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GLAUCOM

A

DEFINITION OF GLAUCOMA

Glaucoma is an optic disc neuropathy which is characterized by:

High intra ocular pressure (IOP) > 21 mmHg,

Optic nerve fibers death optic disc damage, Progressive visual field defect,

  • Glaucoma is the most common cause of blindness worldwide and is the second major cause of blindness in Indonesia

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INCIDENCE

Primary glaucoma is:

hereditary

female > male

especially at age > 40 years

INCIDENCE

Congenital glaucoma Infantile glaucoma Juvenile glaucoma

since in the intrauterine after birth until 2 years age 10 - 15 years

Secondary glaucoma: glaucoma as a complication from other eye disease

AQUEOUS HUMOR SECRETION

80% is secreted by non pigmented ciliary epithelium via active metabolic process that depends on a number of enzymatic systems (carbonic anhydrase enzyme),

20% is produced by passive processes as ultrafiltration and diffusion.

AQUEOUS OUTFLOW

AH fills posterior chamber

  • pupil

AQUEOUS OUTFLOW AH fills posterior chamber pupil anterior chamber uveoscleral route (10%) ciliary body 90 %

anterior chamber

AQUEOUS OUTFLOW AH fills posterior chamber pupil anterior chamber uveoscleral route (10%) ciliary body 90 %

uveoscleral route (10%)

AQUEOUS OUTFLOW AH fills posterior chamber pupil anterior chamber uveoscleral route (10%) ciliary body 90 %

ciliary body

90 %
90 %

Trabecular route

AQUEOUS OUTFLOW AH fills posterior chamber pupil anterior chamber uveoscleral route (10%) ciliary body 90 %

Schlemm’s canal

AQUEOUS OUTFLOW AH fills posterior chamber pupil anterior chamber uveoscleral route (10%) ciliary body 90 %

suprachoroidal space

AQUEOUS OUTFLOW AH fills posterior chamber pupil anterior chamber uveoscleral route (10%) ciliary body 90 %

leaves the eye through episcleral vein

venous system in the ciliary body

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AQUEOUS

OUTFLOW

  • a. Uveal meshwork

  • b. Corneoscleral meshwork

  • c. Schwalbe’s line

  • d. Schlemm’s canal

  • e. Collector channels

  • f. Ciliary body

  • g. Scleral spur

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AQUEOUS OUTFLOWS, INFLUENCED BY:

High intra ocular pressure (IOP), High episcleral pressure, Aqueous viscosity: exudate, blood cell, Ciliary block, pupillary block, posterior synechia, Narrow / closed anterior chamber angle, Narrowing of trabecular meshwork pore, Macrophage, lens cell at the trabecular meshwork.

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TRABECULAR

MESHWORK

• • • • Descemet membrane Sclera Iris Ciliary body
Descemet membrane
Sclera
Iris
Ciliary body

The TM is located at the anterior chamber angle, which consists:

Schwalbe’s line scleral spur iris processus angle recess

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INTRA OCULAR PRESSURE (IOP)

Normal IOP < 21 mm Hg, IOP > 21 mm Hg glaucoma suspect, Diurnal fluctuation of IOP in 24 hours:

IOP higher in the morning

IOP lower in the afternoon and evening

Ocular hypertension: IOP > 21 mmHg without any nerve fiber damage,

Normal tension glaucoma: normal IOP, but presenting glaucomatous signs.

PATHOGENESIS OF GLAUCOMATOUS DAMAGE

There are two current theories:

The indirect ischaemic theory: IOP » -- nerve fiber death + interfering micro

circulation of the optic disc, Direct mechanical theory: IOP » -- damage on retinal nerve fiber at the optic disc.

CLASSIFICATION OF THE GLAUCOMAS

According to:

Outflow impairment: open angle and angle closure glaucoma,

contributing factors to IOP : primary and secondary glaucoma,

Age: congenital, infantile, juvenile, adult.

