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GLAUCOMA

Bagain Ilmu Kesehatan Mata
Fakultas Kedokteran
Universitas Hasanuddin

AQUEOUS HUMOUR
PRODUCTION
ACTIVE SECRETION FROM NON-PIGMENTED EPITHELLIUM OF
THE CILIARY BODY AS RESULT OF A METABOLIC PROCESS
( Na+/K+ ATPase PUMP, CARBONIC ANHYDRASE)

OUTFLOW
 TRABECULAR MESHWORK :
- UVEAL MESHWORK
- CORNEOSCLERAL MESHWORK
- ENDOTHELIAL (JUXTACANALICULAR) MESHWORK

SCHLEMM CANAL, CONNECT IN/DIRECTLY EPISCLERAL
VEINS

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. DEFINITION GLAUCOMA IS AN OPTIC NEUROPATHY WITH CHARACTERISTIC APPEARANCE OF OPTIC DISC AND SPECIFIC PATTERN OF VISUAL FIELD DEFECTS THAT IS ASSOCIATED FREQUENTLY BUT NOT INVARIABLY WITH RAISED IOP .

NON CONTACT TONOMETER = AIR PUFF NON-CONTACT TONOMETER = PULSAIR 2000 KEELER .CONTACT TONOMETER : = GOLDMANN APPLANATION TONOMETER = PERKINS HAND-HELD APPLANATION TONOMETER = TONO-PEN HAND-HELD TONOMETER = SCHIOTZ INDENTATION TONOMETER .. IOP (INTRAOCULAR PRESSURE) RANGE 11-21 MMHG MEASUREMENT BY TONOMETER: .

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ARCUATE-SHAPED DEFECTS .END STAGE CHANGES . VISUAL FIELD MEASSUREMENT BY HUMPHREY PERIMETRY CHARACTERISTIC PATTERN OF THE GLAUCOMATOUS FIELD DEFECT: .A NASAL (ROENNE) STEP SCOTOMA .PERIPHERAL SCOTOMA ..PARACENTRAL SCOTOMA .

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The central retina artery & vein from centrally the disc of the optic nerve and then nasally following the edge of the cup . The optic cup 2. nas.. temporal =ISNT) 4. The neuroretinal rim (the tissue between the outer edge of the cup and the disc margin. normally broadest inferior rim followed by sup. OPTIC NERVE HEAD EVALUATION BY UN/DIRECT FUNDUSCOPY 1. The cup: disc ratio ( normally .3) 3. vertical cup: disc ratio <0.

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1. ACUTE CONGESTIVE ANGLE-CLOSURE GLAUCOMA D.CLASSIFICATION . PRIMARY GLAUCOMA = PRIMARY OPEN ANGLE GLAUCOMA = PRIMARY ANGLE-CLOSURE GLAUCOMA. LATENT ANGLE-CLOSURE GLAUCOMA B. CHRONIC ANGLE-CLOSURE GLAUCOMA F. ABSOLUTE ANGLE-CLOSURE GLAUCOMA . SUBACUTE (INTERMITTEN) ANGLE-CLOSURE GLAUCOMA C. 6 CLINICAL STAGES: A. POSTCONGESTIVE ANGLE-CLOSURE GLAUCOMA E.

TRABECULAR GLAUCOMA. WHICH THE OBSTRUCTION OCCURS AS A RESULT OF CLOGGING UP OF THE MESHWORK BY: + PIGMENT PARTICLES (PIGMENTARY GLAUCOMA) + RED BLOOD CELLS ( RED CELL GLAUCOMA) + DEGENERATED RED CELLS (GHOST CELL GLAUCOMA) + MACROPHAGES AND LENS PROTEINS ( PHACOLYTIC GLAU + PROTEINS ( HYPERTENSIVE UVEITIS) . SECONDARY GLAUCOMA = SECONDARY OPEN ANGLE GLAUCOMA A. PRETRABECULAR GLAUCOMA.. 2. WHICH AQUEOUS OUTFLOW IS OBSTRUCTED BY A MEMBRANE COVERING THE TRABECULUM + FIBROVASCULAR TISSUE (NEOVASCULAR GLAUCOMA) + ENDOTHELIAL CELLS (IRIDOCORNEAL ENDOTHELIAL = ICE SYNDROME) + EPITHELIAL CELLS (EPITHELIAL INGROWTH) B.

WHICH AQUEOUS OUTFLOW IS IMPAIRED AS ARESULT OF ELEVATED EPISCLERAL VENOUS PRESSURE + CAROTID-CAVERNOUS FISTULAE + STURGER-WEBER SYNDROME + OBSTRUCTION OF THE SUPERIOR VENA CAVA = SECONDARY ANGLE CLOSURE GLAUCOMA A. + OEDEMA (HERPES-ZOSTER IRITIS) + SCARRING (POST-TRAUMA ANGLE RECESSION GLAUC) C. POST TRABECULAR GLAUCOMA. POSTERIOR FORCED PUSH THE PERIPHERAL IRIS AGAINST THE TRABECULUM (IRIS BOMBESECLUSIO PUPILLAE) B. ANTERIOR FORCED PULL THE IRIS OVER THE TRABECULUM BY CONTRACTION OF INFLAMMATORY (LATE NEOVASC GL) .+ PSEUDOEXFOLIATIVE MATERIAL (PEX GLAUC) .

