CPD Modules Available

Print this page

Glaucoma 2: Detection

4T in Autralia | 1CD + 1G in New Zealand | 8 December 2018




The goal in glaucoma detection and management is to delay progression of the disease so that the patient still has vision as they get older. The manner and methods of detecting glaucoma have changed significantly over time, as well as, what constitutes standard care for patients with glaucoma. While glaucoma is a primary optic neuropathy, observation of the optic nerve will give the most information regarding who does and who does not have glaucoma.


1. Primary open angle glaucoma and all characteristic features
2. The epidemiology of glaucoma and societal burden of the disease
3. Aqueous humor production and drainage and how it contributed to intraocular pressure elevations
4. Proper optic nerve analysis for the detection of glaucoma
5. The importance of various risk factors in the development of glaucoma and properly assess them in the detection of the disease
6. Functional analysis and interpretation of threshold perimetry.

At one time, everyone with intraocular pressure (IOP) exceeding 21mmHg was diagnosed with glaucoma and medicated, often for many years and to end of life. The cut off for normal IOP at 21 is very inappropriate and based upon an old population based study of approximately 2000 Anglo-Celtic men over the age of 40 years who self reported that they had “normal eyes”.1 It is crucial to remember that people with IOP over 21mmHg may never develop glaucoma and others with IOP never exceeding 21mmHg may become blind. There is no IOP cut off that will accurately separate normal from glaucoma and tonometry is not an acceptable method of screening for glaucoma.

In the past and present, there have been optic nerve anomalies with glaucomatous type vision loss or glaucomatous type appearance, such as hypoplasia, colobomas, buried drusen, optic pits, tilted disc syndrome, and obliquely inserted discs that have been misdiagnosed as glaucoma. Additionally, there are neurological diseases such as optic atrophy, chiasmal syndromes, and compressive lesions of the anterior visual pathway, which may superficially mimic glaucoma and be misdiagnosed. Arteritic anterior ischemic optic neuropathy, compressive tumors, and other entities may have enlargement and deepening of the optic cup superficially similar to glaucoma, but with other features such as sudden vision loss and disc pallor that are not found in glaucoma. There have been spurious glaucoma provocative tests such as the water provocative test, mydriatic provocative test, prone and dark room provocative test, and the pressor-congestion test where patients were exposed to some unnatural situation and if there was a corresponding increase in IOP, they were diagnosed with glaucoma, often independent of any other feature or risk factor.2

When assessing patients and trying to accurately detect glaucoma, it is important to recognise what glaucoma actually is:

Primary open angle glaucoma (POAG) is a progressive, chronic optic neuropathy in adults where intraocular pressure and other currently known and unknown risk factors contribute to damage and in which, in the absence of other identifiable causes, there is a characteristic acquired atrophy of the optic nerve and loss of retinal ganglion cells and their axons, often with characteristic damage to the visual field. This is associated with an anterior chamber angle that is open by gonioscopic appearance.

There exists these caveats: the IOP does not need to be ‘elevated’, just too high for an individual eye and there does not need to be visual field loss.

There is debate upon what constitutes the standard of care for patients with glaucoma. Certainly, with advances in imaging technology and pachymetry, some would argue that these technologies are standard of care today. However, it can be argued that it is much simpler. In order to meet a reasonable standard of care for patients with glaucoma, optometrists should be performing applanation tonometry, threshold perimetry, and gonioscopy. They should also be examining the optic disc, preferably stereoscopically. Any optometrist performing these tasks not only is meeting what would be considered a standard of care for glaucoma management, but is actually delivering good glaucoma care. Beyond this, the optometrist can add pachymetry as part of the glaucoma patient evaluation. Further, beyond this, the practitioner can add optic disc photos to the evaluation. Finally, the highest level will involve a diagnostic imaging device of some type. However, if one were to look at the optic nerve stereoscopically, and additionally perform gonioscopy, applanation tonometry, and threshold perimetry, then patients with glaucoma will be well cared for.


Aqueous is produced at 2-3 microlitres/minute and there is complete turnover every 1-2 hours. A resistance and pressure decrease occurs across the inner wall of Schlemm’s canal causing the pressure in the trabecular meshwork (TM) distal to be greater. At elevated IOP, the TM distends and the inner wall moves towards the outer wall of the canal. Giant vacuoles in the wall of Schlemm’s canal transport aliquots of aqueous. Giant vacuole formation is pressure dependent. Aqueous in the canal is drained to the episcleral venous plexus. Increased episcleral venous pressure will increase outflow resistance as well as resistance at the trabecular meshwork. Even aqueous itself can increase outflow resistance. The cribriform, or juxtacanalicular meshwork represents the principal site of aqueous outflow resistance.

