Aqueous Humor

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

Anatomi Jaringan Trabekular

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

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.

Jaringan Trabekular

a. Jaringan Uveab. Jaringan

Korneosclerac. Garis Schwalbed. Kanal Schlemme. Saluran

pengumpulf. Badan Siliarg. Tonjolan Sclera

Aliran Aqueous

Aliran normal cairan aqueous :

a. Jalur trabekular konvensional

b. Jalur Uveoskleral

c. melalui iris

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

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 %

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

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

Glaukoma

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

Incidence

• 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

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.

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.

Primary glaucomas

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

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

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

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 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).

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

Tonography

• 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.

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:– Identification of abnormal angle structure,– Estimating the width of the chamber angle,– Visualization of the angle during this following

procedures: goniotomy, laser trabeculoplasty.

Indentation Gonioscopy

Identification of angle structures

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

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.

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.

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.

Identification of angle

structures

Identification of angle structures

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

contact.

Shaffer Grading

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.

Ophthalmoscopy of the optic disc

Nerve fiber layer anatomy

Ophthalmoscopy of the optic disc

Normal nerve fiber layer

Ophthalmoscopy of the optic disc

Diffuse nerve fiber atrophyNormal nerve fiber layer

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.

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.

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.

Optic disc changes in glaucoma

Normal disc with small cup

Optic disc changes in glaucoma

Large physiological cups

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,

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

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.

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,

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

Visual Fields in Glaucoma

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.

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 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

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.

PACG stage

• Five overlapping stage:– 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 congestiveangle-closure glaucoma

• Presentation:

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

– Eye ache and frontal headache,

– Congestion, nausea, vomiting.

Acute congestiveangle-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 congestiveangle-closure glaucoma

• Wide pupil, slow / negative light reflex,

• Papilla edema, retinal edema,

Acute congestive angle-closure glaucoma

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

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.

Postcongestiveangle-closure glaucoma

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 gonioplasty 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,

• The iris insertion can be flat or concave,

• Poorly prognosis.

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.

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.

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.

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. - Phacolytic glaucoma• Red cell gl. - Ghost cell glaucoma• Angle recession glaucoma• Iridocorneal endothelial syndrome• Pseudoexfoliative glaucoma

Therapy

• 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.

Indications of Medical Treatment

• Simple glaucoma

• Acute / chronic closed angle glaucoma

• Maintain the diurnal IOP

• Lowering 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 successfull.

• Laser treatment:– iridotomy– gonioplasty– trabeculoplasty

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.

Thank You