Decibels are not true units of luminance but a representation, and vary between visual field machines. B C Fig. This makes the assessment of visual fields more intuitive, as a higher number corresponds with higher retinal sensitivity.
The visual field is therefore a three-dimensional representation of differential light sensitivity at different points. The threshold sensitivity is highest at the fovea and decreases progressively towards the periphery. The retinal sensitivity at any location varies depending on background luminance. Rod CHAPTER Examination Techniques photoreceptors are more sensitive in dim light than cones, and so owing to their preponderance in the peripheral retina, at lower scotopic light levels the peripheral retina becomes more sensitive in proportion to the central retina.
The hill of vision flattens, with a central crater rather than a peak at the fovea due to the high concentration of cones, which have low sensitivity in scotopic conditions. Some diseases give markedly different field results at different background luminance levels, e.
It should be noted that it takes about 5 minutes to adapt from darkness to bright sunlight and 20—30 minutes from bright sunlight to darkness. The HFA see below uses a photopic preferentially cone level of background luminance at A method of assessing fields, usually automated, in which the location of a stimulus remains fixed, with intensity increased until it is seen by the subject threshold is reached — Fig. A stimulus of constant intensity is moved from a non-seeing area to a seeing area Fig.
Points from different meridians are joined to plot an isopter for that stimulus intensity. Stimuli of different intensities are used to produce a contour map of the visual field. Kinetic perimetry can be performed by means of a manual Goldmann or an automated 1 perimeter if the latter is equipped with an appropriate software program. It was formerly the standard method of field testing but has now largely been superseded by automated methods.
It is still used occasionally, particularly in cognitively limited patients unable to interact adequately with an automated system, and for dynamic testing of peripheral fields. These predominantly utilize static testing, though software is available on some machines to perform dynamic assessment. A typical automated strategy is to present a stimulus of higher than expected intensity.
If seen, the intensity is decreased in steps e. The stimulus is then increased again e. If the stimulus is not seen initially, its intensity is increased in steps until seen. Threshold testing is commonly used for monitoring glaucoma. Suprathreshold A Suprathreshold perimetry involves testing with stimuli of luminance above the expected normal threshold levels for an agematched 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 B Fig. A Static — stimulus intensity red arrow at a single location is increased until perceived — areas of lower sensitivity perceive only stimuli of greater intensity longer red arrows ; B kinetic — stimulus of constant intensity is moved from a non-seeing area until perceived 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.
The Octopus Perimeter 11 12 Perimetry Fig. TOP presents each stimulus once at each location, instead of 4—6 times per location with a standard technique.
The number after the hyphen 2 describes the pattern of the points tested. Glaucomatous defects here may threaten central vision. Patterns that include central and peripheral points e. FF are typically limited to the assessment of neurological defects. Esterman strategy is used to assess statutory driving entitlement in many jurisdictions. Analysis SAP provides the clinician with an array of clinically relevant information via monitor display or printout.
General information should be reviewed, such as the type of algorithm performed, the time taken for the test and the order in which the eyes were tested. In patients who consistently fail to achieve good reliability it may be useful to switch to a suprathreshold strategy or kinetic perimetry. 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. In SITA testing, false positives are estimated based on the response time. 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. If significantly unreliable, further evaluation of the visual field printout is pointless.
A grey scale represents the numerical display in graphical form see Fig. Total deviation see Fig. Negative values indicate lower than normal sensitivity, positive values higher than normal. Pattern deviation see Fig.
Probability value plots of the total and pattern deviation see Fig. This may be because an optic nerve head with a large cup is structurally more vulnerable, or it may be that early damage is already present. The higher the PSD value the greater the risk.
This possibly signifies early glaucomatous field change. A Orbscan; B Pachmate Genetics of ocular hypertension A single nucleotide polymorphism in TMC01 appears to be significantly associated with conversion to glaucoma in white people with ocular hypertension 3-fold risk in individuals with two risk alleles compared with those with no risk alleles. A recent meta-analysis has identified genetic loci associated with IOP and suggests a major role for angiopoietin-receptor tyrosine kinase signalling, lipid metabolism, mitochondrial function and developmental processes as risk factors for elevated IOP.
Clinical evaluation History and examination should be carried out as for glaucoma see below. The field-testing modality for this purpose is usually taken as standard achromatic automated perimetry. Management Raised IOP is an important risk factor in the development of glaucoma and can be modified with treatment. However, it is difficult to justify the treatment of all individuals with raised IOP because of the high prevalence of ocular hypertension, the low conversion rate to glaucoma and the cost and side effects of treatment.
