Anatomy

• •
  

  The trabecular meshwork (trabeculum) is a sieve-like structure ( Fig. 10.1 ) at the angle of the anterior chamber (AC) through which 90% of aqueous humour leaves the eye. It has three components ( Fig. 10.2 ).

  
  
  
  
  • ○
    

    The uveal meshwork is the innermost portion, consisting of cord-like endothelial cell-covered strands arising from the iris and ciliary body stroma. The intertrabecular spaces are relatively large and offer little resistance to the passage of aqueous.

    
    
  • ○
    

    The corneoscleral meshwork lies external to the uveal meshwork to form the thickest portion of the trabeculum. It is composed of layers of connective tissue strands with overlying endothelial-like cells. The intertrabecular spaces are smaller than those of the uveal meshwork, conferring greater resistance to flow.

    
    
  • ○
    

    The juxtacanalicular (cribriform) meshwork is the outer part of the trabeculum, and links the corneoscleral meshwork with the endothelium of the inner wall of the canal of Schlemm. It consists of cells embedded in a dense extracellular matrix with narrow intercellular spaces, and offers the major proportion of normal resistance to aqueous outflow.

  
  

  
  

  
  

  

  
  

  
  

  Scanning electron micrograph of the trabecular meshwork

  
  

  
  

  
  

  

  
  

  
  

  Anatomy of outflow channels: A, Uveal meshwork; B, corneoscleral meshwork; C, Schwalbe line; D, Schlemm canal; E, connector channels; F, longitudinal muscle of the ciliary body; G, scleral spur

  
  
  
  
• •
  

  The Schlemm canal is a circumferential channel within the perilimbal sclera. The inner wall is lined by irregular spindle-shaped endothelial cells containing infoldings (giant vacuoles) that are thought to convey aqueous via the formation of transcellular pores. The outer wall is lined by smooth flat cells and contains the openings of collector channels, which leave the canal at oblique angles and connect directly or indirectly with episcleral veins. Septa commonly divide the lumen into 2–4 channels.

Physiology

Aqueous flows from the posterior chamber via the pupil into the AC, from where it exits the eye via three routes ( Fig. 10.3 ).

• •
  

  Trabecular outflow (90%): aqueous flows through the trabeculum into the Schlemm canal and then the episcleral veins. This is a bulk flow pressure-sensitive route so that increasing IOP will increase outflow.

  
  
• •
  

  Uveoscleral drainage (10%): 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.

  
  
• •
  

  Iris : some aqueous also drains via the iris.

Routes of aqueous outflow: A, trabecular; B, uveoscleral; C, iris

Concept of normal intraocular pressure

The average IOP in the general population is around 16 mmHg on applanation tonometry, and a range of about 11–21 mmHg – two standard deviations either side of the average – has conventionally been accepted as normal, at least for a Caucasian population. However, some patients develop glaucomatous damage with IOP less than 21 mm Hg whilst others remain unscathed with IOP well above this level. Whilst reduction of IOP is a key modifiable element in essentially all types of glaucoma, additional incompletely understood factors are critical in determining whether a particular individual or eye develops glaucomatous damage. These include features influencing the IOP reading, such as corneal rigidity, and probably factors affecting the susceptibility of the optic nerve to damage, such as the integrity of its blood supply and structural vulnerability to mechanical stress at the optic nerve head.

Fluctuation

Normal IOP varies with time of day (diurnal variation), heartbeat, blood pressure and respiration. The diurnal pattern varies, with a tendency to be higher in the morning and lower in the afternoon and evening. This is at least partially due to a diurnal pattern in aqueous production, which is lower at night. Glaucomatous eyes exhibit greater than normal fluctuation, the extent of which is directly proportional to the likelihood of progressive visual field damage, and a single reading may therefore be misleading. It is good practice always to note the time of day in conjunction with a recorded IOP.

Definition

It is difficult to define glaucoma precisely, partly because the term encompasses a diverse group of disorders. All forms of the disease have in common a characteristic potentially progressive optic neuropathy that is associated with visual field loss as damage progresses, and in which IOP is a key modifiable factor.

Classification

Glaucoma may be congenital (developmental) or acquired. Open-angle and angle-closure types are distinguished based on the mechanism by which aqueous outflow is impaired with respect to the AC angle configuration. Distinction is also made between primary and secondary glaucoma; in the latter a recog­nizable ocular or non-ocular disorder contributes to elevation of IOP.

Epidemiology

Glaucoma affects 2–3% of people over the age of 40 years; 50% may be undiagnosed. Primary open-angle glaucoma (POAG) is the most common form in white, Hispanic/Latino and black individuals; the prevalence is especially high in the latter. On a worldwide basis, primary angle closure (PAC) constitutes up to half of cases, and has a particularly high prevalence in individuals of Asian descent, although with improved assessment such as the routine performance of gonioscopy in a darkened rather than a bright environment, PAC is known to be more prevalent in Caucasian individuals than previously realized.

Principles

Goldmann applanation tonometry (GAT) is based on the Imbert–Fick principle, which states that for a dry thin-walled sphere, the pressure ( P ) inside the sphere equals the force ( F ) necessary to flatten its surface divided by the area ( A ) of flattening (i.e. P = F / A ). Theoretically, average corneal rigidity (taken as 520 µm for GAT) and the capillary attraction of the tear meniscus cancel each other out when the flattened area has the 3.06 mm diameter contact surface of the Goldmann prism, which is applied to the cornea using the Goldmann tonometer with a measurable amount of force from which the IOP is deduced ( Fig. 10.4 ). The tonometer prism should be disinfected between patients and replaced regularly in accordance with the manufacturer’s instructions. Disposable tonometer prisms and caps have been introduced to address concerns of infection from reusable prisms.

Goldmann tonometry. (A) Physical principles; (B) tonometer

(Courtesy of J Salmon – fig. B)

Technique

• •
  

  Topical anaesthetic (commonly proxymetacaine 0.5%) and a small amount of fluorescein are instilled into the conjunctival sac.

  
  
• •
  

  The patient is positioned at the slit lamp with his or her forehead firmly against the headrest and instructed to look straight ahead (often at the examiner’s opposite ear) and to breathe normally.

  
  
• •
  

  With the cobalt blue filter in place and illumination of maximal intensity directed obliquely (approximately 60°) at the prism, the prism is centred in front of the apex of the cornea.

  
  
• •
  

  The dial is preset at 1 (i.e. 10 mmHg).

  
  
• •
  

  The prism is advanced until it just touches the apex of the cornea ( Fig. 10.5A ).

  
  

  
  

  
  

  

  
  

  
  

  Applanation tonometry. (A) Contact between the tonometer prism and the cornea; (B) fluorescein-stained semicircular mires – the diagram at right shows the correct end-point using mires of appropriate thickness

  
  
  
  
• •
  

  Viewing is switched to the ocular of the slit lamp.

  
  
• •
  

  A pattern of two green semicircular mires will be seen, one above and one below the horizontal midline, which represent the fluorescein-stained tear film touching the upper and lower outer halves of the prism. Mire thickness should be around 10% of the diameter of its total arc ( Fig. 10.5B ). Care should be taken to horizontally and vertically centre the mires so that as far as practically possible two centralized semicircles are observed.

  
  
• •
  

  The dial on the tonometer is rotated to vary the applied force; the inner margins of the semicircles align when a circular area of diameter precisely 3.06 mm is flattened.

