OPHTHALMOLOGY Glaucoma MBChB 4 Prof P Roux 2012. WHAT IS GLAUCOMA? A GROUP OF DISEASES IN WHICH...

OPHTHALMOLOGYGlaucoma

MBChB 4Prof P Roux

2012

WHAT IS GLAUCOMA?

•A GROUP OF DISEASES IN WHICH INTRAOCULAR PRESSURE (IOP) CAUSES DAMAGE TO VISION.COMMON FEATURES:•Optic disc cupping

•Visual field loss

•Raised intraocular pressure (Usually)

AQUEOUS HUMOUR DYNAMICS:

PRODUCTIONOUTFLOW

•SECRETION•ULTRAFILTRATION

•TRABECULAR MESHWORK(ANGLE)

•UVEOSCLERAL PATHWAY

Aqueous outflowAnatomy

a - Uveal meshworkb - Corneoscleral meshworkc - Schwalbe lined - Schlemm canale - Collector channelsf - Longitudinal muscle of ciliary bodyg - Scleral spur

c - Iris outflow

a - Conventional outflowb - Uveoscleral outflow

Physiology

•OPEN-ANGLE•ANGLE-CLOSURE

•PRIMARY•SECONDARY

•CONGENITAL•INFANTILE•JUVENILE•ADULT

CLASSIFICATION:

ACCORDING TO:

ANGLE ASSOCIATED FACTORS AGE OF ONSET

a. Pre-trabecular - membrane over trabeculum

Open-angle

b. Trabecular - ‘clogging up’ of trabeculum

c. With pupil block - seclusio pupillae and iris bombé

Angle-closure

d. Without pupil block - peripheral anterior synechiae

c d

a b

ANGLE

SECONDARY GLAUCOMAS1. Pseudoexfoliation glaucoma

3. Neovascular glaucoma

2. Pigmentary glaucoma

4. Inflammatory glaucomas

5. Phacolytic glaucoma

7. Iridocorneal endothelial syndrome

6. Post-traumatic angle recession glaucoma

8. Glaucoma associated with iridoschisis

ASSOCIATED FACTORS

PATHOGENESIS

•INDIRECT ISCHAEMIC THEORY

(MICROCIRCULATION/ PERFUSION PRESSURE)

•DIRECT MECHANICAL THEORY

(DAMAGE TO NERVE FIBRES)

Theories of glaucomatous damage

Direct damage by pressure Capillary occlusion

Interference withaxoplasmic flow

Risk Factors

1. Age - most cases present after age 65 years

2. Race - more common, earlier onset and more severe in blacks

3. Inheritance• Level of IOP, outflow facility and disc size are

inherited• Risk is increased by x2 if parent has POAG• Risk is increased x4 if sibling has POAG

4. Myopia

5. Diabetes

EXAMINATION

1. TONOMETRY (PRESSURE)

2. GONIOSCOPY (ANGLE)

3. VISUAL FIELD

4. OPTIC DISC(OPTIC NERVE)

Tonometers

GoldmannContact applanation

PerkinsPortable contact applanation

Pulsair 2000 (Keeler)Air-puff

Schiotz

Portable non-contact applanation

Non-contact indentation

Contact indentation

Tono-PenPortable

contact applanation

GoniolensesGoldmann

• Single or triple mirror

Zeiss

• Contact surface diameter 12 mm

• Coupling substance required

• Four mirror

• Coupling substance not required

• Contact surface diameter 9 mm

• Suitable for ALT• Not suitable for indentation gonioscopy• Suitable for indentation gonioscopy

• Not suitable for ALT

Indentation gonioscopy

Differentiates ‘appositional’ from ‘synechial’ angle closure

Press Zeiss lens posteriorly against cornea

Aqueous is forced into periphery of anterior chamber

Humphrey perimetry

Anatomy of retinal nerve fibres

Horizontalraphe

Papillomacularbundle

Optic nerve head

a - Nerve fibre layer

Small physiological cup

b - Prelaminar layer

c - Laminar layer

• Normal vertical cup-disc ratio is 0.3 or less

• 2% of population have cup-disc ratio > 0.7

• Asymmetry of 0.2 or more is suspicious

Total glaucomatous cupping

Large physiological cup

a

c

b

Types of physiological excavation

Small dimple central cup Larger and deeperpunched-out central cup

Cup with sloping temporal wall

Pallor and cupping

Cupping and pallor correspond

Pallor - maximal area of colour contrast

Cupping is greater than pallor

Cupping - bending of small blood vessels crossing disc

TREATMENT OF GLAUCOMA

MEDICAL

SURGERY Trabeculectomy

LASER

1

2

3

ANTIGLAUCOMA DRUGS

1. ALPHA-2 SELECTIVE ADR. AGONISTS - Alphagan

2. BETA-ADRENERGIC BLOCKING AGENTS - Betagan

3. CARBONIC ANHYDRASE INHIBITORS - Trusopt

4. PROSTAGLANDIN DERIVATIVES - Xalatan

5. PILOCARPINE

6. ADRENALINE

DECREASED AH PRODUCTION•ADRENERGIC AGONISTS

-ALPHA-2•ADRENERGIC ANTAGONISTS

-BETA BLOCKERS•CAI

INCREASED OUTFLOW•ADRENERGIC AGONISTS

(NON SELECTIVE)•PILOCARPINE•PROSTAGLANDINE

DERIVATIVES

ANGLE GLOSURE GLAUCOMA• ACUTELY PAINFULL RED EYE !!• LOSS OF VA ,• CLOUDY CORNEA,• NON REACTIVE PUPIL,• LOSS OF RED REFLEX

MANAGEMENT

• DIAGNOSIS

• TOPICAL & SYSTEMIC PRESSURE REDUCTION

• PILOCARPINE (REDUCE PUPIL BLOCK)

• SYSTEMIC ANALGESIC & ANTI-EMETICS

• LASER PI

a. Cutting of deep block - anterior incision

b. Posterior incision

d. Peripheral iridectomy

e. Suturing of flap and reconstitution of anterior chamber

f. Suturing of conjunctiva

c. Excision of deep block

f

d

ba

c

e

SURGERY: Technique

ANGLECLOSURE

SECONDARYGLAUCOMAS

OPEN ANGLE

GLAUCOMA

Sturge-Weber syndrome

• Congenital, does not blanche with pressure• Associated with ipsilateral glaucoma in 30% of cases

Naevus flammeus

• CT scan showing left parietal haemangioma• Complications - mental handicap, epilepsy and hemiparesis

Meningeal haemangioma

Port-winestain

Fibroma molluscum in NF-1

Iris melanoma

• Usually pigmented nodule at least 3 mm in diameter• Invariably in inferior half of iris

• Occasionally non-pigmented• Surface vascularization

• Angle involvement may cause glaucoma

• Pupillary distortion, ectropion uveae and cataract