Diagnostic and treatment of glaucoma

Diagnostic and treatment of glaucoma
Małgorzata Seredyka-Burduk

Introduction Physiology and anatomy
Aqueous secretion Active secretion accounts for approximately 80% of aqueous production. The aqueous is secreted by the non-pigmented ciliary epithelium via an active metabolic process that is dependent on number of enzymatic systems.

Aqueous secretion Passive secretion accounts for the remaining 20%. Aqueous is produced by passive processes such as ultrafiltration and diffusion which are dependent on the level of blood pressure in the cilliary capillaries, the plasma oncotic pressure and the level of intraocular pressure. Bp in cilliary capillaries Plasma oncotic pressure iop

Aqueous outflow Aqueus humour leaves the eye by trabeculum. The trabeculum (trabecular meshwork) is a sieve-like structure. Aqueous outflow Aqueus humour leaves the eye by trabeculum. The trabeculum (trabecular meshwork) is a sieve-like structure.

The trabeculum consists of three portions: 1. The uveal meshwork (a) is the innermost portion which consists of cord-like meshes that extend from the root of the iris to the Schwalbe’s line. The intertrabecular spaces are relatively large and offer little resistance to the passage of aqueous. Root of iris to schwalbes line

2. The corneoscleral meshwork (b) forms the larger middle portion which extends from the scleral spur (g) to Schwalbe’s line (c). The meshes are sheet-like and the intertrabecular spaces are smaller than in the uveal meshwork. Scleral spur to schwalbes line

3. The endothelial meshwork is the narrow outer part of the trabeculum which links the corneoscleral meshwork with the endothelium on the inner wall of Schlemm’s canal (d). Corneoscleral to endoth of schlemms canal

Schlemm’s canal is a circumeferential channel bridged by septa. The inner wall of the canal is lined by irregular spindle-shape endothelial cells which contain giant vacuoles. The outer wall of the canal is lined by smooth flat cells and contain the openings of the collector channels.

Aqueous flows from the posterior chamber into the anterior chamber through the pupil and is drained by the two routes: The trabecular (conventional) route (accounting 90% of aqueous outflow) is through the trabaculum into Schlemm’s canal and episcleral veins. Post chamber – pupil- anterior chamber- trabecular route 90% into schlemm n episcleral veins unconventional route 10% into ciliary bodyand even iris

The uveoscleral (unconventional) route accounts 10%. The aqueous passes across the cilliary body into the suprachoroidal space and is drained by the circulation in the cilliary body, choroid and sclera. Some aqueous also drains via the iris.

The following factors determine IOP: rate of aqueous secretion, resistance encountered in the outflow channels, level of episcleral venous pressure The normal IOP varies between 10mmHg and 21 mmHg. Although there is no absolute cutoff point, 21 mmHg is considered the upper limit of normal, and levels above this are viewed with suspicion.

Fluctuations of IOP occur with the time of day, heartbeat, blood pressure level and respiration. Normal eyes have a smaller diurnal fluctuations (<4mmHg) than eyes with glaucoma in which the fluctuation may be 10mmHg or more.

Introduction Pathogenesis of glaucomatous damage of optic nerve
1. The ischaemic theory postulates that raised IOP causes death of nerve fibres because of too low perfusion pressure (difference between the IOP and the intracapillary pressure). 2. The mechanical theory suggests that elevated IOP directly damages the retinal nerve fibres as they passed through the optic nerve head. It seems likely that both mechanisms play a role in most cases.

Introduction Classification of the glaucomas
1. Open-angle glaucomas 2. Angle-closure glaucomas 1. Primary glaucomas (the elevation of IOP is not associated with any other ocular disorder) 2. Secondary glaucomas (an ocular or non-ocular disorder alters aqueous outflow – this results in elevation of IOP).

There are the following secondary open-angle glaucomas: pre-trabecular (aqueous outflow is obstructed by a membrane covering the trabeculum) trabecular (the obstruction occurs within the trabeculum itself)

There are the following secondary open-angle glaucomas: post-trabecular (the trabeculum by itself is normal but aqueous outflow is impaired as a result of elevation of pressure in episcleral veins)

Secondary angle-closure glaucomas are those in which aqueous outflow is impaired by apposition between the peripheral iris and the trabeculum. This may be the result of: posterior forces which push peripheral iris against the trabeculum anterior forces which pull the peripheral iris over the trabeculum

In generally, primary open-angle glaucoma (POAG) is most common and accounts for 55% of cases, secondary glaucomas are next (30%), followed by primary angle-closure glaucoma (PACG) – 12% and congenital – 3%.

Methods of examination
Tonometry The two main methods of measuring IOP are by applanation (The Goldmann tonometer, The Perkins tonometer, The air-puff, The Pulsair, The Tono-Pen) and indentation (The Schiotz tonometer). Both are based on the principle that the applied force either flattens (applanates) or indents the cornea.

