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the diagnosis of glaucoma is usually made after a comprehensive clinical eye examination that includes biomicroscopy, applanation tonometry, gonioscopy and dilated stereoscopic evaluation of the optic disc and fundus. Further testing including automated perimetery is performed on those suspected to have glaucoma after such an examination. automated perimetry confirms functional damage and provides a baseline for follow-up. Imaging techniques are not essential for the diagnosis but may have a role to play in follow-up. A comprehensive eye examination for every clinic patient can achieve the objective of detecting all potentially sight threatening disease including glaucoma.
An approach to of a glaucoma
The eye-care practitioner should aim to detect all potentially serious ophthalmic pathology, including glaucoma. Screening for glaucoma using imaging or visual fields prior to a clinical examination can have too many false positives and negatives and is not recommended.
the diagnosis is possible, yet intervention can still alter the course of the disease and change the prognosis. Diagnosis at an even earlier stage (pre-perimetric glaucoma) is ideal but far more difficult than and not as critical as in established disease. As early diagnosis comes with implications of ‘labelling’ and life-long treatment,3,9 it is best confirmed by an experienced ophthalmic examiner using the experience and tools at their disposal. The diagnostic importance of concepts such as pretest probability, sensitivity, specificity and likelihood ratios of symptoms, signs and tests and how they can be used to confirm a diagnosis are basic to any test and are dealt with elsewhere.10,11 already on a systemic beta-blocker. As another example topical alpha-2 agonists are contraindicated in a patient on monoamine oxidase inhibitors.
The Essay on Self examination
Self examination is always daunting. This is especially so when taking a sociological study of oneself as having an “addiction”. Shocking as it may seem, I have to admit that I love the TV-schmalz-fest that is "Gilmore Girls". Indeed, I so look forward to my weekly fix that I cannot help wondering if I am addicted. How would I characterize this possible addiction? I suppose, from a ...
Introduction
Glaucoma affects around three per cent of the Australian population over the age of 50 years; of those affected, 50 per cent do not know that they have the disease.1 This article on the evaluation of primary adult glaucomas is targeted at eye-care providers working in Australia with a strategy for prevention of blindness by case detection of established disease. The piece is adapted from an article originally published in the Indian Journal of Ophthalmology and has been revised and updated for presentation here.2 The detection of most ocular pathology including glaucoma is the purview of all eye-care providers.3, 4 The patient usually does not present to an eye-care provider with a diagnosis of glaucoma. The presenting complaints may be trivial but it is responsibility of the examining clinician to rule out all potentially serious ocular pathology, including glaucoma. The diagnosis of glaucoma at a treatable stage can be achieved by a clinical examination using basic instrumentation that should be available in every clinician’s office. Glaucoma is a chronic optic neuropathy with typical structural damage to the optic disc, usually leading to correlating functional changes in the visual field.5-7 ‘Raised’ intraocular pressure is a causal risk factor for glaucoma, the only one that can be treated and does raise suspicion of glaucoma but it is neither sufficient nor necessary for the diagnosis.5-8 It is also important to remember that glaucoma is usually asymptomatic until the late stages, at which time the prognosis is poor. The diagnosis of end stage glaucoma is straightforward and can be made by a trainee using an ophthalmoscope. It is desirable to detect the disease at a stage where
Examination
A comprehensive eye examination is recommended as routine for all ophthalmic patients. Such an eye examination helps detect not just glaucoma but other potentially blinding ocular pathology. Such a comprehensive eye examination comprises: • Vision and refraction • External examination and assessment of ocular motility • Examination of the pupil with special attention to the presence of a relative afferent pupillary defect • Slitlamp biomicroscopy • Intraocular pressure measurement, preferably using applanation tonometry • Gonioscopy to examine the angle of the eye • A dilated examination of the optic disc and retina • Visual fields: if glaucoma is suspected, automated perimetry is performed to detect functional defects in the visual field. The clinical diagnosis of glaucoma is usually based on a combination of intraocular pressure (IOP), gonioscopy, optic disc and visual field examination, and these steps should always be carried out as a part of the comprehensive eye examination, not in isolation. The prevalence of glaucoma is high enough and the implications serious enough to suggest that ALL patients seen in an eye-care professional’s clinic undergo the comprehensive eye examination as well as
The Essay on Glaucoma Symptoms Eye Angle
Glaucoma Glaucoma is a condition whereby the optic nerve is damaged, resulting in vision loss. This damage is usually caused by an increase in the pressure within the eye although damage may occur even if the intra-ocular pressure is normal. There are three types of Glaucoma primary, secondary, and congenital. Primary Glaucoma can be divided in to two different types open angle and closed angle. ...
