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Glaucoma

What is Glaucoma?

Structure and Function of the Eye [ top ]

The eye has special requirements to achieve its role as our organ of sight -

  1. Consisting of soft but tough tissues, in order to hold their shape so as to focus incoming light, the outer coats of the eye need to be inflated like a balloon.
  2. Living structures within the eye have to be nourished by a fluid that, unlike red blood, will allow light to pass through.

Both these needs are met with the internal circulation of a clear fluid called the aqueous. Produced in a doughnut shaped structure called the ciliary body, aqueous percolates around and between the focusing structures of the eye, nourishing them, and then filters out through a meshwork back to the bloodstream. Resistance to outflow at this meshwork produces a pressure higher than the atmosphere, holding the eyeball in shape. The meshwork is a ring-shaped structure tucked into the side of the front of the eye between the cornea (front window of the eye) and the iris (membrane that gives the eye its colour and controls the amount of light entering the eye by varying the size of the black pupil). The space in which the meshwork is located is called the "angle" of the eye.

At the rear of the eye, all the nerve fibres from the retina converge onto the sole opening in the wall of the eyeball where they exit the eye to form the optic nerve. This is how they carry the messages of sight back to the brain for processing. As they exit, these nerve fibres turn through 90 degrees, and as they do so, they are vulnerable to damage.

Different Types of Glaucoma [ top ]

  1. Primary Open-angle Glaucoma (POAG)
    Worldwide, this is the commonest type. Eyes with POAG have open access of aqueous to the meshwork in the front of the eye and an erosion of the retinal nerves as they exit the eye at its rear. Often, but not always, the eye pressure is higher than normal. Whatever the level of pressure, reducing it slows or halts the progress of the condition.
  2. Angle-closure and Angle-closure Glaucoma (AC and ACG)
    Some people inherit eyes that are shorter than usual. This results in crowding of the structures in the front of the eye. As a person ages, the focusing lens grows like a tree trunk, occupying ever more volume - the crowding gets worse. Eventually there can be a risk that the iris makes contact with the meshwork, blocking aqueous outflow. Eye pressure rises and can damage the nerves at the rear of the eye, thus damaging the vision.
  3. Childhood Glaucoma
    See separate section.
Normal vision

Normal vision

Vision damaged by glaucoma

Vision damaged by glaucoma

Cataracts and Glaucoma

For information about Glaucoma, please see the relevant Section.

What is a cataract? [ top ]

In the eye there is a lens which focuses light onto the retina, the nerve membrane at the back of the eye. It is the retina which is responsible for translating the light image that falls onto it, into nerve impulses. These nerve impulses travel along the optic nerve to the brain, where they are interpreted and we see. When the focusing lens becomes cloudy, it is called a cataract.

Cataracts usually form with age, but they can be brought on at an earlier age by many factors - eg diabetes, injuries, steroids (cortisone), eye diseases and inflammations, eye surgery and some medications. Cataracts cause the vision to become blurry - as if the person is looking through a dirty window - and perhaps sensitive to glare. The sufferer notices the problem quite quickly. Treatment is surgical removal, usually with a replacement plastic lens implanted. If all goes well with the surgery and through the healing process, the visual result is usually excellent. The problem is thus curable.

Normal vision

Normal vision

Vision damaged by cataracts

Vision damaged by cataracts

Why do cataracts and glaucoma occur together? What happens when they do? [ top ]

Because both cataracts and glaucoma are more common as people age, they not uncommonly are found together. Sometimes treatment for either of these conditions can contribute to the development of the other. Our population is ageing - the over 85 year olds are the fastest growing segment of our community. Both cataract and glaucoma are becoming more common, therefore.