CONGENITAL GLAUCOMA A. IOP RISED AFTER 3TH BIRTHDAY BUT BEFORE THE AGE OF 16 YEARS.OPEN ANGLE ON GONIOSKOPY . OCULAR HYPERTENSION IOP MORE THAN 21 MMHG & ABSENCES OF DETACTABLE GLAUCOMATOUS DAMAGE 5.. JUVENILE GLAUCOMA. WHICH IOP ELEVATED DURING INTRAUTERINE LIFE B. CHARACTERIZED BY : . WHICH MANIFESTS PRIOR TO THE 3TH BIRTHDAY C. TRUE PRIMARY CONGENITAL GLAUCOMA. INFANTILE GLAUCOMA. 3.IOP EQUAL TO OR LESS THAN 21 MMHG (DIURNAL TESTING) .GLAUCOMATOUS OPTIC DISC DAMAGE & VISUAL FIELD LOSS . 4. NORMAL TENSION GLAUCOMA IS A VARIANT OF POAG.ABSENCES OF SECONDARY CAUSES .

OPEN ANGLE OF NORMAL APPEARANCE .GLAUCOMATOUS OPTIC NERVE HEAD DAMAGE .IOP > 21 MMHG .ADULT ONSET .PRIMARY OPEN ANGLE GLAUCOMA (POAG) SIN. CHRONIC SIMPLE GLAUCOMA GENERALLY BILATERAL CHARACTERIZED BY: . glutamine metabolism.VISUAL FIELD LOSS PATOGENESIS Elevation IOP. Ca + influx into the cell body increase in intracelluler nitric oxide retinal ganglion cell death apoptosis .

central retinal vein occlusion. retinitis pigmentosa . AETIOLOGIES 1. rhegmatogenous retinal detachment. MYOPIA 5. postulates that compromise of the microvasculature with resultant ischaemia in the optic nerve head 2.. POAG . The direct mechanical theory. RETINAL DISASES . FAMILY HISTORY with POAG 4. AGE . The ischaemic theory.Cont…. RACE. After the age of 65 years 2. More earlier & severe in black people than in white 3. raised IOP directly damages the retinal nerve fiber RISK FACTORS 1.

Typical visual field changes .Gonioscopy shows a normal open angle MANAGEMENT .POAG .Trabeculectomy . CLINICAL FEATURES SYMPTOMS….CONT…. prostaglandine analough ) .Optic disc changes .Medical therapy ( timolol maleat.Laser trabeculoplasty ..Raised IOP (> 21 mmHg ) & diurnal fluctuation in IOP (> 5 mmHg) . Asymptomatic until significant loss of visual field has occurred SIGN : .

in caucasians. > 60 years 2. FAMILY HISTORY ANATOMICAL PREDISPOSING FACTORS 1. females : males = 4:1 3. Shallow anterior chamber 3. RACE. GENDER. more common in South-East Asians 4. AGE . Relatively anterior location of the iris-lens diaphragm 2. axial length) .PRIMARY ANGLE-CLOSURE GLAUCOMA (PACG) Is a condition in which elevation of IOP occurs as a result of obstruction of aqueous outflow by partial or complete closure of the angle by the peripheral Iris RISK FACTORS 1. Narrow entrance to the chamber angle (lens size. corneal diameter.

PACG . 1.Cont…. The dilatator muscle theory postulates that contraction of the dilator pupillae exerts a posterior vector. PATHOGENESIS is incompletely understood. 2. The sphincter muscle theory postulates that the sphincter pupillae is the prime culprit in precipating angle closure. .

+ Convex-shaped iris-lens diaphragm + Close proximity of the iris to the cornea -Gonioscopy : Shaffer grade 1 or 0 Treatment .Cont …PACG .Prophylactic peripheral laser iridotomy . LATENT ANGLE-CLOSURE GLAUCOMA Clinical features -Symptoms are absent -Slit lamp biomicroscopy + Axial anterior chamber depth is less than normal. CLASSIFICATION 1.

PACG 2.PROPHYLACTIC PERIPHERAL LASER IRIDOTOMY . Cont….FRONTAL HEADACHE . CLINICAL FEATURES : ..OCULAR DISCOMFORT .THE ANGLE IS NARROW TREATMENT . SUBACUT (INTERMITTEN) ANGLE CLOSURE GLAUCOMA A PREDISPOSED EYE WITH AN OCCLUDABLE ANGLE AN ASSOCIATION WITH INTERMITTENT PUPILLARY BLOCK.BLURRING OF VISION ASSOCIATED WITH HALOES AROUND LIGHTS .CORNEAL EPITHELIAL OEDEMA .

vertically oval + IOP is 50-100 mmHg . ACUTE CONGESTIVE ANGLE-CLOSURE GLAUCOMA This is a sight –threatening emergency. 3.PACG .Slit lamp biomicroscopy + injection the limbal & conjunctival blood vessels + corneal oedema + peripheral iridocorneal contact + pupil is fixed semi-dilated.Symptoms : + rapidly progressive unilateral visual loss + periocular pain & congestion + nausea & vomiting . CLINICAL FEATURE .Cont…….