history
Primary open angle glaucoma (POAG) and primary angle closure disease (PACD) are usually asymptomatic. A history of frequent changes of reading glasses, while suspicious, is not sensitive or specific enough for clinical use. A family history of the disease increases the risk of glaucoma up to eightfold and mandates a careful examination.12-15 A comprehensive eye examination is recommended for all family members of a glaucoma patient. Myopes are at higher risk for POAG and hypermetropes are at higher risk for PACD.16,17 A directed history helps rules out secondary causes for glaucoma such as steroid use (especially topical), trauma, uveitis, sleep apnea, severe blood loss and intracranial disease. It is wise to enquire about the use of systemic medications that may influence glaucoma management. For example a topical beta blocker may not add significantly to the IOP lowering effect for someone
The Term Paper on Mechanical Measurement Lab Manual
To study the working of Bourdon Pressure Gauge and to check the calibration of the gauge in a deadweight pressure gauge calibration set up. 3. To study a Linear Variable Differential Transformer (LVDT) and use it in a simple experimental set up to measure a small displacement. 4. To study the characteristics of a pneumatic displacement gauge. . To measure load (tensile/compressive) using load cell ...
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like any other measurement may be subject to errors; measurements must be carefully preformed to avoid erroneous readings. The measurement is also affected by corneal thickness. A structurally thick cornea overestimates the IOP while a thin cornea underestimates the measurement. We recommend a central corneal thickness (CCT) measurement for all ocular hypertensives and those suspected to have ‘normal tension’ glaucoma, certainly before subjecting the latter to a neurological ‘massage’.19 On the other hand, we should avoid the tendency to consider the CCT-corrected IOP to be ‘accurate’, as all the nomograms remain to be validated and issues such as corneal hysteresis may be as or more important. There are other sources of error that cannot be accounted for by the CCT. Statistically, an IOP measured in the recommended manner, which after ‘correction’ for corneal thickness is raised beyond two standard deviations of the population mean, is suspicious. The two standard deviations value varies between populations but > 22 mmHg is a reasonable cut-off for most populations.20-23 The tonopen, ICARE and air puff tonometers have a place in busy clinics but all abnormal values should be repeated and then confirmed by Goldmann applanation. The Pascal tonometer can provide a closer estimate of the intracameral IOP and seems to have the least variability. As with any measurement and especially in the absence of other signs of glaucoma, we should not rely on a single reading.10,11 A measurement obtained after dilatation may increase the ‘yield’. If the disc is suspicious, other signs of the disease are present or the patient is considered high risk, for example, by virtue of a family history, the IOP measurements continued page 4
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the assessment suspect
‘directed’ investigations. In some instances a diagnosis may not be possible at the initial examination: in suspects and early disease it may be necessary to repeat the entire examination after a period of observation. We briefly describe the essential components of a comprehensive eye examination.18 External examination May detect subtle signs of facial hemangioma or dilated episcleral veins, which indicate a secondary cause. Ciliary conjunctival congestion suggests sinister intraocular pathology including acute angle closure. Ocular motility Detection of amblyopia or sensory exotropia may be the reason for a less aggressive management plan. Examination of the pupil As glaucoma is usually an asymmetric disease, a relative afferent pupillary defect is an important diagnostic clue and a possible prognostic factor as well. A dilated pupil may be a sign of acute angle closure. Slitlamp examination Is performed both before and after dilatation to detect signs of pseudo-exfoliation, pigment dispersion, uveitis or trauma. Pigment liberation following dilatation is very thomas r*† parikh r§ Walland m|| * Queensland Eye Institute, Brisbane, Australia † University of Queensland § Bombay City eye Institute & Research Centre, || Glaucoma Unit, Royal Victorian Eye and Ear Hospital
The Term Paper on International Preliminary Examination
International preliminary examination is an optional feature of the international phase available under Chapter II of the PCT. It is performed by an International Preliminary Examining Authority (IPEA), one of the Offices which are also International Searching Authorities (ISAs) [see Module 7]. The receiving Office with which you filed your PCT application has appointed the IPEA which is “ ...
suggestive of pseudo-exfoliation (or active pigment dispersion) and directs the search for subtle signs of disease like the early ‘brown’ stage of pseudoexfoliation (Figure 1).