  
  
• •
  

  The reading on the dial, multiplied by 10, gives the IOP; a version is available that shows IOP on a digital display.

Sources of error

• •
  

  Inappropriate fluorescein pattern. Excessive fluorescein will result in the mires being too thick, with consequent overestimation of IOP; insufficient will make the semicircles too thin, with consequent underestimation (see Fig. 10.5B , left and centre).

  
  
• •
  

  Pressure on the globe from the examiner’s fingers, eyelid squeezing or restricted extraocular muscles (e.g. thyroid myopathy) may give an anomalously high reading.

  
  
• •
  

  Central corneal thickness (CCT). Calculations of IOP by GAT assume that central corneal thickness is 520 µm, with minimal normal variation. If the cornea is thinner, an underestimation of IOP is likely to result, and if thicker, an overestimation. Corneas tend to be thicker than average in individuals with ocular hypertension, and thinner in normal-tension glaucoma (NTG); following refractive surgery procedures the cornea is both thinner and structurally altered such that IOP is likely to be underestimated. Some methods of IOP measurement (e.g. DCT – see below) may reduce the effect of structural confounding variables. Other corneal mechanical factors may also be important but are less well defined.

  
  
• •
  

  Corneal oedema may result in artificial lowering of IOP, hypothesized to be due to a boggy softening; the associated increased CCT seems to be more than offset.

  
  
• •
  

  Astigmatism , if significant, may give distorted mires as well as leading to mechanically induced errors. If over 3 dioptres, the average reading of two can be taken with the prism rotated 90° for the second, or optimally the prism is rotated so that the red line on the tonometer housing is aligned with the prescription of the minus axis.

  
  
• •
  

  Incorrect calibration of the tonometer can result in a false reading, and calibration should optimally be checked before each clinical session using the manufacturer’s calibration arm.

  
  
• •
  

  Wide pulse pressure. It is normal for there to be a small oscillation of IOP in concert with the rhythm of ocular perfusion. If this ‘pulse pressure’ is substantial, either the midpoint or the highest level observed may be taken.

  
  
• •
  

  Repeated readings over a short period will often be associated with a slight fall in IOP due to a massaging effect on the eye.

  
  
• •
  

  Other factors include a tight collar and breath-holding, both of which obstruct venous return and can raise IOP.

Overview

• •
  

  Gonioscopy is a method of evaluating the AC angle, and can be used therapeutically for procedures such as laser trabeculoplasty and goniotomy.

  
  
• •
  

  Other means of angle assessment such as anterior segment optical coherence tomography (OCT) and high-frequency ultrasound biomicroscopy (UBM) offer advantages in some aspects of angle analysis, but current clinical opinion suggests they should supplement rather than replace visual gonioscopic analysis.

Optical principles

The angle of the AC cannot be visualized directly through the intact cornea because light from angle structures undergoes ‘total internal reflection’ at the anterior surface of the precorneal tear film ( Fig. 10.7, top ). When light travels from a medium of higher to one of lower refractive index (such as cornea to air) it will be reflected at the interface between the two unless the angle of incidence is less than a certain ‘critical angle’ dependent on their refractive index difference (46° for the tear film–air interface). The phenomenon is utilized in optical fibre signal transmission, where it ensures that light is retained within the core of a cable. Because the refractive index of a goniolens is similar to that of the cornea, it eliminates total internal reflection by replacing the tear film–air interface with a tear film–goniolens interface ( Fig. 10.7 , bottom). Light rays can then be viewed as they exit the contact lens, directly or indirectly (see below).

Optical principles of gonioscopy; n = refractive index; i = angle of incidence

Disinfection

Lenses must be cleaned between patients to remove any particulate matter and then sterilized; a suggested regimen is soaking in 2% hypochlorite solution (this has activity against transmissible spongiform encephalopathies) for at least 5 minutes followed by thorough rinsing in sterile saline, then air-drying.

Non-indentation gonioscopy

• •
  

  Goniolenses

  
  
  
  
  • ○
    

    The classic Goldmann lens consists of three mirrors ( Fig. 10.8A ), one of which is specifically for gonioscopy; some goniolenses have one ( Fig. 10.8B ), two or four mirrors.

    
    

    
    

    
    

    

    
    

    
    

    Goldmann goniolens. (A) Three mirrors; (B) single mirror

    
    

    
    

    

    
    
    
    
  • ○
    

    Lenses of similar basic structure but with modifications include the Magna View, Ritch trabeculoplasty and the Khaw direct view.

    
    
  • ○
    

    Because the curvature of the contact surface of the lens is steeper than that of the cornea, a viscous coupling substance of refractive index similar to the cornea is required to bridge the gap between cornea and lens.

  
  
  
  
• •
  

  Technique

  
  
  
  
  • ○
    

    It is essential that the examination takes place in a room in which the ambient illumination is very low – completely dark if possible.

    
    
  • ○
    

    The size and intensity of the slit beam should be reduced to the absolute minimum compatible with an adequate view, in particular avoiding any of the beam being directed through the pupil.

    
    
  • ○
    

    The patient is seated at the slit lamp and advised that the lens will touch the eye but will not usually cause discomfort; the forehead must be kept against the headband and both eyes should remain open.

    
    
  • ○
    

    A drop of local anaesthetic is instilled.

    
    
  • ○
    

    A drop or two of coupling fluid (e.g. hypromellose 0.3%) is placed on the contact surface of the lens.

    
    
  • ○
    

    The patient is asked to look upwards and the lens is inserted rapidly so as to avoid loss of the coupling fluid. The patient then looks straight ahead.

    
    
  • ○
    

    Indirect gonioscopy gives an inverted view of the portion of the angle opposite the mirror.

    
    
  • ○
    

    Once the initial examination has been performed and the findings noted, increasing the level of illumination may help in defining the angle structures.

    
    
  • ○
    

    When the view of the angle is obscured by a convex iris, it is possible to see ‘over the hill’ by asking the patient to look in the direction of the mirror. Only slight movement is permissible, otherwise the structures will be distorted and a closed angle may appear open.

    
    
  • ○
    

    Excessive pressure with a non-indentation lens narrows the angle appearance (in contrast to the effect of pressure during indentation gonioscopy – see below). Excessive pressure also causes folds in the cornea that compromise the clarity of the view.

    
    
  • ○
    

    In some eyes, suction on the cornea from the lens may artificially open the angle; awareness of the need to avoid retrograde, as well as anterograde, pressure on the lens will tend to prevent inadvertent distortion.

  
  

Indentation (dynamic, compression) gonioscopy

• •
  

  Goniolenses include the Zeiss ( Fig. 10.9 ), Posner and Sussman (no handle), all of which are four-mirror gonioprisms.

  
  
  
  
  • ○
    

    The contact surface of the lenses has a curvature flatter than that of the cornea, negating the need for a coupling substance.

    
    
  • ○
    

    The lenses do not stabilize the globe and are relatively unsuitable for laser trabeculoplasty.

    
    
  • ○
    

    A common criticism is that it is easy to inadvertently open the angle, giving a misleadingly reassuring impression, especially if inexperienced.

  
  

  
  

  
  

  

  
  

  
  

  (A) Zeiss goniolens; (B) slit lamp view with lens in place on the cornea

  
  
  
  
• •
  

  Technique

  
  
  
  
  • ○
    

    The first stages are as set out above for non-indentation gonioscopy.