In the OHTS, untreated patients with ocular hypertension had a 9. This helps in deciding on the frequency of testing and whether to start treatment. The decision to treat in patients with varying risk profiles is not straightforward and has to be made on an individual basis. Progressive retinal ganglion cell death and visual field loss are associated with these changes. Intraocular pressure is a key modifiable factor. Openangle 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. It is the second leading cause of blindness in the world. On a worldwide basis, primary angle closure PAC constitutes up to half of cases and has a particularly high prevalence in people of Asian descent.
With improved assessment such as the routine performance of gonioscopy in a darkened rather than a bright environment, PAC is more prevalent in whites than previously realized. Large differences exist among patients and different glaucoma types, but based on the mean rate of change in untreated individuals, visual function in an average individual appears to deteriorate from normal to blindness over a period of approximately 25 years.
This is influenced significantly by using treatment to reduce IOP. It affects both genders equally. POAG is more common in older individuals. It is significantly perhaps four times more common, develops at an earlier age and may be more difficult to control in black individuals than in whites. Family history of POAG. First-degree relatives of patients with POAG are at increased risk.
An approximate risk to siblings is four times and to offspring twice the normal population risk, though surveyed figures vary. Diabetes mellitus. Longitudinal studies show no increased risk of glaucoma. Selection bias probably explains why clinicbased studies report a higher prevalence of glaucoma in people with diabetes.
Myopia is associated with an increased incidence of POAG and myopic eyes may be more susceptible to glaucomatous damage.
Anti-VEGF vascular endothelial growth factor therapy. Patients undergoing anti-VEGF therapy for age-related macular degeneration or diabetic macular oedema are at risk of sustained IOP elevation. This is more likely to occur after recurrent injections with bevacizumab than with ranibizumab.
The risk is significantly greater for patients with glaucoma than for normal individuals. The risk that glaucoma surgery will be needed increases after six injections. Contraceptive pill. Recent research suggests that long-term use of the oral contraceptive pill may increase the risk of glaucoma, perhaps by blocking a protective oestrogen effect. Vascular disease. A range of systemic conditions linked to vascular compromise may be associated, though clear-cut relationships have proved difficult to demonstrate consistently.
Systemic hypertension, cardiovascular disease, diabetes and vasospastic conditions such as migraine have all been implicated. Poor ocular perfusion may be a risk factor for glaucoma progression.
Translaminar pressure gradient. Studies suggest that a difference in the levels of IOP and orbital CSF pressure may increase the likelihood of the development and progression of glaucomatous damage, perhaps due to associated deformation of the lamina cribrosa. Optic disc area. Large discs are more vulnerable to damage. Ocular perfusion pressure is the difference between the arterial BP and the IOP and has been shown in population studies to be linked to increased risk for the development and progression of glaucoma.
Genetics POAG has been associated with at least 20 loci in the human genome, but mutations in only the MYOC gene, coding for the protein myocilin that is found in the trabecular meshwork and the OPTN gene, which codes for optineurin, are broadly accepted as causing glaucoma. A number of different mutations have been described in the MYOC gene, though the normal function of myocilin and its role in glaucoma is as yet undetermined.
Genetic investigation of a patient and family may be considered if three or more first-degree relatives from two generations are affected, or for research purposes. Pathogenesis of glaucomatous optic neuropathy Retinal ganglion cell death in glaucoma occurs predominantly through apoptosis programmed cell death rather than necrosis. The preterminal event is calcium ion influx into the cell body and an increase in intracellular nitric oxide. Glutamine metabolism is intrinsically involved.
After initial injury, a cascade of events results in astrocyte and glial cell proliferation and alterations in the extracellular matrix of the lamina cribrosa, with subsequent optic nerve head remodelling.
The process of glaucomatous damage and the relationship with IOP and other potential influences is still poorly understood. Accumulating evidence of the influence of mechanical deformability in the region of the lamina cribrosa supports this. This may relate to ocular perfusion pressure as a possible risk factor for glaucoma. Both mechanisms might lead to a reduction in axoplasmic flow, interference with the delivery of nutrients or removal of metabolic products, deprivation of neuronal growth factors, oxidative injury and the initiation of immune-mediated damage.