Corneal oedema detected during such an examination may underestimate IOP measurement. Posterior synechiae may explain pupillary distortion. Corneal endothelial or iris pathology may direct the search towards a secondary cause. Intraocular pressure (IOP) The IOP is measured at every visit. The current gold standard is the Goldmann applanation tonometer attached to the slitlamp; the hand-held Perkins instrument can be used. too. It is important to remember that the Goldmann applanation tonometer,
Figure 1
Figure 2
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From page 3
should be repeated. This is necessary not just to detect raised IOP but also to obtain a baseline for treatment. In the presence of disc and field changes, if the IOP is ‘normal’ or ‘low’, multiple readings should be obtained during different times of the day—in come cases, even at night time—if facilities are available. Such multiple readings could be considered before initiating any expensive or invasive investigations to explain the disc and field changes. The principle of multiple readings, preferably obtained at different times of the day applies even after treatment is initiated. Obtaining diurnal curves is difficult; the recent use of the water drinking test to predict the peak IOP and IOP fluctuation requires further study. So-called normal tension glaucoma patients do not routinely require neurological imaging simply by virtue of their IOP; by contrast, any pallor of the optic disc rim and/or disc-field—that is, structure-function—mismatch mandates imaging, irrespective of the IOP.
The Term Paper on Optical Fibre Light Angle Fibres
History of Fibre Optics When Alexander Graham Bell spoke over a beam of light in the 1880's, he never dreamed ofthe possibilities that modern scientists are dreaming up for light. He used sunlight which was focused by means of a reflector and a lens to a device which could be made to vibrate in harmony with speech from a human voice. The light beam was made to vary the focus in and out so that the ...
Figure 3
gonioscopy
POAG is a diagnosis of exclusion. The name itself indicates that the signs of glaucoma must be present with an open angle, in the absence of other causes. The visualisation of an open angle is especially important in re-
gions of the world where PACD is common. Australia is a migrant nation that comprises several ethnic groups that are at risk for PACD; and PACD including acute angle closure does occur in the Caucasian population, too. Detection of PACD in the early stages presents an excellent opportunity for prevention using a simple laser iridotomy.24 Goniosocopy is used to examine the angle of the anterior chamber and is best performed using an ‘indentation’ type of
Figure 4
Figure 5
gonioscope. (Figure 2).
A four-mirror indentation gonioscope is the better choice; the lack of need for coupling fluid also makes the goal of routine gonioscopy easier. In difficult patients and where the four-mirror indentation gonioscope is not available, ‘manipulation’ with a two-mirror gonioscope to try and achieve indentation is an acceptable option. The features of an open angle are shown in Figure 3. When determining if an angle is open or closed, the testing conditions are critical. If the examination is done in a bright room with a long slit beam that impinges on and constricts the pupil, and/or with some pressure applied by the gonioscope, many angles will ‘open’. Figure 4 shows the same angle, open with bright illumination but closed in dim illumination. The ideal gonioscopic testing conditions include: dim room illumination, minimal intensity of the slitlamp illumination, a low slit beam height such that light does not impinge on the pupil and no pressure on the eye with the gonioscope. It is necessary to wait for 30-45 seconds for the pupil to dilate before deciding if the angle is open. • If under these conditions the posterior trabecular meshwork (PTM) is not seen, the patient is asked to look towards the mirror in order to obtain an ‘over the (iris) hill view’ of the angle. If > 180 degrees of the PTM is seen with such an ‘over the hill view’ under the specified testing conditions, without any pressure on the eye, the angle is considered open (Figure 5).
The Essay on Glaucoma Eye Treatment Pressure
Glaucoma The most common eye disease of the eyelid is a sty, which is an infection of the eyelashes. Several congenital defects of the eyelids occur, including colo boma, or cleft eyelid, and ptosis, a drooping of the upper lid. (Eye 4) Defects to the eye are in inner surface of the eyelid to the eyeball, which usually burns. The eyelids are skin diseases such as eczema and acne and malignant ...
If not, the patient is considered a primary angle closure suspect. (The current clinical classification
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optic disc and NFl examination
A magnified, stereoscopic examination of the optic disc using a 60-90 D lens, or a contact lens with the slitlamp is the ideal method of examining the optic disc and nerve fibre layer (NFL).18 Retinal examination also requires an indirect ophthalmoscope but this alone is not good enough to comment on the optic disc. In experienced hands the direct ophthalmoscope can provide valuable information. Stereo-photographs are considered the current gold standard for documentation and monitoring of the optic disc. There is considerable disagreement even between experts for evaluating progression using stereo-photographs and this is likely to be greater with standard disc photographs. Stereo-photographs detect disc haemorrhages more often than routine clinical examinations. It is possible that the same may be true for standard photographs but the data is not available. Finally, while stereo-photographs are still considered the gold standard, optic disc findings should at least be documented with a drawing or imaging for comparison with future examinations. The structural changes in the optic disc in glaucoma are numerous; the diagnosis is based on a combination of signs.27 • The most commonly used sign for the diagnosis of glaucomatous damage is an ‘increased’ cup to disc ratio (CDR).
