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PLEASE READ THIS: The information contained herein is not intended as a
substitute for medical advice and care from qualified, licensed health
care providers. The reader should regularly consult a physician in matters
relating to his or her health and particularly with respect to any symptoms
that may require diagnosis or medical attention. The information is presented
here to educate and inform and to guide you to an understanding of cause,
prevention as well as treatment.
Note: This report will be of value to both practitioners and patients. It necessarily contains a great deal of medical terminology. I've tried to provide in-context explanations and definitions where possible. It is probably a good idea to have the Glaucoma Glossary printed out and accessible as you read this report. There is also a General Glossary that you may find useful. A summary version of this report will be posted as an abstract sometime soon which less medically-inclined readers may find valuable.
(All links are on this page.)
Glaucoma is the diagnosis given to the ocular condition when there is loss of retinal nerve fibers and a corresponding loss of vision. The visual defect is most often observed as enlargement of the physiological blind spot and other visual field losses. Left untreated, the disorder can ultimately result in serious visual field loss with only limited direct central vision, or worse. Treated, and treated early and properly, vision can often be saved. Early treatment may prevent significant vision loss or at least arrest the process, sometimes completely and other times with varying degrees of loss of parts of the visual field.
For clinicians, the major issues are early diagnosing and effectively treating the condition. Unfortunately, unlike some other ocular conditions, glaucoma does not often lend itself to simple diagnosis or treatment. Recently, we have come to understand much more about the mechanisms of glaucoma. And within the last few months there have been a few brand new medications which show great promise for more effectively and conveniently managing the disorder.
Glaucoma occurs as a result of increased intraocular fluid pressure (IOP), as measured by an instrument called a tonometer. The eyeball is basically a rigid sphere filled with fluid. As the total amount of fluid increases, pressure increases, similar to over inflating a tire. Sooner or later, something has to give. It is the retinal nerve fibers that become damaged and die, and with them goes the vision. But 25% of the time, glaucoma can occur in apparent absence of elevated pressure. It is also possible to have increased pressure without nerve damage (ocular hypertension). These are examples of some of the many mysteries of glaucoma.
The two primary causes for increased pressure are increased aqueous fluid production and decreased fluid outflow. In the normal healthy eye, the aqueous fluid is constantly being produced and drained, normally at equal rates. In open angle glaucoma, the tissue producing the fluid becomes over-active. Medications can reduce the fluid production. At other times, the drainage channels can become blocked. This is angle closure glaucoma. There are a number of causes for this anomaly, including anatomical defects, degenerative tissue defects (including possible systemic immune system and connective tissue disease), trauma and internal eye infection. Again, medications can sometimes help open the drainage and increase outflow, and there is a laser surgical procedure to clean out debris, widen the outflow channels or even open a new channel.
Additionally, certain medications (e.g., topical ocular corticosteroid anti-inflammatory drugs, orally administered steroid medications and vasoconstrictor drugs, as well as other pharmaceuticals) can, as a side effect, raise the intraocular pressure.
Researchers are also concerned with a third mechanism of action relating to open angle glaucoma. This has to do with restriction of the blood flow to the nerve fibers which may or may not be related to elevated intraocular fluid pressure.
You can gather from the above that glaucoma has many possible causes, and therefore a variety of treatments. Sometimes the disorder can be completely resolved, sometimes it requires constant medical control with medications and/or surgery---still with very good outcomes as far as saving vision. But sadly, there are times when medical intervention comes too late, or is otherwise ineffective at stemming the course of the disease.
The current understanding of the disease is that there are structures called microtubules within the axons of each of the hundreds of thousands of nerve fibers comprising the optic nerve. These microtubules serve as corridors to remove metabolic waste products and to supply nutrients to maintain the health of the individual nerve fibers. When these tubules are damaged, perhaps crushed by the increased pressure, the nerve fiber becomes functionless---dead. Vision is lost, little by little as the number of damaged nerve fibers increase. By the time we can measure visual field defects, a great deal of damage has already occurred.
Localized loss of blood supply can also cause the nerve cell to die, and this loss of blood flow may be related to elevated pressure or an ischemic event where the blood supply is otherwise mechanically blocked.
The mechanical theory, then, explains how the increased pressure crushes the microtubules, depriving the nerve of nutrients. It also helps explain loss of blood flow as the internal eye pressure exceeds that of the blood vessels' pressure. It does not, however, explain low-pressure glaucoma or why some people can have elevated pressure without damage to the nerves (ocular hypertension. More on that below.).
Two of the riddles of glaucoma are (1) what causes nerve damage in normal-pressure glaucoma and (2) why does lowering the pressure in high-tension glaucoma sometimes not stop the progress of the disease?
One proposed explanation focuses on the premise that normal-pressure glaucoma really is high pressure, only that a number of transient elevations are occurring during the late night when it is not being measured. The other explanation is that an underlying connective tissue disease is damaging the microtubules. Yet another rationale is that there is loss of blood flow (capillary non-perfusion). Clearly this occurs in the presence of elevated pressure. But it also may occur under normal pressure, possibly caused by nutritional deficiencies or systemic disease affecting the strength of the capillary walls.
