwork and

impairs the outflow of the aqueous humor

from the anterior chamber

How to examine the angle of the anterior How to examine the angle of the anterior chamber?chamber?

• Gonioscopy is examination of the angle of the anterior chamber ( the angle between the posterior corneal surface and the anterior surface of the iris)

• It is especially important in the evaluation of glaucoma to determine if the angle is closed or open.

• goniolens : goldmann three-mirror, zeis, or koeppe

Methods of ExaminationMethods of Examination

• Tonometry

• Gonioscopy

• Ophthalmoscopy

• Perimetry

Primary Open angle glaucomaPrimary Open angle glaucoma

• chronic, slowly progressive optic neuropathy characterized by atrophy and cupping of the optic nerve head and associated with characteristic patterns of visual field loss.

• IOP is an important risk factor• Epidemiology

- the most common type of glaucoma in the U.S

- prevalence rate ranges from 1.3 to 2.1% in general population 40 years of age or older.

- blacks are affected more frequently than are whites

Primary Open Angle GlaucomaPrimary Open Angle Glaucoma

• Clinical features:

Symptoms: asymptomatic until significant loss of visual

field has occurred.

Signs: 1. IOP > 21mmhg

2. An open angle of normal appearance

3. Glaucomatous optic N head damage

4. visual field loss


• Risk factors and associations

1. Age – common in older individuals

2. Race – more common in black people

3. Family history and inheritance

4. Myopia

5. Retinal disease like CRVO


• Pathogenesis of glaucomatous damage Trabecular meshwork – resist the aqueous outflow - increase IOP

- 2 theories

1. Ischemic theory

2. Direct mechanical theory

Primary Open Angle GlaucomaPrimary Open Angle Glaucoma• Management:

Goal: to preserve visual function by lowering IOP below

a level that is likely to produce further damage to

the optic nerve

1. Medical therapy

- Ideal drug: fewest side effects, least disruption of patient’s life and effective in its lowest concentrations

- Initial treatment usually with one drug.

2. Surgery : Trabeculectomy, Laser trabeculoplasty

Primary Angle Closure GlaucomaPrimary Angle Closure Glaucoma

- a condition in which elevation of IOP occurs as a result

of obstruction of outflow by partial or complete closure

of the angle by the peripheral iris.- frequently bilateral although presentation of the acute

form is often unilateral.- anatomical predisposing factors:

1. relatively anterior location of the iris-lens diaphragm

2. shallow anterior chamber

3. narrow entrance to the chamber angle

Primary Angle Closure GlaucomaPrimary Angle Closure Glaucoma

• Risk factors

1. age- the ave. age is 60 years,

2. gender – females are more commonly affected

3. race - more common in South-East Asians, Chinese and Eskinos

4. Family history – first degree relatives are at increased risk because predisposing

anatomical factors are often inherited

PACG with pupillary blockPACG with pupillary block

• Classification

1. Latent

2. Subacute ( Intermittent )

3. Acute congestive

4. Chronic

5. Absolute – end stage of glaucoma in which the eye is completely blind.

Latent Angle Closure GlaucomaLatent Angle Closure Glaucoma

• Clinical features

1. symptoms are absent.

2. Slit lamp biomicroscopy

- Axial AC depth is less than normal.

- convex-shaped iris-lens diaphram

- close proximity of the iris to the cornea

3. Gonioscopy shows an occludable angle

4. Clinical course without treatment

IOP may remain normal

Acute or subacute angle closure may develop

Chr. Angle closure may develop w/o passing through subacute or acute stages.

Latent Angle Closure GlaucomaLatent Angle Closure Glaucoma

• Treatment

- pophylactic laser iridotomy

Subacute Angle Closure GlaucomaSubacute Angle Closure Glaucoma

• a condition characterized by episodes of blurred vision, halos around lights, and mild pain caused by elevated IOP.

• These symptoms resolve spontaneously especially during sleep or by physiological miosis ( exposure to bright sunlight.)

• IOP is usually normal between episodes .• This condition can progress to acute or chronic angle

closure glaucoma• Treatment: prophylactic LI

Acute Congestive Angle Closure GlaucomaAcute Congestive Angle Closure Glaucoma

• A condition that occurs when IOP rises rapidly as a result of relatively sudden blockage of the trabecular meshwork by the iris.

• Symptoms: pain

blurred vision

rainbow-colored halos around lights

nausea and vomiting


• Signs: high IOP,

middilated, sluggish, and often irregular pupil

corneal epithelial edema

congested episcleral and conjunctival blood vessels

shallow anterior chamber


• Management:

Initial treatment- to lower IOP

Definitive tx – laser iridotomy - < 180 degree angle closed

trabeculectomy - if LI failed and angle

totally closed

Prophylactic LI on the fellow eye

Chronic Angle Closure GlaucomaChronic Angle Closure Glaucoma

• A condition that may develop either after acute angle closure glaucoma or when the angle closes gradually and IOP rises slowly.

• Permanent peripheral anterior synechiae may or may not be present.