Generally, an arbitrary statistical cut off of 0.7:1 is considered to be suspicious, more so if the cup is vertically oriented. The CDR can be fallacious and should not be used in isolation. The reason is that about a million plus axons exit the eye through the optic disc; they form the ‘neuro-retinal’ rim of the optic disc. Think of the cup as the ‘space’ that is left over after these axons have been ‘accommodated’ in the disc. The size of the optic disc varies considerably; the ‘space left over’, that is the cup, has to vary with the size. Accordingly, a small disc may not be entitled to any cup; and a large disc is entitled to a very large cup, beyond the 0.7:1 cut-off (Figure 7) . continued page 6
Figure 6
uses 270 degrees of PTM non visibility, but data for progression is available only for 180, hence our use of the latter.) In the next step, the illumination and slight beam height are increased to constrict the pupil, and ‘indentation’ is performed with the gonioscope to look for other signs of pathology in the angle. These may include peripheral anterior synechiae (PAS) (Figure 6), a consequence of angle closure or inflammation, signs of PXE, trauma, old haemorrhage, inflammation or new vessels. The authors recently encountered a rare case where trabecular precipitates were the only evidence of inflammation in a patient being treated as POAG;25 investigations led to the diagnosis of sarcoidosis. If other signs are absent AND the angles are open under the conditions described above, then in the presence of disc and/ or field changes we consider a diagnosis of POAG. Gonioscopy is not a once only examination. A patient with POAG can develop an angle closure component over time. Gonioscopy should be repeated at least annually if the signs of the disease change, and also after interventions like iridotomy or trabeculectomy.
role of van herick tests and angle imaging
The van Herick test has been suggested as a screening test for angle closure. The sensitivity and specificity of this test are such that a negative test does not rule out angle closure and a positive test still
requires a gonioscopy.3,26 The presence of a positive van Herrick AND a raised IOP is highly specific and almost pathognomonic of closure but gonioscopy is still required for management.3,26 Accordingly if the philosophy is one of case detection and management, the van Herrick test does not really help. Angle imaging techniques such as the ultrasound bio-microsope (UBM) and anterior segment OCT (ASOCT) are adjunctive tools in the management of PACD, are subject to the general rules guiding such tests and have not replaced the gonioscope. While the ASOCT is easier to use than the UBM, both instruments examine only a few sections of the angle. False positives of PACD are common and most signs in the angle (blood, black balls, blotchy pigment) can be missed. Unless a scanning section has serendipitously passed through an area of peripheral anterior synechia, even this important pathology can be missed. At the moment the ASOCT can at best identify eyes that may harbour such angle pathology but the detection of most such pathology requires a gonioscope. Available data for progression of PACD that currently guides management were obtained using a gonioscope and this data cannot be extrapolated to imaging. There is currently no evidence to base management decisions on imaging alone. It is possible that imaging for PACD will have a role to play in documenting progression and the effect of intervention but at the moment they have not replaced gonioscopy and are not necessary for routine clinical use.
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From page 5 The cup disc ratio can be useful, but only if it is related to the size of the disc. The size of the disc can be easily estimated on the slitlamp with a 60 D lens. A narrow slit beam height is adjusted vertically until it just encompasses the margins of the optic disc and the height is read directly off the graticule: 90 D and 78 D lenses require a conversion factor (x1.3 and x1.1 respectively) (Figure 8).
It is not as important to obtain an actual measurement as it is to get a feel for whether a disc is small (vertical diameter 2 mm).
As with any other examination, that only becomes possible after examining and measuring a large number of discs.The question we ask is: ‘Is this disc physiologically allowed to have this sort of cup?’ A small cup, like 0.3, usually considered to be in the normal range, may not be physiological in a small disc; on the other hand, a large cup may by physiological in a large disc. In other words, a small cup may be abnormal in a small disc and a large cup may be normal for a large disc. The CDR is also useful in two other situations. If, after accounting for a difference in size of the two discs, the CDR in the two eyes differs by more than > 0.2, that is suspicious for glaucomatous damage. A loss of rim tissue (increase in the cup) over time without rim atrophy is pathognomonic of glaucoma. It is important to remember that the cup and the CDR are only a surrogate for the tissue that we really want to examine: the neuro retinal rim (NRR).