Trabecular outflow is through the trabecular meshwork. Uveoscleral outflow is through the interstices of the uveoscleral meshwork located on the ciliary face. Trabecular outflow is approximately 80 per cent of the outflow and uveoscleral is the remainder. The uveoscleral pathway goes to the supraciliary and finally the suprachoroidal space. Uveoscleral flow is pressure independent, representing bulk flow rather than diffusion related phenomena. Flow is unchanged despite elevations in episcleral pressure.3

The anterior chamber angle of all patients undergoes normal aging changes including loss of trabecular cells, an increase in the accumulation of pigment within the endothelial cells of the trabecular meshwork, and thickening of the trabecular lamellae from an accumulation of material in the basement membrane of the endothelial cells and also the addition of extracellular material within the core of the trabecular beam. There is also a loss of ability to form giant vacuoles along the inner wall of Schlemm’s canal. Glaucoma can be viewed as an exaggerated, elevated rate in aging changes.4

Glaucoma also has posterior segment changes including compression of laminar sheets, distortion of laminar pores, posterior and lateral displacement of laminar sheets, blockage of axonal transport with death of ganglion cells, and deepening and enlargement of the optic cup.5

Clinical Pearl:

The anterior segment changes and abnormalities in the aqueous filtration mechanisms occur to some degree in all patients as they age. In glaucoma, these changes occur earlier and more significantly. One might argue that everyone would develop glaucoma if they lived long enough.



In 2013, the number of people (aged 40-80 years) with glaucoma worldwide was estimated to be 64.3 million, increasing to 76.0 million in 2020 and 111.8 million in 2040.6 More than 2.7 million Americans aged 40 and older are affected and half are either unaware or undiagnosed. The prevalence of glaucoma in the United States is 22 percent higher than it was 10 years ago. Approximately 4 per cent of glaucoma patients become blind; however, not everyone with glaucoma has a 4 per cent risk of becoming blind – some may be much higher or lower.

The Thessaloniki Eye Study looked at 2,554 participants aged 60 years or over and found a 50 per cent rate of undiagnosed glaucoma. Primary open-angle glaucoma was found to be four times more likely to be undiagnosed compared with exfoliation glaucoma. Not having seen an eye doctor in the past 12 months and a smaller cup-to-disc ratio were other associated factors with non-diagnosis. Curiously, a prevalence of 66.7 per cent over diagnosed glaucoma was also found. Only one-third of the patients who had been previously diagnosed with glaucoma had the diagnosis confirmed in the study. The vast majority was undergoing treatment, and a smaller proportion already had laser or surgery. The factors associated with over diagnosis were similar to those identified with under-diagnosis. Patients who had seen an eye doctor in the last 12 months had three times increased likelihood to be over diagnosed, and a higher cup-to-disc ratio was associated with a four times increase. Other factors identified were family history, history of cataract surgery and higher IOP. The implications of this population based survey were that one-third of subjects with undiagnosed glaucoma had progressed to advanced stages. On the other hand, fear of blindness, side effects of unnecessary treatment, increased costs for individuals and society, and the waste of clinical resources are consequences of over diagnosis.7


A constellation of risk factors leading to loss of neural tissue with progressive disc damage and functional vision loss makes glaucoma a multifaceted disease. Initially there may not be visual field loss in patients with glaucoma. This is termed “preperimetric glaucoma”. Thus, there is glaucomatous damage to the optic disc and retinal nerve fiber layer (RNFL), but visual field loss has not yet ensued. Glaucoma can be diagnosed based upon disc appearance in the absence of visual field loss.

While technically glaucoma is a disease characterised by progressive disc damage and progressive field loss, diagnostic dilemmas and contradictions exist. In early cases, the progressive nature is important in making the diagnosis. Therefore, in these cases, sequential visual field examinations and optic nerve head photos are often required in order to demonstrate the progressive nature of the disease. However, in moderate and advanced cases, where the patient presents with (or even without) elevated IOP, optic nerves with obvious glaucomatous changes, and advanced visual field defects consistent with glaucoma, the diagnosis is often made upon the initial visit (without waiting to demonstrate progression). In addition, there are a number of conditions (e.g. inflammation, pigment dispersion, etc.), which produce an elevation in IOP and are termed secondary glaucomas, though there may be no field defect or optic nerve defect at the time of diagnosis. So, while not technically glaucoma based on the definition of progressed field loss and optic nerve damage, they are termed glaucoma because, in our best medical opinion, these pathological changes will likely occur if the IOP is not reduced.

Ocular hypertension (OHTN) is defined as IOP of 21mmHg or more in the absence of structural and functional changes. The Ocular Hypertension Treatment Study (OHTS) has shown that approximately 10 per cent of patients with ocular hypertension convert to true glaucoma over the course of 5 years.8 There are far more patients with OHTN than glaucoma and prevalence increases with age; 75 per cent of ocular hypertensives are over 60 years and 24 per cent of people over 70 years may be ocular hypertensive. A patient may also be considered a glaucoma suspect based upon elevated IOP, a suspicious disc appearance, a family history of glaucoma, advanced age, race, suspicious visual field loss, or a suspicious retinal nerve fiber layer (RNFL).

Clinical Pearl:

 The diagnosis of a “Glaucoma Suspect” should come with a Statute of Limitations. After 2 years, the patient needs to be diagnosed as either glaucoma or normal. They shouldn’t be a ‘suspect’ for 10 years.


IOP Variations

Elevated IOP is the most significant risk factor overall for the development and progression of glaucoma. It is important to remember that IOP which is statistically abnormal is not necessarily physiologically abnormal for an individual eye. Conversely, IOP that is statistically normal is not necessarily physiologically healthy for an individual eye. Thus, there is no clinically useful level of IOP to differentiate all normal people from those with glaucoma. Patients with advanced glaucoma may not be able to tolerate even moderate levels of IOP, while those with healthy optic discs and normal visual fields may be able to tolerate elevated IOP for many years.