Screening Universal population screening for glaucoma has not been demonstrated to be cost-effective and current practice restricts casefinding to high-risk groups, such as a older individuals, b those over the age of 40 with a history of POAG in a close family member and c people of African racial background. In these groups, screening tends to be performed sporadically via routes such as commercial optometric eye examinations, which may lead to the relative exclusion of underprivileged economic groups.
Population screening with tonometry alone is unsatisfactory, since it will label as normal a significant number of cases with other features of POAG such as cupping and visual field loss, and routine screening eye examinations should include visual field assessment as well as tonometry and ophthalmoscopy.
Sometimes symptomatic central field defects may occur at an early stage, in the presence of a relatively normal peripheral field. Previous eye surgery, including refractive surgery which may affect IOP readings.
The vertical rather than the horizontal ratio is generally taken Fig. As a basic principle, small diameter optic discs have small cups Fig. Exclude a relative afferent pupillary defect RAPD. Colour vision assessment such as Ishihara chart testing if there is any suggestion of an optic neuropathy other than glaucoma. Slit lamp examination. Exclude features of secondary glaucoma such as pigmentary and pseudoexfoliation. Tonometry prior to pachymetry, noting the time of day.
Optic disc examination for glaucomatous changes see below should be performed with the pupils dilated, provided gonioscopy does not show critically narrow angles.
Red-free light can be used to detect RNFL defects. The neuroretinal rim NRR is the orangepink tissue between the outer edge of the cup and the optic disc margin. The inferior rim is the broadest followed by the B Fig. In any individual, asymmetry of 0. 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, which has been found to be thinner in eyes with NTG.
Disc size varies on average between racial groups and is largest in Africans. 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. Four morphological 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.
Dense superior or inferior scotomas threatening fixation are common. This morphology is most common in younger male patients. 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.
Changes in glaucoma In some cases it is not possible to be certain whether an individual optic disc is glaucomatous. The clinical findings and results of investigation should be considered together to guide management. Glaucomatous damage results in characteristic signs involving a the optic nerve head, b the peripapillary area and c the retinal nerve fibre layer.
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 Fig. If an eye with a small optic disc and A Table IOP is usually significantly elevated at presentation. 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. When screening for glaucoma approximately three out of four people with a disc haemorrhage will not have glaucoma. It is characterized by a space between the neuroretinal rim and a superficial blood vessel Fig.
Collaterals between two veins at the disc Fig. They are probably caused by chronic low-grade circulatory obstruction. Retinal vascular tortuosity may also occur. Loss of nasal NRR Fig. 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. 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. 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. Peripapillary atrophy PPA surrounding the optic nerve head may be of significance in glaucoma Fig. It tends to be larger and possibly more common in glaucomatous eyes. Alpha zone white arrow and beta zone black arrow Papillomacular bundle Temporal retina Nasal retina Horizontal raphe Fig.
They do not cross the horizontal raphe that extends from the foveola to the temporal retinal periphery, demarcating the superior and inferior halves of the retina. The fibres in the papillomacular bundle are the most resistant. Within the optic nerve head, the retinal fibres are arranged as follows Fig. 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. Redfree green light increases the contrast between normal retina and defects on slit lamp biomicroscopy or fundus photography and typically makes identification easier. 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 in apparently normal individuals.
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. An understanding of the distribution of the 1. Within the retina the arrangement is as follows Fig. Imaging has become an indispensable tool in the management of patients with glaucoma.
However, it is important to remember that in order to determine a diagnosis or to determine change, imaging should always be used to supplement clinical examination and visual field results, rather than as the sole investigation.
Stereo photography has historically been regarded as the reference standard in optic disc imaging and remains a valuable option. The images are taken by repositioning slightly between shots, either manually or using a stereo separator built into the camera.
A Red-free photograph arrows show wedgeshaped defect associated with a disc margin haemorrhage ; B corresponding superior arcuate defect in the visual field Fig. A Showing normal angle appearance; B showing closed angle arrow ultrasound and is used for imaging the anterior segment of the eye. It is particularly useful to show the anatomy in patients with primary angle-closure glaucoma Fig.
In comparison to anterior segment OCT, the main strength of UBM is its ability to demonstrate structures behind the iris, particularly the ciliary body and lens. Anterior segment optical coherence tomography has an expanding range of clinical applications primarily in the evaluation of angle-closure glaucoma. It is useful when demonstrating the relationship of the peripheral iris to the filtration angle Fig. Objective measurement of the depth of the AC is often clinically useful in glaucoma management.