Changes in the neuro retinal rim suggest pathology. Rather than the usual cup to disc ratio, we prefer to document the RIM to DISC ratio in the superior, superotemporal, inferotemporal, inferior and nasal areas of the disc. A rim to disc ratio of under 0.1:1 should be considered pathology until proved otherwise. Rim to disc ratio also allows better monitoring.28,29
Figure 8
Figure 7A
changes in the neuro retinal rim
Pattern The NRR is usually thickest inferiorly, followed by superior, nasal and temporal (Figure 9).
This ‘ISNT’ rule holds true in about 80 per cent of normals. While that is not specific enough and there may be normal variations, any change in this pattern should be considered suspicious 27 (Figure 10).
If the inferior rim is thinner than the superior, that could suggest pathology. Certainly, an inferior or superior rim that is equal to or thinner than the temporal rim is highly suspicious. The temporal rim should be the thinnest. Localised narrowing of the inferior or superior rim that does not extend to the rim is also suspicious. A rim that extends to the edge of the disc for a clock hour is called a notch. A notch is characteristic of glaucoma and usually correlates with a functional field defect (Figure 11) . A flame-shaped haemorrhage that touches the neuroretinal rim is specific but not sensitive for glaucoma (Figure 12).
Pallor of the rim is NOT a sign of glaucoma. Pallor of the rim outside the area of loss or out of proportion to the ‘cupping’ suggests other neurological causes and needs to be investigated. Peripapillary choroidal atrophy is a soft sign of glaucomatous damage. It is significant if associated with other signs or if it increases in size.
Figure 7B
Figure 7c
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Figure 9 Nerve fibre layer defect (NFLD) The gold standard for the examination of the NFL is red free photography but it can be examined clinically using the green filter on the slitlamp or ophthalmoscope. It is sometimes clearly seen on indirect ophthalmoscopy too, both with and without the green filter. The normal arcuate nerve fibre layer is seen as fine bright striations. Viewed from the superior to the inferior arcuate area the NFL has a bright, dark, bright pattern, the ‘dark’ being the region between the disc and macula (Figure 13).
The inferior arcuate NFL has a larger area and is more clearly seen than the superior arcuate NFL; this is consistent with the NRR thickness. A localised NFLD appears as a dark wedge that follows the pattern of the nerve fibre layer and widens towards the periph-
Figure 10 ery (Figure 14).
Such a defect should be wider than an arteriole, touch the edge of the disc and increase in width towards the periphery. NFL defects have a strong predictive value for future functional changes. The specificity is very high but the sensitivity is poor. The defects are a definite sign of pathology but can occur in diseases other than glaucoma, too. Diffuse NFLDs are more difficult to detect. The normal bright, dark, bright pattern is lost. The pattern takes on a dark, dark, dark apearance. Better visibility of the superior NFL compared to the inferior is also suspicious. The diagnosis of glaucomatous changes in the optic nerve is usually based on a combination of the above signs.27-29 For example in a disc with a notch as well as a NFLD, the combined specificity is high enough to rule in glaucoma. Similarly, in a disc with a thinning of the rim as well as an optic disc haemorrhage, the specificity is again high enough to rule in glaucoma. On the other hand, the sensitivity of individual signs is not high enough to rule out glaucoma unless most or all the signs are absent. Jost Jonas usually teaches three rules for optic disc examination in glaucoma diagnosis (Jonas JB, personal communication).
Until proved otherwise: l all glaucoma suspects have nerve fibre layer defects l all glaucoma suspects have optic nerve haemorrhage l all myopes have glaucoma (myopes are at higher risk for glaucoma).
continued page 8
Figure 11A
Figure 11B
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From page 7 important area.30,31 The clinical application for such data for diagnosis and progression requires a basic knowledge of how to apply the published sensitivity, specificity and likelihood ratios.10 Their use for screening and in lieu of clinical examination is not based on clinical principle or evidence. localised. A localised defect will show up in both the total deviation and pattern deviation plots. A generalised depression is more characteristic of anterior segment related causes, like cataract affecting the visual field. In such cases the defects are limited to the total deviation plot (Figure 16).