Gonioscopy The main purposes of gonioscopy: identification of abnormal angle structures estimation of the width of the chamber angle visualization of the angle during procedures such us laser trabeculoplasty and goniotomy

The angle of the anterior chamber cannot be visualized directly through an intact cornea because light emitted from angle structures undergoes total internal reflection. A goniolens eliminates this by replacing the cornea/air interface with a new interface which has a refractive index greater than that of the cornea and tears.

The two main types of goniolenses are: 1. indirect (provide a mirror-image view of the opposite angle and can be used only with conjunction with a slitlamp) – the Goldmann goniolens, the Zeiss goniolens

The two main types of goniolenses are: 2. direct (provide a direct view of the angle and is usually used with the patient in the supine position during operations on the angle) – the Koeppe goniolens, the Swan-Jacob goniolens, the Barkan goniolens

The Goldmann goniolens gives an excellent view of the angle structures, stabilizes the globe, is suitable for laser trabeculoplasty. The curvature of the contact surface of the lens is steeper than that of the cornea, so a viscous coupling substance, with the same refractive index as the cornea, that bridges the gap between the cornea and the goniolens is required.

The Zeiss goniolens has four mirrors, so the entire extent of the angle may be visualized with minimal rotation. As the curvature of the contact surface of the lens is flatter than that of the cornea, coupling substance is not required.

The Zeiss goniolens does not stabilize the globe, but if the lens is pushed hard against the cornea, it will distort it and impair visualization of the angle. This will also displace aqueous humour to the periphery of the angle, so that a narrow angle may appear artificially wide. indentation gonioscopy

Methods of examination Identification of angle structures during gonioscopy
Schwalbe’s line is the most anterior structure appearing as an opaque line. It represents the peripheral termination of Descemet’s membrane and the anterior limit of the trabeculum. In locating Schwalbe’s line is useful the corneal wedge. Using a narrow slit beam, two linear reflections can be seen: one from the external surface of the cornea and its junction with sclera, the other from the internal surface of the cornea. The two reflections meet at Schwalbe’s line which forms the apex of the corneal wedge.

The trabeculum has a ground-glass appearance and appears to have a depth. It consists of the two parts: the anterior, non-functional, non-pigmented, lies behind the Schwalbe’s line, has a whitish colour. the posterior, functional, pigmented, lies between the anterior trabeculum and scleral spur, has a greyish-blue colour.

Pigmentation of the trabeculum is very rare before puberty. In senile eyes it involves the trabeculum to a variable extend and is most marked inferiorly. Pathological trabecular hyperpigmentation is caused by excessive shedding of pigment from the posterior layer of the iris. In eyes without trabecular pigmentation Schlemm’s canal can occasionally be identified as a slightly darker line deep to the posterior trabeculum.

The scleral spur is the most anterior part of the sclera and the site of attachment of the longitudinal muscle of the ciliary body. It appears as a narrow, dense, shiny, whitish band. The scleral spur is the most important landmark because it has relatively consistent appearance in different eyes.

The ciliary body stands out just behind the scleral spur as a dull-brown or slate-grey band. Its width depends on the position of the iris insertion and tends to be narrower in hypermetropic eyes and wider in myopic eyes.

Iris processes are small extensions of the anterior surface of the iris which are inserted at the level of scleral spur and cover the ciliary body. Iris processes are present in about one-third of normal eyes and are most prominent during childhood and in brown eyes. Iris processes should not be confused with peripheral anterior synechiae, which are adhesions between the iris and the angle structures!

Methods of examination Grading of angle structures
Its main aims are to evaluate the functional status of the angle, its degree of closure and the risk of future closure.

In the Shaffer system, an estimation of the angle width is achieved by observing the amount of separation between two imaginary lines, constructed to the inner surface of the trabeculum and the anterior iris surface.

Grade 4 (35°-45°) is the widest angle characteristic of myopia and aphakia in which the ciliary body can be visualized. It is incapable of closure.

Grade 3 (20°-35°) is an open angle in which at least the scleral spur can be identified. It is incapable of closure.

Grade 2 (20°) is moderately narrow angle in which only the trabeculum can be identified. Angle closure is possible but unlikely.

Grade 1 (10°) is a very narrow angle in which only Schwalbe’s line and the top of the trabeculum can be identified. The risk of angle closure is high.

Grade 0 (0°) is a closed angle resulting from iridocorneal contact. Indentation gonioscopy with the Zeiss goniolens is neceserry do differentiate between „appositional” and „synechial” angle closure.

