GLAUCOMA (NW).ppt

7/21/2019 GLAUCOMA (NW).ppt

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GLAUCOMA

NW


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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)

OUTFLOWTRABECULAR MESHWORK :

- UVEAL MESHWORK- CORNEOSCLERAL MESHWORK

- ENDOTHELIAL (JUXTACANALICULAR) MESHWORK

SCHLEMM CANAL, CONNECT IN/DIRECTLY EPISCLERAL VEINS


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DEFINITIONGLAUCOMA IS AN OPTIC NEUROPATHY WITH

CHARACTERISTIC APPEARANCE OF OPTIC DISC AND SPECIFIC PATTERN OF VISUAL FIELDDEFECTS THAT IS ASSOCIATED FREQUENTLYBUT NOT INVARIABLY WITH RAISED IOP


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VISUAL FIELD MEASSUREMENT BYHUMPHREY PERIMETRYCHARACTERISTIC PATTERN OF THE GLAUCOMATOUS FIELDDEFECT:

- 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 FUNDUSCOPY1. The optic cup2. The cup: disc ratio ( normally , vertical cup: disc ratio


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GONIOSCOPYEvaluation the angle of the anterior chamber structuresContact between peripheral iris and cornea signifies a closed angle orwide 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 :

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 angle4. GRD 1 (10 dgr) : which only Schwalbe line and perhaps also the top

of the trabeculum can be identified very narrow angle5. SLIT ANGLE : which is no obvious iridocorneal contact but no angle

structures can be identified imminent closure6. GRD 0 (1 dgr) : which iridocorneal contact synechial angle closure


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.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 GLAUCOMAC. ACUTE CONGESTIVE ANGLE-CLOSURE GLAUCOMAD. POSTCONGESTIVE ANGLE-CLOSURE GLAUCOMAE. CHRONIC ANGLE-CLOSURE GLAUCOMAF. ABSOLUTE ANGLE-CLOSURE GLAUCOMA


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.2. SECONDARY GLAUCOMA= SECONDARY OPEN ANGLE GLAUCOMA

A. PRETRABECULAR GLAUCOMA, WHICH AQUEOUS OUTFLOWIS 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 UPOF 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 )


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.+ 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 AGAINST

THE TRABECULUM (IRIS BOMBE SECLUSIO PUPILLAE)B. ANTERIOR FORCED PULL THE IRIS OVER THE TRABECULUM

BY CONTRACTION OF INFLAMMATORY (LATE NEOVASC GL)


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3. CONGENITAL GLAUCOMA A. 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 HYPERTENSION

IOP MORE THAN 21 MMHG & ABSENCES OF DETACTABLE GLAUCOMATOUSDAMAGE 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


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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


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.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


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.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


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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-pheralIris

RISK FACTORS1. AGE , > 60 years

2. 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 diaphragm

2. Shallow anterior chamber3. Narrow entrance to the chamber angle (lens size, corneal diameter, axial

length)


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.Cont.PACG

PATHOGENESIS

is incompletely understood.

1. The dilatator muscle theory postulates that contraction of the dilatorpupillae exerts a posterior vector.

2. The sphincter muscle theory postulates that the sphincter pupillae isthe prime culprit in precipating angle closure.


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.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 0Treatment- Prophylactic peripheral laser iridotomy


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Cont.PACG

2. SUBACUT (INTERMITTEN) ANGLE CLOSURE GLAUCOMA A PREDISPOSED EYE WITH AN OCCLUDABLE ANGLE AN ASSOCIATIONWITH 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


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Cont.PACG

3. ACUTE CONGESTIVE ANGLE-CLOSURE GLAUCOMAThis 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 GLAUCOMACLINICAL 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 GLAUCOMAPATHOGENESIS1. Type 1 (creeping), gradual & progressive synechial angle close-

sure caused by anteriorly situated cilliary process plateau iris2. Type 2, synechial angle closure as a result of intermittent (sub-

acut) attacks secondary pupillary block3. Type 3 (mixed), combination of POAG with narrow angle (the

long term use of miotics)CLINICAL FEATURESsimilar POAG , shows a variable degree of angle closureTREATMENTlaser iridotomy combined with medical therapy


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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 thickenedtrabeculum at or anterior to the scleral spur

2. Concave iris insertion, superficial iris tissue sweeps over the irido-trabecular junction and the trabeculum


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Cont .PCG

CLINICAL FEATURES

- Corneal haze ( epithelial & stromal oedema) lacrimation, photophobia, 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

MANAGEMENTdo not require treatmentonly high risk should be treated because its effective in delaying or preventing 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


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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.


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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

C NTG


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Cont.. NTG

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

1. Medical , betaxolol the drug of choice. Prostaglandin analoues tendto greater ocular hypotensive effect

2. 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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GLAUCOMA (NW).ppt