A warning: visual fields like any other test must NEVER be interpreted in isolation. • The field should usually correlate with structural changes in the optic disc and NFL. • If there is definite structural damage but the field is normal, repeat the visual field. • If there is a visual field defect but no correlating structural damage, examine the disc again. If there is still no correlating structural damage, re-examine the disc using a contact lens to obtain a good stereoscopic view. While the gold standard for perimetry is a full threshold examination, in the presence of other signs of glaucoma the presence of a repeatable defect in the 20-1 screening mode of a frequency doubling perimeter (FDP) (Figure 17) is sufficient evidence for a visual field defect due to glaucoma.35-36 While it is not in the remit of this article, we feel that the demonstration of a repeatable functional defect is usually required before incisional surgery is considered. This can be done even with a Bjerrum’s screen but an automated simple machine like the FDP is more likely to be used. The FDP is also capable of a full threshold test but has no follow-up capability. The initial evaluation of a patient may or may not lead to a confirmed diagnosis or a decision to treat. Follow-up of suspects
As we are serious about detecting glaucoma at a stage when we can prevent visual disability, we have added the following rule: l Unless proved otherwise, ALL optic discs have glaucomatous changes (and all angles are closed).
The rule emphasises that to detect glaucoma, we must have a high index of suspicion and examine ALL patients carefully. The optic disc should be examined at every visit. Depending on the course of the disease, documentation should be performed every six to 12 months.
Visual field
Glaucoma is a potentially blinding disease because it causes functional defects in the visual field. In the presence of a repeatable defect that correlates with the disc and NFL changes, the diagnosis and management decisions become clearer. The detection of field defects and their progression (or stability) is therefore extremely important in glaucoma management. Like any other test, a visual field is obtained ONLy if there is a suspicion of disease. A field ‘defect’ in a person whose examination is normal is likely to be a false positive. If there is no suspicion of disease, do not obtain fields or any other test, including imaging. • The current gold standard for examination of the visual fields is full threshold automated perimetry. Automated perimetry has a learning curve and it is best not to rely on the first two fields. It is best to use the same model of perimeter for the same patient; a perimeter that has a validated progression program like the visual field index is desirable.32,33 • The perimetry printout is analySed systematically in Zones.34 A field with an early glaucomatous defect is shown in Figure 15. • The field defects in glaucoma are usually
Imaging techniques for examining optic disc
The optic nerve and or nerve fibre layer imaging techniques include the Heidelberg Retinal Tomograph (HRT III), Optical Coherence Tomography (OCT) and the Nerve Fiber Layer Analyzer (GDx VCC).
The World Glaucoma Association (WGA) consensus on imaging states that these instruments lack the sensitivity and specificity for routine clinical use but that in the hands of experts, they may provide valuable clinical information.4 These instruments can help corroborate our suspicions and help support our diagnosis but are not required for routine clinical diagnosis. If we have to make a choice between automated perimetery or one of the imaging techniques for diagnosis, we suggest the automated perimeter. We do feel that the imaging devices may have a potential for documenting and detecting change and have a major role to play in this
Figure 12 Figure 13
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Figure 14
and patients at appropriate intervals for detection of progression based on optic disc examination, imaging and serial visual fields is crucial to further decision-making. It is important to obtain baseline documentation of the optic disc and visual fields early in the course of the disease. Baseline fields should exclude the learning curve.
When do we suspect glaucoma?
• Family history of glaucoma • Raised IOP (more than 22 mmHg) • Non-visibility of the trabecular meshwork on goniosocpy • A ‘suspicious’ optic disc (anything that looks out of the ordinary or outside the normal range or a rim to disc ratio
Figure 15
Figure 16
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Summary
The diagnosis of established glaucoma at a stage where treatment can prevent blindness involves the strategy of case detection. The eye-care practitioner should aim to detect all potentially serious ophthalmic pathology, including glaucoma. This requires a comprehensive eye examination including slitlamp, IOP, gonioscopy and a dilated disc and fundus examination on all clinic patients. Automated perimetry should be obtained for all suspects and programs like a visual field index (VFI) should be used for follow-up. FDP is an alternative to confirm the presence of glaucomatous visual field defects. Screening for glaucoma using imaging or visual fields prior to a clinical examination can have too many false positives and negatives and is not recommended. Acknowledgement The authors are grateful to the Indian Journal of Ophthalmology for permission to reproduce photographs and text.
