Aqueous Humor

4 - Glaukoma

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Aqueous Humor

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Sekresi Aqueous humor

• 80% disekresi oleh epitel badan silier yang tidak berpigmen melalui proses metabolik aktifs yang tergantung pada jumlah enzim (carbonic anhydrase enzyme),

• 20% diproduksi oleh proses pasif melalui ultrafiltrasi dan difusi

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Anatomi Jaringan Trabekular

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Jaringan Trabekular

• Jaringan trabekular terletak di sudut bilik mata depan yang terdiri dari : – Membran Descemet Garis Schwalbe– Sklera tonjolan sklera– Iris tonjolan iris– Badan Siliar angle recess

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Jaringan Trabekular

• The TM is devided into three portions:– Uveal meshwork, large spaces, resistance «,– Corneoscleral meshwork, smaller space,– Endothelial meshwork, major proportion of

normal resistance to aqueous outflow.

• Obstruction of aqueous flow usually at trabecular meshwork high IOP.

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Jaringan Trabekular

a. Jaringan Uveab. Jaringan

Korneosclerac. Garis Schwalbed. Kanal Schlemme. Saluran

pengumpulf. Badan Siliarg. Tonjolan Sclera

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Aliran Aqueous

Aliran normal cairan aqueous :

a. Jalur trabekular konvensional

b. Jalur Uveoskleral

c. melalui iris

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Aliran Aqueous

• AH mengisi bilik mata belakang (BMB) pupil bilik mata depan (BMD) keluar dari dalam mata melalui 2 cara :– 90% melalui jalur trabekular kanalis

Schlemm’s vena episklera keluar mata– 10% melalui jalur uveosklera: melewati badan

silier ronga suprachoroidal sistim vena dalam badan silier

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Aliran Aqueous

AH mengisi BMB pupil

Jalur trabekular BMD

Kanalis Schlemm jalur uveosklera (10%)

rongga suprakoroid badan silier Keluar mataMelalui vena episklera sistim vena dalam badan silier

90 %

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Aliran Aqueous, dipengaruhi oleh:

• Tekanan intra okular (TIO) yg tinggi

• Tekanan episklera yg tinggi

• Kekentalan Aqueous : eksudat, sel darah

• Blok Siliar, blok pupil, sinekia posterior

• Sudut bilik mata depan sempit/tertutup

• Penyempitan pori-pori jaringan trabekula• Macrofag, sel lensa di jaringan trabekula

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Tekanan Intra Okular (TIO)

• Normal 15 - 21 mm Hg,• TIO > 21 mm Hg diduga glaukoma• Perubahan Diurnal TIO selama 24 jam :

– TIO lebih tinggi pada pagi hari– TIO lebih rendah pada sore & malam hari

• Hipertensi Okular : TIO > 21 mmHg tanpa kerusakan serabut saraf

• Glaukona tensi normal : normal TIO, ada gejala glaukoma

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Definisi Glaukoma

• Neuropati diskus optikus yg ditandai dengan :– TIO tinggi > 21 mHg– Kematian serabut saraf optik kerusakan

diskus optik– Kerusakan lapang pandang progresif

• Penyebab kebutaan permanen ketiga terbanyak

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• Congenital glaucoma age 0 - 2 years

• Infantile glaucoma age > 2 years

• Juvenile glaucoma age > 15 year

• Secondary glaucoma: glaucoma as a complication from other eye disease

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Pathogenesis of Glaucomatous Damage

• There are two current theories:– The indirect ischaemic theory: IOP » -- nerve

fiber death + interfering of micro circulation of the optic disc,

– Direct mechanical theory: IOP » -- damage 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,– Factor contributing IOP » : primary and

secondary glaucoma,– Age: congenital, infantile, juvenile, adult.

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Primary glaucomas

• High IOP is not associated with any ocular disorder– Open angle– Angle closure– Congenital (developmental)

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Secondary glaucomas

• 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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Secondary Glaucoma

Mechanism of obstruction in secondary glaucoma:

a. Pre-trabecular obstruction (membrane)

b. Trabecular obstruction (pigment granules)

c. Secondary angle closure by pupil block

d. Secondary angle closure without pupil block

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• 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.

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• 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 specific weight,

5 mm indentation represent as each scale of Schiotz which 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 of the plunger is smaller (3.06 mm),• Disadvantages: cannot be applied to

– Corneal edema

– Keratitis, corneal ulcer

– Keratokonus

– High astigmatic

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• To estimate outflow facility of HA,• Principal: to express fluid from the eye by

continuous pressing to the eye, maximal flows,

• Placing Schiotz type tonometer 2-4 minutes, • Compare IOP at 0 and after 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

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• Three main purposes of gonioscopy:– Identification of abnormal angle structure,– Estimating the width of the chamber angle,– Visualization of the angle during this following

procedures: goniotomy, laser trabeculoplasty.

