Glaucoma and Draining the Eye.

Factual Questions
1

I know glaucoma is a terrible disease. My mother and I both had it. But thankfully, there are now some very effective medicines for it. That’s good, because it literally can cause blindness if untreated.

Anyways, this may sound simplistic to some. But I’ve wondered this for some time now. For glaucoma (which by defn. is high intraocular pressure), why can’t they just literally drain the eye? I mean just set up a little shunt or valve on the eye, and you’re good-to-go. The person can even perform the draining procedure at home. And furthermore, the technology to do this was probably around since the 19th century–if not way before! Think about it.

Where am I wrong in this?

:slight_smile:

2

They actually do have such devices and procedures, and they are commonly done in people who don’t respond well to treatment via medication.

Downsides are about what you’d expect, including the risk of it becoming “clogged” in some fashion as well as the chance of the area around the shunt eroding.

The draining process is ongoing such that it mixes in with normal eye lubrication.

3

I have Glaucoma, I have lost some side sight, I use drops to keep the pressure down, One eye doctor put in Puntim plugs but that didn’t help. The specialist said the drops were like using a Drano like product. I have to hold the drops in my eye for 3 minutes To give the medication time to desolve any blockage. My pressure has been good for many years. I haven’t lost any more sight. I had it many years before I knew it. It never showed up on the earlier eye tests.

4

[nitpick] Glaucoma is not elevated intraocular pressure.

Glaucoma by definition is damage to the optic nerve. Generally the mechanism is elevated intraocular pressure. If elevated pressure is identified and not treated appropriately, it may lead to glaucoma. But if there’s no damage to the optic nerve, and hence no visual loss, it’s not glaucoma. [/nitpick]

So, monavis unfortunately does have actual glaucoma.

Otherwise, Ferret Herder has answered the question admirably.

5

Thank you, QtM. :slight_smile: Some WAGs about monavis’ case, which may lead to a less-generous evaluation of my understanding… (IANAD/N, but do work in ophthalmology.)

The only early warning sign for the potential for developing glaucoma that I’m aware of is a measurement of increasing eye (intraocular) pressure, which can progress to glaucoma and thus causing slow damage to the optic nerve over time. (There are versions of glaucoma that come on rapidly, but IIRC these are less common.)

IOP (intraocular pressure) is typically considered OK until you get into or past the low 20s. (Too-low IOP, hypotony, is another matter.) IOP ideally should probably be tested in some fashion* at an eye appointment just because it is a simple way to check for this damaging problem.

However, cornea thickness can throw off this reading - a thick cornea can make it look like you have a high IOP, while a thin one can read lower than the real pressure inside. So this is why a full, dilated eye exam (where the optic nerve is examined) may sometimes be what catches glaucoma even if the IOP readings appear normal.

Other tests like OCT (optical coherence tomography: a weak laser that gives a cross-sectional scan of the back of the eye) or visual fields (having the patient press a button when a light is seen; testing that all over the scope of vision can turn up blind spots and loss of peripheral vision) can help diagnose it as well.

Without regular eye exams to give a chance at an early warning, typically the only symptom someone might potentially notice is the gradual loss of peripheral vision. Since this usually happens slowly, some people don’t notice until they’re nearly down to tunnel vision. The rarer rapid-onset cases often have strong sensations of pressure or pain in the eye(s) and a faster loss of peripheral vision, so they’re more obvious.

So anyway, a variety of things like not checking IOP, a thin cornea producing incorrect “normal” results when pressure was actually high, and/or lack of full dilated eye exams where the optic nerve was closely examined might have all contributed. Or perhaps there was just a rapid onset of the disease.

  • If you’re wondering if you’ve had it done, the tests for this include the “puff of air on the eye” method (non-contact or air-puff tonometry), the “tap on the (numbed) eye with something that looks like an in-ear thermometer” (Tonopen) method, or the “doctor puts a stingy (yellow-tinted) drop in your eye, you put your chin in the chin rest, and the doctor brings a blue light up to your eye” (Goldmann applanation tonometry) method. There are others but these seem to be the most common.