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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
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