To confirm many of the posterior staphylomas I've observe over the years have not progressed.
My experience with extreme myopia began like yours, with nearsightedness that worsened every year since I was a child. Luckily the progression stopped around age 40 (I'm 50 now) and stabilized around -14 for contacts and -16.5 for glasses.
The symptom that sent me running to various doctors until I found a person I'm comfortable with was an episode like central serous retinopathy, although it was never confirmed to be CSR w/ imaging. I developed sudden, painless distortion (vertical lines kinked/bent), blurring and decreased contrast in one eye, in the literal blink of an eye. Over the past 3 months the distortion has gradually lessened (although vertical lines still have a slight curve), but the blurring and lower contrast persist. That eye is about 20/50 now. I also have had and still have floaters for years, which you probably have too.
My retinas were always evaluated as 'stable and normal' with no sign of peripheral detachment and no symptoms. Aside from warning that I was at higher risk of RD, I never knew anything else bad was going on. As you say, ignorance is (was) bliss.
However, in the past few years I started hearing 'slight lattice degeneration' during exams so I knew something was up, although both my OD and RD said not to worry. It wasn't until I saw actual color photos of my retinas recently and had them evaluated by a different retina specialist that I understood the extreme nature of the degeneration.
I have the typical 'tigroid fundus' appearance of DM, along with a Fuch's Spot in one eye (off-center from the macula, thankfully), visible thinning in numerous areas, tilted disc, myopic crescent, vitreal degeneration, etc. The images were horrifying, frankly. The Heidelberg spectral-domain OCT also showed the pronounced tilt of the retina (especially the macular zone) in each eye due to staphylomas.
The last retina specialist also did a contact lens biomicroscopy of my eyes and said he could see the staphylomas at the rear just by looking at the magnified, lighted view of the inner retina surface.
FYI you can find online images of staphyloma shown in CT/MRI scans. I think they can also be imaged by ultrasound. However, as Dr Hagan said it's apparently atypical to have them measured regularly, or even mapped at all. I'm not sure why doctors don't track this, except that for the most part it's assumed there is nothing that can be done.
There have been a few patients here on MedHelp who have had the posterior pole buckle / scleral reinforcement surgery to reduce the chance of future damage from increasing staphyloma depth. A side benefit to the surgery in theory would be a slowing of the myopic progression, but that alone is probably not a reason to face the expense and risk of surgery.
If you get an axial length measurement of your eyes every year, you could at least track how much longer your eye is growing over time, even if you can't determine whether any length increase is due to overall eye stretching or localized staphyloma growth.
As ValveJob said, cataracts can also affect prescription changes, as can any alteration in the cornea shape/thickness/transparency. It would be good to know if the blurring you have now might be attributable to a cataract rather than increased myopia. If there has been a big change in the cataract in the past year, that could be partially responsible.
Like ValveJob, I also had the axial length measurement done w/ the Carl Zeiss IOL Master. The second retina specialist I saw did it to establish a baseline, as the first time he was seeing me was when I had pronounced symptoms in the left eye and he could see I was severely myopic w/ a lot of degeneration.
The machine is interesting as it measures the depth in various areas on the macula. I asked for a printout of the results, which shows six different depth values and a resulting average.
In my case one eye varied from 30.50 to 30.59 (OD avg 30.55) and the other was 30.24 to 30.30 (OS avg 30.27, all in millimeters). I don't know across how wide an area of the retina the machine scans, although I know the measurements are targeted around the macula because you stare at a single pinpoint of light while the machine is chunking away.
Depending on how broad the scan area is, it may or may not be a helpful tool for tracking posterior staphyloma.
Of course, an axial measurement does help determine the degree to which your retina is under more or less stress. If there was a lot of lengthening year over year in your results, it might prompt your doctor to be more vigilant about watching for symptoms. But most RDs seem to feel that they can't really do anything unless/until the patient complains of DM symptoms, at least two of which (retinal detachment/tearing/schisis and CNV/bleeding) can potentially be treated.