Indications include assessment of PAC risk and monitoring of progression in conditions where the AC is shallow, such as post-trabeculectomy hypotony and ciliolenticular block. Older methods used a slit lamp with or without a special attachment, but an accurate and repeatable measurement can be obtained using OCT, ultrasonographic or optical interferometric methods e. Zeiss IOLMaster. Optical coherence tomography is most useful when the patient is either C Fig.
A Thickened iris; B abnormal iris insertion; C peripheral iris roll on pupil dilatation a glaucoma suspect or has early—moderate disease Fig. It can be used to detect damage and progression Fig.
Macular thickness measurements may be more helpful in these circumstances. This involves the acquisition of a circular scan of the retina around the optic nerve head. Because different OCT devices use different scanning protocols, caution should be taken when comparing RNFL thickness between machines. The left optic disc shows no abnormality membrane opening rather than the optic disc margin, centration of the imagine can be enhanced. The results are compared to a colour-coded normative database.
When assessing structural changes over time, it is often difficult to distinguish between glaucomatous change and measurement variability or age-related structural loss. A new defect, widening of an established defect or deepening of a defect are important features of glaucomatous change. Radial cross-sectional scans permit an objective and repeatable assessment of disc morphology, with reasonable discriminatory value. This function is less commonly used than RNFL.
A At presentation; B after 2 years showing progressive RNFL thinning Primary Open-Angle Glaucoma and the inner plexiform layer at the macula in an attempt to detect early stage glaucomatous damage. This is as effective for diagnosing glaucoma and assessing progression as analysis of the RNFL.
OCT signal quality is good, particularly in the elderly and diseased eye. Trend-based analysis using a number of scans, measures the shape of change and is particularly useful when confirming that progressive change has occurred. This employs a scanning laser ophthalmoscope SLO to build a threedimensional image of the optic nerve head and retina. As with the OCT, it is used to distinguish normal from glaucomatous eyes by comparison against a normative database Moorfields regression analysis and to monitor disease progression.
High-quality images can usually be acquired without pupillary dilatation and through mild—moderate lens opacity. After image capture, for greatest accuracy the operator should manually mark the contour line that defines the edge of the neuroretinal rim. The amount of alteration is directly related to the thickness of the layer.
Deviation maps show the location and magnitude of RNFL defects as tiny colour-coded squares and parameters for each eye are displayed in a table Fig. Standard automated perimetry SAP is relatively insensitive in the early stages of the disease.
Special modalities such as frequency doubling technology FDT and short wavelength automated perimetry SWAP may demonstrate defects at an earlier stage.
They are more commonly seen in NTG. The defect is bounded by the horizontal midline, corresponding to the retinal nerve fibre layer horizontal raphe. Inferior optic disc and OCT changes with a corresponding superior nasal step are shown in Fig. With time, they tend to elongate circumferentially along the distribution of arcuate nerve fibres Fig.
The perimetry pattern facilitates monitoring of the residual central field. On average, an annual deterioration in mean total deviation of just over 1. This provides information concerning differences between superior and inferior halves of the visual field by evaluating threshold at mirror-image points above and below the Fig. This program also compares the overall height of the hill of vision with age-adjusted normal values. The duration and magnitude of decrease in nocturnal blood pressure below the daytime mean blood pressure predicts progression in NTG.
Obstructive sleep apnoea syndrome may be associated, perhaps via an effect on ocular perfusion. Autoantibody levels have been found to be higher in some groups of NTG patients by some investigators. Series2 5 Series1 3. Previous retinal vascular occlusion should also be considered. Prior refractive surgery and corneal ectasia also lead to falsely low IOP readings. Plotting a diurnal IOP curve over an 8-hour period phasing during office hours may detect daytime elevation, but detection of nocturnal IOP spikes requires substantial resource commitment.
Previous episodes of raised IOP may have occurred as a result of ocular trauma, uveitis or local or systemic steroid therapy. Masking by systemic treatment such as an oral beta-blocker, commenced after glaucomatous damage has already been sustained. Spontaneously resolved pigmentary glaucoma. The typical examination features of pigmentary glaucoma tend to become less evident with increasing age.
