What is ocular hypertension?

Infact, ocular hypertension is not glaucoma. It is a "pre-glaucoma" condition. Not all cases lead to glaucoma. If you have raised eye pressure, but no other sign of glaucoma, then you have ocular hypertension. Glaucoma is defined by visual field loss and consistent optic nerve signs. If the optic nerve shows characteristic signs, or of there is nerve fiber layer loss, then "pre-perimetric glaucoma" is diagnosed in some circumstances.

Raised eye pressure may occur for many years without causing a problem. With time, however, it can lead to damage to the optic nerve. The largest studies in the world (eg OHTS) permit the approximate calculation of risk of glaucoma onset in certain patients. If you are in a high risk category, then treatment is considered. For example, those with an exceptionally thin cornea or a significantly increased "cup to disc ratio" might be deemed appropriate to treat.

More detailed information about Ocular Hypertension

Ocular hypertension refers to any situation in which the eye pressure (or 'intraocular' pressure) is higher than normal, and primarily refers to raised pressure without any optic nerve damage or vision loss.  Some eye conditions can increase the pressure inside the eye. Ocular hypertension is not a disease in itself, merely a term that is used to describe those who should be observed more closely to detect glaucoma or other ocular diseases that could be causing elevated intraocular pressure. Glaucoma is diagnosed when increased intraocular pressure, optic nerve damage, and vision loss are all present together.

High pressure inside the eye is caused by an imbalance in the production and drainage of fluid in the eye (aqueous humor). In ocular hypertension, the channels that normally drain the fluid from inside the eye do not function properly. If more fluid is continually being produced inside the eye, but cannot be drained because of improperly functioning drainage channels, then this results in an increased amount of fluid inside the eye, thus raising the eye pressure.

Eye pressure is measured in millimeters of mercury (mmHg). Normal eye pressure ranges from 10-21 mmHg; ocular hypertension is defined by an eye pressure greater than 21 mmHg.  

RISK FACTORS
Ocular hypertension cannot be prevented, but through regular eye examinations with an ophthalmologist, its progression to glaucoma can be delayed or prevented.  Elevated intraocular pressure is a concern in people with ocular hypertension because it is one of the main risk factors for glaucoma. Studies have shown that those at risk of ocular hypertension are:

• people over the age of 40
• women after the menopause
• people with primary open-angle glaucoma
• black people – because they are prone to thinner corneas (the transparent membrane covering the eye which admits light) 
• pigment dispersion syndrome

RISK FACTORS AND THE PROGRESSION TO GLAUCOMA
Recent studies have shown that there is a risk on average of 10% of people with ocular hypertension developing glaucoma over 5 years. If eye pressure is lowered by medications or laser surgery, this risk may be decreased to 5% (a 50% decrease in risk).

Those affected with ocular hypertension who are at greatest risk of developing glaucoma include people with intraocular pressures of over 24 mmHg, and those with thinner corneas (this is more prevalent in black people).

RISK FACTORS AND THE PROGRESSION TO EYE DEFECTS
A small percentage of people with ocular hypertension will develop retinal vein occlusion (less than 5%), a condition where veins in the retina can become blocked. This can lead to vision loss. Keeping pressures below 25 mmHg in people with ocular hypertension, and who are older than 65 years, is beneficial.

SYMPTOMS   Most people with ocular hypertension do not experience any symptoms. Clearly, therefore, regular eye examinations with an ophthalmologist are very important to rule out any damage to the optic nerve caused by a raise in pressure.

SIGNS   Investigations to determine possible causes of eye pressure and rule out early primary open-angle glaucoma or secondary causes of glaucoma, will be carried out by an ophthalmologist using some or all of the following techniques
• a visual acuity assessment (how well you can see an object) will determine the range of visual acuity by reading letters from across a room using an eye chart a tonometer will measure intraocular pressure; a reading of greater than 21 mmHg measured in one or both eyes will be re-examined on two or more occasions. A visual field test will assess the peripheral (side) vision
• gonioscopy (using a special contact lens) will determine if the drainage channels in the eye are open, narrowed or closed
• fundus photographs (pictures of the back of the eye) will determine possible changes and / or damage to the optic nerve and
• pachymetry (a simple measurement of corneal thickness) will determine the accuracy of intraocular pressure readings because a thinner cornea can give falsely low pressure readings, whereas a thick cornea can give falsely high pressure readings
• a slit lamp (a special microscope) will determine damage or changes to the front of the eye which includes the cornea, anterior chamber, iris, and lens.