Glaucoma does not provoke symptoms until the damage it has caused is very extensive. Such damage is irreversible - treatment can stop or slow more damage, but cannot regain what's been lost. Treatment needs to start as early as possible, and needs to be effective. Eye drops are usually the first line of treatment. Most of them have no effect on the vision itself, but some, such as pilocarpine, may constrict the pupil. This may exaggerate the effects of any cataract on the person's vision. Surgery for glaucoma can also hasten the development of cataracts, or make an existing cataract "thicken" faster.

So, the presence of a cataract may influence the treating ophthalmologist to modify the glaucoma treatment program.

If both conditions are present, and surgery is needed, what is the approach? [ top ]

If a patient has both glaucoma and a cataract in an eye, surgery for either condition also needs to be assessed differently from when only one problem is present.

If a patient with glaucoma which is controlled with drops and/or laser, needs to have a cataract extraction operation to restore sight blurred by that cataract, the ophthalmologists may recommend that only the cataract operation is performed, with the glaucoma treatment continued afterwards just the same as before. Sometimes this treatment can be made a little simpler because eye pressure may be easier to control after the cataract has been removed. While this is most pleasant when it occurs, it cannot be counted upon, as any such improvement is quite unpredictable.

An alternative is to combine a glaucoma drainage operation (eg trabeculectomy) with the cataract operation so that, once the healing process is complete, the glaucoma may be able to be controlled without ongoing medications at all, or perhaps with a greatly reduced anti-glaucoma program. Such a combined operation is somewhat longer and more complicated than a cataract operation on its own, and the post-operative care is more demanding. The patient and the ophthalmologist may feel that this short-term disadvantage is more than compensated for by the long-term benefits.

If such a person requires a trabeculectomy operation at a later date, the modern cataract extraction techniques should not diminish the chances of that operation succeeding. The older style cataract operations did interfere with the likely success of later glaucoma surgery, because they caused more scarring around the eye. Such scarring could interfere with drainage success.

A patient with glaucoma may be found to have insufficient protection from the available treatment, with progressive visual damage documented. The decision is made that drainage surgery is needed. Such a patient may have a cataract which has not yet caused enough visual disturbance to justify removal in its own right. However, it is common experience, that after glaucoma drainage surgery, an existing cataract is likely to thicken - up to 12% of patients who undergo trabeculectomy will need a cataract extraction within 12 months of their glaucoma operation. The patient and the ophthalmologist may decide therefore that it would be simpler and wiser to combine the removal of the cataract and insertion of an intra-ocular lens with the planned drainage operation - aiming "to kill two birds with one stone".

The other option for such a patient is to have the glaucoma operation first, and then to undergo a cataract operation as a separate procedure. With modern techniques this later cataract operation is far less likely to compromise the glaucoma operation than were the older style cataract operations. There is still a risk, however, that the later cataract operation will stimulate enough inflammation in the eye to lead to blockage of the glaucoma drain.

In summary [ top ]

Each patient's situation is different. If you are in the situation of having both cataract and glaucoma, you are encouraged to discuss these options with your ophthalmologist and together you can determine which course of action is likely to be best for you in the longer term.

Childhood Glaucoma

"Childhood Glaucoma" describes the different types of glaucoma sometimes referred to separately as Congenital or Juvenile or Developmental Glaucoma. There is usually an abnormal development of the eye's aqueous outflow system. Although most of the patients with this condition come under treatment in infancy or early childhood, some may not have their glaucoma diagnosed until adulthood.

Even though childhood glaucoma is uncommon, when it occurs the effect on vision can be devastating. Early diagnosis and appropriate treatment can make a significant difference to the child's sight. Any vision during a child's development is worth fighting for, even if it may be lost in the end in severe cases.

There are three major types of childhood glaucoma:

  1. The aqueous drainage pathways are developed imperfectly as an isolated abnormality;
  2. There are abnormalities of the eye and/or body together with the imperfect development of the drainage pathways;
  3. Other eye diseases such as inflammation, growths or injury can lead to glaucoma.