Progressive retinal nerve fibre defects not due to glaucoma such as may occur in myopic degeneration and optic disc drusen. Congenital disc anomalies simulating glaucomatous cupping, such as a disc pit or coloboma. Neurological lesions causing optic nerve or chiasmal compression can produce visual field defects that may be misinterpreted as glaucomatous and neuroimaging should be performed if there is any suspicion, particularly in young patients.
A Clinical features History and examination are essentially the same as for POAG but specific points warrant attention. In asymmetrical disease the more damaged disc typically corresponds to the eye with the higher IOP. These are often missed if the disc is not photographed or is examined without magnification see Fig. In more than half of patients, field changes are non-progressive over a period of 5 years or more without treatment. However, perhaps because of delayed diagnosis, patients tend to present with more advanced damage than in POAG.
A high level of suspicion for a deficit pattern suggesting a lesion posterior to the optic nerve is important. Betaxolol is the beta-blocker of choice in these circumstances. Surgery should be considered if progression occurs despite IOP in the low teens. Antimetabolite enhancement of trabeculectomy is likely to be indicated in order to achieve a satisfactorily low pressure and to prevent IOP spikes.
Control of systemic vascular disease such as diabetes, hypertension and hyperlipidaemia may be important, in order to optimize optic nerve perfusion. Systemic calcium-channel blockers to address vasospasm have been advocated by some authorities.
Antihypotensive measures. If significant nocturnal dips in BP are detected, it may be necessary to reduce antihypertensive medication, especially if taken at bedtime.
Effects of sleeping in a head-up position. Neuroprotective agents of proven benefit are not yet available. Memantine is used to retard neuronal death in some central nervous system CNS disorders, but has not been shown to be beneficial in glaucoma. Some cases of NTG progress more rapidly than others and because further lowering of IOP is effective in reducing progression, treatment should be considered in patients with advanced glaucomatous damage, particularly if central vision is threatened and in those with a long life expectancy.
Regular assessment including perimetry should be performed at 6-monthly intervals initially. Patients should be encouraged to take regular exercise. Yoga exercises that involve head-stands should be avoided. Prostaglandins are usually prescribed as initial treatment. Brimonidine may have a neuroprotective effect in addition to an IOP-lowering effect. Angle closure can be primary, when it occurs in an anatomically predisposed eye, or secondary to another ocular or systemic factor.
PACG may be responsible for up to half of all cases of glaucoma globally and is particularly common in Asia. It progresses rapidly and is more likely to result in visual loss than POAG. Gonioscopy see Ch. The angle is usually narrowest superiorly. The main aims are to evaluate the functional status of the angle, the degree of closure and the risk of future closure. 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. The ciliary body can be visualized without tilting the lens. It allows formal description of the position of iris insertion, the angular approach and peripheral iris curvature. In contrast to common clinical use, in the original system a higher numeral e. IV actually signifies a narrower angle. Classification As knowledge about the epidemiology and mechanisms of angle closure has increased, classification has moved away from a symptom-based approach acute, subacute and chronic to reflect the stages in the natural history of the disease.
The ZAP study a large community-based randomized controlled trial shows an incidence rate of 8. Table Bilateral laser iridotomy is performed once an attack has been broken, signified by a clear cornea and preferably normal IOP.
Topical steroids are continued for at least a week. Gonioscopy needs to be repeated to ensure that the angle is open.
A low threshold may be adopted for cataract surgery, particularly if a significant phacomorphic element is suspected. Trabeculectomy is occasionally necessary for persistent IOP elevation despite a successfully opened angle. If symptomatic cataract is present, lens extraction usually opens the angle Fig. Urgency and intensity of treatment and frequency of review is tailored to the individual patient, considering IOP, extent of angle closure and glaucomatous damage, if present. It is easily overlooked in the early stages, as the signs are not always obvious.
It is more common in women than men and although the condition is found worldwide, the prevalence is highest in Scandinavia. Not all patients with PXS will develop glaucoma and there is no reliable method of determining which patients with the condition will subsequently develop optic disc damage.
Pathogenesis Pseudoexfoliative material is a grey-white fibrillary substance deriving from abnormal extracellular matrix metabolism in ocular and other tissues. The material is deposited on various ocular structures including the lens capsule Fig. Pseudoexfoliative material has been found in skin and visceral organs, leading to the concept that PXS is the ocular manifestation of a systemic disorder.