Primary open angle glaucoma frequently occurs at statistically normal IOP and population based surveys show 50 per cent of POAG patients rarely have IOP exceeding 21mmHg. Thus, the risk factor is not “elevated” IOP, but an IOP level exceeding tolerability for an individual that matters most. The higher the IOP, the greater the risk. Ocular hypertension is a risk factor for glaucoma, not a prerequisite. The level of IOP which causes damage to an optic nerve varies significantly between individuals and even in the same person as she/he ages.

Glaucoma patients tend to have greater IOP variations, which may be even more pronounced with secondary glaucomas. It was once thought that IOP peaked in the morning and decreased throughout the day. It was also thought that IOP dropped during sleep due to aqueous production suppression; however, we have recently learned that the highest IOP occurs when the patient is sleeping in the supine position.9,10 This is likely due to increased episcleral venous pressure and not circadian rhythm. It has been shown that the diurnal IOP curve is not consistent over time and is not symmetrical between eyes of the same person.11
Glaucoma is predominately a disease of older people of African, Asian and Hispanic descent, and Indigenous people groups. Older Hispanics have a higher prevalence of glaucoma than people of African descent. In these demographics, POAG tends to occur earlier and follow a more aggressive natural history than in Anglo-Celtic patients.12

Family history should also be considered, especially if there is a direct relative such as a parent, sibling, or child. Prevalence of glaucoma is especially high in mothers and siblings and a family history of blindness is very important. One out of eight patients with POAG has a direct, first-degree undiagnosed family member. Hence, likely the best screening for glaucoma is to examine family members of glaucoma patients.13

The OHTS Study showed that central corneal thickness (CCT) was a strong predictor of conversion to glaucoma from OHTN.14 Thick corneas overestimate true applanation pressure and thin corneas underestimate true applanation pressure. However, beyond errors imparted by applanation, patients with thin corneas have greater risk of converting to glaucoma from ocular hypertension, are more likely to progress in glaucomatous damage, and are more likely to have structural and functional changes. This is possibly indicative of other structural weaknesses within the eye predisposing to glaucoma, but this is only speculative and not proven. Thin cornea is a risk factor for glaucoma at all levels of IOP, thus seems an independent risk factor. It should be remembered that there is no scientifically validated conversion factor to adjust for the role of CCT on IOP.


Diabetes is a very controversial risk factor for glaucoma. Various studies are contradictory with some supporting diabetes as a risk factor and others not. The best evidence from meta analyses indicate that diabetes is likely a positive risk factor for glaucoma. It could be that diabetes predisposes to vascular compromise and thus poor optic disc blood flow. Or, conversely, it may be that diabetics are referred for retinopathy screening and thus are more apt to be diagnosed with glaucoma based upon an increased sheer number of eye exams.15

Blood pressure likely has a role in glaucoma development. Hypertension can cause vascular compromise and arteriolosclerosis with poor blood vasculature. Conversely, hypotension may lead to poor blood flow to the optic nerve and chronic ischemia. This has all been examined as an indirect measurement of ocular perfusion pressure (OPP), which is simply the difference between systemic blood pressure and intraocular pressure. It has been speculated as an indirect measure of retinal and optic nerve perfusion.16 Numerous population based survey studies have identified low OPP being highly associated with glaucoma.

Obstructive sleep apnea (OSA) has been speculated as a risk factor for glaucoma, possibly contributing to a chronic hypoxic state that deprives the optic nerve of oxygen. Various studies have shown a high glaucoma prevalence in patients with obstructive sleep apnea.17 However, numerous studies have seen no association between glaucoma and OSA and this remains an unknown entity in glaucoma risk factors.18


As glaucoma is a primary optic neuropathy, observation of the optic nerve will give the most information regarding who has and who doesn’t have glaucoma. In glaucoma, there is a characteristic glaucomatous neuropathy involving focal rim damage in the form of notching and not a generalized concentric enlargement of the optic disc. It is important to be able to diagnose, or at least strongly suspect, glaucoma based solely upon disc appearance. That involves looking for focal rim defects as well as RNFL damage.

When assessing the optic disc, particular attention must be paid to these five features: Disc size, rim contour, parapapillary area, retinal nerve fiber layer, and disc hemorrhages.19 Additionally, neuroretinal rim color should be assessed and pallor should not be present.

Discs that are not of average size may be prone to over-or-under diagnosis. There are approximately one million retinal ganglion cell axons comprising the optic disc. The blood supply comes mostly from the short posterior ciliary arteries (SPCA). The average disc size ranges from 1.7 and 2.0mm vertically and 1.6 to 1.8 horizontally (1.9mm x 1.7 mm is a good average). Physiologically large nerves have large cups and occur more commonly in patients with normally large chorioscleral canals. One million axons need only so much room and in cases of megalopapillae, there can easily be an over diagnosis of glaucoma. Conversely, physiologically small nerves have small cups and even moderate cupping can indicate significant loss of tissue, resulting in an under diagnosis of glaucoma.

The neuroretinal rim should have pink colouration due to axons and capillaries and in glaucoma, the rim is always pink (except in very end stage disease where everything seems pale and you cannot distinguish rim from cup). There should be no rim pallor in glaucoma; if this occurs, it is not glaucoma (alone).

