Last week I described my cataract surgery and the disappointing outcome. I had set my hopes of better vision on that surgery, and although the procedure itself was successful, it did nothing to improve my sight. My eye problems started back in April 2017 after experiencing a vitreous hemorrhage. For those of you just joining this topic, you can follow my journey and find detailed information about retinal detachments here or you can catch up with my recent updates here.
When I saw my regular ophthalmologist a few weeks after cataract surgery, I asked what could be causing the worsening vision, if it wasn’t the cataract or the silicon oil residue. He said it was likely damage to the optic nerve from sustained elevated intraocular pressure. The cataract ophthalmologist had told me the silicon oil still in the eye cavity could raise ocular pressure. This ophthalmologist disagreed, saying the residue was too minimal to cause problems, although the oil could’ve originally plugged the drainage tubes.
My pressure was 18 that day, which is upper normal. In the past year it’d often reached the high 20s or 30s, and this can harm the optic nerve. He suggested I have regular pressure checks, and see him periodically. I didn’t know much about optic nerves, so did some online research. I learned:
-The retina and the optic nerve are two of the most important components of vision. The retina creates the image, and the optic nerve sends it to the brain for interpretation.
-Optic nerve damage can cause vision distortion, vision loss, and blindness. Seek immediate medical care if you experience sudden vision loss, halos around lights, any vision distortion or severe eye pain. These symptoms could result in optic nerve damage and permanent vision impairment.
-There are several causes of optic nerve damage, one being glaucoma or high pressure within the eye. Because glaucoma has no symptoms, optic nerve damage might not be detected until vision becomes impaired.
-There’s no cure for optic nerve damage, and various treatments may only prevent further vision loss.
When I had my pressure checked ten days later, it was up to 37. The ophthalmologist wasn’t in the office that day, but the tech contacted him, and he had her take an image of my eyes. He also prescribed an oral medication, Methazolamide, which eases pressure by slowing production of fluid in the eye.
I was already taking three sets of eye drops:
Latanoprost, which increases fluid drainage from the eye.
Timolol, which lowers the amount of fluid the eye makes.
Brimonidine, which helps with drainage. It also lessens the amount of fluid produced.
My blood pressure had been hovering in a lower than normal range, which the pharmacist said could be caused by the eye drops. At 108/59, it wasn’t a concern as long as I felt okay, which I did. Immediately after taking the Methazolamide pills, I began feeling dizzy and spacey, especially in the morning or after the slightest exertion. My blood pressure dropped to an average of 101/54.
Three days after starting Methazolamide, my intraocular pressure was up to 39. Three days after that it was down to 18. Ten days later, it was back up to 28. Despite all that medication, my eye pressure wouldn’t stabilize.
The ophthalmologist showed me the image of my eyes he’d had taken earlier that month. The orb on the left side (which is actually my right eye) reveals an increased whitening in the center, which indicates optic nerve damage. This damage is permanent, and would worsen if the intraocular pressure isn’t controlled. The white mass on the upper right side is damage to the retina from the initial trauma.
There was an invasive surgery in Vancouver to consider, but first he wanted to try a simple laser procedure that’s often successful in lowering ocular pressure. The procedure could be done by the ophthalmologist who did my cataract surgery.
So I waited for that call. Meanwhile I crossed my fingers and hoped this procedure would work so I could stop taking that nasty Methazolamide.
And the saga continues.