The exception is Dr Brian Ward in San Jose, CA who is doing posterior pole buckle surgery in the US. He feels it's beneficial to arrest staphyloma growth to help delay major retina deterioration, despite the risk of surgery. But he is in the minority. You can search this forum for a few users' experiences with this procedure.
Thank you for your comments. I believe you when you say that you have seen many staphylomas remain stable over great lengths of time. But is this usually the case or is there more of a general tendancy for them to increase in size with age?
Also, with all the various types of eye scanning equipment (OCT scans etc...) typically found in most opthalmologists offices is it possible to accurately measure and track progression of staphylomas? Is this usually done or is the general consensus not to bother since not much can be done about them anyway? My doc seemed to really not want to give it much attention.
Thank you for your comments as well. As for your comments on staphylomas, I am well aware of what they are and how they contribute to the pathogenesis of degenerative myopia. What I'm trying to guage is what the typical tendancy for progression (if there is anything typical about them) is with regards to them. Just look at one single picture online of an eye with a deep staphy and common sense screams that a retina WOULD easily be damaged a hundred different ways from such a thing. And yet there appears to be little interest in attempting to surgically stabilize them. I don't understand that - and it scares me. I really was shocked by how nonchalant my RS was about my staphy. Maybe I'm making more of it then I should be. I don't know.
BTW, at age 40, I don't think I've ever directly commmunicated with another myope anywhere near my prescription. You mentioned you suffer from "symptoms of DM". May I ask what symptoms you have? For me, the constant prescription changes alone are tough on me mentally. I know it means further stress on my retinas which will lead to further problems down the road. Also, if I were to keep going back to my optometrist and buy new glasses every time I began recognizing prescrip changes - I'd be broke by now! Seriously, I last updated my glasses 11 months ago. I noticed my vision starting to become slightly blurry again a little over a month ago. Prescrip change confirmed at recent opth visit but I will purposely endure slightly blurred vision until the spring and get a new pair then so I can have decent vision for the summer months. Just a tiny part of what I'm constantly living with.
These days, the bigger concern is with regards to the actual health of my eyes. Despite being told that currently my myopia is "normal" I just don't buy it anymore. I'm told I'm "normal" and then in the same breath I'm also told "Lattice degeneration, nuclear cataracts, vitreal degeneration, tilted discs, staphylomas, retinal cysts, areas of thinning... and my favorite: I can always tell your age from your prescription and your prescription from your age!". Oi. This isn't normal. Not at my age.
I will admit though, that what "knowledge" I have about DM comes only from what info is available online since I can't get any answers from my doctors. As I'm sure you're well aware, you won't find any words of encouragement in any online articles pertaining to degenerative myopia. However, I recognize that inferences on one's own future cannot be made by reading online articles and study postings (many of which are from the 70's and 80's anyway). On one hand knowledge is powerful, on the other it can be dangerous. Part of me wishes the internet didn't exist. It's true what they say: Ignorance IS bliss.
Generally repeat measurements of staphyloma are not done. Difficult to do accurately and not give you useful information nor is there any highly successful treatment.
Although I am much older than you, my prescription is also very strong (OD: -18.75, OS: -17) and changes all the time especially in the last several years. I definitely have myopic macular degeneration. However, I also have nuclear cataracts which create a myopic shift. I had an A-scan (measures the axial length among other things) at the end of May and at the beginning of November. Thank goodness, there was absolutely no change for the right eye and only 0.02 change in the left. So my recent change in prescription must be due to my cataracts.
Is it possible that you also have cataracts? I know you are young, but I have heard of young people who get them.
I feel your pain; I'm in a similar situation with a posterior staphyloma in both of my eyes. You are exceptionally, fortunate to still have good vision despite the degree of your myopia. That's great news.
Although I am less myopic than you at -14.0, I am having symptoms as a result of degenerative myopia. I've done a lot of reading after my diagnosis and have a few things to add on the topics you raised.