PXS is associated with an increased prevalence of high-tone hearing loss and cardiovascular disorders. The pathogenesis is multifactorial, but in some populations almost all patients with PXS have single nucleotide polymorphisms SNPs in the LOXL1 gene on chromosome 15, which codes for an enzyme that is involved in crosslinking of tropoelastin and collagen and is therefore important for the formation and maintenance of elastic fibres and extracellular matrix.
Plasma and aqueous humour homocysteine levels tend to be higher than controls and inadequate dietary folate intake folate reduces homocysteine may be a risk factor.
Open-angle glaucoma Fig. Curiously, despite the systemic nature of the condition and the fact that biopsy reveals subclinical pseudoexfoliative material in the apparently unaffected eye, glaucoma remains confined to one eye in about two-thirds of patients. Clinical features Diagnosis is usually incidental, but can follow vision loss from advanced glaucoma. Pseudoexfoliative material may be deposited on the endothelium and scattered pigment deposits are common.
A vertical Krukenberg spindle may rarely form, similar to that seen in pigment dispersion syndrome. Endothelial cell abnormality, such as low density, is more common than average. Pseudoexfoliative material particles are sometimes seen. Mild aqueous flare from an impaired blood— aqueous barrier is common. Granular pseudoexfoliative material deposits, pupillary ruff loss and patchy transillumination defects at the pupillary margin Fig.
The anterior lens capsule typically shows a central disc and a radially indented peripheral layer of pseudoexfoliative material, separated by a clear zone maintained by pupillary abrasion Fig. Peripheral capsular deposition is often visible only with pupillary dilatation Fig. Deposits may be flaky, with scrolled edges. Cataract is more common in an eye with pseudoexfoliative material, probably because of reduced ascorbate levels in the aqueous.
Phacodonesis lens instability due to zonular weakness may be present, but spontaneous subluxation is rare. It is not pathognomonic and can be found in pigment dispersion syndrome. In most eyes the presence of glaucomatous damage is associated with elevated IOP.
The majority of patients have a chronic open-angle glaucoma that is usually unilateral at first. Occasionally the IOP may rise acutely despite a wide angle, mimicking acute angle closure.
Severe damage may be present at diagnosis and can develop rapidly. In the long term, these patients are at significant risk of visual loss and blindness. It is therefore important to monitor patients closely and it may be prudent for review in patients with PXS to take place at intervals of no more than 6 months.
Care should be taken not to apply excessive energy, as trabecular pigmentation may confer higher absorption resulting in transient IOP spikes.
There is a high risk of complications, due to poor mydriasis, increased fragility of the zonules and lens capsule and endothelial deficiency. There is also an increased risk of a postoperative IOP spike, postoperative corneal oedema, inflammation, capsular opacification, capsulorhexis contraction capsular phimosis and late IOL decentration or dislocation. Secondary pigmentary glaucoma PG is common. PDS and PG are more common in males, particularly young myopic white men.
In Africans, where it is rare, the condition tends to affect older hypermetropic women. AD inheritance with incomplete penetrance seems to be present in at least some families and a range of genetic loci have been linked.
Myopia is a risk factor for clinical manifestation, higher degrees of myopia being associated with earlier and more severe glaucoma. Secondary pigment dispersion can occur as a consequence of trauma, intraocular tumour and rubbing of a malpositioned IOL on the iris pigment epithelium. Occasionally symptoms from glaucomatous visual loss lead to attendance, or from corneal oedema due to an acute IOP rise following the release of pigment granules particularly after physical exercise.
Signs of PDS are usually bilateral but may be subtle and go undetected. Pigment is deposited on the endothelium in a vertical spindle shape Krukenberg spindle; Fig. The AC is deep and melanin granules may be seen in the aqueous. Characteristic radial spoke-like transillumination defects Fig. To best demonstrate these, the room should be minimally illuminated and a short, narrow but intense slit beam directed through the pupil. Visualization may be aided by asking the patient to look up.
Melanin granules may be present on the surface of the iris, usually inferiorly, which become less obvious with age. There may be partial loss of the pupillary ruff Fig. It is believed that an increase in anterior chamber pressure relative to the posterior chamber occurs due to reverse pupillary block, supported by the observation that peripheral iridotomy flattens the iris and decreases iridozonular contact Fig.
The pigment epithelium itself may be abnormally susceptible to shedding in affected individuals. Pigment shedding decreases from middle age onwards due to physiological changes resulting in decreased iridozonular contact. Acute IOP elevation can occur due to direct trabecular obstruction by released melanin granules.
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