Methods of examination Ophthalmoscopy of the optic nerve head
The key to the interpretation of visual field loss in relation to optic nerve cupping in glaucoma is an understanding of the distribution of the 1,2 million axons. Fibres arising from the macula an from the nasal retina follow a straight course to the optic nerve head. Those from macula form a spindle-shape area (papillomacular bunge).

Fibres arising from the retina temporal to the macula follow an arcuate path around the papillomacular bundle to reach the optic nerve head.

The arcuate fibres reaching the superotemporal and inferotemporal parts of the optic nerve head are most vulnerable to damage in glaucoma and the fibres of the papillomacular bundle are the most resistant.

The scleral canal is an opening through which nerve fibres leave the eye. The diameter of this canal is related to the size of the optic disc – eyes with small canals have small optic discs (hypermetropia), with large canals – large discs (myopia).

The optic cup is a pale depression in the centre of the optic nerve head which is not occupied by neural disc tissue. Cupping is best evaluated by observing the bending of the small blood vessels as they cross the disc.

The size of the cup is related to the diameter of the disc – a small disc have a small cup because the nerve fibres are bunched and crowded up as they leave the eye.

In adult glaucoma, pathological cupping is caused by a decrease in the number of nerve fibres, glial cells and blood vessels. In young children, cupping may be caused by an increase in the diameter of scleral canal and be reversible with early treatment.

The neuroretinal rim is a tissue between the outer edge of the cup and the outer margin of the disc. A normal rim should be orange or pink and constant, irrespective of the overall diameter of the disc.

The normal c/d ratio in the horizontal meridian in most eyes is 0,3 or less. Only 2% of normals have a ratio of more than 0,7. In 70% of patients with early glaucoma the difference between two eyes is more than 0,1.

The spectrum of disc damage in glaucoma ranges from highly localized tissue loss with notching of the neuroretinal rim to diffuse concentric enlargement of the cup. Concentric expansion of the optic cup is caused by a diffuse loss of nerve fibres. When this occurs the excavation simply enlarges concentrically without associated localized notching of neuroretinal rim.

Localized expansion of the optic cup is caused by localized damage to the neuroretinal rim at the superior or – more commonly – inferior poles of the optic disc.

In advanced cupping occurs the double angulation of the blood vessels – they dive sharply backwards and then turn along the steep wall of the excavation before angling again onto the floor of the disc – bayonetting sign

Progression of glaucomatous damage of optic disc

Methods of examination Visual fields
The visual field is an island of vision surrounded by a sea of darkness.

The outer aspect of the visual field extends: 60° nasally, 90° temporally, 50° superiorly, 70° inferiorly.

The visual field isn’t a flat plane but a three-demensional structure. The visual acuity is sharpest at the top of the island and then declines progressively towards the periphery. The nasal slope is steeper than the temporal. The blind spot is located temporally between 10° and 20°.

An isopter enclosses an area within which a target of a given size is visible. As a size of target is decreased, the area within which it can be perceived becomes smaller, so a series of isopters is formed.

A scotoma is either an absolute or a relative defect in the visual field. Absolute scotoma represents total loss of vision. Relative scotoma is an area of partial visual loss within which some targets can and others cannot be seen. Sometimes an absolute scotoma is surrounded by a relative scotoma.

Perimetry is a method of evaluating the visual field. Kinetic perimetry involves the presentation of a moving stimulus of known intensity from a non-seeing area to a seeing area, until the patients reports that the stimulus has been perceived. It can be performed by simple confrontation, as well as using perimeters, such as the tangent screen, the Lister and the Goldmann.

Static perimetry involves the presentation of stimuli of varying intensity in the same position to obtain vertical boundary of the visual field. Although it is slower than kinetic perimetry, it is much better suited to quantitative testing. It can be performed by an automatic perimeters, such as the Humphrey, the Octopus, the Optopol.

Methods of examination Visual field defects in glaucoma
Early defects: 1. The earliest clinically significant field defect is a scotoma that develops between 10° and 20° of fixation. Initially the defects do not connect with the blind spot itself but, with the passage of time, they tend to elongate circumferentially along the distribution of arcuate nerve fibres.

2. Baring of the blind spot may occur in association with other nerve fibre bundle defects, but it is too non-specific a sign to be of diagnostic importance by itself.

3. Isolated paracentral nasal scotomata may also be find. Although they are frequently absolute when first detected, they may ocassionally disappear after normalization of IOP.

4. A nasal (Roenne) step or a temporal wedge is frequently associated with other defects and may rarely be present by itself.

Late defects 1. The scotomata in Bjerrum’s area (between 10° and 20° of fixation) change to form an arcuate-shaped defect which arches from the blind spot around the macula, reaching to within 5° of fixation nasally.

2. A ring of double arcuate scotoma develops when defects arising in opposite halves of the visual field join together.

3. The visual field loss gradually spreads to the periphery and also centrally, so that eventually only a small island of central vision and a temporal island are left.

