GLAUCOMABagain Ilmu Kesehatan Mata Fakultas Kedokteran Universitas Hasanuddin

AQUEOUS HUMOURPRODUCTION 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

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

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

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.OPTIC NERVE HEADEVALUATION BY UN/DIRECT FUNDUSCOPY 1. The optic cup2. The cup: disc ratio ( normally , vertical cup: disc ratio

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.CLASSIFICATION

1. PRIMARY GLAUCOMA = PRIMARY OPEN ANGLE GLAUCOMA = PRIMARY ANGLE-CLOSURE GLAUCOMA, 6 CLINICAL STAGES:A. LATENT ANGLE-CLOSURE GLAUCOMAB. SUBACUTE (INTERMITTEN) ANGLE-CLOSURE GLAUCOMAC. ACUTE CONGESTIVE ANGLE-CLOSURE GLAUCOMAD. POSTCONGESTIVE ANGLE-CLOSURE GLAUCOMAE. CHRONIC ANGLE-CLOSURE GLAUCOMAF. ABSOLUTE ANGLE-CLOSURE GLAUCOMA

.2. SECONDARY GLAUCOMA = SECONDARY OPEN ANGLE GLAUCOMA A. PRETRABECULAR GLAUCOMA, WHICH AQUEOUS OUTFLOW IS OBSTRUCTED BY A MEMBRANE COVERING THE TRABE-CULUM+ FIBROVASCULAR TISSUE (NEOVASCULAR GLAUCOMA)+ ENDOTHELIAL CELLS (IRIDOCORNEAL ENDOTHELIAL = ICE SYNDROME) + EPITHELIAL CELLS (EPITHELIAL INGROWTH) B. TRABECULAR GLAUCOMA, WHICH THE OBSTRUCTION OCCURSAS 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)

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

.3. CONGENITAL GLAUCOMAA. TRUE PRIMARY CONGENITAL GLAUCOMA, WHICH IOP ELEVATED DURING INTRAUTERINE LIFEB. INFANTILE GLAUCOMA, WHICH MANIFESTS PRIOR TO THE 3TH BIRTHDAYC. JUVENILE GLAUCOMA, IOP RISED AFTER 3TH BIRTHDAY BUT BEFORE THE AGE OF 16 YEARS.4. OCULAR HYPERTENSIONIOP MORE THAN 21 MMHG & ABSENCES OF DETACTABLE GLAUCOMATOUS DAMAGE5. NORMAL TENSION GLAUCOMA IS A VARIANT OF POAG, CHARACTERIZED BY :- IOP EQUAL TO OR LESS THAN 21 MMHG (DIURNAL TESTING)- GLAUCOMATOUS OPTIC DISC DAMAGE & VISUAL FIELD LOSS- OPEN ANGLE ON GONIOSKOPY- ABSENCES OF SECONDARY CAUSES

PRIMARY OPEN ANGLE GLAUCOMA (POAG)SIN. CHRONIC SIMPLE GLAUCOMA

GENERALLY BILATERALCHARACTERIZED BY:- ADULT ONSET- IOP > 21 MMHG- OPEN ANGLE OF NORMAL APPEARANCE- GLAUCOMATOUS OPTIC NERVE HEAD DAMAGE- VISUAL FIELD LOSS

PATOGENESISElevation IOP, glutamine metabolism, Ca + influx into the cell body increase in intracelluler nitric oxide retinal ganglion cell death apoptosis

.Cont.. POAG

AETIOLOGIES1. The ischaemic theory, postulates that compromise of the microvas-culature with resultant ischaemia in the optic nerve head2. The direct mechanical theory, raised IOP directly damages the retinal nerve fiber

RISK FACTORS1. AGE . After the age of 65 years2. RACE. More earlier & severe in black people than in white3. FAMILY HISTORY with POAG4. MYOPIA5. RETINAL DISASES , central retinal vein occlusion, rhegmatogenous retinal detachment, retinitis pigmentosa

.CONT..POAG

CLINICAL FEATURESSYMPTOMS. Asymptomatic until significant loss of visual field has occurredSIGN : - Raised IOP (> 21 mmHg ) & diurnal fluctuation in IOP (> 5 mmHg) - Optic disc changes - Typical visual field changes - Gonioscopy shows a normal open angle MANAGEMENT- Medical therapy ( timolol maleat, prostaglandine analough )- Laser trabeculoplasty- Trabeculectomy

PRIMARY ANGLE-CLOSURE GLAUCOMA (PACG)Is a condition in which elevation of IOP occurs as a result of obstruction ofaqueous outflow by partial or complete closure of the angle by the peri-pheral Iris

RISK FACTORS1. AGE , > 60 years2. GENDER, females : males = 4:13. RACE, in caucasians, more common in South-East Asians4. FAMILY HISTORY

ANATOMICAL PREDISPOSING FACTORS1. Relatively anterior location of the iris-lens diaphragm2. Shallow anterior chamber3. Narrow entrance to the chamber angle (lens size, corneal diameter, axial length)

.Cont.PACG

PATHOGENESISis incompletely understood.