MEDICATION TREATMENT   The aim in preventing the onset of glaucoma is by reducing the raise in intraocular pressure, and medical treatment, in the form of eye drops, has proven to be very beneficial.  Sometimes, more than one medicine is required.  Initially, eye drops may be required only in one eye to see how effective the drug is in lowering the pressure and, if effective, the drops may be used in both eyes.

Symptoms such as haloes, blurred vision, pain, or if intraocular pressures have recently increased and then continue to increase on subsequent visits, will most likely require medical treatment. However, it is not always necessary to prescribe these initially, and it may be that observing by routine eye examination is all that is required unless, however, pressures are consistently higher than 28-30 mmHg and there is evidence of optic nerve damage, or if intraocular pressure is steadily increasing. Once medication is prescribed, regular follow-up visits with the ophthalmologist (initially  3-4 weeks after starting medication) for pressure checks will be required to ensure the drug is helping to lower intraocular pressure. If the drug is working and is not causing any side effects, then it is continued for a further 2-4 months. If the drug is not helping to lower the pressure, or is causing an allergic reaction, then that drug will be withdrawn and a new drug will be prescribed.

SURGICAL TREATMENT   Generally, if the pressure inside the eye cannot be lowered with one or two medicines, then surgical or laser therapy may be the next step. Laser trabeculoplasty is a reasonable first option in selected patients with ocular hypertension, if the drainage angle is open and shows no sign of scarring. Otherwise, very occasionally, surgery (Trabeculectomy with 5FU) is the best option.

FOLLOW-UP   Once ocular hypertension has been detected, routine examinations will be necessary. If the intraocular pressure is 28 mmHg or higher, medication will usually be prescribed. After one month of taking the drug a follow-up visit with the ophthalmologist will determine if the drug has been effective in lowering the pressure and that there are no side effects. If the drug is working, then follow-up visits may only be necessary every 3-4 months. If intraocular pressure is 26-27 mmHg, the pressure is rechecked in 2-3 weeks after the initial visit. If, on the second visit, the pressure is still within 3 mmHg of the reading at the initial visit, then follow-up visits will be recommended every 3-4 months. If the pressure is lower on the second visit, then the length of time between follow-up visits is longer. At least once a year, visual field testing will be carried out and the optic nerve examined. If the intraocular pressure is 22-25 mm Hg, the pressure is rechecked in 2-3 months. At the second visit, if the pressure is still within 3 mm Hg of the reading at the initial visit, then a six-month follow-up review may be recommended and may include a visual field test and an optic nerve examination. Testing may then be repeated at least yearly. Follow-up visits may also be necessary if there is concern during a visual field test because this may be a sign of early primary open-angle glaucoma.

OUTCOME
By early detection and treatment, the risk of the onset of glaucoma will decrease and, in the vast majority of cases, medication will be effective.

Eye drops are used to treat ocular hypertension.

Steroid-induced glaucoma affects the trabecular meshwork of the eye, caused by the effects of corticosteroids - any of several steroid hormones secreted by the cortex of the adrenal glands, or any synthetic forms with similar properties. With this form of glaucoma, raised intraocular pressure is due to the reduced outflow facility of the pigmented trabecular meshwork and is usually seen within two to four weeks after starting topical steroids (medication applied to the surface of the body).

Raised intraocular pressure may also occur after prolonged use of large doses of steroids in other forms, eg., inhalers for asthma, steroid tablets taken for arthritis, skin creams, and nasal inhalers: with oral or intravenous steroid use, raised intraocular pressure may occur within a few days.

SYMPTOMS

Any unexlplained raise in intraocular pressure whilst using steroid medication, such as Maxidex (dexamethasone) and Pred Forte (prednisolone being more likely to cause a pressure rise) may show developing signs of primary open-angle glaucoma, together with a cup-shaped depression in the head of the optic nerve (optic-nerve cupping) and peripheral (field) loss in an eye with an open anterior-chamber angle.

DIAGNOSIS

The level of rise in intraocular pressure will relate to the strength of the steroid drop being taken.  Because steroids are used to treat eye inflammation, it may be difficult to determine the exact cause of increase in pressure.  The ophthalmologist will therefore carry out a complete eye examination to assess the degree of inflammation and measure intraocular pressure (recorded in millilitres of mercury (mmHg)).