Figure 17
Suspected Glaucoma Slitlamp examination IOP (applanation tonometry) Gonioscopy DISC & RNFL evaluation (60 D/ 78 D/ 90D) Automated perimetry if indicated (WWP)
Raised IOP (≥ 22 mmHg) CCT diurnal variation*
• Open angles • Secondary glaucoma ruled out
‘Normal’ IOP with optic disc changes & corresponding visual field defects
CCT diurnal variation** Normal optic disc & visual field Definite disc & RNFL changes normal field Definite disc & RNFL changes with corresponding field defect IOP ≥ 22 mm Hg Definite disc & RNFL changes with corresponding field defect IOP
OHT
Pre-perimetric glaucoma
POAG
? FDT/ ?? SWAP Optic disc & RNFL imaging for follow-up
? FDT ?? SWAP Optic disc & RNFL imaging for diagnosis & follow-up
WWP Optic disc & RNFL imaging for follow-up OHT: Ocular hypertension CCT: Central corneal thickness
IOP: Intraocular pressure POAG: Primary open angle glaucoma
RNFL: Retinal nerve fibre layer WWP: White on white perimetry
* Multiple IOP readings at different times on different days is easier to obtain than a diurnal variation of tension. ** Multiple IOP readings at different times on different days / 24 hour diurnal variation of IOP
Figure 18
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1. Mitchell P, Smith W, Attebo K, Healey PR. Prevalence of open-angle glaucoma in Australia. The Blue Mountains Eye Study. Ophthalmology 1996; 103: 1661–1669. 2. Thomas R, Loibl K, Parikh R. Evaluation of a glaucoma patient. Indian J Ophthalmol 2011; 59: Suppl S43-52. 3. Thomas R, Parikh R, Paul P, Muliyil J. Populationbased screening versus case detection. Indian J Ophthalmol 2002; 50: 233-237. 4. Glaucoma Diagnosis: Structure and Function. Eds: Greve E, Wienreb R. Hague, Netherlands: Kugler Publication; 2004. 5. American Academy of Ophthalmology. Primary Open- Angle Glaucoma. Preferred Practice Pattern. San Francisco, CA: American Academy of Ophthalmology; 1996. 6. SEAGIG Asia Pacific Glaucoma Guidelines. 2nd ed; 2008-2009. www.seagig.org. 7. The Fast Facts in Glaucoma. Healey P, Thomas R. Oxford UK: Health Press Ltd. In press. 8. Walland MJ. Editorial. How to save the sight of Australians with glaucoma. Med J Aust 2008; 188: 269-270. 9. Sackett DL, Haynes RB, Guyatt GH, Tugwell P. Clinical Epidemiology: A Basic Science for Clinical Medicine. Early Diagnosis. Boston: Little Brown and Co; 1991. p 168. 10. Parikh R, Parikh S, Arun E, Thomas R. Likelihood ratios: clinical application in day-to-day practice. Indian J Ophthalmol 2009; 57: 217-221. 11. Parikh R, Mathai A, Parikh S, Chandra Sekhar G, Thomas R. Understanding and using sensitivity, specificity and predictive values. Indian J Ophthalmol 2008; 56: 45-50. 12. Green CM, Kearns LS, Wu J, Barbour JM, Wilkinson RM, Ring MA, Craig JE, Wong TL, Hewitt AW, Mackey DA. How significant is a family history of glaucoma? Experience from the Glaucoma Inheritance Study in Tasmania. Clin Experiment Ophthalmol 2007; 35: 793-799. 13. Mitchell P, Rochtchina E, Lee AJ, Wang JJ. Bias in self-reported family history and relationship to glaucoma: the Blue Mountains Eye Study. Ophthalmic Epidemiol 2002; 9: 333-345. 14. Sommer A. Glaucoma risk factors observed in the Baltimore Eye Survey. Curr Opin Ophthalmol 1996; 7: 93-98. 15. Nemesure B, He Q, Mendell N, Wu Sy, Hejtmancik JF, Hennis A, Leske MC; Barbados Family Study Group. Inheritance of open-angle glaucoma in the Barbados family study. Am J Med Genet 2001; 103: 36-43. 16. Mitchell P, Hourihan F, Sandbach J, Wang JJ. The relationship between glaucoma and myopia: the Blue Mountains Eye Study. Ophthalmology 1999; 106: 2010-2015. 17. Dandona L, Dandona R, Mandal P, Srinivas M, John RK, McCarty CA, Rao GN. Angle-closure glaucoma in an urban population in southern India. The Andhra Pradesh eye disease study. Ophthalmology 2000; 107: 1710-1716. 18. Thomas R, Parikh RS. How to assess a patient for glaucoma. Community Eye Health 2006; 19: 36-37. 19. Parikh RS, Parikh SR, Navin S, Arun E, Thomas R. Practical approach to medical management of glaucoma. Indian J Ophthalmol 2008; 56: 223-230. 20. Jacob A, Thomas R, Koshi SP, Braganza A, Muliyil J. Prevalence of primary glaucoma in an urban south Indian population. Indian J Ophthalmol 1998; 46: 81-86. 