Other diseases can cause “cupping”, though there will be other features inconsistent with glaucoma such as central acuity loss and disc pallor. Non-glaucomatous cupping includes arteritic anterior ischemic optic neuropathy and possibly some others such as orbital or chiasmal masses, inflammatory diseases, trauma, and hereditary conditions.20

It is critically important to examine the optic disc contour for focal damage, which is commonly termed ‘notching of the neuroretinal rim’. This focal loss of tissue is very specific for and indicative of glaucoma. While other conditions can cause optic atrophy and increased in cup size, they don’t notch the nerve like glaucoma does. This focal damage manifests as vertical elongation of the optic cup. Ganglion cell axons are looser in the inferior and superior lamina and have less structural support. This is the reason for vertical elongation. Thus, one should look for narrowing of neuroretinal rim superiorly and inferiorly. There may often be an associated RNFL defect in areas of disc notching. In areas of notching, a hemorrhage may be present or was possibly an antecedent event. This aspect of disc analysis is the most compelling in diagnosing glaucoma.21,22

Clinical pearl:

Notching does not occur initially on the temporal or nasal aspect of the disc. Temporal thinning of the disc is most commonly an anomaly of disc insertion and not glaucoma. The term “temporal thinning”, in the absence of other glaucomatous disc changes, is meaningless.


Clinical Pearl:

It has been said that the temporal rim is the last to go in glaucoma. This is not technically true, but is practically accurate. When the temporal rim degrades, the papillomacular bundle is damaged and visual acuity decreases. This is easy to identify. In actuality, the nasal rim is preserved more than the temporal rim with a “temporal island of vision”. However, we typically don’t discover this “temporal island of vision” because when visual acuity drops significantly, we stop doing fields. This is the reason that an eye that is “No Light Perception” from glaucoma will still have a direct light reactive pupil.


Parapapillary observations should be part of the optic disc analysis. An atrophic peripapillary retina should make you consider glaucoma. This occurs often due to tissue misalignment and a possible shifting of tissues during the glaucomatous process. Parapapillary atrophy may change over time, but has been documented so infrequently that no statements can be made on significance. It still isn’t clear if parapapillary atrophy represents susceptibility to damage or the result of damage from glaucoma. It is unclear if this is a cause of glaucoma or an epiphenomenon of glaucoma. Adjacent to the optic disc may be an area of parapapillary atrophy known as Zone Beta and this involves scleral tissue showing through and is more associated with glaucoma. Further out one may find Zone Alpha; a pigment adjacent to Zone Beta, which is not highly associated with glaucoma.23

Clinical Pearl:

There are many normal eyes with parapapillary atrophy and glaucomatous eyes with no parapapillary atrophy.


 Retinal nerve fibre layer evaluation is as important as optic disc evaluation when assessing patients for glaucoma. Normal RNFL has a striate appearance with underlying vessels modestly obscured as if covered by transparent tape. An alteration in appearance of this normal striated pattern of RNFL, which may be diffuse or focal, can indicate glaucomatous damage. This may occur in the presence of a normal appearing optic disc and typically precedes disc and visual field changes. RNFL defects often appear as a dull area to the fundus which allows a better observation of the underlying choroidal details. However, RNFL defects can be difficult to detect in dark, tessellated, and myopic fundi, and when the damage is diffuse. Importantly, the RNFL can be very obviously focally damaged yet the disc (and possibly visual field) may appear perfectly normal. RNFL analysis and detection of damage is critically important in glaucoma diagnosis.

Hemorrhages are an important facet of optic disc analysis for glaucoma. In glaucoma, they are found inferior, inferior temporal, superior, superior temporal regions of the disc which are most susceptible to glaucomatous damage and account for virtually all true disc hemorrhages.24 Disc hemorrhages resolve within about six weeks, making it difficult to determine incidence in glaucoma. Also, many disc hemorrhages are missed in clinical observation.

Disc hemorrhages do not constitute a diagnosis of glaucoma nor a progression or conversion to glaucoma or an endpoint for any major glaucoma study. They can be recurrent and, if so, tend to recur in the same place on the disc each time. The best evidence through OCT study of laminar tissue indicates mechanical shifting of tissue as the cause of disc hemorrhages. This explains recurrent nature, characteristic location, and occurrence of unilateral hemorrhages. Numerous studies have indicated that that disc hemorrhages are strongly associated with risk of progression.25-27 Recurrent disc hemorrhages are no more associated with progression risk than single hemorrhage, unless it recurs in different part of disc.

Clinical Pearl:

A proper optic disc analysis involves assessment of optic disc size, assessment of neuroretinal rim color, and an inspection for the presence or absence of disc hemorrhages, retinal nerve fibre layer (RNFL) defects, parapapillary atrophy, and focal neuroretinal rim defects (notches).



Determination of functional loss through automated threshold perimetry is a key component in detecting glaucoma and predicting the potential for visual disability in a patient’s lifetime. There are numerous visual field changes that occur in glaucoma. Damage may be extensive (widespread) in end stage disease or focal in early-moderate disease. Initially, there will be relative scotomas (mild compared to adjacent points) which can easily be misinterpreted as normal. Similar are fluctuating scotomas (which are highly variable and may or may not be present on subsequent tests) representing very early damage. As the disease progresses, these may become absolute scotomas with no perception of lighted stimulus.