    
    
  • ○
    

    Indentation is performed by gently pressing the lens posteriorly against the cornea; this forces aqueous into the angle, pushing the peripheral iris posteriorly.

    
    
  • ○
    

    If the angle is closed only by apposition between the iris and cornea it will be forced open, allowing visualization of the angle recess ( Fig. 10.10 ).

    
    

    
    

    
    

    

    
    

    
    

    Indentation gonioscopy in appositional angle closure. (A) Total angle closure prior to indentation; (B) during indentation the entire angle becomes visible (arrow) – the corneal folds seen are typical

    
    

    (Courtesy of W Alward, from Color Atlas of Gonioscopy , Wolfe 1994)

    
    
    
    
  • ○
    

    If the angle is closed by adhesions between the peripheral iris and cornea – peripheral anterior synechiae (PAS) – it will remain closed.

    
    
  • ○
    

    Dynamic gonioscopy can be invaluable in helping to define the structures in angles that are difficult to assess, such as in distinguishing an extensive or double highly pigmented Schwalbe line from the pigmented meshwork.

  
  

Shaffer system

The Shaffer system records the angle in degrees between two imaginary lines tangential to the inner surface of the trabeculum and the anterior surface of the iris about one-third of the distance from its periphery. The system assigns a numerical grade to each quadrant of the angle.

• •
  

  Grade 4 (35–45°) is the widest angle, characteristic of myopia and pseudophakia; the ciliary body can be visualized without tilting the lens.

  
  
• •
  

  Grade 3 (25–35°) is an open angle in which the scleral spur is visible.

  
  
• •
  

  Grade 2 (20°) is an angle in which the trabeculum but not the scleral spur can be seen.

  
  
• •
  

  Grade 1 (10°) is a very narrow angle in which only the Schwalbe line and perhaps the top of the trabeculum can be identified.

  
  
• •
  

  Slit angle is one in which there is no obvious iridocorneal contact but no angle structures can be identified.

  
  
• •
  

  Grade 0 (0°) is closed due to iridocorneal contact.

  
  
• •
  

  Indentation will distinguish appositional from synechial angle closure.

Other systems

• •
  

  The Spaeth system is detailed but underused. It allows formal description of the position of iris insertion, the angular approach and peripheral iris curvature.

  
  
• •
  

  The Scheie classification refers to the angle structures visible and allocates a Roman numeral accordingly. In contrast to common clinical use, in the original system a higher numeral (e.g. IV) actually signifies a narrower angle.

  
  
• •
  

  The van Herick method ( Table 10.1 ) uses the slit lamp alone to estimate the AC angle width:

  
  
  
  
  • ○
    

    A thin but bright slit beam is set approximately perpendicularly to the corneal surface (offset from the optics by about 60°) to the patient’s temporal side for each eye.

    
    
  • ○
    

    The beam is used to estimate the ratio of the corneal thickness to the most peripheral part of the AC.

    
    
  • ○
    

    It is useful as a screening tool, but overestimates angle width in a proportion of patients, particularly those with a plateau iris conformation.

  
  

Neuroretinal rim

The neuroretinal rim (NRR) is the orange-pink tissue between the outer edge of the cup and the optic disc margin. The inferior rim is the broadest followed by the superior, nasal and temporal (the ‘ISNT’ rule – Fig. 10.15 ); this has high sensitivity for glaucoma but is not very specific, i.e. eyes without glaucoma often do not respect the rule.

Normal disc that obeys the ‘ISNT’ rule (see text)

Cup/disc (C/D) ratio

The C/D ratio indicates the diameter of the cup expressed as a fraction of the diameter of the disc; the vertical rather than the horizontal ratio is generally taken. Small diameter optic discs have small cups ( Fig. 10.16A ) and vice versa ( Fig. 10.16B ); only 2% of the population have a C/D ratio greater than 0.7. In any individual, asymmetry of 0.2 or more between the eyes should also be regarded with suspicion, though it is critical to exclude a corresponding difference in overall disc diameter (see next).

Normal discs. (A) Small disc with a low cup/disc ratio; (B) larger disc with a proportionally larger cup

Optic disc size

Optic disc size is important in deciding if a cup/disc (C/D) ratio is normal (see above), and is also a prognostic indicator. Large discs are believed to be more likely to sustain damage, particularly in NTG. This may be the result of the larger diameter conferring relative mechanical weakness and hence greater vulnerability to IOP-induced displacement of the lamina cribrosa; the lamina cribrosa has been found to be thinner in eyes with NTG. Disc size varies on average between racial groups, and is largest in black individuals. Imaging can objectively measure disc area, but vertical diameter is the parameter most frequently used clinically; normal median vertical diameter (for non-glaucomatous discs) is 1.5–1.7 mm in a white population.

• 
  
  
  
  
  
  • ○
    

    A narrow slit beam is focused on the disc using a fundus lens.

    
    
  • ○
    

    The height of the beam is adjusted until it matches the distance between the superior and inferior limits of the NRR (not the scleral rim surrounding the neural tissue), and the diameter in millimetres is read from the slit lamp graticule.

    
    
  • ○
    

    A correction factor may be necessary, depending on the lens used ( Table 10.2 ). Refractive error affects measurement only minimally, although myopia above −8 dioptres may distort the result.

    
    
    
    

    Table 10.2

    
    

    Correction factors for estimating optic disc diameter

    
    

    
    
    
    
    
    
    
    
    
    
    
    
    
    
    
    
    
    
    
    
    
    

    Lens	Correction factor
    Volk 60 D	×0.88–1.0
    Nikon 60 D	Around 1.0
    Volk 90 D	×1.3
    Volk 78 D	×1.1
    Goldmann 3-mirror	×1.27

     
    
    

  
  

Optic nerve head

Pathological cupping is caused by an irreversible decrease in the number of nerve fibres, glial cells and blood vessels. A documented increase in cup size is always significant. If an eye with a small optic disc and correspondingly small cup develops glaucoma, the cup will increase in size, but even in the presence of substantial damage may still be smaller than that of a large physiological cup.

Subtypes of glaucomatous damage

Four ‘pure’ glaucomatous disc appearances have been described, and although the majority of discs are unclassifiable the descriptions encompass a useful overview of patterns of glaucomatous damage, and may provide clues to underlying pathological processes.

• •
  

  Focal ischaemic discs ( Fig. 10.17A ) are characterized by localized superior and/or inferior notching and may be associated with localized field defects with early threat to fixation.

  
  

  
  

  
  

  

  
  

  
  

  Classic subtypes of glaucomatous damage. (A) Focal ischaemic – inferior notch and disc haemorrhage; (B) myopic; (C) sclerotic; (D) concentrically enlarging

  
  

  
  

  

  
  

  
  

  

  
  

  
  

  

  
  
  
  
• •
  

  Myopic disc with glaucoma ( Fig. 10.17B ) refers to a tilted (obliquely inserted), shallow disc with a temporal crescent of parapapillary atrophy, together with features of glaucomatous damage. Dense superior or inferior scotomas threatening fixation are common. This morphology is most common in younger male patients.