How does childhood glaucoma present itself? High eye pressure in babies stretches the soft eyeball wall so that the eye is usually large. The child often dislikes light and if older may hide its head to escape brightness. Watering of the eye is also often noticed. Sometimes the condition is only noticed when the deepest layer of the stretched cornea splits allowing the aqueous fluid to enter the cornea, turning it white. If the glaucoma is particularly severe, the child may be born with cloudy corneas for this reason, indicating that the eye pressure has already been significantly raised in the womb.

Assessment of the affected child needs to identify whether glaucoma is present or not, and if it is, to decide which type of glaucoma is involved. This assessment can be difficult in babies or little children who usually do not co operate with the ophthalmologist! Often, therefore, examination under anaesthesia is required. In such an examination, the size and shape of the eye is measured, the eye pressure is recorded, and the structures of the tissues in the front and back of the eye are assessed.

Once a firm diagnosis has been made, and these baseline measurements recorded, treatment can be planned. Inflammation, injuries and growths are treated specifically; if they are the cause of the glaucoma, these measures should lower the eye pressure.

If there is an abnormal development of the drainage pathways then this may be managed firstly by drops and/or liquids by mouth to reduce eye pressure, and then by operation. If the cornea, the window of the eye, is normal in structure, and clear, the usual operation performed is called a goniotomy. This consists of passing a special knife needle across the inside of the front of the eye (the anterior chamber) and gently cutting the abnormal tissue that is blocking the flow of aqueous fluid from the anterior chamber of the eye through the drainage tissues (the trabecular meshwork).

The drain is a ring that extends for 360 degrees right round the inside of the front of the eye. In a single goniotomy operation about 120 degrees of the abnormal tissue can be cut. If one operation does not lower the eye pressure sufficiently, a second and even a third goniotomy may be needed for each eye.

If the cornea is cloudy and the surgeon cannot see across the anterior chamber to cut the abnormal tissue, then a trabeculotomy is needed. In this operation the tiny canal into which the aqueous should be flowing is identified, an instrument is inserted into it, and delicately swept into the anterior chamber. This opens the drain into the anterior chamber, and allows the aqueous fluid an easier exit. Trabeculotomy too may need to be performed more than once to lower eye pressure effectively.

Occasionally these operations cannot be performed for technical reasons, or they do not succeed in reducing the eye pressure. Then either a trabeculectomy drainage operation, or the placement of an artificial plastic tube and plate on the outside of the eye is needed. This depends on the condition of each eye.

The success of any of these operations has to be determined for the life of the child. Initially this means regular checks in the ophthalmologist's surgery or the hospital outpatients together with examinations under anaesthesia until the child can cooperate fully. On each occasion the structures of the tissues of the eye and the pressure are measured. The cornea should be clear (unless there is an underlying abnormality of this tissue too) and not increasing in size, the eye pressure should be in the normal range of 10 20 mm Hg, and the shape of the nerve fibres in the optic disc at the back of the eye should be stable.

The need of the eye for glasses is also assessed. If one eye is affected more severely than the other the child may need to wear an eye patch. The end result sought is not just a normal eye pressure (although this is the first important goal without which nothing much else can be achieved) but if possible a seeing eye in a happy child.

Treatment of childhood glaucoma is therefore complicated, and is needed for the life of the patient. There are no short cuts. The range of severity of these diseases is wide. Some affected children will achieve and maintain normal vision; some will lose their sight no matter what is tried for them; and some will achieve partial but effective sight.

Because childhood glaucoma is relatively uncommon, and covers such a wide variety of very different diseases, there has been no clear cut pattern of inheritance identified. In the kind of childhood glaucoma without other eye or general problems, the chances of two unrelated parents with an affected child having another affected baby is between 3% and 15%. (If the parents are related to one another, this risk may be much higher.) In some of the glaucomas associated with other diseases, this risk may be as high as 50%. If a child is diagnosed as having glaucoma, then his/her brothers and sisters need to be examined too.

