GLAUCOMA

AQUEOUS HUMOUR PRODUCTION OUTFLOW 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

Second most commonly cause of visual loss in elderly Affects - 10 % african American > 70 - 2% Caucasian > 70 Early detection and treatment can prevent blindness

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

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GONIOSCOPY Evaluation the angle of the anterior chamber structures . GONIOSCOPY Evaluation the angle of the anterior chamber structures Contact between peripheral iris and cornea signifies a closed angle or wide separation between the two signifies an open angle. Two type goniolenses instruments: 1. Indirect goniolenses ( goniomirrors) - Goldmann three-mirrors - Zeiss four mirrors - Posner –Sussman four mirrors 2. Direct goniolenses - Koeppe - Swan-Jacob

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Grading of angle width,used by the Shaffer system: . Grading of angle width,used by the Shaffer system: 1. GRD 4 (35-45 dgr) : which the cilliary body can be visualised  widest angle 2. GRD 3 (25-35 dgr) : which at least the scleral spur can be indentified  open angle 3. GRD 2 (20 dgr) : which only the trabeculum can be identified  moderately narrow angle 4. GRD 1 (10 dgr) : which only Schwalbe line and perhaps also the top of the trabeculum can be identified  very narrow angle 5. SLIT ANGLE : which is no obvious iridocorneal contact but no angle structures can be identified  imminent closure 6. GRD 0 (1 dgr) : which iridocorneal contact  synechial angle closure

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

. + PSEUDOEXFOLIATIVE MATERIAL (PEX GLAUC) + OEDEMA (HERPES-ZOSTER IRITIS) + SCARRING (POST-TRAUMA ANGLE RECESSION GLAUC) C. POST TRABECULAR GLAUCOMA, 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. 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)

. 3. CONGENITAL GLAUCOMA A. TRUE PRIMARY CONGENITAL GLAUCOMA, WHICH IOP ELEVATED DURING INTRAUTERINE LIFE B. INFANTILE GLAUCOMA, WHICH MANIFESTS PRIOR TO THE 3TH BIRTHDAY C. JUVENILE GLAUCOMA, IOP RISED AFTER 3TH BIRTHDAY BUT BEFORE THE AGE OF 16 YEARS. 4. OCULAR HYPERTENSION IOP MORE THAN 21 MMHG & ABSENCES OF DETACTABLE GLAUCOMATOUS DAMAGE 5. 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 BILATERAL CHARACTERIZED BY: - ADULT ONSET - IOP > 21 MMHG - OPEN ANGLE OF NORMAL APPEARANCE - GLAUCOMATOUS OPTIC NERVE HEAD DAMAGE - VISUAL FIELD LOSS PATOGENESIS Elevation IOP, glutamine metabolism, Ca + influx into the cell body increase in intracelluler nitric oxide retinal ganglion cell death apoptosis

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

- Typical visual field changes - Gonioscopy shows a normal open angle . CONT…..POAG CLINICAL FEATURES SYMPTOMS…. Asymptomatic until significant loss of visual field has occurred SIGN : - 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

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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 peri-pheral Iris RISK FACTORS 1. AGE , > 60 years 2. GENDER, females : males = 4:1 3. RACE, in caucasians, more common in South-East Asians 4. FAMILY HISTORY ANATOMICAL PREDISPOSING FACTORS 1. Relatively anterior location of the iris-lens diaphragm 2. Shallow anterior chamber 3. Narrow entrance to the chamber angle (lens size, corneal diameter, axial length)

is incompletely understood. Cont….PACG PATHOGENESIS is 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.

1. LATENT ANGLE-CLOSURE GLAUCOMA Clinical features Cont …PACG CLASSIFICATION 1. 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

2. SUBACUT (INTERMITTEN) ANGLE CLOSURE GLAUCOMA 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

3. ACUTE CONGESTIVE ANGLE-CLOSURE GLAUCOMA 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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- Gonioscopy, perform until the corneal oedema resolved by topical . 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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4. POSTCONGESTIVE ANGLE-CLOSURE GLAUCOMA CLINICAL FEATURES 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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5. CHRONIC ANGLE-CLOSURE GLAUCOMA PATHOGENESIS 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 % boys Sporadic, 10 % autosomal recessive PATHOGENESIS Isolated 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 spur 2. Concave iris insertion, superficial iris tissue sweeps over the irido- trabecular junction and the trabeculum

- Corneal haze ( epithelial & stromal oedema)  lacrimation, photopho . 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) TERMINOLOGY When the IOP is found to be > 21 mmHg on two consecutive occa- sions, 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. 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

- IOP 24-29 mmHg without NFL defects . Cont……OH 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 perimetry is 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

- IOP to reduce by at least 30 % 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 effect 2. Trabeculectomy, in at least one eye, if progressive field loss occurs 3. 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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