Meanwhile, we now appreciate that glaucoma is a complex disorder that can have more than one cause---and sometimes more than one remedy.
Contrary to popular belief, a glaucoma test measuring the fluid pressure (tonometry), is not the predictor of the final diagnosis. Of more importance is the direct observation of damage to the optic nerve itself and sometimes the nerve fiber layer of the retina. Quantifying a loss of vision in part of the visual field consistent with observed nerve fiber loss is the true definitive diagnosis for glaucoma.
We believe that probably 75% of glaucoma sufferers do indeed have elevated intraocular pressure. So careful measurement of the eye pressure on a regular basis (for high risk people) is a crucial step in early detection. Direct observation of the optic nerve with the ophthalmoscope, fundus lens or retinal camera is vital. In suspected angle closure glaucoma, a gonioscopic lens is placed on the eye which then allows direct observation of the outflow channels. Additionally, mapping of the integrity of the peripheral and central visual fields using an automated perimeter is required to quantify visual field loss and thereby monitor the clinical effects of the treatment.
In the USA, both optometrists and ophthalmologists may perform these tests. However not all practitioners have the necessary equipment or the skills to make the diagnosis or manage the treatment.
It is perfectly reasonable for the doctor to repeat these tests over a period of time before committing to the diagnosis of glaucoma. In suspected ocular hypertension, an informed decision must be made regarding initiating treatment in absence of visual field loss. If ocular hypertension might be a precursor to glaucoma, and 25% of the time it is, then early treatment can prevent nerve damage. But medical intervention at this stage nevertheless commits the patient to many years of ongoing treatment, never knowing for certain if glaucomatous nerve damage has been prevented or if it might not have occurred without the medicine in any event. Many practitioners take the wait-and-see approach, carefully monitoring pressure and visual fields and initiating treatment at the first signs of trouble. An informed, compliant patient and attentive doctor can be a successful co-management team.
Argon Laser Trabeculoplasty
This laser microsurgical procedure helps to increase fluid outflow. Somewhat controversial of late, some doctors may choose this as the initial therapy and others reserve it as a last resort. The downside is that almost half the patients who have this procedure will experience diminishing IOP lowering effects within 5 years. And sometimes repeated laser treatment is not nearly as effective as the initial therapy. The positive considerations: for patients non-compliant with oral and topical medications, laser might be the ideal choice.
Topical Medications
The traditional therapy has been the use of beta-blocker eye drops, such as timolol (Timoptic, Betimol), betaxolol (Betoptic), levobunolol (Betagan), carteolol (Ocupress), and metipranolol (OptiPranol).
Epinephrine derivatives, dipivefrin (Propine) is another drug sometimes added to another topical medication to enhance the effect.
Beta-blockers and carbonic anhydrase inhibitors (CAI) reduce aqueous production. Dipivefrin reduces production and may also increase outflow.
Pilocarpine, another older medication, has been used to increase aqueous outflow.
Orally Administered Medications
Oral carbonic anhydrase inhibitor (CAI), acetazolimide (Diamox) may be used along with topical medications.
A number of new medications have become available recently. The most exciting addition to the management of glaucoma has been lantanoprost (Xalatan), a prostaglandin analog. This drug represents a totally new approach to lowering intraocular pressure by increasing aqueous outflow. It appears, unlike most of the other medications, to be without side effects. (One minor side effect without symptomology or other consequences has been darkening of light colored irises.) Many practitioners feel that this new drug may revolutionize the treatment of glaucoma and soon become the drug of choice.
Other new medications include the adrenergic agonists apraclondine (Iopidine) and brimonidine (Alphagan) and the topical CAIs dorzolamide (Trusopt) and methazolamide (Neptazane).
Many practitioners are beginning treatment of new glaucoma patients with Xalatan and, when necessary, the addition of Trusopt or Neptazane. Most doctors feel that patients already under treatment and successful with beta-blockers should continue with that protocol.
The principal of the management of glaucoma is to reduce the intraocular pressure to the point whereby the remaining healthy nerve fibers are able to receive proper nourishment and therefore maintain function. The key to the success with medication therapy is patient compliance, and the key to compliance is patient education.
The use of the medication must be consistent with the patient's ability to properly administer and tolerate the drug, taking into account lifestyle, dexterity and awareness of side effects.
The doctor is responsible for diagnosing a difficult to diagnose disorder and provide medical treatment often using drugs that are variably effective and not without side effects. This requires a keen sense of communication with the patient, attention to the regulation of dosage and type(s) of medication and active follow-up care.
With the new understanding of the mechanisms causing vision loss in glaucoma patients, the accessibility to diagnostic equipment at optometrists and ophthalmologists everywhere, and the availability of extremely effective new medications, the management of glaucoma has come a long way in the last year. We look forward to an even greater understanding of the underlying causes of the disorder, new instrumentation to aid in early detection and new medicines to help manage glaucoma in the near future.
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