  
  
• •
  

  Sclerotic discs ( Fig. 10.17C ) are characterized by a shallow, saucerized cup and a gently sloping NRR, variable peripapillary atrophy and peripheral visual field loss. The peripapillary choroid is thinner than in other disc types. Patients are older, of either gender, and there is an association with systemic vascular disease.

  
  
• •
  

  Concentrically enlarging discs (verified by serial monitoring) are characterized by fairly uniform NRR thinning ( Fig. 10.17D ) and are frequently associated with diffuse visual field loss. IOP is often significantly elevated at presentation.

Non-specific signs of glaucomatous damage

Other disc signs of glaucomatous damage include:

• •
  

  Disc haemorrhages ( Figs 10.18A and B , and see Fig. 10.17A ) often extend from the NRR onto the retina, most commonly inferotemporally. Their presence is a risk factor for the development and progression of glaucoma. They are more common in NTG, but can also occur in healthy individuals as well as patients with systemic vascular disease.

  
  

  
  

  
  

  

  
  

  
  

  Non-specific signs of glaucomatous damage. (A) and (B) Disc haemorrhages; (C) baring of inferior circumlinear blood vessel; (D) bayoneting of blood vessels; (E) collateral vessels; (F) loss of nasal neuroretinal rim and laminar dot sign

  
  

  (Courtesy of S Chen – fig. A)

  
  

  
  

  

  
  

  
  

  

  
  

  
  

  

  
  

  
  

  

  
  

  
  

  

  
  
  
  
• •
  

  Baring of circumlinear blood vessels is a sign of early thinning of the NRR. It is characterized by a space between the neuroretinal rim and a superficial blood vessel ( Fig. 10.18C ).

  
  
• •
  

  Bayoneting is characterized by double angulation of a blood vessel. With NRR loss, a vessel entering the disk from the retina may angle sharply backwards into the disk and then turn towards its original direction to run across the lamina cribrosa ( Fig. 10.18D ).

  
  
• •
  

  Collaterals between two veins at the disc ( Fig. 10.18E ), similar to those following central retinal vein occlusion (CRVO), are relatively uncommon. They are probably caused by chronic low-grade circulatory obstruction. Retinal vascular tortuosity may also occur.

  
  
• •
  

  Loss of nasal NRR ( Fig. 10.18F ) is a sign of moderately advanced damage; a space may develop between the NRR and the central retinal vasculature.

  
  
• •
  

  The laminar dot sign occurs in advancing glaucoma. Grey dot-like fenestrations in the lamina cribrosa (see Fig. 10.18F ) become exposed as the NRR recedes. The fenestrations sometimes appear linear, and this itself may be a sign of advanced damage, indicating distortion of the lamina. The dots may be seen in normal eyes.

  
  
• •
  

  ‘Sharpened edge’ or ‘sharpened rim’ is a sign of advancing damage. As NRR is lost adjacent to the edge of the disc, the disc margin contour assumes a sharper angle backwards. Bayoneting of vessels is often seen at a sharpened edge. This should not be confused with a ‘sharpened nasal polar edge’, which refers to the sharp angulation of the NRR at the nasal margin of a focal vertical polar notch.

Peripapillary changes

Peripapillary atrophy (PPA) surrounding the optic nerve head may be of significance in glaucoma ( Fig. 10.19 ), and may be a sign of early damage in patients with ocular hypertension.

• •
  

  Alpha (outer) zone is characterized by superficial retinal pigment epithelial changes. It tends to be larger and possibly more common in glaucomatous eyes.

  
  
• •
  

  Beta (inner) zone is characterized by chorioretinal atrophy; it is distinct from the scleral rim, the white band of exposed sclera central to the beta zone. The beta zone is larger and more common in glaucoma, and is a risk factor for progression; the location of beta-zone PPA seems to indicate the orientation of likely visual field loss.

Parapapillary changes. Alpha zone (white arrow) and beta zone (black arrow)

Retinal nerve fibre layer

In glaucoma subtle retinal nerve fibre layer (RNFL) defects precede the development of detectable optic disc and visual field changes; their onset often follows disc haemorrhages. Two patterns occur: (a) localized wedge-shaped defects and (b) diffuse defects that are larger and have indistinct borders. Defects are sometimes evident following disc haemorrhages ( Fig. 10.20A ). Red-free (green) light increases the contrast between normal retina and defects on slit lamp biomicroscopy or fundus photography ( Fig. 10.20B ) and typically makes identification easier. OCT and scanning laser polarimetry are highly effective means of quantifying the RNFL. It should be noted that RNFL defects are not specific to glaucoma, and can be seen in a range of neurological disease, as well as apparently normal individuals.

Retinal nerve fibre layer defects. (A) Superotemporal wedge-shaped defect associated with a disc margin haemorrhage; (B) red-free photograph of the same eye

(Courtesy of P Gili)

Threshold

Threshold perimetry is used for detailed assessment of the hill of vision by plotting the threshold luminance value at various locations in the visual field and comparing the results with age-matched ‘normal’ values. A typical automated strategy is to present a stimulus of higher than expected intensity; if seen, the intensity is decreased in steps (e.g. 4 dB) until it is no longer seen (‘staircasing’). The stimulus is then increased again (e.g. 2 dB steps) until seen once more ( Fig. 10.26 ). If the stimulus is not seen initially, its intensity is increased in steps until seen. Essentially, the threshold is crossed in one direction with large increments, then crossed again to ‘fine-tune’ the result with smaller increments. Threshold testing is commonly used for monitoring glaucoma.

Determination of threshold

Suprathreshold

Suprathreshold perimetry involves testing with stimuli of luminance above the expected normal threshold levels for an age-matched population to assess whether these are detected; in other words, testing to check that a subject can see stimuli that would be seen by a normal person of the same age. It enables testing to be carried out rapidly to indicate whether function is grossly normal or not and is usually reserved for screening.

Fast algorithms

In recent years strategies have been introduced with shorter testing times, providing efficiency benefits with little or no detriment to testing accuracy. The HFA offers the SITA (Swedish Interactive Thresholding Algorithm), which uses a database of normal and glaucomatous fields to estimate threshold values, and takes responses during the test into account to arrive at adjusted estimates throughout the test. Full threshold values are obtained at the start of the test for four points. SITA-Standard and SITA-Fast ( Fig. 10.27 ) versions are available; their relative superiority is subject to debate. The Octopus Perimeter uses G-TOP (Glaucoma Tendency Oriented Perimetry), which again estimates thresholds based on information gathered from more detailed assessment of adjacent points. TOP presents each stimulus once at each location, instead of 4–6 times per location with a standard technique.

Humphrey perimetry – SITA-Fast printout (see text)

Reliability indices

Reliability indices (see Fig. 10.27, top left corner) reflect the extent to which the patient’s results are reliable, but it is important to note that there is relatively little research-based evidence in this area, with limited absolutes in branding a field as clearly reliable or unreliable. With SITA strategies, false negatives or false positives over about 15% should probably be regarded as highly significant, and with full-threshold strategies, fixation losses over 20% and false positives or negatives over 33%. In patients who consistently fail to achieve good reliability it may be useful to switch to a suprathreshold strategy or kinetic perimetry.

• •
  

  Fixation losses indicate steadiness of gaze during the test. Methods of assessment include presentation of stimuli to the blind spot to ensure no response is recorded, and the use of a ‘gaze monitor’.