PRIMARY GLAUCOMAS

High IOP is not associated with any ocular disorder

Open angle

Angle closure

Congenital (developmental)

SECONDARY

GLAUCOMA

Aqueous outflow alters by ocular / non ocular disorders IOP » :

Secondary open angle glaucoma: pretrabecular, trabecular and post-trabecular,

Secondary angle closure glaucoma caused by apposition between the peripheral iris and trabeculum,

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Pathogenesis: anterior forces / posterior forces

TONOMETRY

Two main methods of measuring IOP:

 

applanation force to flatten the cornea

indentation force to indent the cornea

The main types of tonometer:

The Schiotz tonometer uses a plunger with a preset weight to indent the cornea. The amount of indentation is converted into mmHg by use of Friedenwald tables.

TONOMETRY

The main types of tonometer:

Goldmann tonometer consists of double prism with 3.06 mm in diameter, applanation, more accurate,

Perkins tonometer, hand held, applanation,

The air puff tonometer, non contact, applanation, jet of air to flatten the cornea.

Tono-pen

Gas Tonometer

Electrical Tonometer

SCHIOTZ TONOMETER

  • Portable, simple, low cost,

  • Measure the depth of indentation of cornea by a plunger with specific weight (5 gr; 7,5 gr ; 10 gr)

  • The indentation represented in Schiotz scale is converted into mmHg by Freidenwald table,

  • Low accuracy because it is influenced by ocular rigidity (high myop, DM, corneal leucoma).

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GOLDMANN’S APPLANATION TONOMETER • More accurate, not influenced by ocular rigidity • The foot plate is

GOLDMANN’S APPLANATION TONOMETER

More accurate, not influenced by ocular rigidity

The foot plate is smaller (3.06 mm)

Disadvantages: cannot be applied to

Corneal edema

Keratitis, corneal ulcer

Keratokonus

High astigmatism

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TONOGRAPHY

To estimate outflow facility of HA,

Principle: to express the fluid flow from the eye by continuous pressing to the eye

Place Schiotz tonometer for 2-4 minutes,

Compare IOP at 0 to 4 minutes outflow facility (C),

Normal C > 0.18.

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PROVOCATION TEST

Water drinking test, dark room test, midriatic test, steroid test,

Positive if IOP at the end of the tests are more than 8 mmHg,

Indications:

Narrow / closed angle glaucoma

Normal tension glaucoma

Bias IOP

GONIOSCOPY

Three main purposes of gonioscopy:

GONIOSCOPY • Three main purposes of gonioscopy: • To Identify the abnormal angle structure, • To

To Identify the abnormal angle structure,

To Estimate the width of the chamber angle,

To Visualize the angle during these following procedures: goniotomy, laser trabeculoplasty.

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IDENTIFICATION OF ANGLE STRUCTURES

Trabecular meshwork has a ground glass

appearance stretching from Schwalbe’s line to scleral

Schwalbe’s line (an opaque line) is a peripheral

termination of Descemet membrane,

spur.

Consists of two parts:

The anterior: nonfunctional, non pigmented

part, whitish color,

The posterior: functional, pigmented part,

greyish-blue translucent.

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IDENTIFICATION OF ANGLE STRUCTURES

Schlemm’s canal: slightly darker line,

behind the posterior trabeculum,

Scleral spurs: anterior of sclera, narrow, dense, often

Ciliary body stands behind the scleral spur as dull

shiny, whitish band. As a landmark for laser

trabeculoplasty.

brown band. The width depends on iris insertion.

Curve of the corner at the margin of the ciliary body

Iris processes

Iris processes, small extension of the anterior surface

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of the iris, inserted at the level of scleral spur.

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ANGLE CLASSIFICATION BY SHAFFER

Grade IV: 45 degrees angle

III

: 20 - 25 degrees angle

 

II : 20 degrees angle closed

I

: 10 degrees angle closed

Grade 0 : closed angle, iridocorneal contact.

OPHTHALMOSCOPY OF THE OPTIC DISC

1.2 million axons passes across the retina and enter the

optic disc,

Fibers from the macula papillomacular bundle, straight

to the optic disc, most resistant,

Fibers from temporal of macula an arcuate path around

the papillomacular bundle supero and inferotemporal

of the optic disc, vulnerable to glaucomatous damage.