• The clinical course resembles that of open angle glaucoma in its lack of symptoms, modest elevation of IOP, progressive cupping of the optic nerve head and characteristic visual field loss

• Gonioscopic examination – to determine the correct diagnosis

Chronic Angle Closure GlaucomaChronic Angle Closure Glaucoma

• Management:

Initial – medical

Definitive - depends on gonioscopic findings:

if angle partially closed, LI

if angle is totally closed with permanent peripheral anterior synechiae,

Trabeculectomy

Primary Congenital Glaucoma Primary Congenital Glaucoma (PCG)(PCG)

• Most common of the congenital glaucoma but still very rare condition

• 1:10,000 births

• 65% - boys

• Autosomal recessive

Pathogenesis of PCGPathogenesis of PCG

Maldevelopment of the angle of the anterior

chamber ( Trabeculodysgenesis )

impaired aqueous outflow

Classification of PCGClassification of PCG

• True Congenital Glaucoma- increase IOP during intrauterine life

• Infantile glaucomaglaucoma before the 3 y/o

• Juvenile glaucoma - least common- glaucoma after the 3y/o but before

age of 16

Clinical Features of PCGClinical Features of PCG

1. Corneal Haze

- 1st sign

- caused by epithelial and stromal edema

- associated with lacrimation, photophobia and blepharospasm

2. Buphthalmos

- large eye as a result of stretching due to elevated IOP before

age of 3

3. Haab striae

- healed breaks of the Descemet membrane

4. Optic disc cupping

- may regress once the IOP is normalized

Differential DiagnosisDifferential Diagnosis

• Cloudy cornea at birth- causes: birth trauma, intrauterine rubella infection

• Congenital large cornea (megalocornea)• Lacrimation

- due to delayed canalization of the

nasolacrimal duct

• Secondary Infantile Glaucoma

- causes: tumors, trauma, ROP, Ectopia lentis

Management PCGManagement PCG

• Initial Evaluation- under GA using IV ketamine- Examination:

1. Optic discs exam

2. IOP measurement

3. Corneal diameter measurement

4. Gonioscopy

Management PCGManagement PCG

• Surgery

1. Goniotomy

2. Trabeculotomy

3. Trabeculectomy

Neovascular GlaucomaNeovascular Glaucoma

• occurs as a result of iris neovascularization• 3 stages: 1. Rubeosis iridis

- presence of new vessels at the pupillary margin

- IOP normal

2. Secondary open angle glaucoma

- presence of fibrovascular membrane covering the trabecular meshwork

- high IOP

Neovascular GlaucomaNeovascular Glaucoma

• stages: 3. Secondary angle closure glaucoma

- caused by contraction of fibrovascular tissue

in the angle with pulling of the peripheral iris over the trabeculum

• Causes: Ischemic CRVO

PDR

Carotid Obstructive disease

Lens-Induced GlaucomaLens-Induced Glaucoma

• Phacolytic glaucoma• Phacomorphic glaucoma

Phacolytic GlaucomaPhacolytic Glaucoma

• Secondary open angle glaucoma• occurs in pt with hypermature cataract• Pathogenesis:

Trabecular obstruction caused by high- molecular-weight lens proteins


• Clinical features

symptoms: Eye pain, one sided HA

signs: Cornea edematous

anterior chamber deep

conjunctival injection

hypermature cataract

high IOP

open angle


• Mgt: Initial – medical

Definitive- cataract surgery

Phacomorphic GlaucomaPhacomorphic Glaucoma

• Acute secondary angle-closure glaucoma precipitated by an intumescent cataractous lens

• Presentation similar to acute PACG• Mgt: initial: medical

definitive: cataract surgery

Anti- Glaucoma DrugsAnti- Glaucoma Drugs

• Beta blockers• Alpha-2 agonists• Prostaglandin analogues• Miotics• Topical carbonic anhydrase inhibitors• Combined topical preparations• Systemic carbonic anhydrase inhibitors• Hyperosmotic agents

Anti-Glaucoma DrugsAnti-Glaucoma Drugs

• A. Beta-blockers

– reduce IOP by decreasing aqueous secretion

- 1. non-selective – equipotent at beta 1 and beta 2 receptors

2. cardioselective – more potent at beta-1

receptors

- Drugs: Timolol, Betaxolol, Levobunolol, Carteolol

Metipranolol

- Contraindications: Asthma, COPD, CHF Bradycardia


• B. Alpha-2 agonists

- decrease IOP by both decreasing aqueous secretion and enhancing uveoscleral outflow

- Drugs: Brimonidine, Apraclonidine

C. Prostaglandin analogues

- reduce IOP by enhancing uveoscleral outflow

- Drugs: Latanoprost, Travoprost, Bimatoprost

Unoprostone


• D. Miotics

- Parasympathomimetic drugs that act by stimulating muscarinic receptors in the sphincter pupillae

and ciliary body.

- In POAG, miotics reduce IOP by contraction of the ciliary muscle, which increases the facility of aqueous outflow through the trabecular meshwork.

- In PACG, contraction of the sphincter pupillae and the resultant miosis pulls the peripheral iris away from the trabeculum, thus opening the angle.

-Drug: Pilocarpine


• E. Topical carbonic anhydrase inhibitors

- lower IOP by inhibiting aqueous secretion

- Drugs: Dorzolamide, Brinzolamide

F. Combined Topical Preparations

- Drugs: Cosopt ( timolol + dorzolamide )

Xalacom ( timolol + Latanoprost )


• G. Systemic carbonic anhydrase inhibitors

- useful as short treatment

- Preparations: Acetazolamide tab 250mg

Dichlorphenamide tab 50mg

Methazolamide tab 5omg

- Systemic side effects: Paresthesia , malaise, renal stone formation GI complex,

Steven-

Johnson syndrome, blood dsycrasias


• H. Hyperosmotic agents– lower the IOP by creating an osmotic gradient between blood

and vitreous so that water is drawn out from the vitreous. The higher this gradient the greater the reduction of IOP.

- Preparations:

Mannitol – most widely used

Isosorbide

Glycerol

Glaucoma

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