Combined Mechanism Glaucomas

This term refers to an eye with elevated pressure in which both open angle and angle closure glaucoma mechanisms are present.

Usually the structure of the eye is similar to that found in eyes with angle closure glaucoma i.e. the globe is somewhat smaller than ideal, with the result that the internal ocular components are crowded together. This means that the coloured part of the eye, the iris, is very close to the trabecular drainage tissues, making it difficult for the aqueous fluid to gain access to the drain, and raising the possibility that the iris tissues can completely block the drain.

A peripheral iridectomy procedure, usually performed with a laser, permits the iris to fall back, away from the drain, allowing the aqueous freer access to the drain, and thereby permitting the pressure to fall to normal levels.

However, if iris tissue because of its previous proximity has blocked the drain intermittently or repeatedly, the drain may become functionally impaired and thus will abnormally resist the drainage of aqueous even when opened by laser peripheral iridectomy.

Occasionally the affected eye also has an open angle glaucoma mechanism causing raised pressure, so that once the angle closure component has been eliminated, the drain still does not operate efficiently, and the pressure remains too high for the safety of the optic nerve fibres. Long term drops, laser treatment to the drain itself, or even drainage surgery may become necessary to preserve sight, just as in the open angle glaucomas.

These situations are known as "combined mechanism glaucomas". Often the diagnosis can only be made once the angle closure element has been removed, and the pressure subsequently monitored. It means that when angle closure has been treated successfully, long term care and observation remain vital to ensure that, should open angle glaucoma occur, it is promptly detected, thus minimising the risk of unnecessary blindness.

Normal Pressure Glaucoma

The level of pressure inside the eye is usually the major risk factor for the development of damage to the optic nerve fibres the damage that leads to the loss of vision from glaucoma. In the normal population the level of this intra ocular pressure is within the range of 10 to 20 mm Hg above atmospheric pressure. In the majority of eyes with glaucoma the pressure is higher; it is this raised pressure, which leads to nerve destruction.

There are eyes, however, which suffer nerve damage even though the eye pressure lies within this normal range. Such eyes are said to suffer from a special type of open angle glaucoma known as "normal tension glaucoma". In the past terms like "low tension" or "normal pressure" or "pseudo glaucoma" were used to describe the same condition.

Because the pressure in this group of eyes is within the so called "normal" range, the presence of glaucoma cannot be detected by a simple eye pressure test. Considerable damage may occur before the diagnosis is made. Sufferers from normal tension glaucoma show no differences from other glaucoma patients with respect to factors such as family history of glaucoma, short sightedness and diabetes.

Patients with normal tension glaucoma form a most important group. Their evaluation needs to be especially thorough both to confirm the diagnosis and to exclude other possible conditions that may mimic glaucomatous damage to the optic nerves. They are of research interest because they demonstrate that factors other than an abnormally raised eye pressure can cause glaucomatous nerve damage. There is much work underway around the world to identify these factors so they can be treated. They also require an extra degree of caution in monitoring the disease because eye pressure levels which would be regarded as likely to be safe in other glaucoma patients may not be safe for them they pose a greater challenge for the treating ophthalmologist.

The principles of treatment for normal tension glaucoma are the same as for other types of glaucoma medications alone or in combination, laser techniques and/or surgery are used to reduce the eye pressure as much as possible in an attempt to halt the progress of the disease. Even in this condition, reducing eye pressure has been shown to be effective in halting or slowing the rate of disc and therefore visual damage. As with all glaucomas, early detection and prompt, effective treatment is vital to reduce visual damage.

Glaucoma and Uveitis (Iritis)

The tissue called the iris determines the colour of our eyes. It forms the aperture (the pupil) through which light passes to reach the retina, allowing us to see. The uvea or uveal tract consists of the iris together with the ciliary body (where the clear aqueous fluid is pumped into the eye) and the choroid (which lies behind the retina and supplies it with most of its nutrients). It is a continuous layer in the eyeball, which is rich in blood vessels.