Nerve fiber layer

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anatomy

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OPHTHALMOSCOPY OF THE OPTIC DISC

OPHTHALMOSCOPY OF THE OPTIC DISC Normal nerve fiber layer Diffuse nerve fiber atrophy 11/16/17 26
OPHTHALMOSCOPY OF THE OPTIC DISC Normal nerve fiber layer Diffuse nerve fiber atrophy 11/16/17 26

Normal nerve fiber layer

Diffuse nerve fiber atrophy

OPHTHALMOSCOPY OF THE OPTIC DISC

The optic cup, pale depression in the center of the optic

cup, absent of nerve fiber,

The neuroretinal rim, tissue between the outer edge of the

cup and the outer margin of the disc, the color is pinkish

orange, uniform width, contains nerve fibers,

Nerve fibers death thinning of retinal rim,

High IOP posterior bowing of lamina cribrosa,

nasalisation of central retinal vessels.

OPHTHALMOSCOPY OF THE OPTIC DISC

The cup-disc ratio: fraction of vertical and horizontal diameter cup and diameter of the disc, normal c/d ratio is 0.3 or less.

OPHTHALMOSCOPY OF THE OPTIC DISC • The cup-disc ratio: fraction of vertical and horizontal diameter cup

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OPTIC DISC CHANGES IN GLAUCOMA

OPTIC DISC CHANGES IN GLAUCOMA Normal disc with small cup 11/16/17 29

OPTIC DISC CHANGES IN GLAUCOMA

Cup and disc ratio > 0.6, Peripapillary atrophy at temporal region, Splinter-shaped hemorrhage on the disc margin.

OPTIC DISC CHANGES IN GLAUCOMA • • • Cup and disc ratio > 0.6, Peripapillary atrophy

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OPTIC DISC CHANGES IN GLAUCOMA

OPTIC DISC CHANGES IN GLAUCOMA 11/16/17 31
OPTIC DISC CHANGES IN GLAUCOMA 11/16/17 31
OPTIC DISC CHANGES IN GLAUCOMA 11/16/17 31
OPTIC DISC CHANGES IN GLAUCOMA 11/16/17 31
OPTIC DISC CHANGES IN GLAUCOMA 11/16/17 31
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NORMAL VISUAL FIELD EXAMINATION

Nasally

: 60 degrees

Temporally

: 95 degrees

Superiorly

Inferiorly

: 50 degrees

: 70 degrees

The blind spot is located temporally 10-20 degrees

Visual field is an island of vision surrounded by the sea of

NORMAL VISUAL FIELD EXAMINATION • Nasally : 60 degrees • Temporally : 95 degrees • Superiorly

darkness, the sharpest is at the top of the island.

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VISUAL FIELDS IN GLAUCOMA

Baring of the blind spot

Localized paracentral scotoma at 10 - 20 degrees of

fixation at superior and inferior quadrant extension to

VISUAL FIELDS IN GLAUCOMA • Baring of the blind spot • Localized paracentral scotoma at 10

the blind spot Byerrum scotoma ring scotoma with

nasal step of Roenne,

VISUAL FIELDS IN GLAUCOMA

Peripheral scotoma that spreads and coalesces to the

paracentral scotoma

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Leaving central island and accompanying temporal island,

even if the central vision is still normal

Temporal island total blindness

VISUAL FIELDS IN GLAUCOMA • Peripheral scotoma that spreads and coalesces to the paracentral scotoma 11/16/17
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CLASSIFICATION

Primary open-angle glaucoma

Secondary open-angle glaucoma

Primary closed-angle glaucoma

Secondary closed-angle glaucoma

Primary congenital glaucoma

Secondary congenital glaucoma

PRIMARY OPEN-ANGLE GLAUCOMA (SIMPLE GLAUCOMA)

Bilaterally, not necessarily symmetrical,

absence of secondary causes of high IOP,

Glaucomatous optic nerve damage,

Open and normal angle, IOP > 21 mmHg,

Adult onset, hereditary, steroid

responsiveness,

Glaucomatous visual field defects, central

tunnel vision,

Minimal clinical signs.

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MANAGEMENT OF PRIMARY OPEN ANGLE GLAUCOMA

Initial therapy is usually medical, except in advanced cases,

Argon laser trabeculoplasty (ALT) if IOP is uncontrolled despite maximal tolerated medical therapy,

Trabeculectomy with / without antimetabolic drug in refractory glaucoma,

Artificial filtering shunt: Achmed valve, Molteno tube, Krupin- Denver valve.