Regarding a staphyloma, these apparently form most often as a result of the thinning of the scleral 'shell' on the outside of the eyeball. Since the most common cause of high myopia is elongation or stretching of the globe of the eye, as the eye enlarges the sclera and the retinal layers inside it get thinner and thinner.
When these tissues get very, very thin, local areas form where the fluid pressure within the eye pushes out against the thinnest areas, forming an outward bulge or staphyloma. The posterior section of the eye tends to be the thinnest area of sclera around the eye, which is why a staphyloma tends to form there first. Unfortunately that is where the macula/fovea is located too, which is why central vision can so often be involved in cases of myopic degeneration with staphyloma.
FYI, I was told by my retina specialist that the scleral stretching in high myopes is due to genetic weakness in the collagen bonds in the sclera. The weakened scleral collagen allows the eye to stretch out in response to normal pressure of the fluid within the eye. The gene causing the weakened scleral collagen is more common in Asian populations than in Caucasians, which is why high myopia and degenerative myopia are most common in Asian countries.
A deep staphyloma directly behind the central vision could in theory add to one's degree of visual myopia, since it would move the focus point on the retinal surface farther away from the natural lens inside the eye. However, a shallow staphyloma would probably not add much overall 'depth' to your eye, given that the total length of your eye is probably on the order of 26-30mm or longer.
I do remember one user on MedHelp who commented that after their 'posterior pole buckle' surgery, they needed slightly less correction for myopia. The surgery involved having a donor scleral reinforcement segment sewn onto the back of their sclera, in an attempt to reduce the depth of any staphyloma behind the macula. In that patient's case, the scleral buckle must have pushed back against the bulge and made the staphyloma a bit more shallow, resulting in bit less correction needed.
However, from the little I've read from patients who have had this surgery, it sounds like the total diopters of correction typically do not change after this procedure. So a shallow staphyloma might not have much to do with how nearsighted you are.
My doctor's opinion is that a staphyloma typically does increase in depth with age, again due to the normal pressure of fluid inside the eye pushing outward against the weakened scleral wall. But if Dr. Hagan knows of patients in which this has not occurred, that is good news for all of us degenerative myopes.
I think staphylomas are also not common in patients with mild myopia, as their eyes are 'shorter', the sclera thicker and the potential for bulging decreased as a result.
Best of luck with your vision in the future!
Yes I have nuclear cataracts as well. However, they were only diagnosed last year and I believe they are still in the very early stages. I don't think they are affecting my vision yet. One thing that is very stable about my prescription is the RATE at which it progresses. Pretty much 0.5D annually each eye. That hasn't changed. I'm sure it will increase much more rapidly though once the cataracts start to mature. Can't wait!!
I'm sorry to hear you have MMD. Are you receiving anti-VEGF shots and if so, are they helping? May I ask your age and what your vision is correctable to? When were you diagnosed?
Also, what prompted your doc to measure your axial length? This is one aspect of my eyes that I do not know (and probably don't want to). I've asked my opthalmologist for that measurement in the past but he's shrugged it off telling me he already knows my eyes are very long. Fab.
Regarding cataract, to help delay the time when you might need surgery you might also want to look into any medications or other factors that can promote or worsen cataract formation.
I was very surprised to find corticosteroids on the list of meds that can cause or worsen cataracts. In my case I started developing cataracts at age 46 - the year after I was prescribed a steroid nasal spray for severe allergy. Doh.
There are many other factors than can cause cataracts of course, including simple aging, but if there were a lifestyle change that might help slow down cataract growth it might be worth investigating.
As for your question about anti-VEGF shots, at the beginning of 2012, I developed a CNV (choroidal neovascularization) so I had two injections (one month apart) of Avastin. That stopped it. However, I was left with a scar which distorts the vision of my left eye!
You don't have to have a CNV to have MMD (as in AMD, there is the dry form and the wet form). So, I have the dry form in both eyes simply because my retina is so stretched and atrophied. The wet form can start because of this, and it did in 2012. Luckily, everything has been stable with that since that was taken care of.