Any part of this layer can become involved in a process of inflammation. Sometimes this can be caused by an infection with bacteria, viruses, fungi or parasites, but most commonly the cause is unknown. The location of this inflammation determines its label iritis, anterior or posterior uveitis, cyclitis (the ciliary body), iridocyclitis, and choroiditis.

Whatever the cause, and particularly if the resulting inflammation is located in the front parts of the eye, the effects on the eye pressure can be similar. The inflammatory process breaks down the normal barriers between the blood and eye tissues, so that white blood cells and various large molecules can spill into the aqueous fluid circulating within the eye. This increases the viscosity (thickness) of the aqueous fluid, slowing its drainage through the trabecular meshwork, and raising the eye pressure. Because the glaucoma that results is associated with an underlying eye disease process, it is termed a "secondary glaucoma".

The inflamed eye is often, but not always, red and uncomfortable (even painful), with blurred vision and sensitivity to light (photophobia). The sticky aqueous and inflamed iris tissues can lead to abnormal adhesions (synechiae) between the iris and the lens and/or the trabecular meshwork of the drain. Such adhesions may interfere with the normal flow of aqueous from one compartment of the eye to another, leading to raised pressures from various mechanisms.

If a cause can be identified, it can be treated directly. Usually this is not the case. In any event, the principles of treatment of the resulting eye problems are the same: suppress the inflammation, minimise the risks of scar and adhesion formation, and reduce the eye pressure as necessary.

Suppressing the inflammation is attempted with steroid medications such as prednisone, dexamethasone, fluorometholone, and non steroidal anti inflammatories such as indomethacin, flurbiprofen and diclofenac. For minimising the risks of scar formation, and also to reduce pain, atropine, homatropine or cyclopentolate are used. For reducing the eye pressure, any one or more of betaxolol, timolol, laevo bunolol, dipivefrin, apraclonidine, dorzolamide, brinzolamide and/or acetazolamide may be prescribed. Most of these are eye drops; the last is in tablet form.

Occasionally injections around the eye of steroids, or steroid tablets orally, may be used. If pressure control is difficult to achieve, an operation such as a trabeculectomy (usually with the help of anti scarring medications like 5 fluoro uracil or mitomycin C) or the insertion of a drainage tube device such as the Molteno implant, may be necessary. Often the inflammatory process can be controlled, and the secondary glaucoma is not a threat to sight. Sometimes the problem is a recurring one most classically the Posner Schlossmann Syndrome (Glaucomatocyclitic crisis). Sometimes it is devastating in the damage it can cause both directly and indirectly through the glaucoma process.

Treatment has therefore to be varied to meet the particular attack in the individual eye.


How is glaucoma diagnosed?

Glaucoma is defined as a progressive optic neuropathy characterised by changes in the appearance of the optic nerve (cupping and loss of nerve fibre layer) and loss of visual field (blind spots or scotomas). A substantial amount of vision can be lost before the patient becomes aware of any defect. This is why population studies reveal that up to 50% of glaucoma in the community is undiagnosed.

Glaucoma has classically been diagnosed by testing for raised intraocular pressure (IOP), measured by tonometry. However we now know that at least a third of glaucoma patients never have a high pressure, yet they develop the typical disease features. The latter has been termed Normal Tension Glaucoma (NTG), and therefore screening for the disease cannot rely on raised IOP alone.

Clinically, the first changes usually occur at the optic nerve head (optic disc) and it remains vital that the clinician looks for the characteristic sign of optic disc cupping. Increasing size of the optic cup is characteristic of glaucoma. Unfortunately evaluation of the cup is subjective and suffers from a large amount of inter and intra observer variability. Even more importantly, the size of the cup to disc ratio is directly related to the size of the optic disc, and there is a wide variety of optic disc sizes and shapes in the community.