  
  
• •
  

  False positives are usually assessed by decoupling a stimulus from its accompanying sound. If the sound alone is presented and the patient still responds, a false positive is recorded. With a high false-positive score the grey scale printout appears abnormally pale ( Fig. 10.28 ). In SITA testing, false positives are estimated based on the response time.

  
  

  
  

  
  

  

  
  

  
  

  High false-positive score (arrow) with an abnormally pale grey scale display

  
  
  
  
• •
  

  False negatives are registered by presenting a stimulus much brighter than threshold at a location where the threshold has already been determined. If the patient fails to respond, a false negative is recorded. A high false-negative score indicates inattention, tiredness or malingering, but is occasionally an indication of disease severity rather than unreliability. The grey scale printout in individuals with high false-negative responses tends to have a clover leaf shape ( Fig. 10.29 ).

  
  

  
  

  
  

  

  
  

  
  

  High false-negative score (arrow) with a clover leaf-shaped grey scale display

  
  

Sensitivity values

• •
  

  A numerical display (see Fig. 10.27 , upper left display) gives the measured or estimated (depending on strategy) threshold in dB at each point. In a full-threshold strategy, where the threshold is rechecked either as routine or because of an unexpected (>5 dB) result, the second result is shown in brackets next to the first.

  
  
• •
  

  A grey scale represents the numerical display in graphical form (see Fig. 10.27 , upper right display) and is the simplest display modality to interpret: decreasing sensitivity is represented by darker tones – the physiological blind spot is a darker area in the temporal field typically just below the horizontal axis. Each change in grey scale tone is equivalent to a 5 dB change in sensitivity at that location.

  
  
• •
  

  Total deviation (see Fig. 10.27 , middle left display) shows the difference between a test-derived threshold at a given point and the normal sensitivity at that point for the general population, correcting for age. Negative values indicate lower than normal sensitivity, positive values higher than normal.

  
  
• •
  

  Pattern deviation (see Fig. 10.27 , middle right display) is derived from total deviation values adjusted for any generalized decrease in sensitivity in the overall field (e.g. lens opacity), and demonstrates localized defects.

  
  
• •
  

  Probability value plots of the total and pattern deviation (see Fig. 10.27 , left and right lower displays) are a representation of the percentage (<5% to <0.5%) of the normal population in whom the measured defect at each point would be expected. Darker symbols represent a greater likelihood that a defect is significant.

Summary values

Summary values (‘global indices’ on the HFA – see Fig. 10.27 , right of middle row) represent distilled statistical information, taking into account age-matched normal data, and are principally used to monitor progression of glaucomatous damage rather than for initial diagnosis.

• •
  

  Visual field index (VFI) in the HFA is a measure of the patient’s overall visual field function expressed as a percentage, the normal age-adjusted value being 100%.

  
  
• •
  

  Mean deviation (MD) on the HFA ( mean defect on the Octopus) gives an indication of the overall sensitivity of the field. It is derived from averaging the total deviation values.

  
  
• •
  

  Pattern standard deviation (PSD) is a measure of focal loss or variability within the field taking into account any generalized depression in the hill of vision. An increased PSD is therefore a more specific indicator of glaucomatous damage than MD.

  
  
• •
  

  Loss variance (LV) is a summary measure on the Octopus perimeter similar to PSD.

  
  
• •
  

  Probability values. Abnormal summary values are followed by a probability value, representing the percentage likelihood that an abnormal value of this level will occur in a normal subject; the lower the P value, the more likely the result is abnormal.

  
  
• •
  

  The glaucoma hemifield test (GHT) used with some HFA testing patterns assesses the visual field for damage conforming to a pattern commonly seen in glaucoma.

Computer analysis of serial fields

Computed analysis of serial visual fields for progression is now becoming more widespread. A disadvantage is the requirement for several reliable fields to be carried out before analysis is effective. The quality of available software has been improving steadily, with integrated programs such as GPA (Guided Progression Analysis) on the HFA and several trend analysis options on the Octopus.

Introduction

The major mode of prostaglandin (PG) action is the enhancement of uveoscleral aqueous outflow, although increased trabecular outflow facility and other mechanisms have been identified. Their IOP-lowering effect is typically greater than alternatives, though beta-blockers (see below) are sometimes equivalent. A prostaglandin derivative is now typically preferred to a beta-blocker as first-line treatment for glaucoma due to the latter’s potential for systemic side effects. Duration of action may extend for several days, though administration once every day (at bedtime) is generally recommended. Systemic side effects are few; the most commonly troublesome ocular side effect is conjunctival hyperaemia. Periorbital fat loss is common, especially with bimatoprost, manifestations including deepening of the upper lid sulcus. If one prostaglandin fails to show adequate efficacy, inter-individual receptor variation means that an alternative preparation may be superior in a given patient. Although some research has suggested that using more than one PG at a time may have an additive effect, consensus currently is that PG overdosing – twice a day or more – raises the IOP in many patients.

Agents

• •
  

  Latanoprost may cause fewer ocular adverse events than other PG agents and so is often used first line, although as a proportion of patients show no response many practitioners prefer initial use of an alternative.

  
  
• •
  

  Travoprost is similar to latanoprost, though it may lower IOP to a slightly greater extent, particularly in black patients. Polyquad® is a novel proprietary preservative introduced by a major pharmaceutical manufacturer in its travoprost formulation that may reduce ocular surface-related adverse effects.

  
  
• •
  

  Bimatoprost has been shown to have a greater IOP-lowering effect than the other PG agents in several studies, but may cause more conjunctival hyperaemia but fewer headaches and perhaps also less iris hyperpigmentation. A newer 0.01% (versus the older 0.03%) preparation may have a comparable IOP-lowering effect but with less hyperaemia. Preservative-free bimatoprost is now available.

  
  
• •
  

  Tafluprost is a newer prostaglandin derivative, and was the first available in preservative-free form. Its IOP-lowering efficacy may be slightly less than that of other PG agents, but it is well tolerated and seems to cause less disruption of the ocular surface.

Side effects

• •
  

  Ocular

  
  
  
  
  • ○
    

    Conjunctival hyperaemia is very common.

    
    
  • ○
    

    Eyelash lengthening, thickening, hyperpigmentation ( Fig. 10.32A ) and occasionally increase in number.

    
    

    
    

    
    

    

    
    

    
    

    Side effects of topical medication. (A) Lengthening and hyperpigmentation of lashes with prostaglandin analogue treatment; (B) monocular prostaglandin analogue treatment – darkening of left iris and eyelid skin; (C) allergic conjunctivitis due to brimonidine; (D) blepharoconjunctivitis due to topical carbonic anhydrase inhibitors

    
    

    (Courtesy of S Chen – figs A and B; J Salmon – fig. C)

    
    

    
    

    

    
    

    
    

    

    
    

    
    

    

    
    
    
    
  • ○
    

    Irreversible iris hyperpigmentation ( Fig. 10.32B ) occurs in up to a quarter of patients after 6 months. The highest incidence is in green–brown irides, less in yellow-brown irides and least in blue-grey/brown irides. It is caused by an increase in the number of pigmented granules within the superficial stroma rather than an increase in the number of melanocytes. Iris naevi and freckles are not affected.

    
    
  • ○
    

    Hyperpigmentation of periocular skin (see Fig. 10.32B ) is common but reversible.

    
    
  • ○
    

    Preoperative use of PG agents may increase the likelihood of cystoid macular oedema following cataract surgery.