As for your cataracts, I have read (if I am wrong, Dr. Hagan, please correct me) that even when cataracts are very mild and just starting that the index of refraction is changing and can cause a myopic shift.
What prompted my RS to have my axial length measured was the fact that I gave him a print-out of all my eyeglass changes in a short period of time. I brought up (as I had before) cataract surgery. Although he is very conservative about that for people like me (which I totally understand), my quality of life plus the constant changes in my glasses is driving me crazy! So, he said in April that he would send me for the first A-scan. He said to come back to see him in six months which I did in October, and then he sent me for another A-scan which I had at the beginning of November so he could compare them. I have another appointment on December 4 to discuss this with him, but I already know the results since I BEGGED the technician!!! As I said before, thank goodness, there was no change. I am sure that in the past there has been a lot of change because my prescription has changed SOOO much in 10 years, and my axial length is SOOO long (OD: 30.74 OS: 30.27 the first time and 30.29 the second) that it could only be from my eye stretching, in my humble opinion.
Anyhow, we are at the point where we are discussing cataract surgery, and to have cataract surgery, an A-scan has to be done in any case. By the way, this past time, it was done with the "IOL Master" which is the best.
Sorry I went on for so long, but you asked...!!! :-)
What your ophthalmologist told you is correct. Many don't progress, many have no effect on vision. Be grateful for the good news.
Tilted disk has no effect on vision. Its rotation of the optic nerve due to size of eyeball
I noticed in a post of yours in another thread that you mentioned you have actually met with Dr Ward and are considering having Posterior Pole Buckling procedure done next year? If you go through with it I wish you the absolute best of luck and I hope you will post on how things go in both the short term and update every once in a while in the years to come. The few members of this forum that had it done seemed to stopped posting shortly afterwards. Hopefully that means they are out enjoying life rather then spending it obessing over their eyes.
Also if you don't mind, I may send you a PM in a few days with some questions on your dealings with Dr Ward. I've been aware of his work with high myopes for some time and have been considering traveling to see him for an examination.
Yes, please PM me or post here regarding questions about Dr. Ward. I do have a surgery date a few months away, but candidly I haven't yet decided whether to go forward.
Almost every other retina specialist I have asked directly (or through friends) feels it is ill-advised to operate on an eye that isn't in dire straits, and that the risk of complications outweighs any benefit from the surgery. One ophthalmologist I asked through a friend said he thought the anti-VEGF injections to treat bleeding should really be the first line treatment in DM, rather than scleral support surgery. He noted that it's risky and that as no other doctors have published findings in support of the technique, he felt it might not be scientifically valid.
I did ask Dr. Ward why other doctors weren't doing the procedure. He said he had tried to train a few but that they 'gave up' as it's technical, fiddly work and just referred their patients to him. I do know that people come from outside the US to have the operation done by him, and that there is a lengthy wait list. But none of that give it scientific credence, of course.
IMHO I'd rather prevent symptoms than treat them, but it's a hard decision. I'm aware of the potential for major complications, and can't decide whether the risks are worth any incremental benefit I'd derive from supporting the area under my macula, given how stretched out and thin my retinas already are. There is clearly damage there already that 'propping up' the posterior pole cannot alleviate.
Still, given the staphyloma issue and general progression of this disorder, the idea of the surgery makes sense to me. I just don't know what to do.
I completely understand the struggle with regards to the descision making on this issue. On one hand, you don't want to risk surgical complications on an eye with good vision. On the other, if you wait too long, then a time may come when neither such a procedure or anything else may be able to help.
Two areas of questions I have at the moment are:
1) Does Dr Ward have specific criteria he uses in recommending the procedure? Does the mere presence of a staphyloma warrant surgery or does he look for other specific findings (certain axial length, laquer cracks, CNV etc...)? Overall, did he give you the impression that he takes an aggressive position (i.e., do it while the eye still sees well and atrophy is minimal) or should it be left as more of a last resort when all else seems to be failing?