Standard methods [ top ]

  1. Optic disc photographs are used to document the nerve, and provide a baseline for future comparison. At subsequent visits the appearance of the nerve can be compared to look for subtle changes that might suggest progression of the disease. Stereo photos can provide 3D assessment of the disc structure.
  2. Visual field testing - Perimetry. Most patients complain that they do not like doing field tests, but they are important for monitoring the disease. The shape of glaucoma blind spots tends to be curved or "arcuate" which corresponds to the distribution of the nerve fibres that are damaged. The defects usually start in the mid periphery. Ultimately when superior and inferior arcuate defects join up the patient is left with tunnel vision. When we test distance vision using a visual acuity chart with letters in rows we are only testing central vision, a patient can have perfect central vision till very late in glaucoma.
    Our conventional approach of looking for visual field defects is with subjective white-on-white automated perimetry where the patient is asked to detect small light targets projected into their peripheral field of view. The Humphrey field machine is the standard and Eye Associates has 3 of these available. It is limited by the fact that a large proportion of the nerve fibres can be lost before an initial defect is seen. While some subjects are very good at field tests, we recognise that they are difficult and performance can be variable. This has to be taken into consideration when interpreting the result.
  3. Intraocular pressure is measured with a Goldman tonometer - a pressure sensor that is gently placed against the cornea (front of the eye) after an anaesthetic drop has been instilled. It can also be measured with a small handheld Tonopen, which our technicians frequently use when they are testing.

What are the new methods available? [ top ]

The newer methods are specifically designed to detect change at earlier stages of the disease or to be less subjective. Field tests have been developed which target smaller subpopulations of ganglion cells (the retinal cells that are damaged in glaucoma), such as Frequency Doubled Technology (FDT), and Short Wavelength Automated Perimetry (SWAP or blue/yellow). Objective perimetry records signals from the visual part of the brain and removes the need for patients' subjective responses. Optic disc and nerve fibre imaging techniques using scanning laser ophthalmoscopes (eg Heidelberg or GDx) can provide objective measures of structural change in the optic nerve and retina.

It has recently been determined that the thickness of an individual's cornea can influence the pressure reading and lead to under or over-estimates. For this reason we now perform Ultrasound Corneal Pachymetry on all our patients as a baseline, to determine corneal thickness. This test is simple, painless and takes a few seconds. Please let us know if you haven't had it done - it is very important for determining an accurate pressure. We are also currently assessing a new pressure measuring system called Dynamic Contour Tonometry.

All of the following tests are available at Eye Associates:

New visual field techniques [ top ]

Frequency Doubling Technology (FDT)

Frequency Doubling Technology works by flickering a coarse pattern of vertical dark and bright bars at a very high frequency. This produces the appearance of twice as many bars than are physically present. The advantages of the FDT are that it is a compact, transportable perimeter with tolerance to refractive errors and rapid test times (less than 4 minutes per eye). In some cases it shows defects before they are seen on standard tests. It is very useful for visual field screening in the community. It is not as useful for long term monitoring.

The development of the new FDT Matrix with smaller targets spaced over narrower intervals improves the ability of the FDT to determine the spatial extent of visual field defects, making it more suitable for staging and monitoring the progression of disease. It gives an assessment similar to the Humphrey standard field.

Short Wave Automated Perimetry (SWAP or Blue/yellow Perimetry)

Short Wavelength Automated Perimetry is similar to standard automated perimetry except it utilizes a blue light stimulus projected onto a bright yellow background. As with FDT above, the concept is to isolate a smaller subpopulation of ganglion cells so it is therefore easier to detect defects. Previous investigations have established that SWAP is a more sensitive indicator of early damage than standard automated perimetry. Clinically, it is recommended for those with early disease or who are at high risk. Unfortunately, it is harder to perform than standard fields, takes 12-15 minutes per eye to perform, the results are more susceptible to the effects of cataracts, and many older patients find the discrimination of colour between the stimuli and background a further difficulty, increasing fatigue. Despite this, SWAP has demonstrated the ability to predict the onset and progression of glaucomatous visual field deficits. It is better suited to younger patients. A newer version of the test will soon be on trial at Eye Associates which has a much faster test time (around 5-6 minutes).

