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a Glaucoma @ INTRODUCTION 193 Physiology of aqueous production ‘Aqueous outflow 193 Incraocular pressure 194 Classification 194 © TONOMETRY Goldmann tonometry Other tonometers GONIOSCOPY Introduction 198 Goniolenses 199 Gonioscopic technique 200 Identification of angle structures Grading of angle width 202 © THE OPTIC NERVE HEAD Applied anatomy 202 The normal optic nerve head Glaucomatous damage 205 Imaging techniques 208 © PERIMETRY 209 Introduetion 209 | Humphrey perimetry 210 Glaucomatous damage 212 Other psychophysiological tests. 217 @ OCULAR HYPERTENSION — 217 © PRIMARY OPEN-ANGLE GLAUCOMA Introduction 218 Screening 219 Clinical features 220 Management 220 © NORMAL-TENSION GLAUCOMA © PRIMARY ANGLE-CLOSURE | GLAUCOMA 223 Introduction 223 Latent angle-closure glaucoma 224 Subacute angle-closure glaucoma 225 Acute congestive angle-closure glaucoma Postcongestive angle-closure glaucoma Chronic angle-closure glaucoma 228 Plateau iris 229 © PSEUDOEXFOLIATIVE GLAUCOMA Pseudoexfoliation syndrome 229 Pseudoexfoliative glaucoma 231 © PIGMENTARY GLAUCOMA | Pigment dispersion syndrome Pigmentary glaucoma 233 | @ NEOVASCULAR GLAUCOMA Introduction 233 | Rubeosis iris 234 Secondary open-angle glaucoma Secondary angle-closure glaucoma 193 196 196 197 198 201 202 204 218 222 225 27 229 234 231 233 235 235 236 © INFLAMMATORY GLAUCOMA Introduction 236 ‘Angle-closure glaucoma with pupil block 236 ‘Angle-closure glaucoma without pupil block 237 ‘Open-angle glaucoma 237 Glaucoma in Fuchs uveitis syndrome Posner-Schlossman syndrome 238 © LENS-RELATED GLAUCOMA Phacolytic glaucoma 239 Phacomorphic glaucoma 239 © TRAUMATIC GLAUCOMA Red cell glaucoma 240 ‘Angle recession glaucoma 240 @ IRIDOCORNEAL ENDOTHELIAL SYNDROME — 241 @ MISCELLANEOUS SECONDARY GLAUCOMAS = 243 Ghost cell glaucoma 243 Glaucoma in carotid-cavernous fistula 243 Glaucoma in intraocular tumours 244 Glaucoma in cillochoroidal detachment Glaucoma in epithelial ingrowth 244 Glaucoma in iridoschisis 245 © PRIMARY CONGENITAL GLAUCOMA @ IRIDOCORNEAL DYSGENESIS 248 Axenfeld-Rieger syndrome 248 Peters anomaly 250 Aniridia 254 © GLAUCOMA IN PHACOMATOSES Sturge-Weber syndrome 252 Neurofibromatosis-1 252 © ANTI-GLAUCOMA DRUGS Beta-blockers 253 ‘Alpha-2 agonists 254 Prostaglandin analogues Miotics 255 ‘Topical carbonic anhydrase inhibitors ‘Combined topical preparations 255, Systemic carbonic anhydrase inhibitors Hyperosmotic agents 256 @LASERTHERAPY 256 ‘Argon laser trabeculoplasty 256 Diode laser trabeculoplasty 258 Nd:YAG laser iridotomy 258 Diode laser cycloablation 259 @ TRABECULECTOMY 259 Surgical techniques 259 Postoperative complications 264 © NON-PENETRATING FILTRATION SURGERY 267 @ ADJUNCTIVE ANTIMETABOLITES @ ARTIFICIAL DRAINAGE SHUNTS 238 239 240 244 4s 252 253 254 255 255 267 268 badly consists of the anterior pars plicata (2 mm nd the posterior pars plana (4 mm wide). ‘The pars bears 70 radially orientated ciliary processes which {nto the posterior chamber, Each ciliary process is a pigmented epithelial layer continuous with the ent epithelium and a non-pigmented epithelial ous with the neuroretina, Each process also has arteriole ending in a rich capillary network. Tight ns between adjacent non-pigmented epithelial cells the blood-aqueous barrier. Aqueous humour Is sseeeted by the non-pigmented epithelium as. result elabolic process that depends on several enzyme Gs especially the Na*/K*-A\TPase pump, which secretes Into the posterior chamber. Water follows passively the osmotic gradient. Carbonic anhydrase also plays ut the precise mechanism is uncertain. Aqueous jon is diminished by factors that inhibit a such as hypoxia and hypothermia but it is inde~ gato the level of intraocular pressure (JOP). Analysis of drstatic and osmotic pressures across the ciliary jim reveals that under normal conditions passive plays litte, if any, role in the genesis of aqueous Aqueous secretion is diminished by the following: p such as beta-blockers. sympathomimeties and car- plestructive procedures such as eyelocryotherapy and ablation itis and retinal trabecular meshwork (trabeculum) is a sieve Ssiructure at the angle of the anterior chambe! agh which 90% of the aqueous humour leaves we (Fig. 9.1). It consists of the following three veal meshwork (Fig, 9.2a) is the innermost which consists of cord-like meshes that extend isto Schwalbe line (Fig. 9.2c). The cular spaces are relatively large and offer ite ce to the passage of aqueous. ‘corneoscleral meshwork (Fig. 9.2b) forms the middle portion which extends from the scleral (Fig. 9.2g) to Schwalbe line, The meshes are sheet- ‘and the intertrabecular spaces are smaller than in veal meshwork ‘Aratotny ef the cuniiow charows (a) Ured|ieaircrie (b) corneoscleral meshwork; (¢) Schwalbe line; (d) Schlemm ‘anal; (@) collector channels; (f) longitudinal muscle of the «iliary body (g) scleral spur ¢. The endothelial (juxtacanalicular) meshwork is. the outer part of the trabeculum which links the corneo- scleral meshwork with the endothelium of the inner wall of Schlemm canal (Fig. 9.2d). ‘The juxtacanali- cular tissue offers the major proportion of normal resistance to aqueous outllow. . Schlemm canal is a circumferential channel in the peri- limbal sclera, bridged by septa. The inner wall of the canal islined by irregular spindle-shaped endothelial cells which contain infoldings (giant vacuoles). The outer wall of the canal is lined by smooth flat cells and contains the open- ings of the collector channels (Fig. 9.2e) which leave Schlemm canal at oblique angles and connect directly or indirectly with episcleral veins. Fig. 9.3 Normal outflow of aqueous humour. (a) Conventional trabecular route; (b) uveoseleral route; (c) through the iris Physiology Aqueous flows from the posterior chamber via the pupil into the anterior chamber, from where it exits the eye by two different routes: |. Trabecular (conventional) route accounts for approx- imately 90% of aqueous outflow (Fig. 9.3a). The aqueous flows through the trabeculum into Schlemm canal and is then drained by the episcleral veins. This is a bulk-flow pressure-sensitive route so that increasing the pressure head will increase outflow, ‘Trabecular outllow can be increased by drugs (miotics, sympathomimeties), laser trabeculoplasty and trabeculotomy. 2. Uveoscleral (unconventional) route accounts for the remaining 10% of aqueous outflow (Fig. 9.3b). The aqueous passes across the face of the ciliary body into the suprachoroidal space and is drained by the venous circulation in the ciliary body, choroid and sclera. Uveoscleral outflow is decreased by miotics and increased by atropine, sympathomimetics and prostaglandins. Some aqueous also drains via the iis (Fig. 9.3c) Intraocular pressure Determining factors 1. Rate of aqueous secretion. 2. Rate of aqueous outflow, which isin turn related to the resistance encountered inthe outflow channels and the level of epscleral venous pressure. ‘The rate of aqueous outflow is proportional to the difference between the intraocular and Jeral venous pressure. The relationship between these factors can be expressed as follows = C(Po— Pe) where F =rate of aqueous outflow (normal 2 l/min) facility of aqueous outflow (normal 0.2 l/min, per mmilg) Po=10P in mmHg, Pe=episcleral venous pressure (normal 10 mmllg) For example: ‘If episcleral venous pressure is 20 mmHg the IOP} (2/0.2) + 20 = 30 mmiig. © If the facility of outflow is 0.05 the IOP wil (2/0,05) + 10 = 50 mmiig, Distribution ‘The distribution of IOP within the general population range of 11-21 mmHg, Although there is no absolute: point, 21 mmHg is considered the upper limit of normal levels above this are viewed with suspicion. However in patients glaucomatous damage occurs with OPS less 21 mmbg (normal-tension glaucoma), while others’ ‘unscathed with LPs up to 30 mmlig (ocular bypert ‘Although the actual level of IOP is important in the ment of glaucomatous damage, other factors also play a ‘The level of IOP is inherited so that first-degree relat patients with primary oper-angle glaucoma have bis ops. Fluctuation Normal JOP varies with the time of day. heartbeat, pressure level and respiration. The pattern of diurnal of 1OP varies, with a tendency to be higher in the and lower in the afternoon and evening, Normal eyes {est a mean diurnal pressure variation of 5 mmHg: hypertensive or glaucomatous eyes, however, exhibit a fluctuation, In normal-tension glaticoma the fluctuation the same asin normals. A single normal reading, parti if taken during late afternoon, may therefore be mis and it may be necessary to take several readings at di times of day (phasing). In clinical practice phasing during) morning hours may be suficient because 80% of pa peak between 8 and 12 au Classification Glaucoma is an optic neuropathy with characte ances of the optic dise and specific pattern of visual defects that is associated frequently but not invariably raised TOP, Because the pathophysiology, clinical presen and treatment of the different ty varied, there is no single definition that adeq encompasses all forms. Understanding this concept hel explain, for example, why one patient with ‘glaucoma’ have no symptoms while another experiences sudden and redness. Glaucoma may be (a) congenital (develo or (b) acquired, Further subclassification into open-angle angle-closure types is based on the mechanism by aqueous outflow is impaired. The glaucoma may als (a) primary or (b) secondary depending on the pr absence of associated factors contributing 10 the rise, In primary glaucomas the elevation of 10P fs