SURGICAL INDICATIONS FOR SIMPLE GLAUCOMA

Uncontrolled IOP by maximal medical treatment

Progressive disc damage and visual field defect

Drugs intolerance

Unable to buy the drugs

Poor compliance

Unable to do the regular control

PRIMARY CLOSED- ANGLE GLAUCOMA

Obstruction of aqueous outflow as a result of closure of

the angle by the peripheral iris

Anatomically predisposed, bilateral,

Predisposition:

Crowded anterior segment

Relatively anterior location iris lens diaphragm,

Shallow anterior chamber,

 

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Narrow entrance to the chamber angle.

PACG STAGE

Five overlapping stages:

Latent

Intermittent (sub acute)

Acute (congestive and post congestive)

Chronic

Absolute

LATENT ANGLE-CLOSURE GLAUCOMA

Shallow anterior chamber, convex-shape iris lens diaphragm, close iris to cornea, normal IOP, occludable angle,

Treatment:

 

Good fellow eye without treatment, follow up,

PACG fellow eye laser iridotomy.

INTERMITTENT ANGLE-CLOSURE GLAUCOMA

Rapid partial closure anterior chamber angle and reopening of the angle after some rest,

Precipitating factors: physiological mydriasis, watching TV in dark room, prone position, reading, sewing, emotion, stress,

Transient blurring of vision, halo, headache,

Recovery after some rest.

ACUTE CONGESTIVE ANGLE-CLOSURE GLAUCOMA

Presentation:

Rapidly progressive impairment of vision, sometimes the vision 1/300 – 0,

Eye ache and frontal headache, Congestion, nausea, vomiting.

ACUTE CONGESTIVE ANGLE-CLOSURE GLAUCOMA

Examination

Ciliary and conjunctival injection

IOP > 50 mmHg, dilated pupil, unreactive.

Cornea: epithelial edema, KP(+), vesicle

Ant chamber: shallow PAS, flare / cell (+),

ACUTE CONGESTIVE ANGLE-CLOSURE GLAUCOMA

Wide pupil, slow / negative light reflex, Papilla edema, retinal edema,

ACUTE CONGESTIVE ANGLE-CLOSURE GLAUCOMA • Wide pupil, slow / negative light reflex, • Papilla edema, retinal

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ACUTE CONGESTIVE ANGLE-CLOSURE GLAUCOMA

ACUTE CONGESTIVE ANGLE-CLOSURE GLAUCOMA 11/16/17 46

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ACUTE CONGESTIVE ANGLE-CLOSURE GLAUCOMA

Differential diagnosis:

Red eyes:

 

conjunctivitis, iridocyclitis

Silent eyes:

simple glaucoma, ocular hypertension

Glaucomatous visual field defect:

anomaly of the optic nerve and retina

Papillary atrophy:

anomaly at optic nerve

Congenital megalocornea without high IOP

ACUTE CONGESTIVE ANGLE-CLOSURE GLAUCOMA

Treatment:

 

Immediately decrease IOP with maximal drugs,

Wait for 24 hours evaluation,

Normal IOP, deep AC, open angle iridectomy,

High IOP, permanent AC closure > 50% trabeculectomy,

The fellow eye: preventive iridectomy.

POSTCONGESTIVE ANGLE-CLOSURE GLAUCOMA

POSTCONGESTIVE ANGLE-CLOSURE GLAUCOMA 11/16/17 49

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CHRONIC CLOSED-ANGLE GLAUCOMA

Clinical features of chronic CAG are similar as POAG except gonioscopy of the angle is closed,

There are three mechanism of CCAG:

Creeping PAS laser iridotomy / trabeculectomy

After intermittent and laser iridotomy drug >

Combination of POAG with narrow angle laser

iridotomy + medical trabeculectomy

CHRONIC CLOSED-ANGLE GLAUCOMA

Signs and therapy are similar as simple glaucoma:

Trabeculectomy,

Laser iridoplasty to make an angle,

Argon Laser Trabeculopasty (ALT)

PRIMARY CONGENITAL GLAUCOMA

65% of patients are male, 1: 10.000,

Inheritance is autosomal recessive, bilateral,

Maldevelopment of the trabeculum and iridotrabecular

junction, abscent of angle recess, trabeculodysgenesis,

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The iris insertion can be flat or concave,

Poor prognosis.

