glaucoma koas

7/27/2019 Glaucoma Koas

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Glaucoma

Dr. Andika Prahasta, SpM


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Definition of Glaucoma

Glaucoma is an optic disc neuropathy which ischaracterized by:

High intra ocular pressure (IOP) > 21 mmHg,

Optic nerve fibers death

optic disc damage,Progressive visual field defect,

Cause of third permanent blindness.


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Incidence

Primary glaucoma is:

hereditary

female > male

especially at age > 40 years


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Incidence

Congenital glaucoma since in the intrauterine

Infantile glaucoma after birth until 2 years Juvenile glaucoma age 10 - 15 years

Secondary glaucoma: glaucoma as a complication

from other eye disease


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Aqueous humor secretion

80% is secreted by non pigmented ciliaryepithelium via active metabolic process thatdepends on a number of enzymatic systems(carbonic anhydrase enzyme),

20% is produced by passive processes asultrafiltration and diffusion.


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Aqueous outflow

AH fills posterior chamber pupil

Trabecular route anterior chamber

Schlemms canal uveoscleral route (10%)

suprachoroidal space ciliary body

leaves the eye

through episcleral vein venous system in the ciliary body

90 %


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Aqueous outflow

a. Uvealmeshwork

b. Corneoscleralmeshwork

c. Schwalbes line

d. Schlemmscanal

e. Collectorchannels

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

The TM is located at the anterior chamber

angle, which consists:

Descemet membrane Schwalbes line

Sclera scleral spur

Iris iris processus

Ciliary body 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.


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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.


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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.


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Primary glaucomas

High IOP is not associated with any ocular

disorderOpen angle

Angle closure

Congenital (developmental)


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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,

Pathogenesis: anterior forces / posterior forces


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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 amountof indentation is converted into mmHg by use

of Friedenwald tables.


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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


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Schiotz Tonometer

Portable, simple, low cost,

Measure the depth of indentation of

cornea by a plunger with specificweight (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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Goldmanns Applanation

Tonometer

More accurate, not influenced by ocularrigidity

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 aremore than 8 mmHg,

Indications:

Narrow / closed angle glaucomaNormal tension glaucoma

Bias IOP


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Gonioscopy

Three main purposes of gonioscopy:

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

Schwalbes line (an opaque line) is a peripheral

termination of Descemet membrane,

Trabecular meshwork has a ground glassappearance stretching from Schwalbes line to scleral

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

Schlemms canal: slightly darker line,behind the posterior trabeculum,

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

shiny, whitish band. As a landmark for laser

trabeculoplasty. Ciliary body stands behind the scleral spur as dull

brown band. The width depends on iris insertion.

Curve of the corner at the margin of the ciliary bodyIris processes

Iris processes, small extension of the anterior surface

\ 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.


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Ophthalmoscopy of the optic disc

1.2 million axons passes across the retina and enter the

optic disc,

Fibers from the macula

papillomacular bundle, straightto 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

anatomy


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Diffuse nerve fiber atrophyNormal nerve fiber layer


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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.


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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.


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Optic disc changes in glaucoma

Normal disc with small cup


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Cup and disc ratio > 0.6,

Peripapillary atrophy at temporal region,

Splinter-shaped hemorrhage on the discmargin.


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Normal Visual Field Examination

Nasally : 60 degrees Temporally : 95 degrees

Superiorly : 50 degrees

Inferiorly : 70 degrees

The blind spot is located temporally 10-20 degrees

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

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

the blind spot Byerrum scotoma ring scotoma with

nasal step of Roenne,


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Visual Fields in Glaucoma

Peripheral scotoma that spreads and coalesces to the

paracentral scotoma

Leaving central island and accompanying temporal island,

even if the central vision is still normal

Temporal island total blindness


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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


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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 inadvanced cases,

Argon laser trabeculoplasty (ALT) if IOP isuncontrolled despite maximal tolerated medicaltherapy,

Trabeculectomy with / without antimetabolic drug

in refractory glaucoma, Artificial filtering shunt: Achmed valve, Molteno

tube, Krupin- Denver valve.


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Surgical Indications for

Simple Glaucoma

Uncontrolled IOP by maximal medicaltreatment

Progressive disc damage and visual fielddefect

Drugs intolerance

Unable to buy the drugs Poor compliance

Unable to do the regular control

Primary Closed Angle


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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,

Narrow entrance to the chamber angle.


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PACG stage

Five overlapping stages:

Latent

Intermittent (sub acute)

Acute (congestive and post congestive)

Chronic

Absolute


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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.


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Intermittent

angle-closure glaucoma

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

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

Transient blurring of vision, halo, headache,

Recovery after some rest.


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Acute congestive


Presentation:

Rapidly progressive impairment of

vision, sometimes the vision 1/3000,

Eye ache and frontal headache,

Congestion, nausea, vomiting.


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Acute congestive


Examination

Ciliary and conjunctival injection

IOP > 50 mmHg, dilated pupil,unreactive.

Cornea: epithelial edema, KP(+), vesicle

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


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Acute congestive


Wide pupil, slow / negative lightreflex,

Papilla edema, retinal edema,


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Acute congestive



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Acute congestive


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


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Acute congestive


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.

P t ti


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Postcongestive



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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


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Chronic closed-angle glaucoma

Signs and therapy are similar as simple

glaucoma:

Trabeculectomy,

Laser iridoplasty to make an angle,

Argon Laser Trabeculopasty (ALT)


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Primary Congenital Glaucoma

65% of patients are male, 1: 10.000,

Inheritance is autosomal recessive, bilateral,

Maldevelopment of the trabeculum and iridotrabecularjunction, abscent of angle recess, trabeculodysgenesis,

The iris insertion can be flat or concave,

Poor prognosis.


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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


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Primary Congenital

Glaucoma

Examinations:

Corneal haze, lacrimation, photophobia and

blepharospasm,

Buphthalmos if IOP before the age of 3 usuallyassociated with axial myop, subluxated lens,

Break of Descemet membrane, endothelial

decompensation permanent stromal edema,

Reversible glaucomatous cupping.


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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.


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Secondary Glaucoma

Inflammation and residual inflammation ofthe uveal tissue: iridocyclitis, posterior

synechia, Immature cataract, hipermature cataract,

Lens luxation, lens subluxation,

Ischemic retina, Sub choroidal bleeding,

Congenital anomaly of the eye


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Secondary Glaucoma

Pigmentary gl. - Neovascular gl.

Inflammatory gl. - Phacolytic glaucoma

Red cell gl. - Ghost cell glaucoma

Angle recession glaucoma

Iridocorneal endothelial syndrome

Pseudoexfoliative glaucoma


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Therapy

Nerve fiber damage caused by glaucoma isirreversible,

Principle of the therapy is to decrease IOPmedically or surgically to maintain the currentcondition,

The purpose of decreasing the IOP is to reduce

progressivity of the nerve fiber damage and visualfield defect,

Early findings.


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Indications of Medical Treatment

Simple glaucoma

Acute / chronic closed angle glaucomaMaintain the diurnal IOP

Lower IOP before operation


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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.


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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.


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Surgical treatment

Peripheral iridectomy:

Acute attack glaucoma, with good trabecularmeshwork,

Preventive treatment from acute attack for the felloweye.

Trabeculectomy for all types of glaucoma,

Goniotomy for congenital glaucoma if the corneais still clear,

Trabeculotomy for congenital glaucoma if thecornea is edema.


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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


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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.


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