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

.Cont PACG

CLASSIFICATION1. LATENT ANGLE-CLOSURE GLAUCOMA Clinical features -Symptoms are absent -Slit lamp biomicroscopy + Axial anterior chamber depth is less than normal. + Convex-shaped iris-lens diaphragm + Close proximity of the iris to the cornea -Gonioscopy : Shaffer grade 1 or 0 Treatment - Prophylactic peripheral laser iridotomy

.Cont.PACG

2. SUBACUT (INTERMITTEN) ANGLE CLOSURE GLAUCOMA A PREDISPOSED EYE WITH AN OCCLUDABLE ANGLE AN ASSOCIATION WITH INTERMITTENT PUPILLARY BLOCK.

CLINICAL FEATURES : - BLURRING OF VISION ASSOCIATED WITH HALOES AROUND LIGHTS - CORNEAL EPITHELIAL OEDEMA - OCULAR DISCOMFORT - FRONTAL HEADACHE - THE ANGLE IS NARROW

TREATMENT - PROPHYLACTIC PERIPHERAL LASER IRIDOTOMY

.Cont.PACG

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

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.Cont ..PACG - Gonioscopy, perform until the corneal oedema resolved by topical glicerine or hypertonic saline ointment , shows complete periphe- ral iridocorneal contact (Shaffer grade 0) - Ophthalmoscopy, optic disc oedema & hyperaemia

IMMEDIATE TREATMENT - Acetasolamide 500 mg/IV, 500 mg orally - Topical therapy : + pilocarpine 2 % + beta blocker (timolol maleat 0,5 %) - Glyserol 50 % (1g/Kg bw) orally or 20% mannitol IV - Analgesia & anti-emetics - YAG laser iridotomy : effective in relatively mild cases - Trabeculectomy

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.Cont..PACG

4. POSTCONGESTIVE ANGLE-CLOSURE GLAUCOMA CLINICAL FEATURES - 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, subnormal or elevated - Gonioscopy , shows narrow angle, trabecular hyperpigmentation - Ophthalmoscopy, congestion or atropic optic disc, choroidal folds

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.Cont.PACG

5. CHRONIC ANGLE-CLOSURE GLAUCOMA PATHOGENESIS 1. Type 1 (creeping), gradual & progressive synechial angle close- sure caused by anteriorly situated cilliary process plateau iris 2. Type 2, synechial angle closure as a result of intermittent (sub- acut) attacks secondary pupillary block 3. Type 3 (mixed), 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

PRIMARY CONGENITAL GLAUCOMA (PCG)Affecting 1:10.000 births, 65 % boysSporadic, 10 % autosomal recessive

PATHOGENESISIsolated trabeculodysgenesis absence of the angle recess with the Iris inserted directly into the surface of the trabeculum :

1. Flat iris insertion, iris inserteds flatly and abruptly into the thickened trabeculum at or anterior to the scleral spur2. Concave iris insertion, superficial iris tissue sweeps over the irido- trabecular junction and the trabeculum

.Cont .PCG

CLINICAL FEATURES- Corneal haze ( epithelial & stromal oedema) lacrimation, photopho bia, blepharospasm- Buphthalmos, large eye as result of stretching due to elevated IOP Scleral thinner ( blue appearance), AC deep, lens subluxasion (zo- nular fibres stretch), axial myopia (increase axial length)- Breaks in Descemet membrane (Haab striae)- Optic disc cupping

SURGERY- Goniotomy- Trabeculotomy- Trabeculectomy

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OCULAR HYPERTENSION (OH)TERMINOLOGYWhen the IOP is found to be > 21 mmHg on two consecutive occa-sions, in the absence of detactable glaucomatous damageMANAGEMENTdo not require treatmentonly high risk should be treated because its effective in delaying orpreventing the development of POAG1. High risk factors - retinal nerve fiber layer defects - parapapillary changes - IOP 30 mmHg or more - IOP 26 mmHg or more & central corneal thickness < 555 um - vertical CDR 0,4 or more & CCT < 588 um

.ContOH

2. Moderate risk factors - IOP 24-29 mmHg without NFL defects - Vertical CDR > 0,3 & CCT > 588 um - Family history of POAG in a first degree relative - high myopia

In these patients annual examination of the optic disc and perimetryis appropriate. Treatment is withheld until damage is documented.

NORMAL TENSION GLAUCOMA (NTG)SIGN- IOP usually in the high teens, but rarely the low teens- 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}- VF defects, to be closer to fixation, deeper, steeper and more localized.- peripheral vascular spasm- migraine- Nocturnal systemic hypotension, over treated systemic hypertension- Reduced blood flow velocity in the a. ophthalmic- Paraproteinaemia

.Cont.. NTG

TREATMENT- progressive VF loss- IOP to reduce by at least 30 %

1. Medical , betaxolol the drug of choice. Prostaglandin analoues tend to greater ocular hypotensive effect2. Trabeculectomy, in at least one eye, if progressive field loss occurs3. Systemic calcium channel blockers (nifedipine) in younger patients with peripheral vasospasm.4. Monitoring of systemic blood pressure for 24 hours, if nocturnal drop may be necessary to avoid anti-hypertensive medication

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