Types of glaucomatous visual field defects include paracentral scotomas, occurring from 5–15 degrees from fixation. These defects represent a relatively small visual field abnormality (a cluster or a single point) in the nerve fibre bundle region that is generally not contiguous with the blind spot or the nasal meridian. In particular, it does not involve points outside 15 degrees that are adjacent to the nasal meridian. There are also central scotomas with visual field loss that is predominantly in the macular region. The foveal threshold must have a p < 5 per cent value. These defects can be associated with a single hemifield and paired with another defect.

There are also nasal steps, which are limited field loss adjacent to the nasal horizontal meridian with at least one abnormal point (p < 5 per cent) at or outside 15 degrees on the meridian. More extensive are arcuate scotomas (also known as Bjerrum’s scotomas). There may be a partial arcuate where visual field loss in the nerve fibre bundle region that extends incompletely from the blind spot to the nasal meridian. The defect is generally contiguous with either the blind spot or the nasal meridian and must include at least one abnormal location in the temporal visual field. Full arcuate defects have significant visual field loss in the nerve fiber bundle region, extending across contiguous abnormal points from the blind spot to at least one point outside 15 degrees adjacent to the nasal meridian.

Less commonly are altitudinal defects, which manifest severe visual field loss throughout the entire superior or inferior hemifield that respects the horizontal midline, with the majority of points in the hemifield having a p < 0.5 per cent value on the total deviation plot and the entire horizontal midline demonstrating abnormality.

General depression and overall depression in sensitivity (diffuse loss) is actually very rare in glaucoma and more indicative of cataract, miosis, or other media/refractive issues.

 Figure 11a Left visual field

Clinical Pearl:

The earliest visual field defect in glaucoma is increased short term fluctuation. However, it is not practical to measure this on contemporary visual fields (only done if the Full Threshold strategy is chosen). The next is a shallow fluctuating scotoma, which can be measured practically, though is often not recognised clinically as a true defect.


A significant amount of retinal ganglion cell fibres can be destroyed in a glaucoma patient who may demonstrate full fields. It may take several years before ganglion cell damage will be detectable on conventional visual fields. Patients may have optic nerve, RNFL damage, or ganglion cell loss and thus have glaucoma, but not manifest a visual field loss. This is termed, “pre-perimetric glaucoma”.28

Swedish Interactive Thresholding Algorithm

Most commonly used is the Swedish Interactive Thresholding Algorithm (SITA), which is a threshold strategy which reduces threshold test time down to 5–7 minutes from original 15–18 minutes (for Full Threshold algorithm) without sacrificing accuracy. Two longstanding and well tested algorithms are SITA Standard and SITA Fast. SITA standard threshold field is considered the best test for diagnosing and following glaucoma. SITA Fast is a good screening test and for those patients who cannot maintain attention for long. It is also reasonable for use in neuro-ophthalmic diseases which are typically not presenting with subtle defects. SITA algorithms employ an Error Related Factor (ERF) in order to reduce test times. Perfect determination of threshold (that is, the sensitivity where the patient will see the stimulus 50 per cent of time) is extremely time consuming, fatiguing, and impractical. SITA allows for some “error” based upon known data and patient responses. SITA fast differs from SITA Standard in that there is decreased test time because the ERF is greater. That is, SITA Fast allows for a greater degree of uncertainty about threshold when deciding to end the test.

SITA Faster is the newest addition to the SITA family of testing strategies for the Humphrey Field Analyzer 3 (HFA3) perimetre. SITA Faster testing takes about two thirds of the time required by SITA Fast and about half the time required by SITA Standard. Test time reductions are largest in eyes with severe field loss. Many patients are able to complete SITA Faster 24–2 testing in about two minutes (SITA Faster is only available for 24–2). SITA Faster reduces “dead time” by no blind spot monitoring or False Negatives assessment and instead uses Gaze Monitoring and False Positives for test quality monitoring. Clinical testing has shown that SITA Faster produces results that are clinically equivalent to SITA Fast with no loss of repeatability. However, SITA Standard does in fact detect visual field progression slightly sooner.

Visual field results historically have been considered either reliable or unreliable, meaning that they are either helpful or utterly useless. It is more realistic is to consider that they come in a continuum of degrees and types of reliability and unreliability. A test determined “reliable” may be misleading, while those considered “unreliable” may still contain sufficient information to establish or rule out certain diseases, or to establish whether the disease has worsened. Reliability falls along a continuum with a multitude of different degrees of dependability, rather than just two. It is better to think in terms of a range from “Highly useful information” to “No useful information” based upon results.

The newest evidence based assessment of visual field reliability has shown that Fixation Losses do not affect VF reliability meaningfully in experienced field takers. Any level of False Positive decreases VF reliability, but one should be especially cautious when FPs occur in advanced disease or are found in >20 per cent of catch trials. False Negatives have less of an impact than False Positives. False Negatives do not significantly affect reliability in advanced disease unless they are high (at least 35 per cent, but oftentimes more than this value). Large increases in Test Duration (>2–3 minutes beyond what is typical) are an indicator of poor reliability and should be taken into consideration.29


Optical coherence tomography is a non-invasive diagnostic imaging technique providing high resolution cross-sectional and topographic images of retinal and optic nerve tissues. The Stratus OCT (Carl Zeiss Meditec, Dublin, CA) is the third generation time-domain device, which has been in clinical use since 2002. Newer designs such as Spectral Domain OCT (Cirrus, Optovue, Spectralis, etc.) have taken over the market.

