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Glaucoma: The Perils of High Pressure
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Glaucoma: The Perils of High Pressure

Dr. Levin is Clinical Assistant Professor, Department of Ophthalmology, Loma Linda University.

It's possible you may be going blind and don't even realize it. A leading cause of irreversible blindness, glaucoma, can happen without any noticeable warning signs or symptoms. Because doctors now have very effective technologies for early diagnosis, as well as new medicines and high-tech treatments (such as lasers), much can be done to slow down and control glaucoma in most patients before vision is permanently damaged. But early diagnosis is critical.

What Is Glaucoma?
The eyeball is bathed by fluid ("aqueous humor") that is produced by cells behind the colored part of the eye ("iris"). Not only does the fluid wash the eye but it helps the eye maintain its shape. When there is either over-production of aqueous humor or problems with the outflow drainage channels, the presence of too much fluid causes the pressure in the eye ("intraocular pressure") to rise. At the back of the eye sits the optic nerve, which connects to the brain and is the key component of sight. High intraocular pressure can permanently damage the optic nerve and result in vision loss. Glaucoma is the name given to the group of diseases that usually involve high intraocular pressure and produce optic nerve damage.

The presence of too much fluid causes the pressure in the eye ('intraocular pressure') to rise.

There are two main types of glaucoma — open angle and closed angle. In typical open angle glaucoma,(1) the outflow channels become blocked over time with aging or other disease processes. In closed angle glaucoma, the blockage occurs suddenly, raising the eye pressure rapidly. This is a true medical emergency requiring immediate treatment. Though eye pressure is not connected to blood pressure, the presence of high blood pressure can worsen the harmful effects of elevated intraocular pressure.

Glaucoma is frequently a complication of changes in the blood supply to the eye such as from a blocked central vein, diabetes and/or multiple surgical interventions. Tumors and some medicines (for example, antihistamines and H2 antagonists to reduce stomach acids) may worsen chronic open angle glaucoma. Severe acute angle closure glaucoma and acute myopia have been reported with topimarate, a drug used to treat epilepsy. The use of oral, injectable and inhaled corticosteroids causes an elevation of intraocular pressure in about 15% of the normal population. Medications prescribed for a variety of conditions (e.g., depression, allergies, Parkinson's Disease) can produce pupillary dilation and initiate an attack of acute angle-closure glaucoma in patients who have eyes with narrow angles.

Diagnosing Glaucoma
We know that certain populations are at higher risk of visual field loss from optic nerve damage. Hispanics, African Americans, patients with diabetes and patients who also have high blood pressure(2) all are at greater risk of glaucomatous visual field loss. Ophthalmologists now define glaucomatous visual field loss as a loss of peripheral vision. While we are born with approximately one million optic nerve fibers, the classic early visual field loss occurs only after half of these fibers are lost.

To make the diagnosis of glaucoma, it is necessary to measure intraocular pressure. It is now also standard practice to measure corneal thickness in all glaucoma suspect patients. The cornea is the transparent covering of the front of the eye. The measurement takes about 30 seconds or less.(3) The eye doctor will also shine a light in your eye with an ophthalmoscope and examine your retina, which is at the back of your eye, and specifically look at the optic disc (the head of the optic nerve) to see if any signs of damage are present. Damage to the optic nerve is called "cupping" and, if present, the doctor will measure and compare the optic nerve of the right eye and the left eye. The doctor will also plot your field of vision, carefully recording gaps in the field of vision for future comparison.

Signs and Symptoms of Angle Closure Glaucoma
The very sudden sudden and extreme rise in intraocular pressure is the significant event that defines angle closure glaucoma. Associated symptoms — headache at the front of the head, halos around lights, nausea — do not, however, always precede the attack. A small eye may be seen since the front of the eye, because of the increased pressure, is smaller, or crowded. A red eye with pain and a mid-sized fixed pupil are also very suspicious of this event. Intraocular pressures will often exceed 50 mm of mercury and this is a true medical emergency to be treated medically with a laser or surgically making a slit to allow drainage.

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Readers Comments
(5) Comments have been made

Normal pressure is 10-21 mm Hg. Increased pressure can reach above 30 mm Hg.
Posted Sat, Mar. 12, 2011 at 9:35 pm EST
Camille Torraco
What is the normal pressure? At what number should one be treated?
Posted Thu, Feb. 24, 2011 at 12:59 pm EST
Is dizziness associated with eye pressure?
Posted Thu, Apr. 8, 2010 at 10:38 am EDT
Darrin Hamilton
What is he skinny if your eye pressure is 60 in one eye and 20 in the other there is no pain,i have had a cornia trans plant due to trama to the eye 15 years ago have destroyed pretty much the eye. scratched the same eye,went to doctor he said the pressure was at 60. what can i look for in life or is there some way to reduce the pressure i have had a heart attack ,do have high blood pressure taking meds for that.
Posted Tue, Mar. 9, 2010 at 1:52 pm EST
My experiences have shown a very disturbing trend of financial considerations affecting quality (and integrity) in treatment. My first doctor had invested in an argon laser, and so declined to educate me on the considerably more benign SLT procedure. My second doctor has, only now, after 5 years of seeing him, administered a visual field test. This, due to my financial limitations and increasing medical bill. The damage to my left eye has progressed substantially. I am now looking for a third doctor.
Posted Fri, Jan. 22, 2010 at 9:30 pm EST

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