    
    
  • ○
    

    Anterior uveitis is rare, but prostaglandins should be used with caution in inflamed eyes.

    
    
  • ○
    

    Promotion of herpetic keratitis can occur, so prostaglandins should be used with caution in patients with a history of the condition.

  
  
  
  
• •
  

  Systemic side effects include occasional headache, precipitation of migraine in susceptible individuals, malaise, myalgia, skin rash and mild upper respiratory tract symptoms.

Introduction

Beta-blockers reduce IOP by decreasing aqueous production, mediated by an effect on the ciliary epithelium. In approximately 10% of cases the response decreases with time (tachyphylaxis), sometimes within only a few days. There may be limited supplementary effect if a topical beta-blocker is added when a patient already takes a systemic beta-blocker; the combination may also involve a relatively high risk of systemic side effects. Beta-blockers should not be instilled at bedtime as they may cause a profound drop in blood pressure while the individual is asleep, thus reducing optic disc perfusion and potentially causing visual field deterioration; the IOP-lowering effect is also believed to be less marked during sleep, as nocturnal aqueous production is normally less than half the daytime rate. However, a beta-blocker may be preferred under some circumstances such as monocular treatment to avoid the cosmetic disadvantage of the asymmetrical periocular skin darkening and/or conjunctival hyperaemia with prostaglandins. Beta-blockers are also preferred in conditions such as ocular inflammation and cystoid macular oedema, or where there is a history of herpes simplex keratitis.

Side effects

• •
  

  Ocular. Ocular side effects are few but include allergy and punctate keratitis. Granulomatous uveitis has been reported with metipranolol.

  
  
• •
  

  Systemic. Though severe problems are extremely rare, numerous deaths have been associated with topical beta-blocker use.

  
  
  
  
  • ○
    

    Bronchospasm. This may be fatal in asthma or other reversible airways disease, and it is critical to exclude a history of asthma before prescribing a beta-blocker. About 1 in 50 patients without asthma will develop reversible airways disease requiring treatment within 12 months of commencing a topical beta-blocker.

    
    
  • ○
    

    Cardiovascular. There is a strong suggestion that cardiovascular mortality is higher in patients taking a topical beta-blocker. Effects include heart block, bradycardia, worsening of heart failure and hypotension, induction of the latter by topical beta-blocker having been reported as a common cause of falls in elderly patients. The pulse should be assessed before prescription. A peripheral vasoconstrictive effect means that they should be avoided or used with caution in patients with peripheral vascular disease, including Raynaud phenomenon.

    
    
  • ○
    

    Unpleasant but less severe side effects include sleep disorders, reduced exercise tolerance, hallucinations, confusion, depression, fatigue, headache, nausea, dizziness, decreased libido and dyslipidaemia.

  
  

Agents

• •
  

  Timolol is available in various forms, including 0.25% and 0.5% solutions used twice daily; there is no evidence of a clinically significant difference in efficacy between the two solution concentrations. Gel-forming preparations of 0.1%, 0.25% and 0.5% are used once daily.

  
  
• •
  

  Betaxolol twice daily has a lower hypotensive effect than timolol. However, optic nerve blood flow may be increased due to a calcium-channel blocking effect, so that visual field preservation may be superior. Betaxolol is relatively cardioselective (beta-1 receptors), so causes less bronchoconstriction.

  
  
• •
  

  Levobunolol once or twice daily has a broadly similar profile to timolol.

  
  
• •
  

  Carteolol twice daily is similar to timolol and also exhibits intrinsic sympathomimetic activity. It has a more selective action on the eye than on the cardiopulmonary system and so may have a lower systemic side effect incidence.

  
  
• •
  

  Metipranolol twice daily is similar to timolol but has been linked with granulomatous anterior uveitis.

Introduction

Ocular alpha-2 receptor stimulation decreases aqueous synthesis via an effect on the ciliary epithelium, and increases uveoscleral outflow. There is probably a neuroprotective effect. They cross the blood–brain barrier and should be used with great caution in young children, in whom severe central nervous system (CNS) depression and hypotension been reported, and are contraindicated under the age of 2 years. They may potentiate vascular insufficiency. They should not be given with oral monoamine oxidase inhibitor antidepressants due to the risk of hypertensive crisis.

Agents

• •
  

  Brimonidine 0.2% twice daily in isolation generally has a slightly less marked IOP-lowering effect than timolol. Allergic conjunctivitis ( Fig. 10.32C ) is relatively common; its onset may be delayed for up to 18 months after commencement of therapy. Granulomatous anterior uveitis can occur, but is rare. Systemic side effects include xerostomia and fatigue, the latter sometimes being severe. A brimonidine preparation, Alphagan-P®, containing a proprietary preservative, Purite®, has been introduced as an alternative to the more common benzalkonium-containing forms and may have greater ocular surface tolerability.

  
  
• •
  

  Apraclonidine 1% (or 0.5%) is used principally to prevent or treat an acute rise in IOP following laser surgery on the anterior segment. The 0.5% concentration is typically used as a temporizing measure over the course of several weeks, such as whilst a patient is awaiting glaucoma surgery. It is generally not suitable for long-term use because of a loss of therapeutic effect over weeks to months and a high incidence of local side effects.

Introduction

The carbonic anhydrase inhibitors (CAI) are chemically related to sulfonamide antibiotics. They lower IOP by inhibiting aqueous secretion, and via the topical route are used three times daily as monotherapy or twice daily as adjunctive treatment. In general, they are slightly less effective than beta-blockers but are hypothesized to have a supplementary neuroprotective effect. They may precipitate corneal decompensation in patients with corneal endothelial dysfunction, but some benefit has been reported in the treatment of cystoid macular oedema. Idiosyncratic bone marrow suppression can occur. Though cross-reaction is uncommon, topical (and systemic) CAI are relatively contraindicated in patients allergic to sulfonamide antibiotics. Research suggests that concomitant treatment with a topical and systemic CAI does not usually give an additive effect.

Agents

• •
  

  Dorzolamide . The main adverse effects are stinging and a transient bitter taste following administration; allergic blepharoconjunctivitis ( Fig. 10.32D ) is not uncommon.

  
  
• •
  

  Brinzolamide is similar to dorzolamide, but with a lower incidence of stinging and local allergy. It is a suspension, and a white residue may be left on the eyelids after instillation if excess is not wiped away.

Introduction

Miotics are cholinergic agonists that are now predominantly used in the treatment of angle closure, though were formerly a mainstay of the treatment of open-angle glaucoma. In angle-closure glaucoma, miotic-induced contraction of the sphincter pupillae pulls the peripheral iris away from the trabeculum, opening the angle. Miotics also reduce IOP by contraction of the ciliary muscle, which increases the facility of aqueous outflow through the trabecular meshwork. Local side effects include miosis, brow ache, myopic shift and exacerbation of the symptoms of cataract. Visual field defects appear denser and larger. Systemic side effects are rare but include confusion, bradycardia, bronchospasm, gastrointestinal symptoms and urinary frequency.

Agents

• •
  

  Pilocarpine 0.5%, 1%, 2%, or 4% solution as four times daily monotherapy is equal in efficacy to beta-blockers. Pilocarpine gel (Pilogel®) 4% is instilled once daily at bedtime so that induced myopia and miosis are predominantly confined to sleep. Gel, or drops twice daily, may be used to prevent angle closure following laser iridotomy in the presence of a substantial non-pupillary block element.