The OCT is able to distinguish precisely the interface between the vitreous cavity and retinal nerve fibre surface anteriorly and the retinal nerve fibres and the retinal ganglion cells posteriorly. Measurements are taken and results are analyzed to calculate average RNFL thickness. The devices then perform an RNFL analysis, making bilateral comparisons, serial comparisons, and comparisons to a proprietary normative database.

Clinical Pearl:

Though OCT technology can discern various tissues, it can and does make errors occasionally. This is one of the reasons that glaucoma cannot be diagnosed solely upon imaging. Also, conditions other than glaucoma can damage the RNFL.


Key elements in OCT printouts include RNFL Peripapillary Thickness profile, Neuro-retinal Rim Thickness profile, and RNFL Quadrant and Clock Hour average thickness, all compared to a normative database. Additionally, several devices also measure the ganglion cell complex (GCC). The RNFL distribution in the macula depends on individual anatomy, while the GCC appear regular and elliptical for most normal patients. Thus, deviations from normal are more easily appreciated in the thickness map by the practitioner, and arcuate defects seen in the deviation map may be less likely to be due to anatomical variations. There is evidence that changes in the GCC may precede changes in the RNFL.

Clinical Pearl:

Retinal abnormalities (such as macular degeneration) involving the macula can affect and artificially depress the GGC analysis while other conditions such as vitreomacular traction and epiretinal membranes can artificially elevate the RNFL scan and make things seem better than they really are. Clinical correlation is essential when using OCT technology.


Interpreting OCT Results

When interpreting OCT scans, it is desirable to have an adequate signal strength or quality index that meets the manufacturer’s recommendations. For the Cirrus OCT, it should be seven or above. For the Optovue OCT, 30 or above is recommended and the Heidelberg Spectralis should be 15 or above. It is also important to have good illumination, focus clarity, image centration, avoid any signs of eye movement, segmentation accuracy, and appropriate B Scan centration.

There can be issues in imaging leading to misinterpretation of results. Media opacity or irregular corneal surface can cause suboptimal OCT image quality that also affects the RNFL or macular thickness measurements. Coexisting posterior segment pathologies including epiretinal membrane and retinoschisis may cause overestimation of RNFL or macular thickness, leading to false-negative results. Additionally, optometrists should also consider age-related decline of RNFL and macular thickness when assessing glaucoma progression.

The normative database itself can be a source of misinterpretation. SD-OCT measurements are compared against an age-matched normative database. Due to this relatively small normative database and wide variation of distribution of RNFL, many results obtained by SD-OCT may be flagged as abnormal statistically in patients who are not represented in the database and thus not necessarily representing real disease, but are actually normal. Optometrists should use caution to avoid over treating “red disease” in these situations.

Additionally, it is critical to carefully assess the clinical findings as well as the OCT Indeed, when OCT assesses patient results and compares to a normative database, there are patients who may have clinical disease but, as a result of averaging significant amount of anatomical detail into the Quadrant or Clock-Hour, results may fall within the normative database of the device. These patients are said to have “Green Disease”; that is, everything about the scan of the patient falls within the normative range and thus everything is printed in green, while true disease is being missed.

An SD-OCT RNFL scan consists of multiple single A-scans side by side to represent a B-scan cube. With eye movement or blinking, these scans do not align correctly, which can lead to an erroneous RNFL thickness measurement, which may be misinterpreted as progressive thinning. The new SD-OCT versions have a built-in eye tracking function which can help compensate for eye movement by relying on blood vessel registration or iris tracking.

It is important to look at the segmentation lines produced by any SD-OCT machine’s software algorithm to ensure that they are appropriately placed. Lines should not come together (go to zero). Occasionally, one will find that the segmentation lines are misplaced along the retina leading to errors in the calculation of RNFL thickness. These segmentation errors are more common in the presence of poor signal strength, tilted discs, staphyloma, large peripapillary atrophy, epiretinal membrane, and posterior vitreous detachment.30 Axial (myopia) length has been shown to influence SD-OCT measurements of both RNFL thickness and ONH parameters due to axial-length induced ocular magnification. The longer the eye, the thinner the RNFL.

Clinical Pearl:

Interpretation of any diagnostic imaging device is a three part process. 1. Understand that the printout identifies how the patient’s measured data differs from the normative database and to what statistical degree, 2. Use personal clinical experience to determine if the results are consistent with normal or abnormal anatomy and, 3. Incorporate everything into the entire clinical picture.

Clinical Pearl:

 In early and moderate glaucoma, progressive thinning of RNFL thickness measured by SD-OCT is a very useful tool to judge progression of disease. At advanced stages however, SD-OCT is less clinically useful due to a “floor effect” of RNFL thickness. RNFL thickness rarely falls below 50μm and almost never below 40μm due to the assumed presence of residual glial or non-neural tissue including blood vessels. At this level of disease, serial 10–2 visual fields are more useful to judge progression.