4. The temporal island is usually extinguished before the central island, although occasionally this sequence is reversed.

Types of glaucomas 1. Primary glaucomas (the elevation of IOP is not associated with any other ocular disorder) 2. Secondary glaucomas (an ocular or non-ocular disorder alters aqueous outflow – this results in elevation of IOP).

Primary open-angle glaucoma
Primary open-angle glaucoma (POAG) is generally a bilateral, although not necessarily symmetrical, disease characterized, in least one eye, by the following: glaucomatous optic nerve damage glaucomatous visual field defects repeated IOP>21 mmHg (in 15% IOP<21 mmHg) adult onset open and normal appearing angle absence of secondary causes of open-angle glaucoma

POAG is the most prevalent of all glaucomas, affecting 1 in 200 of the general population over the age of 40 years. It increases with age. It affects both sexes equally. It is more common in black than in white individuals.

POAG is freqently inherited. First-degree relatives of patients with POAG are at increased risk of developing it. In general risk is 10% in siblings (brothers and sisters) and 4% in offspring (parents).

Ocular risk factors of POAG: high myopia central retinal vein occlusion Fuchs’ endothelial dystrophy rhegmatogenes retinal detachment retinitis pigmentosa

Systemic risk factors of POAG: increasing age diabetes elevated systolic blood pressure

POAG is a chronic, slowly progressive, usually bilateral but asymmetrical disease with an insidious onset. It is usually asymptomatic until it has caused a significant loss of visual field. Patients frequently present with significant visual field loss in one eye and less advanced or without any damage in the other.

Ocassionally, patients with very high IOPs may complain of eye ache, headache and even haloes caused by transient corneal epithelial oedema.

Treatment There should be a treatment goal in terms of ideal IOP level. Unfortunately, the actual safe level of IOP is still unknown, although, in general, the more advanced the damage the lower the IOP required to halt a progression of the disease.

Treatment Only the long-standing stability of visual fields, and the appearance of the optic nerve head, are proof that the IOP is at a safe level. If control is good and the appearance of the optic disc stable, twice-yearly perimetry is sufficient.

The initial therapy is usually medical, except in advanced cases. We use: β-blockers α2-sympathomimetics carbonic anhydrase inhibitors prostaglandins miotics

The chosed drug should be used at its lowest concentration, as infrequently as possible, to achieve the desire effect. If possible, the drug with the fewest potential side effects should be chosen.

If the IOP is not reduced to satisfactory level the following options should be considered: increase the strength of the drug, withdraw the initial drug and substitute to another, add another drug (when a combination of drugs is used, the patient should be instructed to wait 10 minutes before instilling the second drug to prevent washout)

If the decrease of IOP is not reduced to a satisfactory level laser trabeculoplasty or filtration surgery should be considered. Laser trabeculoplasty is a method of lowering IOP by the application of discrete laser burns to the trabeculum. We use two types of lasers to realize trabeculoplasty: argon laser (ALT – argon laser trabeculoplasty) Nd:YAG Q-switch (SLT – selective laser trabeculoplasty)

Indications to a trabeculoplasty: open-angle glaucomas which are uncontrolled despite maximal tolerated medical therapy, primary therapy in patients with open-angle glaucoma who do not comply with medical therapy, open-angle glaucoma following filtration surgery in which a further lowering of IOP is required

Contraindications to a trabeculoplasty: closed of extremely narrow angle (trabeculum is not visible) corneal clouding advanced and rapidly progressive glaucoma–there is insufficient time to assess the response to LT active intraocular inflammation or blood in AC bad cooperation with patient

During trabeculoplasty, the burns are applied to the junction of the non-pigmented with the pigmented trabeculum. The pigmented Schwalbe’s line should not be confused with posterior pigmented trabeculum!

It is extremely important to identify the scleral spur because the application of burns posterior to it will result in greater inflammation and therefore increased risk of early post-laser rise in IOP, as well as the formation of peripheral anterior synechiae.

Trabeculectomy is a surgical procedure which lowers the IOP by the creation of a new channel for aqueous outflow between the anterior chamber and sub-Tennon’s space.

Technique of trabeculectomy: 1. A conjunctival flap is fashioned superonasally. It may be based at limbus or at fornix.

2. The scleral flap is cut by first outlining a rectangle based at the limbus (some surgeons make a square or triangular flap). Than incisions are made along the marks through two-thirds of sleral thickness and the flap is prepared.