  
  
• •
  

  Carbachol is an alternative to pilocarpine.

Introduction

Systemically administered CAI are generally used for short-term treatment, particularly in patients with acute glaucoma. Because of their systemic side effects, long-term use is reserved for patients at high risk of visual loss. Sulfonamide (‘sulfa’) allergy is a relative contraindication.

Agents

• •
  

  Acetazolamide is available as 250 mg tablets (250–1000 mg daily in divided doses), sustained-release 250 mg capsules (250–500 mg daily) and 500 mg powder vials for injection (single dose, typically used in acute angle-closure glaucoma).

  
  
• •
  

  Dichlorphenamide 50 mg tablets (50–100 mg two or three times daily).

  
  
• •
  

  Methazolamide 50 mg tablets (50–100 mg two or three times daily); this has a longer duration of action than acetazolamide but is less widely available.

Side effects

• •
  

  Ocular. Choroidal effusion, particularly after cataract surgery. Angle closure may result.

  
  
• •
  

  Systemic. Paraesthesia (‘pins and needles’ sensation in the extremities), hypokalaemia (reduced blood potassium level – common), malaise and lowered mood, gastrointestinal symptoms, renal stones, Stevens–Johnson syndrome (very rare), dose-related bone marrow suppression, idiosyncratic aplastic anaemia (exceptionally rare but with 50% mortality).

Introduction

Osmotic agents lower IOP by creating an osmotic gradient so that water is ‘drawn out’ from the vitreous into the blood. They are employed when a short-term reduction in IOP is required that cannot be achieved by other means, such as in resistant acute angle-closure glaucoma or when the IOP is very high prior to intraocular surgery. They are of limited value in inflammatory glaucoma, in which the integrity of the blood–aqueous barrier is compromised. Side effects include cardiovascular overload as a result of increased extracellular volume (caution in patients with cardiac or renal disease), urinary retention (especially elderly men), headache, backache, nausea and confusion.

Agents

• •
  

  Mannitol is given intravenously (1 g/kg body weight or 5 ml/kg body weight of a 20% solution in water) over 30–60 minutes; peak action occurs within 30 minutes.

  
  
• •
  

  Glycerol is an oral agent (1 g/kg body weight or 2 ml/kg body weight of a 50% solution) with a sweet and sickly taste, and can be given with lemon (not orange) juice to avoid nausea. Peak action occurs within 1 hour. Glycerol is metabolized to glucose, and careful monitoring with insulin cover may be required if administered to a (well-controlled only) diabetic patient.

  
  
• •
  

  Isosorbide is a metabolically inert oral agent with a minty taste; the dose is the same as for glycerol. It may be safer for diabetic patients.

Introduction

Laser trabeculoplasty (LTP) involves the delivery of laser to the trabecular meshwork with the aim of enhancing aqueous outflow and thereby lowering IOP.

• •
  

  Selective laser trabeculoplasty (SLT) has increased in popularity over recent years and is now widely performed. A 532 nm frequency-doubled, Q-switched Nd:YAG laser is used to selectively target melanin pigment in trabecular meshwork (TM) cells, leaving non-pigmented structures unscathed. It is probably similar in efficacy to medical monotherapy and argon laser trabeculoplasty (see below). The mechanism is incompletely understood, but potentially includes stimulation of TM cell division, macrophage recruitment and extracellular matrix recruitment. Laser application is made easier by a broad targeted and treated area ( Fig. 10.33 , left), which may lead to more consistent results. Reported protocols (e.g. 180° or 360° TM treatment) and results vary markedly, but IOP reductions of 10–40% can be expected after 6 months in responsive patients, with 25% being common. Probably around two-thirds of patients will achieve a reasonable IOP fall within 6 months of 180° TM treatment. The contralateral untreated eye also tends to sustain a small IOP fall. The effects generally wane over time, but as there is no thermal tissue damage, treatment can be repeated with a successful outcome, even if initial treatment has been unsuccessful. The prior use of topical glaucoma medication does not seem to affect results. Energy delivered to the TM is much lower than with argon laser, and complications are relatively mild but include transient mild inflammation with mild discomfort, PAS formation and IOP elevation; the latter is usually mild but substantial rises have been reported, especially in heavily pigmented angles, for which overtreatment should be avoided. The concern has been raised that the extensive treated area causes damage to corneal endothelial cells, with rare reports of endothelial decompensation. Herpes simplex keratitis reactivation has been reported, as has macular oedema.

  
  

  
  

  
  

  

  
  

  
  

  Targeted area in selective (left) and conventional argon (right) and micropulse laser trabeculoplasty

  
  
  
  
• •
  

  Argon laser trabeculoplasty (ALT) is a long-established procedure that uses laser burns to achieve IOP reduction comparable to SLT; there is an extensive body of published research reporting good outcomes. Mechanisms are likely to overlap with those of SLT, and there may also be a mechanical opening of the trabecular spaces. As the TM sustains thermal damage, repeat treatment is of limited benefit and is infrequently performed. Complications include peripheral anterior synechiae, acute elevation of IOP (should be monitored carefully over subsequent weeks in patients with severe glaucomatous damage), cystoid macular oedema and anterior uveitis (usually mild); there is concern that there may be an adverse effect on the outcome of subsequent filtration surgery.

  
  
• •
  

  Micropulse laser trabeculoplasty (MLT) is a relatively new modality that uses extremely short duration pulses of laser to deliver thermal energy to the TM to stimulate cells without damage. Unlike SLT and ALT, there is no visible tissue reaction. A smaller area is targeted than in SLT ( Fig. 10.33 , right), limiting potential collateral effects on adjacent tissue. Initial results suggest a benign safety profile with results comparable to other LTP forms.

Indications

• •
  

  Type of glaucoma. LTP can be used in a range of open-angle glaucomas including primary, pseudoexfoliative and pigmentary, and can also be used in ocular hypertension. Success has been reported in less common circumstances, e.g. steroid-induced glaucoma has been treated with SLT.

  
  
• •
  

  Primary therapy. As SLT has increasingly demonstrated a favourable safety profile, its use as a primary alternative to topical medication has increasingly been considered.

  
  
• •
  

  Failure of compliance with medical therapy.

  
  
• •
  

  Adjunctive treatment to avoid polypharmacy.

  
  
• •
  

  Intolerance of topical medication including allergy.

  
  
• •
  

  Failure of medical therapy , as a less aggressive treatment measure than surgery.

Technique

• •
  

  LTP is performed under topical anaesthesia.

  
  
• •
  

  A drop of apraclonidine or brimonidine is instilled 30–60 minutes pre-procedure with the aim of preventing or minimizing an early post-laser IOP rise. A similar drop is instilled post-procedure.

  
  
• •
  

  Some practitioners instil a drop of pilocarpine prior to the procedure, particularly if the angle is not wide. There is likely to be greater potential for PAS formation in narrower angles, particularly with ALT, and this should be borne in mind when considering a particular patient’s suitability for LTP.

  
  
• •
  

  A goniolens is inserted; with the mirror at the 12 o’clock position, the inferior angle is visualized.