Often neglected in the glaucoma evaluation is gonioscopy. Gonioscopy must be done on every glaucoma patient and suspect (at least at some point in the evaluation). You cannot accurately diagnose any glaucoma until you know the anatomic status of the angle. Von Herrick estimation is not enough and is misleading. While gonioscopy is often deferred until the last part of the initial evaluation, it should be done urgently if a patient is symptomatic or with high initial IOP (> 40mmHg).

Gonioscopy should also be periodically repeated. Do not assume that the configuration of the angle remains the same. As the patient ages, cataracts develop, the lens thickens, the apposition between the anterior lens capsule and posterior iris the pupil becomes firmer (pupil block), aqueous egress from the posterior to the anterior chamber becomes hindered, and the angle shallows (or closes). There are patients that slowly convert from open angle glaucoma to chronic (or even acute) angle closure. The intervals to repeat are debatable, but 2–3 years is reasonable. Any patient that has had any form of angle closure or been prophylactially treated to prevent angle closure should have gonioscopy done annually.

Be aware of possible artifacts when performing gonioscopy. The use of flanged gonioscopic lenses artifactually opens angles by creating a suction cup effect, stretching the scleral-corneal ring and displacing the iris and ciliary body backwards. Indentation with a non-flange 4–mirror lens can open closed angles. This is called depression gonioscopy or dynamic gonioscopy. Pressure from the gonioscopy lens forces aqueous into angle and potentially opens the angle. If no peripheral anterior synechiae (PAS) exists, the anterior chamber angle will change configuration (appearing more open). This can give a false impression of the angle being more open than it truly is. In reality, depression/indentation can warp the cornea and negatively impact your ability to visualize the angle in some cases. This happens more commonly if IOP is low to mid–teens. If IOP is around 20mm, then corneal warping isn’t as much of a problem.

Gonioscopic findings, going from posterior to anterior, in a normal open angle would be the iris, ciliary body, scleral spur, pigmented and non-pigmented trabecular meshwork, and finally Schwalbe’s line. Abnormalities indicative of a secondary glaucoma to examine for include recession, PAS, iris processes, heavy trabecular meshwork pigmentation, neovascularization, and exfoliative material. A tremendous resource containing numerous gonioscopy videos can be found at http://www.gonioscopy.org

Clinical Pearl:

Combined assessment of IOP, anterior chamber angle anatomy, optic nerve, nerve fibre layer, and visual field function is essential for the diagnosis and management of ocular hypertensive and glaucoma patients.



Joseph Sowka, OD, FAAO, Diplomate
Dr. Sowka is a Professor of Optometry at Nova Southeastern University College of Optometry where he serves as Chief of The Advanced Care Service and Director of the Glaucoma Service at the College’s Eye Institute. He is also Chair of the Department of Optometric Sciences. He is the longest tenured faculty member at the College.
Dr. Sowka is a founding member of both the Optometric Glaucoma Society and Optometric Retina Society. He is also the Chair of the Neuro-Ophthalmic Disorders in Optometry Special Interest Group for the American Academy of Optometry. Dr. Sowka is a Glaucoma Diplomate of the American Academy of Optometry. He is the lead author of the annual Handbook of Ocular Disease Management published by Review of Optometry. He is a partner and co-owner of Optometric Education Consultants.   