3. The deep block of slera and trabeculum is excised.

4. A peripheral iridectomy is performed to prevent blockage of the internal opening by the peripheral iris.

5. The superficial scleral flap and the conjunctival flap are sutured.

Primary angle-closure glaucoma
Primary angle-cosure glaucoma (PACG) is a condition in which aqueous outflow is obstructed solely as a result of closure of the angle by the peripheral iris. It occurs in anatomically predisposed eyes and is frequently bilateral. It affects 1 in 1000 individuals over the age of 40. Its prevalence increases with age. Women are affected more commonly than men by a ratio of 4:1.

Anatomical predisposition to the disease is inherited and consist of the following three factors: A relatively anterior location of the iris-lens diaphragm A shallow anterior chamber A narrow entrance to the chamber angle

The proximity of the cornea to the peripheral iris enables angle closure to occur more easily than in a normal eye. The following three interrelated factors are responsible for these characteristics: axial growth of the lens small corneal diameter short axial length A short eye, which is also frequently hypermetropic, has a small corneal diameter, and a thick lens that is located in an anterior position.

Mechanism of angle closure in PCAG 1. the dilator muscle of the iris contracts, which increases the amount of apposition between the iris and the anteriorly located lens (reliative pupil block)

Mechanism of angle closure in PCAG 2. increase the pressure in posterior chamber and the flaccid peripheral iris bows anteriorly (iris bombe) 3. the angle becomes obstructed by the peripheral iris and the IOP raises

PACG can be divided into five overlapping stages: latent PACG subacute (intermittent) acute chronic absolute The condition does not necessarily progress from one stage to the next in an orderly sequence.

Latent PACG Examination shows a shallow anterior chamber, a convex-shaped iris-lens diaphragm, close proximity of the iris to the cornea, a normal IOP and a narrow angle capable of closure. Without treatment, an eye with latent PACG may remain normal or it may develop subacute, acute or chronic angle closure with or without passing through the other stages.

Treatment of latent PACG depends on the state of fellow eye. If it has had acute or subacute PACG, treatment is by a laser iridotomy. It lowers the risk of an acute angle closure.

Subacute PACG It occurs when the angle is narrow in only one part. A rapid partial closure and reopening the angle occurs. The level of elevation of IOP is proportional to the extend of angle closure.

Subacute PACG The attacks may be precipitaded by: physiological mydriasis (watching TV in a dark room, stress) physiological shallowing of the anterior chamber (when the patient assumes a prone or semiprone position to see or read)

Subacute PACG The attacks are recurrent and usually broken after 1-2 hours by physiological miosis (exposure to bright sunlight or sleep). Presentation is with transient blurring of vision associated with haloes around lights resulting from corneal epithelial oedema. They may also be some eye ache or frontal headache.

Subacute PACG Examination during an attack shows corneal epithelial oedema. In some cases pupil may be semidilated but the globe itself is uncongested. In between attacks the eye looks perfectly normal although the angle is narrow.

Subacute PACG Treatment is with intensive miotic therapy of both eyes. Also bilateral laser peripheral iridotomies should be performed.

Acute congestive angle-closure glaucoma Acute congestive PACG is characterized by a sudden and severe elevation of IOP as a result of total closure of the angle. Presentation is with rapidly progressive impairment of vision associated with periocular pain and congestion. In severe cases nausea and vomiting may occur.

Acute congestive angle-closure glaucoma Examination during the acute stage shows a ciliary flush caused by injection of the limbal and conjunctival blood vessels. The IOP is elevated and the cornea is oedematous.

Acute congestive angle-closure glaucoma The anterior chamber is shallow with peripheral iridocorneal contact. The pupil is vertically oval, fixed in the semidilated position. It is unreactive to both light and accommodation.

Acute congestive angle-closure glaucoma After the corneal oedema has cleared, examination shows: aqueous flare and cells dilated and congested blood vessels on the iris oedema of optic nerve head iridocorneal contact in gonioscopy

Acute congestive angle-closure glaucoma Initial treatment is aimed primarily at lowering IOP through systemic medication with hyperosmotic agents (glycerol p.o., mannitol i.v.). Hyperosmotic agents lower IOP by increasing blood osmolality, thereby creating an osmotic gradient between the blood and vitreous, and drawing water from the vitreous.

Acute congestive angle-closure glaucoma Subsequent treatment is aimed at re-establishing the communication between the posterior and anterior chambers by making an opening in the peripheral iris. A peripheral iridotomy is successful only if no more than 50% of the angle is permanently closed by peripheral anterior synechiae. If more than half the angle is permanently closed, the filtration surgery is usually required.

Acute congestive angle-closure glaucoma After lowering the IOP topical therapy with anti-glaucomatous drops, especially miotics may be helpful in reducing IOP and topical steroids may be useful in decongesting the eye.

Acute congestive angle-closure glaucoma It is very important to treat the fellow eye prophylactically with pilocarpine drops until a prophylactic iridotomy has been performed.