TREATMENT

Optic disc photographs may be taken to assess the degree of damage - if any -  to the optic nerve, plus a visual-field test to determine the range of peripheral vision. Advice may be given to gradually discontinue topical medication in one eye to see if the pressure improves. Reduce the concentration or dosage of the steroid. Change to a less potent steroid such as FML (fluorometholone), Vexol (rimexalone) or Lotemax (loteprednole). Change to an oral nonsteroidal anti-inflammatory drug, eg. ibuprofen. Treat as for open-angle glaucoma. Where inflammation is moderate to severe, steroids are usually increased initially to reduce the inlammation using a topical hypotensive agent such as a prostaglandin analogue or a beta-blocker.

OUTLOOK

Patients with a family history of glaucoma, diabetes, high myopia (nearsightendness) or from a black race, are more likely to develop a steroid response and subsequent glaucoma.  Any sudden, unexplained eye symptom whilst taking steroid medication should seek medical advice immediately.

Prostaglandin analogues (eg lumigan, travatan, xalatan) are preferred first line agents for glaucoma. They are usually very well tolerated but may cause increased pigmentation (such as darker, and longer, eyelashes in some people; and some darkening of the iris). More frequently, some minor irritation may be experienced with drop instillation (which applies to all glaucoma medications) and in addition some redness of the eyes may develop when the medication is started for the first time. This generally reduces over the subsequent weeks, and improves with time.

Alpha agonists (eg alphagan). These drops work mainly by reducing the production of aqueous fluid in the eye. Typically, these drops are used twice a day. Possible side-effects include a dry mouth, and dizziness. Alphagan is not given to children as it may cause marked drowsiness in children. Alphagan is now available in combination with timolol (Combigan).

Cosopt (timolol + trusopt) is a preferred second line agent for glaucoma. It is usually very well tolerated but may cause some stinging on instillation. It contains beta blocker medication, and this is avoided in patients with any respiratory problems such as asthma. Also a possible side effect of beta blockers is dizziness, and this drug is therefore avoided in patients experiencing such a symptom.

Carbonic anhydrase inhibitors (eg Trusopt, Azopt). These drops reduce the production of fluid in the eye and are used 2-3 times daily. Trusopt sometimes stings on instillation, and generally is preferred in combination with a beta-blocker (eg cosopt).

Miotics (parasympathomimetics) eg pilocarpine
These drops are usually used four times a day (Pilogel is taken once daily). They increase the drainage of fluid out of the eye. These drops cause a small pupil which may mean that they cause a reduction in vision. They may give rise to headache, particularly in the first 2 weeks of taking. These drops were the original drops to be used for glaucoma but are now less commonly used as others are often better tolerated.

Other glaucoma treatments

Should I Use Marijuana to Treat Glaucoma?

The American Academy of Ophthalmology http://www.aao.org/ offer the following advice: "Based on a lack of scientific evidence, the American Academy of Ophthalmology does not endorse the use of marijuana to treat glaucoma. The Academy believes there is no evidence to date that shows that marijuana is safer or more effective than the drugs currently available to lower IOP to prevent optic nerve damage from glaucoma. This conclusion is based on reviews from the National Eye Institute (NEI) and the Institute of Medicine, as well as on available scientific evidence."

Putting in eye drops - try to keep your eyes open and allow drop to fall into corner of the eye nearest the nose.

Pigment dispersion syndrome is associated with the development of glaucoma (known as pigmentary glaucoma). The lifetime risk of developing glaucoma in those affected by pigment dispersion syndrome has previously been recorded at around 50%. Pigment from the back of the iris is released into the front chamber of the eye and is deposited in various areas - onto the back of the cornea, and also onto the trabecular meshwork - the part of the eye that drains fluid out of the eye. Over many years, pigment dispersion within the eye can lead to elevated eye pressure, and this can lead to glaucoma. The reason why some people get pigment dispersion is that the shape of the iris tends to bow back towards the lens (that lies behind the iris). This concavity of the iris means that the pigment layer on the back of the iris can rub against the lens more readily. Performing an iridotomy (a tiny dot opening in the iris created by laser) is known to flatten the iris contour, presumably reducing pigment release. Laser is not performed in all cases. Another type of laser, laser trabeculoplasty is particularly effective in this condition.

To read a personal account of what it is like to have pigment dispersion with some excellent illustrations, http://www.krukenbergs-spindle.co.uk

Example of visual field test showing field loss in glaucoma (black patches = lights not seen)