  
  
• •
  

  ALT: initial settings are commonly 50 µm spot size, 0.1 s duration, and 700 mW power (range of 400–1200 mW, largely dependent on angle pigmentation). The aiming beam is focused at the junction of the pigmented and non-pigmented TM ensuring that the spot is round and has a clear edge. The optimal reaction is a very light blanching or the appearance of a minute gas bubble. If the reaction is inadequate, the power is increased by 50–200 mW. Fifty burns are applied at regularly spaced intervals over 180° of the angle. Many practitioners apply initial treatment of 180° of the angle, treating the other 180° if the initial response is unsatisfactory; primary treatment of the entire circumference is associated with a higher risk of IOP spikes. Topical fluorometholone or prednisolone 0.5% four times daily for one week is prescribed post-laser.

  
  
• •
  

  SLT: a common initial power setting is 0.8 mJ; as with ALT, this should be varied depending on angle pigmentation (range 0.3–1.0 mJ); the spot size and duration are fixed at 400 µm and 0.3 ns respectively. The TM is brought into focus rather than the aiming beam; the beam is centred on the pigmented TM and then fired, an optimal reaction consisting of a few tiny (‘champagne’) bubbles with adjustment of the power higher or lower as required to achieve this. The number of burns applied is as for ALT. The total energy used for SLT is considerably less than for ALT, and it is common not to prescribe any post-laser anti-inflammatory drops, though non-steroidal or weak steroid drops can be used if significant inflammation occurs.

  
  
• •
  

  With practice it is possible to perform LTP by continually rotating the goniolens and applying each burn through the centre of the mirror; using this technique, treatment of the entire inferior half of the angle is accomplished by first rotating the lens to one side (e.g. anticlockwise) by 90° whilst applying 25 shots, then returning to the 12 o’clock position before applying an additional 25 shots whilst rotating the lens to the opposite side (clockwise in this example).

  
  
• •
  

  An IOP check should be performed 30–60 minutes after the laser to exclude a substantial early spike, with further IOP measurement, treatment and review as appropriate if this occurs, depending on each patient’s risk profile.

  
  
• •
  

  Medical glaucoma therapy is generally continued.

  
  
• •
  

  Follow-up is dependent on the perceived level of risk; 1–2 weeks is typical in the absence of pertinent considerations.

Introduction

Laser iridotomy is used principally in the treatment of primary angle closure, but may also be indicated in secondary angle closure with pupillary block. It is also sometimes performed in pigment dispersion syndrome, though its effectiveness in this scenario remains under investigation.

Technique

• •
  

  A topical anaesthetic agent is instilled.

  
  
• •
  

  Apraclonidine or brimonidine is given prophylactically as for LTP.

  
  
• •
  

  The pupil is miosed with topical pilocarpine (e.g. one drop of 2%).

  
  
• •
  

  A special iridotomy contact lens (e.g. Abraham – Fig. 10.34A , Volk MagPlus) is inserted.

  
  

  
  

  
  

  

  
  

  
  

  Nd:YAG iridotomy. (A) Abraham lens; (B) approximately appropriate iridotomy size; (C) probably too small; (D) probably too large – may also be insufficiently peripheral

  
  
  
  
• •
  

  Many practitioners target a site under the upper eyelid between 11 and 1 o’clock, though some prefer 3 or 9 o’clock. The highest risk of monocular diplopia or glare (see below) occurs when an iridotomy is half-covered by the lid margin. Radially, the iridotomy should be located within the outer third in order to reduce the risk of damage to the crystalline lens (see Fig. 10.34D ). Targeting an iris crypt, if present, is usually associated with much easier achievement of an adequate opening.

  
  
• •
  

  It is critical to note that effective power settings vary somewhat between machines. The spot size and duration are fixed. Most iridotomies are made with power settings of 4–5 mJ; the risk of crystalline lens damage may be higher at 5 mJ or above. For a thin blue iris the typical required energy level is 2–4 mJ. Some practitioners prefer single pulse shots, others shots of up to three pulses.

  
  
• •
  

  Pre-treatment with thermal (argon or diode) laser is often required in thick dark irides. Suitable parameters include power of 600–900 mW using a small spot size of 50 µm and relatively short duration of 0.03–0.05 s, though larger, lower power, longer duration settings can be equally effective.

  
  
• •
  

  The beam is focused precisely and the laser fired. Successful penetration is characterized by a gush of pigment debris. The number of shots required to produce an adequate iridotomy is very variable. The optimal size is uncertain, recommendations ranging from 150 to 500 µm ( Figs 10.34B–D ).

  
  
• •
  

  Over-treatment should be avoided due to the risk of substantial postoperative inflammation and pressure spikes; further treatment can be applied after a few days; in urgent circumstances re-treating the same site after allowing a few minutes for pigment and debris to clear, or moving to a different site, may be adequate.

  
  
• •
  

  A second drop of apraclonidine is instilled following the procedure; oral acetazolamide may also be given in patients at high risk such as those with advanced glaucomatous damage or high IOP pre-treatment.

  
  
• •
  

  A potent topical steroid (e.g. dexamethasone 0.1%) is prescribed post-procedure. Varying regimens have been described, with a limited evidence base for the optimal approach; four times daily for 1 week is typical, though instillation every hour for several hours immediately post-laser is common.

  
  
• •
  

  The IOP should be checked 1–2 hours after the procedure to exclude an early spike. Routine review is usually at 1 or 2 weeks, with subsequent monitoring according to individual circumstances. Patients with marked glaucomatous damage may require extended ocular hypotensive cover and earlier review.

Complications

• •
  

  Bleeding occurs in around 50% but is usually mild and stops after only a few seconds; persistent bleeding can be terminated by increasing contact lens pressure.

  
  
• •
  

  IOP elevation . Usually early and transient but occasionally persistent.

  
  
• •
  

  I ritis . Especially if excessive laser is applied or post-laser steroid therapy is inadequate, or in darker irides (including those due to prostaglandin derivative treatment).

  
  
• •
  

  Corneal burns may occur if a contact lens is not used or if the AC is shallow; these usually heal very rapidly without sequelae.

  
  
• •
  

  Cataract. Localized lens opacities occasionally develop at the treatment site; age-related cataract formation may be accelerated by iridotomy.

  
  
• •
  

  Glare and/or diplopia due to a ‘second pupil’ effect are rare (see above).

Technique

• •
  

  A sub-Tenon or peribulbar anaesthetic is administered.

  
  
• •
  

  Laser settings are 1.5–2 s and 1500–2000 mW; the spot size is fixed.

  
  
• •
  

  The power is adjusted over sequential shots until a ‘popping’ sound is heard and then reduced to just below that level.

  
  
• •
  

  Approximately 12–24 burns are placed posteriorly to the limbus over 360°, avoiding the neurovascular bundles at 3 and 9 o’clock ( Fig. 10.35 ). Fewer shots (e.g. treatment of only one or two quadrants) can be used for eyes with good vision, in order to reduce the risk of complications; more treatment sessions are likely to be required using this approach.

  
  

  
  

  
  

  

  Only gold members can continue reading. Log In or Register to continue

  Share this:

  • Click to share on Twitter (Opens in new window)
  • Click to share on Facebook (Opens in new window)

  Related

  Related posts:

  1. Orbit
  2. Ocular side effects of systemic medication
  3. Strabismus
  4. Uveitis

  

  Stay updated, free articles. Join our Telegram channel

  Join