Objective Perimetry - AccuMap (mVEP)

Due to the variability of subjective techniques above, an objective measure of the visual field loss has been sought. The AccuMap technique involves recording brain signals in response to a flickering pattern visual stimulus displayed on a computer screen. The patient is required to look at a changing number or figure in the centre of the screen for the duration of the recording, about 7-8 minutes per eye. Four electrode sensors are placed over the back of the head to record responses from the brain.

The advantages of this method are that it removes subject indecision, and patients find it easier to perform. It eliminates the learning curve and anxiety associated with subjective tests. Limitations of the mVEP are that it is not specific for glaucoma, it is more technician dependant, and visual acuity is important (patients need to focus on the centre). The mVEP is ideal for patients who find standard fields difficult to perform. It is also very useful in detecting and monitoring optic neuritis.

New Structural tests - Imaging of the optic disc and nerve fibre layer

The advantage of these new technologies is that they move beyond optic disc photographs as a means of documenting what a nerve looks like for future comparisons. They not only give an image of the nerve's appearance, but actual measurements of its structure which can be compared with future scans to detect changes over time. The retinal nerve fibre layer (RNFL) thickness is measured in the different techniques. In glaucoma, the retinal nerve fibre layer becomes thinner. This correlates with the visual field defects: thinner inferiorly with superior visual field defects and thinner superiorly with inferior field defects. By measuring the RNFL the test can detect abnormal regions in the optic disc and look for disease progression.

When assessing an individual's optic nerve, there is such great variability among the normal population that we cannot always be certain that strangely shaped optic discs or thin nerves are not just normal variants. Therefore, while a scan can tell us whether an individual's nerve is thinner than average, it cannot say for certain whether the patient has definite glaucoma - only highlight it as abnormal. However the scanning techniques are excellent for follow up over time so repeat scans done at a later date can be directly compared to look for change.

Heidelberg Retinal Tomograph (HRT)

The HRT (Heidelberg Engineering, Heidelberg, Germany) is a scanning laser ophthalmoscope. This means that it uses a laser light beam to scan across the back of the eye and take measurements using the light that is reflected back to its sensors, much the same as a laser scanner reads a bar code. The HRT rapidly projects a laser grid across the retina and records with multiple layers of focal depth. From this the HRT is able to generate a 3 dimensional image of the optic disc and surrounding retina, using 16 to 64 consecutive images each with 384 x 384 picture elements. The accuracy of the height measurements is around 20 micrometers. The scan itself takes only 1-2 seconds to capture the information. Usually 3 quick scans are made and an average calculated. It is easy to use and has good patient acceptance.

Scanning Laser Polarimeter- GDx VCC

This technology provides quantitative assessment of the retinal nerve fibre layer (RNFL), using a polarised laser. It measures the change in direction of the alignment of the light (polarisation shift) after it passes through the RNFL which is birefringent. The GDx (Laser Diagnostic Technologies, San Diego, Ca,USA) then calculates the thickness of the RNFL based on the amount of change in polarization. Eye Associates has the newest version of the GDx with a Variable Corneal Compensator to overcome the problems found in the older machine. The test duration is very short and it is easy for technicians to use. It can be performed on undilated pupils. Serial scans can be reviewed to look for progression.

Conclusion [ top ]

When diagnosing glaucoma examination of the optic disc, measurement of intraocular pressure and assessment of visual field loss are necessary. The rapid advances in technological development provides us with important additional diagnostic information, that enables us to detect subtle visual field defects earlier, as well as quantify retinal and optic disc structural changes caused by glaucomatous disease. There is no uniform agreement in the most appropriate new diagnostic technology however, the additional information provided by accurately quantifying glaucomatous changes is fundamental both for early diagnosis and monitoring of our patients.