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5 %) . perform until the corneal oedema resolved by topical glicerine or hypertonic saline ointment .Ophthalmoscopy.Trabeculectomy . . optic disc oedema & hyperaemia IMMEDIATE TREATMENT .Acetasolamide 500 mg/IV..Glyserol 50 % (1g/Kg bw) orally or 20% mannitol IV .Analgesia & anti-emetics . shows complete peripheral iridocorneal contact (Shaffer grade 0) .YAG laser iridotomy : effective in relatively mild cases .Cont …. 500 mg orally .PACG .Gonioscopy.Topical therapy : + pilocarpine 2 % + beta blocker (timolol maleat 0.

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Cont…. trabecular hyperpigmentation ..Gonioscopy . congestion or atropic optic disc.PACG . subnormal or elevated .Slit lamp biomicroscopy + Descemet membrane folds (if IOP reduced rapidly) + fine pigment granules (on the corneal endothelium & iris) + aqueous flare & cells + stroma iris atrophy (spiral like configuration) + fixed & semi-dilated pupil (paralysis sphincter & post synechiae) + glaukomflecken + IOP normal. shows narrow angle. 4. choroidal folds .Ophthalmoscopy. POSTCONGESTIVE ANGLE-CLOSURE GLAUCOMA CLINICAL FEATURES .

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combination of POAG with narrow angle (the long term use of miotics) CLINICAL FEATURES similar POAG . shows a variable degree of angle closure TREATMENT laser iridotomy combined with medical therapy .Cont…. Type 3 (mixed). CHRONIC ANGLE-CLOSURE GLAUCOMA PATHOGENESIS 1. Type 1 (creeping). Type 2.PACG . synechial angle closure as a result of intermittent (subacut) attacks  secondary pupillary block 3. 5. gradual & progressive synechial angle closesure caused by anteriorly situated cilliary process  plateau iris 2.

10 % autosomal recessive PATHOGENESIS Isolated trabeculodysgenesis  absence of the angle recess with the Iris inserted directly into the surface of the trabeculum : 1. superficial iris tissue sweeps over the iridotrabecular junction and the trabeculum .PRIMARY CONGENITAL GLAUCOMA (PCG) Affecting 1:10. iris inserteds flatly and abruptly into the thickened trabeculum at or anterior to the scleral spur 2. Concave iris insertion. Flat iris insertion.000 births. 65 % boys Sporadic.

photopho bia.Breaks in Descemet membrane (Haab striae) .Trabeculotomy . CLINICAL FEATURES . blepharospasm .Corneal haze ( epithelial & stromal oedema)  lacrimation. AC deep. lens subluxasion (zonular fibres stretch).Goniotomy .Cont ….PCG . large eye as result of stretching due to elevated IOP  Scleral thinner ( blue appearance).Buphthalmos.Optic disc cupping SURGERY .Trabeculectomy . axial myopia (increase axial length) .

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IOP 30 mmHg or more .parapapillary changes .IOP 26 mmHg or more & central corneal thickness < 555 um .4 or more & CCT < 588 um .retinal nerve fiber layer defects .OCULAR HYPERTENSION (OH) TERMINOLOGY When the IOP is found to be > 21 mmHg on two consecutive occasions. in the absence of detactable glaucomatous damage MANAGEMENT do not require treatment only high risk should be treated because it’s effective in delaying or preventing the development of POAG 1.vertical CDR 0. High risk factors .

2.Cont……OH . Treatment is withheld until damage is documented. Moderate risk factors . .IOP 24-29 mmHg without NFL defects .Family history of POAG in a first degree relative .Vertical CDR > 0.high myopia In these patients annual examination of the optic disc and perimetry is appropriate.3 & CCT > 588 um .

VF defects. to be closer to fixation. steeper and more localized. deeper.Paraproteinaemia . ophthalmic .migraine .ONH + both glaucomatous cupping or parapapillary changes are identical POAG + splinter haemorrhages at the disc margin  progressive damage of NFL + acquired optic disc pits (localized excavations of the lamina cribrosa} .Nocturnal systemic hypotension. .peripheral vascular spasm .NORMAL TENSION GLAUCOMA (NTG) SIGN .Reduced blood flow velocity in the a. over treated systemic hypertension . but rarely the low teens .IOP usually in the high teens.

Systemic calcium channel blockers (nifedipine) in younger patients with peripheral vasospasm. if progressive field loss occurs 3..IOP to reduce by at least 30 % 1. in at least one eye. if nocturnal drop may be necessary to avoid anti-hypertensive medication . Monitoring of systemic blood pressure for 24 hours. Trabeculectomy. TREATMENT . Prostaglandin analoues tend to greater ocular hypotensive effect 2. NTG .progressive VF loss . Medical .Cont…. betaxolol the drug of choice. 4.

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