2) Did you discuss with Dr. Ward potential long term issues with regards to the donor scleral buckle? I'm not in any way trying to scare you, but can the buckle be removed in the future if problems occur down the road? And if so, did he give you any sense as to whether he felt another surgeon would be able to remove it (should Dr Ward be long retired)?
You are reading my mind with the questions you raise. I need to schedule an appointment w/ Dr. Ward to discuss these points and others, but have been putting it off while I do more online research. It may also be a bit of 'head in sand' on my part too, because once I have his take on the surgery in addition to all the research, I have to make the call on whether to be operated on.
The surgical questions on my list so far are:
- At what point does he recommend the surgery - once problems start to develop, or while an eye is still asymptomatic? Does the depth of any staphyloma affect his recommendation? [My impression from the comments in his published paper is that he feels early intervention makes the most sense, but I haven't asked directly.]
- If a patient with DM has a stable degree of refractive error and few present symptoms, does he recommend the PPB surgery? [I'm in this category; pretty stable prescription but symptomatic in one eye and not in the other].
- What are the risks associated with donor sclera tissue? (tissue rejection, CJD or other disease transmission, etc). What is the long-term biological prognosis for this material? Which scleral graft material (brand) does he use?
- Has he ever had a surgical failure with this operation such as inability to suture the buckle material to a thinned sclera? Have there been any other intraoperative incidents where the procedure was curtailed?
- What percentage of his surgical patients have had persistent, vision-affecting diplopia?
- How many were unable to return to contact lens use?
- What percentage of his surgical patients had complications requiring repositioning or removal of the buckle? Can it be removed or re-tensioned at a later date?
- Does the PPB surgery restrict treatment options for later vision-threatening incidents such as retinal detachment or macular hole?
- Has any patient developed a retinal/choroidal bloodflow restruction or bleeding incident tied to the buckling? Has any PPB patient developed other negative side effects of surgery?
I'd also like to know whether he is still following the patients in his initial study, and what is their current status. Of course he cannot disclose specific patients' medical records, but I would be surprised if someone in his office was not following up with these patients.
I also do worry about what would happen when Dr. Ward retires or is no longer able to perform the procedure. I cannot find one single other surgeon in the US who does it. The next-closest would probably be a surgeon who has experience with segmented buckles for RD or foveoschisis repair - which I haven't found either.
Every US based resource or paper I can find about pathological/degenerative myopia cites treatment of addressable symptoms (ie, anti-VEGF injections for CNV or other bleeding) as the only recommended intervention.
One doctor I consulted pointed out that he felt if Dr. Ward has a breakthrough to offer with demonstrable results and proven safety, he would have published a follow-up by now and other surgeons would be adopting his techniques. It's very hard to discern if he is on the leading edge - or the fringe.
Don't worry about frightening me with any questions. I'm scared enough on my own.
That is a very well thought out list of questions. When you get the answers, please be sure to post them here in this thread for others to see.
BTW, I sent you a PM.
"Glad" to hear i am not the only one. My myopia problems started at 6. By the time i was 16 it stabilised at around -18 diopters ( contact lenses). My condition remained stable up to the age of 42 until almost overnight Instarted seeing all lines bent, all shapes distorted both veryically & horizontally in my good eye ( the other one has a vision of 5/10 corrected.) the situation remained stable for over 1,5 years when cataracts developed , dropping the vision to my good eye to 3/10 corrrected). Cataract surgery improved the vision to 11/10! But lasted only for 2 months. I started seeing zebra like stripes in all shining surfaces , then a stable cobweb. The parlial PVD diagnosed 2 years ago caused extensive makular traction and eventually foveoschisis. My doctor advised me vitrectomy with ILM peeling and gas tamponade. I just cancelled the operation scheduled out of fear of the outcome since if I lose the 8/10 vison i know have i wont be able to work ( in front of a computer the whole day). I am seeking other opinions, one stating that foveoschisis should be observed until it causes a retina detachemnt or vision deteriorates to 3/10. In the last 4 days the big shadow in my area of focus moved away, or shifted , my floaters are that big and very little moving that obstract me heavily when i read covering some letters , almost making them partially dissapear. Any advice?