1. Luntz MH, Sevel D, Lloyd JP. The Oxford glaucoma survey: Statistical analysis of the results. Br J Ophthalmol. 1965 Mar;49:128-36.
2. The provocative tests in the diagnosis of the glaucomas. Sugar HS. Am J Ophthalmol. 1948 Oct;31(10):1193-1202.
3. Tamm ER, Braunger BM, Fuchshofer R. Intraocular Pressure and the Mechanisms Involved in Resistance of the Aqueous Humor Flow in the Trabecular Meshwork Outflow Pathways. Prog Mol Biol Transl Sci. 2015;134:301-14.
4. Song MM, Lei Y, Wu JH, Sun XH. The progress of studies on aqueous humor dynamics abnormality induced by trabecular meshwork and Schlemm canal endothelial cell senescence and its relation with glaucoma. Zhonghua Yan Ke Za Zhi. 2017 Nov 11;53(11):868-73.
5. Downs JC, Girkin CA. Lamina cribrosa in glaucoma. Curr Opin Ophthalmol. 2017 Mar;28(2):113-19.
6. Tham YC, Li X, Wong TY, et al. Global prevalence of glaucoma and projections of glaucoma burden through 2040: a systematic review and meta-analysis. Ophthalmology. 2014 Nov;121(11):2081-90.
7. Topouzis F, Wilson MR, Harris A, et al. Prevalence of open-angle glaucoma in Greece: the Thessaloniki Eye Study. Am J Ophthalmol. 2007 Oct;144(4):511-9.
8. Kass MA, Heurer DK, Higginbotham EJ, et al. The Ocular Hypertension Treatment Study. A randomized trial determines that topical ocular hypotensive medication delays or prevents the onset of primary open angle glaucoma. Arch Ophthalmol 2002;120:701-13.
9. Grippo TM, Liu JH, Zebardast N, et al. Twenty-four-hour pattern of intraocular pressure in untreated patients with ocular hypertension. Invest Ophthalmol Vis Sci. 2013 Jan 17;54(1):512-7.
10. Mansouri K, Weinreb RN, Liu JH. Effects of aging on 24-hour intraocular pressure measurements in sitting and supine body positions. Invest Ophthalmol Vis Sci. 2012 Jan 10;53(1):112-6.
11. Liu JH, Realini T, Weinreb RN. Asymmetry of 24-hour intraocular pressure reduction by topical ocular hypotensive medications in fellow eyes. Ophthalmology. 2011 Oct;118(10):1995-2000.
12. Kim E, Varma R. Glaucoma in Latinos/Hispanics. Curr Opin Ophthalmol. 2010 Mar;21(2):100-5.
13. O’Brien JM, Salowe RJ, Fertig R, et al. Family History in the Primary Open-Angle African American Glaucoma Genetics Study Cohort. Am J Ophthalmol. 2018 Mar 17. pii: S0002-9394(18)30112-0. doi: 10.1016/j.ajo.2018.03.014. [Epub ahead of print].
14. Gordon MO, Beiser JA, Brandt JD, et al. The Ocular Hypertension Treatment Study: baseline factors that predict the onset of primary open angle glaucoma. Arch Ophthalmol 2002; 120:714-20.
15. Song BJ, Aiello LP, Pasquale LR. Presence and Risk Factors for Glaucoma in Patients with Diabetes. Curr Diab Rep. 2016 Dec;16(12):124.
16. Tham YC, Lim SH, Gupta P, et al. Inter-relationship between ocular perfusion pressure, blood pressure, intraocular pressureprofiles and primary open-angle glaucoma: the Singapore Epidemiology of Eye Diseases study. Br J Ophthalmol. 2018 Jan 13. pii: bjophthalmol-2017-311359. doi: 10.1136/bjophthalmol-2017-311359. [Epub ahead of print].
17. Friedlander AH, Graves LL, Chang TI, et al. Prevalence of primary open-angle glaucoma among patients with obstructive sleep apnea. Oral Surg Oral Med Oral Pathol Oral Radiol. 2018 Jan 31. pii: S2212-4403(18)30057-9. doi: 10.1016/j.oooo.2018.01.021. [Epub ahead of print].
18. Swaminathan SS, Bhakta AS, Shi W, et al. Is Obstructive Sleep Apnea Associated With Progressive Glaucomatous Optic Neuropathy? J Glaucoma. 2018 Jan;27(1):1-6.
19. Fingeret M, Medeiros FA, Susanna R Jr, Weinreb RN. Five rules to evaluate the optic disc and retinal nerve fiber layer for glaucoma. Optometry. 2005 Nov;76(11):661-8.
20. Greenfield DS, Siatkowski RM, Glaser JS, et al. The cupped disc. Who needs neuroimaging? Ophthalmology. 1998 Oct;105(10):1866-74.
21. Spaeth GL. A new classification of glaucoma including focal glaucoma. Surv Ophthalmol. 1994 May;38 Suppl:S9-17.
22. Kitaoka Y, Tanito M, Yokoyama Y, et al. Estimation of the Disc Damage Likelihood Scale in primary open-angle glaucoma: the GlaucomaStereo Analysis Study. Graefes Arch Clin Exp Ophthalmol. 2016 Mar;254(3):523-8.
23. De Moraes CG, Murphy JT, Kaplan CM, et al. β-Zone Parapapillary Atrophy and Rates of Glaucomatous Visual Field Progression: African Descent and Glaucoma Evaluation Study. JAMA Ophthalmol. 2017 Jun 1;135(6):617-23.
24. Ozturker ZK, Munro K, Gupta N. Optic disc hemorrhages in glaucoma and common clinical features. Can J Ophthalmol. 2017 Dec;52(6):583-91.
25. Budenz DL, Anderson DR, Feuer WJ, et al. Detection and prognostic significance of optic disc hemorrhages during the Ocular Hypertension Treatment Study. Ophthalmology. 2006 Dec;113(12):2137-43.
26. Drance S, Anderson DR, Schulzer M, Collaborative Normal Tension Glaucoma Study Group. Risk factors for the progression of visual field abnormalities in normal tension glaucoma. Am J Ophthalmol 2001; 131: 699-708.
27. Anderson DR, Drance SM, et al. Factors that predict the benefit of lowering intraocular pressure in normal tension glaucoma. Am J Ophthalmol 2003; 136:820-9.
28. Shin JW, Sung KR, Park SW. Patterns of Progressive Ganglion Cell-Inner Plexiform Layer Thinning in Glaucoma Detected by OCT. Ophthalmology. 2018 Apr 25. pii: S0161-6420(18)30044-7. doi: 10.1016/j.ophtha.2018.03.052. [Epub ahead of print].
29. Yohannan J, Wang J, Brown J, et al. Evidence-based Criteria for Assessment of Visual Field Reliability. Ophthalmology 2017; 124(11): 1612-20.
30. Miki A, Kumoi M, Usui S, et al. Prevalence and Associated Factors of Segmentation Errors in the Peripapillary Retinal Nerve Fiber Layer and Macular Ganglion Cell Complex in Spectral-domain Optical Coherence Tomography Images. J Glaucoma. 2017 Nov;26(11):995-1000.

' While technically glaucoma is a disease characterised by progressive disc damage and progressive field loss, diagnostic dilemmas and contradictions exist '