Postcongestive angle-closure glaucoma Examination shows a combination of the following signs: the IOP is normal, subnormal or elevated folds in Descemet’s membrane pigment granules on the corneal endothelium and iris

Postcongestive angle-closure glaucoma stromal iris atrophy semidilated pupil small, grey-white anterior capsular or subcapsular opacites (glaukomflecken) in gonioscopy - open angle or varying degrees of angle closure

Chronic angle-closure glaucoma The clinical features of chronic PACG are those of POAG except that gonioscopy shows a variable amount of angle closure.

Chronic angle-closure glaucoma The management depends on the mechanism of angle closure: 1. A gradual and progressive synechial angle closure, usually starting superiorly and spreading inferiorly. Treatment is by laser iridotomy to eliminate any element of pupil block, prevent the development of new peripheral anterior synechiae and make medical control easier.

Chronic angle-closure glaucoma 2. angle closure is a result of subacute attacks These cases will already have had a laser iridotomy so that the medical therapy should be added as necessary.

Absolute angle-closure glaucoma is the end stage of acute congestive PACG in which the eye is completely blind.

Secondary glaucomas: 1. Common secondary glaucomas: pseudoexfoliative glaucoma pigmentary glaucoma neovascular glaucoma inflammatory glaucomas

Secondary glaucomas: 2. Uncommon secondary glaucomas: phacolytic glaucoma lens-related pupil block glaucomas red cell glaucoma angle-recession glaucoma ghost cell glaucoma iridocorneal endothelial syndromes

Common secondary glaucomas Pseudoexfoliative glaucoma
Pseudoexfoliative glaucoma is chronic trabecular – block open-angle glaucoma, caused by pseudoexfoliation syndrome (PXS, PEX). PXS typically affects elderly patients and is bilateral only in about one-third cases. In patients with unilaterated PXS, the propability of the normal fellow eye also developing PXS after 10 years is 20%. More than 50% of patients with PXS present with glaucoma which is usually unilateral.

PXS is characterised by the secretion of a grey-white fibrillogranular material by ageing endothelial cells in anterior segment of the eye. This material is abnormal basement membrane and is histologically similar to amyloid.

The most commonly recognized feature of PXS is pseodoefoliation material (PXM) on pupillary border and anterior lens surface. The constant rubbing of the pupil scrapes the PXM off the midzone of the lens, giving rise to a central disc, a peripheral band and a clear zone in between. Peripheral band can be detected only after the pupil has been dilated.

Iris changes consist of PXM on the pupillary border, pigment dispersion and atrophy of the sphincter pupillae, which gives rise to transilumination defects (sphincter has ‚moth-eaten’ pattern).

The cornea may show deposits of both PXM and pigment. The pigment is usually distributed diffusely. The zonules and cilliary processes are covered by PXM and zonules themselves may be weak (high risc of development of a zonular dialysis during cataract surgery!).

Gonioscopy shows hyperpigmentation of trabeculum (pigment lies on the surface of trabeculum). Also Schwalbe’s line is pigmented and is called Sampaolesi’s line.

Other gonioscopic findings consist of deposits of PXM which have been rubbed off the anterior lens capsule by the iris float in the aqueous and come to rest in the inferior trabecular meshwork. On gonioscopy the PXM has a dandruff-like appearance.

The prognosis of pseudoexfoliative glaucoma is not as good as in POAG because: the IOP is usually higher and more difficult to control visual field loss may develop more rapidly.

All patients with PXS and raised IOP should be treated even in the presence of normal fields and disc, because, if untreated, a large percentage of cases will develop damage. (medical treatment, laser trabeculoplasty, filtration surgery)

Common secondary glaucomas Pigmentary glaucoma
Pigmentary glaucoma is chronic trabecular block open-angle glaucoma, caused by the pigment dispersion syndrome (PDS). PDS is a bilateral condition characterized by the deposition of pigment granules throughout the anterior segment. Glaucoma develops in 10% of patients with PDS. Affected individuals are typically myopic men in the third or fifth decades of life. The male:female ratio is 5:1.

PDS is caused by shedding of pigment, resulting from mechanical rubbing between the posterior pigment layer of the iris and the anterior surface of the zonular fibrils. This state is caused by excessive posterior bowing of the peripheral portion of the iris. The pigment granules are released into the aqeous humour and deposited on all anterior chamber structures, including trabecular meshwork.

Slitlamp examination shows: 1. Krukenberg’s spindle, which consists of pigment deposits on the corneal endothelium. The size and density of deposits are usually proportional to the extent of associated iris atrophy. 2. The anterior chamber is very deep, particularly in the midperiphery where the iris tends to bow posteriorly.

3. The anteror surface of iris is coated with pigment granules. The loss of pigment from the midperiphery of the iris gives slit-like iris defects seen on transillumination. 4. The lens and extreme periphery of the retina also show pigment deposits.