Forgot to mention that i have huge posterior staphylomas seen with naked eye and axial lengths of 33 & 36 if i remember correctly- but at these lengths what difference can ti make ? ( irony)
I am 38 years old extremely nearsighted -14 in both eyes. My distortion started march 2013 , it was first lines, now its shapes and progressing. I have posterior staphyloma. How is your vision now? Just trying to find how long distortion continues (or) how the vision will be as time goes by.Please share if you have any info.
I am jumping into the mix as I have recently discovered that I have posterior staphyloma in both eyes. I am impressed with the knowledge of contributors to this blog, and equally concerned that Dr. Brian Ward may be the only one around who thinks their is a remedy for posterior staphyloma. My ophthamologist told me there's a 25% success rate.
About 15 years ago I had a detached vitreous in the right eye and this January I had the same occur in the left eye. I had gone to my ophthamologist in December after my optometrist saw a small hemorrhage in my left eye. That turned out to be due to the process of vitreous detachment in that eye. By the way, I'm 64; 65 in December.
Over these past 15 years, my right eye has become uncorrectable to any better than 20-35, but even those numbers are 'fuzzy' as I'm guessing at the eye chart. I always attributed it to the detached vitreous, thinking I hope I never have detached vitreous in the left eye. When that happened to me in January, my ophthamoloist said that detached vitreous has no effect on vision. That didn't convince me and on the next visit I told him the sight in my left eye had deteriorated, so he put me on a scanning machine and saw the posterior staphyloma in both eyes. It appeared that the angle formed by the bulge in the right eye was about 45 degrees off the eye curvature, and about 20 degrees in the left eye. He said both would get worse with time.
It may be just my imagination, but it is getting harder and harder to read, use the computer, watch golf tournaments on TV (where's the ball on the green?). I've searched the internet for information on treatment, and this blog thread is the best I've come up with. I've printed out the entire thread and may set an appointment to see my ophthamologist to discuss treatment. As mentioned, he's not optimistic and we currently are on a 'see him once a year' schedule, the next time being May 2016.
Any thoughts would be appreciated.
Hi there, I realize it has been a while since this discussion started but I do have good hope to get my questions answered here as it seems that you all know quite well what you are talking about. I am a 37 years old female and I am wearing glasses of -13 for both eyes (highly myopic, though with no staphylomas). My ophtamologist always warned me for a retinal detachment as there is an increased risk. But I was completely unprepared for what I experienced 3 weeks ago.
It came quickly and from one moment to another I saw a black spot with my left eye just left to the point where I tried to focus. It gradually grew in the next couple of minutes causing straight lines to bend dramatically. As it happened, I called my neurologist who put me on 4 mg/day oral dexamethasone (a strong corticosteroid like prednisone) in the 4 weeks just prior to the, what I now know was a, retinal bleeding. The only thing my neurologist did was prescribe some more prednisone, what I found quite surprising. Realizing this would not help me, I immediately called my ophtamologist and within half an hour I was in his office. I told him that I have been taking a high dose of prednisone for 4 weeks, because of a faint pressure/pain behind my left eye that I already had for at least 6 months (accompanied by a decreased visual aquity, which used to be above average and still is above average for my right eye, despite being strong myopic) and more recently also caused migraine-like headackes. I eventually went to the neurologist, because my ophtamologist could not find anything at first. Based on an MRI my neurologist concluded I had a neuritis of the optical nerve of my left eye and this is how I started treatment with prednisone.
According to my opthamologist it is not uncommon for prednisone users to develop retinal edema. But when he looked into my eye and saw that there was blood involved, his demeanor changed to more serious. He explained I had blood underneath my retina adjacent to my yellow spot. This caused my retina to bulge inwards into my eyeball, as seen on the scan, which explained the bending of straight lines in my sight. The next day a fluorescence angiogram (FAG) was sceduled to establish the exact cause of the bleeding.