Medical treatment of Glaucoma

Glaucoma can be treated with medicines, laser or surgery. By far the most common form of treatment is with medicines (topical medication).

All current glaucoma medications act in the front half of the eye to lower the intraocular pressure (IOP). The best way to get them there is to put a drop of the medication on the eye surface. That is why most glaucoma medications are eye drops.

The wall of the eye is very soft, so the pressure in the eye comes from the difference between the production and drainage of a special fluid called aqueous humour. Production and drainage (inflow and outflow) of aqueous changes constantly. So the eye pressure can vary quite a lot during the course of a day. In some people it might vary up to 10mmHg. The 'normal' range for IOP is between 10-21mmHg.

Medicines are grouped in classes, according to their chemical structure or the way they work. Current glaucoma medications either increase outflow (drainage) of aqueous, reduce inflow (production), or both. The effect of a glaucoma medication depends on its class, strength (potency) and half life.

Most glaucoma medications only come in one strength.

The half life is the time it takes for half the medicine (or the effect of the medicine) to be lost after you take it. This depends of the chemistry of the drug, not its strength and therefore will determine the frequency of use (how often you have to use the medication).

A strong drug that lasts only a few hours still needs to be taken several times a day for its effect on IOP to be sustained. A drug with a very long half life will not work any better if it is taken more often.

Below is a list of common glaucoma medications.

Class Drug name Action Half life Brand names
Prostaglandin Analogues Latanoprost Outflow Long Xalatan
  Travoprost Outflow Long Travatan
  Bimatoprost* Outlflow Long Lumigan
Beta blockers Timolol Inflow Moderate (longer in gel form) Timoptol, Tenopt, Nyogel
  Laevobunalol Inflow Moderate Betagan
  Betaxolol Inflow Moderate Betoptic
Alpha-agonists Brimonidine Inflow/ Outflow Moderate Alphagan
Carbonic Anhydrase Inhibitors Acetazolamide (tablet) Inflow Short Diamox
  Dorzolaminde Inflow Shorter Trusopt
  Brinzolamide Inflow Shorter Azopt
Miotics Pilocarpine Outflow Short Pilopt, PV Carpine
  Carbacholine Outflow   Carbachol

* may be chemically different to prostaglandins

Instilling glaucoma medication is not easy. We practice putting things in our mouths every day. Putting eye drops in our eyes also requires practice. Currently glaucoma medications come in dropper bottles. Because drops fall down from the bottle you need to turn the bottle upside down and to have your head horizontal to get a drop into the eye. Pulling the eyelids back makes the target (the front surface of the eye) a little larger. The aim is to get the drop onto the surface of the eye, where it can be absorbed straight into the eye. It is important NOT to blink after instilling the eye drops as blinking pumps the drops out of the eye and into the nose. Just close your eyes gently. If you keep you eyes closed for a few minutes you increase the amount of medication getting into the eye and reduce the amount going down the nose. Using a clean fingertip to compress the inner part of the eyelids onto the nose works even better. This blocks the canalicular duct that drains tears into the nose.

If you stop taking glaucoma medication, the eye pressure goes back up to the level prior to treatment. It is vital that you continue to take your drops as prescribed. Remember your eye doctor can't treat your glaucoma with medications. He or she can only write a prescription. It is you who has the power to lower your eye pressure by taking your medications properly.

General Ophthalmology

Subspecialties

Glaucoma
Cataracts
Cornea
Pterygium
Retinal Vein Occlusion
Macular Degeneration
Diabetic Eye Disease
Uveitis
Ocular Pain

Associated Sites

Glaucoma Australia
AMD Alliance
Vision Australia
Guide Dogs Association (NSW)
Stepping Out with Confidence (Western Australian Blind Assoc)
Seeing Eye Dogs Assoc.
The Fred Hollows Foundation

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