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Indentation Gonioscopy

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Identification of angle structures

• Schwalbe’s line as an opaque line is a peripheral termination of Descemet membrane,

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Identification of angle structures

• Trabecular meshwork has a ground glass appearance, stretches from Schwalbe’s line to scleral spur.Consists of two part:– 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, deep to the posterior trabeculum,

• Scleral spurs, most anterior of sclera, narrow, dense, often shiny, whitish band. As a landmark for laser trabeculoplasty.

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Identification of angle structures

• 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 body– Iris processes

• The angle recess dipping of the iris, it inserts into the ciliary body.

• Iris processes, small extension of the anterior surface of the iris, inserted at the level of scleral spur.

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Identification of angle


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Identification of angle structures

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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• Slit angle : less than 10 degrees,• Grade 0 : closed angle, iridocorneal


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Shaffer Grading

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Ophthalmoscopy of the optic disc

• 1.2 million axons pass 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.

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Ophthalmoscopy of the optic disc

Nerve fiber layer anatomy

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Ophthalmoscopy of the optic disc

Normal nerve fiber layer

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Ophthalmoscopy of the optic disc

Diffuse nerve fiber atrophyNormal nerve fiber layer

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Ophthalmoscopy of the optic disc

• Scleral canal, the opening of 1.2 million nerve fiber leaves the eye, oval, vertical, 1.75 mm in diameter,

• The lamina cribrosa, plate of collagenous connective tissue, 200-400 pore, containing retinal nerve fiber bundles,

• The large pores have thin connective tissue supports, and large nerve fibers, vulnerable to glaucomatous damage.

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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 outer edge of the cup and the outer margin of the disc, the color is pink 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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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.

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Optic disc changes in glaucoma

Normal disc with small cup

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Optic disc changes in glaucoma

Large physiological cups

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Optic disc changes in glaucoma

• Progressive loss of the retinal nerve fibers notching / thinning of neuroretinal rim (NRR)

• The cup is enlarged :– concentrically diffuse thinning of NRR

– localized expansion notching of NRR

• Double angulation of the blood vessel bayoneting sign,

• Arterial and vein nasalisation,

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Optic disc changes in glaucoma

• Cup and disc ratio > 0.6,

• Peripapillary atrophy at temporal region,• Splinter-shaped hemorrhage on the disc


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Optic disc changes in glaucoma

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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

sea of darkness, the sharpest is at the top of 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 coalesce 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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Visual Fields in Glaucoma

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• Primary open-angle glaucoma

• Secondary open-angle glaucoma

• Primary closed-angle glaucoma

• Secondary closed-angle glaucoma

• Primary congenital glaucoma

• Secondary congenital 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 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.

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Surgical Indications forSimple 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

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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 stage:– 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 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.

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Acute congestiveangle-closure glaucoma

• Presentation:

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

– Eye ache and frontal headache,

– Congestion, nausea, vomiting.

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Acute congestiveangle-closure glaucoma

• Examination– Ciliary and conjunctival injection– IOP > 50 mmHg, dilated pupil,


– Cornea: epithelial edema, KP(+), vesicle– Ant chamber: shallow PAS, flare /

cell (+),

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Acute congestiveangle-closure glaucoma

• Wide pupil, slow / negative light reflex,

• Papilla edema, retinal edema,

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Acute congestive angle-closure glaucoma

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Acute congestiveangle-closure glaucoma

• Differential diagnosis:– Red eyes:

• acute glaucoma, 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 congestiveangle-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.

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Postcongestiveangle-closure glaucoma

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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 gonioplasty 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 iridotrabecular junction, abscent of angle recess, trabeculodysgenesis,

• The iris insertion can be flat or concave,

• Poorly prognosis.

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Primary Congenital Glaucoma

• Clinical signs:– Depends on the age of onset and the level of

IOP,– According to age of onset there are 3 types:

• True congenital glaucoma (40%). IOP elevated intrauterine buphthalmos,

• Infantile glaucoma (55%) manifest after birth,

• Juvenile glaucoma: IOP » at 2-16 years of age, with clinical manifestation the same as POAG.

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Primary Congenital Glaucoma

• Examinations:– 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

• Treatment:– 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 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

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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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• Nerve fiber damage caused by glaucoma is irreversible,

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

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

• Early finding.

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Indications of Medical Treatment

• Simple glaucoma

• Acute / chronic closed angle glaucoma

• Maintain the diurnal IOP

• Lowering 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 trabecular

meshwork,– Preventive treatment from acute attack for the fellow


• 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.

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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 successfull.

• 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 for checking their IOP and use medical treatment,

• Case finding among glaucoma family.

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Thank You