My ophtamologist called me right after the FAG and told me I have a Fuchs spot and that I should get treatment with VEGF-inhibitor to be injected into my eyeball. But he also told me that he already saw an improvent in just one day and that the spot got smaller. I confirmed this as the bending of lines was already way less. In the next couple of days the spot decreased even more to the point I would not even notice it anymore. The bending was nearly gone and the darkening/discoloration was also nearly gone. Exactly one week later another scan was taken and my ophtamologist concluded that the progress was very good. Even better than could be expected after treatment with an anti-VEGF injection. Also he told me that the FAG shows no leakage nor signs of neovascularization, so a VEGF-inhibitor would not have any effect. A follow-up was sceduled for 2 weeks later. I was especially relieved that day to hear that the photoreceptors would not die, which has been my greatest concern.
Unfortunately I experienced a setback shortly after. I cought a serious cold and was couching uncontrollably last week. I suspect this caused again a small bleeding on exactly the same spot. It therefore took me a day or so to realize this. The original nearly deminished spot got suddenly more apparent i.e. a bit darker and maybe also a bit bigger and, worst of all, even closer to where I focus. This was confirmed with a scan and now my ophtamologist urges me to have the anti-VEGF injections anyway, even though the FAG did not show any signs of neovascularization. I won't dispute the fact that I am dealing with macular degeneration (MD), but I definately question the proposed treatment in my case.
So far it seems to recover the same way as it did after the initial bleeding. I really hope it will not happen again (luckily the cold is retreating), but to be honest I am quite scared it will hit my central vision. What should I do? I just don't see how treatment with anti-VEGF will be effective without neovascularization being the underlying cause. Besides I am not convinced it will aid in recovery of the current damage (the spot is there and will hopefully be resorbed), nor do I expect it to avoid further bleeding. Moreover the injections are not unlikely to cause complications such as retinal detachment and/or cataract. I don't even talk about the risk of an infection, for me that is of less relevance and not a reason not to undergo treatment. As long as neovascularization is not proven to be the cause of the bleeding in my eye, I really see no reason to take anti-VEGF injections, unless someone can convince me otherwise.
To my opinion the cause of the bleeding is still the dexamethasone pills I took for 4 weeks. Chronologically it fits and drugs like these are known to weaken veins and cause hemorrhages. I just got unlucky to have one in my eye. On the other hand, I already experienced some trouble with my left eye for quite a while. Was it really a neuritis? Maybe not, even my neurologist now doubts his diagnosis. So maybe I had this coming anyway, corticosteroids or not. I don't know. I do know that I for sure need some answers to be able to make my decision.
Therefore, does anyone know (perhaps from experience) if:
- my eyes being highly myopic is the only reasonable cause for the retinal bleeding to occur? Even though they do not represent staphylomas?
- dexamethasone, prednisone or any corticosteroid alike is known to cause retinal bleeding?
- another cause (e.g. artery occlusion) must be considered to explain the retinal bleeding and slight pressure/pain behind my eye?
- a retinal bleeding can cause pain? I still do experience some vague pain behind my eye.
- neovascularisation can be missed on a FAG?
- there will be any permanent damage to the photoreceptors (or otherwise loss of visual function) due to the retinal hemorrhage? What can be done to minimize the damage? Supplements? Vitamins?
- a beta-blocker will reduce the risk for a retinal bleeding to recur?
- anti-VEGF is effective to treat MD without neovascularization?
- anti-VEGF instantly closes leaking bloodvessels on the retina?
- anti-VEGF aids in resorbtion of retinal hemorrhages?
- anti-VEGF aids in complete recovery, without scarring, of Fuchs spots?
- eye injections may cause retinal hemorrhages?
I hope that the second bleeding will recover as well as the first. I still highly suspect the prednisone as the original cause of the bleeding and not neovascularization. So I try to stay calm, avoid physical activity and I check my left eye several times on a day to see if there is any change. I hope there is someone among you that can point out whatever relevant information I missed here and that I definately should consider. That would help me for sure to make a wise decision.
Thanks a lot.