Gonioscopy shows a wide open and heavily pigmented angle. The peripheral iris root shows a mild concavity close to its insertion.

The symptoms and treatment of pigmentary glaucoma are usually those of POAG, but in some patients the IOP may initially be very unstable. In general, the long-term prognosis is relatively good but some patients have very high levels of IOP so that, at the time of diagnosis, it is common for advanced visual field to be present in one eye and relatively mild damage in the other.

Common secondary glaucomas Neovascular glaucoma
In neovascular glaucoma (NVG) elevation of IOP is caused by synechial angle closure through contraction of fibrovascular tissue. The common factor in all eyes with NVG is severe, diffuse and chronic retinal ischaemia, caused by: ischaemic retinal vein occlusion, proliferative diabetic retinopathy, carotid obstructive disease, carotid-cavernous fistula, intraocular tumours, chronic intraocular inflammation, ROP (rare causes).

NVG is divided into three stages: 1. rubeosis iridis 2. secondary open-angle glaucoma 3. synechial angle-closure glaucoma

1. rubeosis iridis Slitlamp examination of early stage of rubeosis iridis shows tiny dilated capillary at the pupillary margin. The new blood vessels grow radially over the surface of the iris towards the angle. At this stage the IOP is usually normal and neovascularization may regress (spontaneously or with treatment).

Treatment of rubeosis iridis: 1. panretinal laser photocoagulation (PRP) 2. ppV (especially in eyes with residual retinal detachment)

2. secondary open-angle glaucoma Slitlamp examination shows continued growth of new blood vessels across the iris surface, across the face of ciliary body and scleral spur to the angle. Gonioscopy shows the formation of a fibrovascular membrane which blocks the trabeculum, giving rise of IOP. Treatment options include: medical therapy and PRP even if IOP is controlled adequately by eye drops).

3. synechial angle-closure glaucoma The fibrovascular tissue in the angle contracts and pulls the peripheral iris over the trabeculum in a zipper-like fashion.

Examination shows: reduced visual acuity, very high IOP with pain of the globe, congestion of the eye, corneal oedema, aqueous flare, severe rubeosis iridis, distorted pupil with ectropion uveae (caused by contraction of fibrovascular tissue).

Gonioscopy shows synechial angle-closure with inability to see any of the angle structures posterior to Schwalbe’s line.

Visual prognosis is extremely poor!!! Treatment is mainly to relieve pain and congestion of the eye by the following methods: PRP (if media are clear) or peripheral retinal cryotherapy (if media are hazy), medical therapy (the same as that for POAG, steroids and atropine) – may make the eye more comfortable and less congested, artificial filtering shunts, cyclodestructive procedures, enucleation (if all else fails)

Common secondary glaucomas Inflammatory glaucomas
There are three main types of inflammatory glaucomas: 1. angle closure with pupil block 2. angle closure without pupil block 3. open angle

1.angle-closure glaucoma with pupil block Secondary angle closure is caused by 360 iridolenticular adhesions – seclusio pupillae. The pupil block obstructs the passage of aqueous humour from the posterior to the anterior chamber, and the increased pressure in the posterior chamber causes an anterior bowing of the peripheral iris – iris bombe.

If iris bombe occurs in an eye with active inflammation, the iris sticks to the trabeculum and iridocorneal contact becomes permanent with the development of peripheral anterior synechiae (PAS). Slitlamp examination shows seclusio pupillae, iris bombe and very shallow anterior chamber. Gonioscopy shows angle closure from iridotrabecular contact.

Treatment involves the following measures: prevention of synechial angle closure (intensive topical steroids), lowering of IOP (B-blockers, sympathomimetics, carbonic anhydrase inhibitors), laser iridotomy ( will be effective in lowerring IOP, if at least 25% of angle is open)

2. angle closure glaucoma without pupil block The deposition and subsequent contaction of inflammatory debris in the angle (during chronic anterior uveitis) pull the peripheral iris over the trabeculum, causing a gradual and progressive synechial angle closure. The rise of IOP is usually gradual and even severe elevations of IOP may be asymptomatic!!!

Slitlamp examination shows a deep anterior chamber and variable amounts of angle closure by peripheral anterior synechiae are found in gonioscopy. Exacerbations of intraocular inflammation in eyes with chronic iridocyclitis are frequently associated with lowering IOP!!!

Treatment options: medical therapy (the same as that for secondary angle closure caused by pupil block), filtration surgery, combined with anti-metabolites or artificial filtering shunts, cyclodestructive procedures

3. open angle glaucoma In acute anterior uveitis the trabecular-block may be caused by either inflammatory cells and debris or acute trabeculitis. In chronic anterior uveitis the facility of outflow is impaired by trabecular scarring and sclerosis secondary to chronic trabeculitis.