21. Dandona L, Dandona R, Srinivas M, Mandal P, John RK, McCarty CA et al. Open-angle glaucoma in an urban population in southern India: the Andhra Pradesh Eye Disease Study. Ophthalmology 2000; 107: 1702-1709. 22. Vijaya L, George R, Arvind H, Baskaran M, Paul PG, Ramesh SV et al. Prevalence of angle-closure disease in a rural southern Indian population. Arch Ophthalmol 2006; 124: 403-409. 23. Vijaya L, George R, Paul PG, Baskaran M, Arvind H, Raju P, Ramesh SV, Kumaramanickavel G, McCarty C. Prevalence of open-angle glaucoma in a rural south Indian population. Invest Ophthalmol Vis Sci 2005; 46: 4461-4467. 24. Thomas R, Sekhar GC, Parikh R. Primary angle closure glaucoma: a developing world perspective. Clin Experiment Ophthalmol 2007; 35: 374-378. 25. Chandler and Grant’s Glaucoma. Eds: Epstein DL, Allingham RR, Schuman JS. 4th ed, 1986. p 383384. 26. Thomas R, George T, Braganza A, Muliyil J. The flashlight test and van Herick’s test are poor predictors for occludable angles. Aust NZ J Ophthalmol 1996; 24: 251-256. 27. J o n a s J B , B u d d e W M , Pa n d a – J o n a s S . Ophthalmoscopic evaluation of the optic nerve head. Surv Ophthalmol 1999; 43: 293-320. 28. Harasymowycz P, Davis B, Xu G, Myers J, Bayer A, Spaeth GL. The use of RADAAR (ratio of rim area to disc area asymmetry) in detecting glaucoma and its severity. Can J Ophthalmol 2004; 39: 240-244. 29. Spaeth GL, Lopes JF, Junk AK, Grigorian AP, Henderer J. Systems for staging the amount of optic nerve damage in glaucoma: a critical review and new material. Surv Ophthalmol 2006; 51: 293-315. Review. 30. Chauhan BC, McCormick TA, Nicolela MT, LeBlanc RP. Optic disc and visual field changes in a prospective longitudinal study of patients with glaucoma: comparison of scanning laser tomography with conventional perimetry and optic disc photography. Arch Ophthalmol 2001 Oct; 119: 10: 1492-1499. 31. Alencar LM, Zangwill LM, Weinreb RN, Bowd C, Vizzeri G, Sample PA, Susanna R Jr, Medeiros FA. Agreement for detecting glaucoma progression with the GDx guided progression analysis, automated perimetry, and optic disc photography. Ophthalmology 2010; 117: 3: 462-470. Epub 2009 Dec 24. 32. Bengtsson B, Patella VM, Heijl A. Prediction of glaucomatous visual field loss by extrapolation of linear trends. Arch Ophthalmol 2009; 127: 12: 1610-1615. 33. Casas-Llera P, Rebolleda G, Muñoz-Negrete FJ, Arnalich-Montiel F, Pérez-López M, FernándezBuenaga R. Visual field index rate and event-based glaucoma progression analysis: comparison in a glaucoma population. Br J Ophthalmol 2009; 93: 12: 1576-1579. Epub 2009 Jun 16. 34. Thomas R, George R. Interpreting automated perimetry. Indian J Ophthalmol 2001; 49: 125-140. 35. Thomas R, Bhat S, Muliyil JP, Parikh R, George R. Frequency doubling perimetry in glaucoma. J Glaucoma 2002; 11: 46-50. 36. Clement CI, Goldberg I, Healey PR, Graham S. Humphrey matrix frequency doubling perimetry for detection of visual-field defects in open-angle glaucoma. Br J Ophthalmol 2009; 93: 582-588. Epub 2008 Jul 31.
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Suspected glaucoma Slitlamp examination Gonioscopy IOP (Applanataion tonometry) Disc and RNFL evaluation (60 D/ 78 D/ 90 D) Automated perimetry if indicated (WWP) Angle: posterior trabecular meshwork not visible > 180 degrees Causes for secondary glaucoma ruled out No PAS Normal disc PACS PAS / ± high IOP Normal disc PACS + PAS / ± high IOP Glaucomatous disc/ ± corresponding visual defect PACG
? Follow up IOP, gonioscopy etc ? Iridotomy: Consider family history, symptoms, extent of non-visibility, need for repeated dilatation, availability of care IOP: Intraocular pressure PACG: Primary angle closure glaucoma
Iridotomy ± Iridoplasty Follow up with IOP, gonioscopy & disc field if indicated. If raised IOP, remains POAG suspect.
Usually iridotomy ± other measures to open the angle. Then manage as POAG
RNFL: Retinal nerve fibre layer PAC: Primary angle closure
PACS: Primary angle closure suspect WWP: White on white perimetry
Figure 19
OPTOMETRy pharma JUNE 2011
