the glaucomas 1

THE GLAUCOMAS 1

Dr Russell J Watkins

Anterior Chamber Anatomy Chamber volume is about 200l Chamber depth is about 3.2mm

Deeper in myopes Shallows with age

Schwalbe’s line marks end of DM Scleral spur receives insertion of the

longitudonal ciliary fibres - contraction opens TM spaces

TM lined by trabeculocytes which have contractile properties which may influence outflow resistance

Anterior Chamber Anatomy Canal of Schlemm is oval in cross-section (200-

400m) Canal is lined by endothelial cells which on inner

wall have giant vacuoles Number & size of vacuoles varies with IOP

This is the mechanism of the bulk transfer of aqueous to Canal of Schlemm

Anterior Chamber Anatomy With age, there is

2-3 fold thickening of trabecular sheets Loss of endothelial cellularity Increase in connective tissue Increased accumulation of TM debris Increased accumulation of GAGs

Such changes are exaggerated in OAG

Autonomic Control of Aqueous Secretion

Cholinergic mechanisms probably not involved in control of IOP

Adrenergic (1, 1 2, & 2) receptors do regulate IOP receptor stimulation inhibits AC (IOP)

aqueous production PGF2

receptor stimulation activates AC (IOP) aqueous production

Aqueous Humour Drainage ~90% aqueous leaves eye via trabecular

meshwork ~10% leaves eye via “unconventional” routes

most important = “uveoscleral” Trabecular meshwork modulated by GAGs & Ca2+

in ECM Inner wall endothelium of Schlemm’s canal

provides most of TM resistance to outflow Intrascleral & episcleral venous flow also

provides resistance to outflow

Aqueous Outflow

Classification All forms of glaucoma are classified into primary &

secondary forms based on Gonioscopic findings ONH findings VF defects

Major risk factors IOP (the major risk factor but not the whole story) Vascular risk factors

• Local• Systemic

Race

Classification Associated conditions

Ocular Extraocular

Additional useful clinical data BP, pulse, blood glucose, blood lipids Migraine, cold hands/Raynaud’s Thyroid disease, neurological diseases History of blood loss, smoking FOH +ve for visual loss FOH +ve for glaucoma

Glaucoma Classification

Primary Congenital Forms Primary Congenital

Glaucoma Primary Infantile

Glaucoma Glaucoma associated

with congenital anomalies

Glaucoma Classification

Primary Open Angle Glaucomas Primary juvenile

glaucoma Primary open angle

glaucoma Normal tension

glaucoma Ocular hypertension

Glaucoma Classification Secondary Open Angle Glaucoma

Pseudoexfoliation glaucoma Pigmentary glaucoma Lens-induced OAG Glaucoma associated with intraocular

haemorrhage Uveitic glaucoma et al ++

Glaucoma Classification

Primary Angle Closure Glaucomas Pupillary block

mechanism Plateau iris mechanism Malignant glaucoma Chronic ACG

Glaucoma Classification Secondary Angle Closure Glaucomas

Secondary ACG with pupil block Secondary ACG due to “pulling” of AC

• NVG• Aniridia• Inflammatory membrane• et al++

Primary Congenital Forms Primary congenital glaucoma

Aetiology is angle dysgenesis Pathomechanism is aqueous outflow Onset from birth to second year of life Usually sporadic; 10% may be AR with

variable penetrance; specific chromosomal abnormalities (1p36 & 2q21)

1 in 10,000 live births M>F (65%:35%)

Primary Congenital Forms Primary congenital glaucoma (cont.)

Photophobia, tearing, blepharospasm Eye rubbing, EUA for IOP unreliable Buphthalmos (cornea >11mm) Corneal oedema (±ruptures in DM Haab’s striae) ONH: pressure distension/uniform enlargement VCDR>0.3 Gonio: open angle but poorly differentiated structures;

trabeculodysgenesis; anterior iris insertion

Primary Congenital Forms Primary infantile glaucoma

Probably late onset congenital glaucoma Same aetiology & pathomechanism as PCG Onset 3rd to tenth yr of life Similar genetics to PCG Pain unusual; no buphthalmos or corneal oedema Often presents late with symptomatic VF loss Peak IOP > 24mmHg without Rx ONH shows pressure distension & generalised cup

enlargement with diffuse rim damage Gonio as PCG

Primary Congenital Forms Glaucoma associated with congenital anomalies

Aniridia Sturge Weber syndrome Neurofibromatosis Marfan syndrome Homocystinuria Goniodysgenesis

• Axenfeld-Rieger syndrome & Peter’s anomaly Rubella Microcornea PHPV et al.