Definitive diagnosis of inflammatory open angle glaucoma is difficult because of the variable appearance of the angle. In theory, the angle should be open with gelatinous exudate on the trabeculum – ‚mashed potatoes’. Treatment is the same as that for secondary synechial angle-closure glaucoma.

Uncommon secondary glaucomas Phacolytic glaucoma
This is trabecular-block open-angle glaucoma which occurs in eyes with hypermature cataracts. It is caused by trabecular obstruction with high-molecular, soluble lens proteins which have leaked through an intact capsule into the aqueous humour. Macrophages that have phagocytosed some of the proteins may also contribute to trabecular blockage.

Phacolytic glaucoma should not be cofused with phacoanaphylactic uveitis which is an autoimmune granulomatous reaction to lens proteins occuring in eyes with ruptured capsules.

Slitlamp examination shows an eye with a hypermature cataract. The anterir chamber is deep and contain floating white particles, some of which may settle inferiorly to form a ‚pseudohypopyon’. Gonioscopy shows an open angle with white particles in trabeculum.

Treatment – cataract extraction!

Uncommon secondary glaucomas Ghost cell glaucoma
Trabecular obstruction is caused by degenerated red blood cells. 2 weeks after haemorrhage into the vitreous, the haemoglobin leaks out of the red blood cells, turning them into ‚ghost cells’. They pass through a defect in the anterior vitreous face into the anterior chamber and obstruct aqueous outflow.

Uncommon secondary glaucomas Ghost cell glaucoma
Slitlamp examination shows reddish-brown or khaki particles in anterior chamber. Treatment is initially medical. If this is ineffective, irrigation of the anterior chamber should be performed and the ghost cells washed out.

Congenital glaucomas Congeniatal glaucomas are divided into: Primary congenital glaucoma Secondary congenital glaucoma

Primary congenital glaucoma (PCG)
PCG affects 1 in births, with 65% patients being boys. In 75% of cases both eyes are affected. Aqueous outflow is impaired as the result of a maldevelopment of the trabeculum and the iridotrabecular junction, which is not associated with other major ocular anomalies – isolated trabeculodysgenesis.

Primary congenital glaucoma
Clinically, trabeculodysgenesis is characterised by the absence of the angle recess, with the iris inserted directly into the surface of the trabeculum. The iris insertion can be either flat or concave.

The clinical features depend on the age of onset and the level of IOP. Examination of patients shows the following: 1. Corneal haze – resulting from epithelial oedema and corneal clouding is an important sign of elevated IOP. It is often associated with lacrimation, photophobia and blepharospasm.

2. Buphthalmos – occurs if the IOP becomes elevated before the age of 3 years. As the sclera enlarges, it also becomes thinner and takes on a blue appearance as a result of enhanced visualisation of the underlying choroid. In advanced cases, when the anterior chamber deepens the zonules become stretched and the lens may subluxate. The ocular enlargement causes axial myopia.

3. Breaks in Descemet’s membrane may be associated with endothelial decompensation and a sudden influx of aqueous into the corneal stroma. Healed breaks in Descemet’s membrane are called Haab’s striae and appear as a horizontal lines in cornea.

4. Glaucomatous cupping in infants may occur early, although it may regress once the IOP is normalized. In contrast to adults eyes, the scleral canal in infants enlarges with high IOPs because of the generalized enlargement of the globe. The lamina cribrosa may also bow posteriorly. In infants, the cup/disc ratio may be increased from either neuronal loss or enlargement of the scleral canal, or both.

Treatment of PCG: 1. Goniotomy – should be done as soon as it’s possible! In this procedure an incision is made in the angle to establish a communication between the anterior chamber and Schlemm’s canal. Although goniotomy may have to be repeated, the eventual success rate is about 85%.

2. Trabeculotomy may be necessary if either corneal clouding prevents visualization of the angle or goniotomy has failed. In this procedure, part of the trabecular meshwork is removed to establish a communication between the anterior chamber and Schlemm’s canal.

The prognosis is good in about 60% of cases. The remainder develop visual loss from a combination of: optic nerve damage, anisometropic amblyopia (myopia!), corneal scarring, cataract, lens subluxation. A buphthalmic eyes are also susceptible to traumatic damage!!!

Rare conditions which may be associated with glaucoma are:
Congenital glaucomas Secondary congeniatal glaucomas occur in patients with congenital disorders involving the cornea and iris - iridocorneal disgenesis. Rare conditions which may be associated with glaucoma are: Axenfeld’s anomaly, Rieger’s anomaly, Rieger’s syndrome, Peter’s anomaly, aniridia, nanophthalmos, phacomatoses.

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Diagnostic and treatment of glaucoma

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Diagnostic and treatment of glaucoma

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