PRIMARY CONGENITAL GLAUCOMA

Clinical signs:

Depends on the age of the onset and the level of IOP,

According to the age of the onset there are 3 types:

 

True congenital glaucoma (40%). IOP elevated since in the intrauterine buphthalmos, Infantile glaucoma (55%) manifesting after birth,

Juvenile glaucoma: IOP » at 10-35 years of age, with clinical manifestation same as POAG.

PRIMARY

CONGENITAL

GLAUCOMA

Examinations:

PRIMARY CONGENITAL GLAUCOMA • Examinations: • Corneal haze, lacrimation, photophobia and blepharospasm, • Buphthalmos if IOP

Corneal haze, lacrimation, photophobia and

blepharospasm,

Buphthalmos if IOP » before the age of 3 usually

associated with axial myop, subluxated lens,

Break of Descemet membrane, endothelial

decompensation permanent stromal edema,

Reversible glaucomatous cupping.

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PRIMARY CONGENITAL GLAUCOMA

Treatments:

Initial drug treatment,

Goniotomy if cornea is still clear,

Trabeculotomy at corneal clouding,

Trabeculectomy and trabeculotomy,

Trabeculectomy with antimetabolic agent,

--Outcome of the operation is poor.

SECONDARY GLAUCOMA

Inflammation and residual inflammation of the uveal tissue: iridocyclitis, posterior synechia,

Immature cataract, hipermature cataract,

Lens luxation, lens subluxation,

Ischemic retina,

Sub choroidal bleeding,

Congenital anomaly of the eye

SECONDARY GLAUCOMA

Pigmentary gl.

- Neovascular gl.

 

Inflammatory gl. Red cell gl.

- Phacolytic glaucoma - Ghost cell glaucoma

Angle recession glaucoma

Iridocorneal endothelial syndrome

Pseudoexfoliative glaucoma

THERAPY

Nerve fiber damage caused by glaucoma is irreversible,

Principle of the therapy is to decrease IOP medically or surgically to maintain the current condition,

The purpose of decreasing the IOP is to reduce progressivity of the nerve fiber damage and visual field defect,

Early findings.

INDICATIONS OF MEDICAL TREATMENT

Simple glaucoma

Acute / chronic closed angle glaucoma Maintain the diurnal IOP

  • Lower IOP before operation

REDUCING AQUEOUS PRODUCTION

Carbonic anhydrase inhibitor

 

acetazolamide 250 mg qid orally,

dorzolamide eye drop tid,

Beta-adrenergic antagonist:

 

beta-blocker (timolol maleat 0.25-0.5%) bid,

betaxolol 0.25% - 0.5% bid.

Adrenergic agonist:

depefeprine 0.5% - 2% bid.

OTHER ANTIGLAUCOMA DRUGS

Parasympathomimetic agents:

pilocarpin eye drop 2-4%, 2-6 x / day

carbachol 0.75% used after cataract operation

Increase the latanoprost uveoscleral flow Hyperosmotic fluid

glycerol 50% 1-2 ml/kg body weight, drink all at once,

manitol 20% swift infusion preoperative, 1.5-3 ml/kg body weight.

SURGICAL TREATMENT

Peripheral iridectomy:

Acute attack glaucoma, with good trabecular meshwork,

Preventive treatment from acute attack for the fellow eye.

Trabeculectomy for all types of glaucoma,

Goniotomy for congenital glaucoma if the cornea is still clear,

Trabeculotomy for congenital glaucoma if the cornea is edema.

SURGICAL TREATMENT

Treatment for absolute glaucoma:

 

cyclocryo coagulation destroys the ciliary body to decrease HA production,

enucleation if all treatment is not successful.

Laser treatment:

iridotomy

gonioplasty

trabeculoplasty

GOOD

PROGNOSIS

Early and right diagnosis,

Adequate control of IOP by medical / surgical treatment,

Compliance of the patients to check their IOP and use medical treatment,

Case finding among glaucoma family.

Thank

you