IPL at Univ of MI - Ann Arbor Kellogg Eye Center

[Guest]

Last reading was 18. Thursday i see the local doctor. Will get another.

Ive been at 17-18. No change. For years.

My local doctor suggested stopping steroids, getting punctul plugs and giving up looking to save my glands. Just try to go without oil and sclerals from here on out.

Obviously im not ready for that quite yet.

The guy at northwestern, my third doc, just wanted to toss me into sclerals. I think if you get a diagnosis you can spin things around. Without that, you’re barely managing the problem.

[ebi1368]

My local doctor suggested stopping steroids, getting punctul plugs and giving up looking to save my glands.

Is plug bad for Gland? How does it affect it?

[Rebecca Petris]

Good news: I went to Dallas for the Dr G laserfit sclerals and they are amaxing. I wore them 10+ hours today. Great day.

Super. So glad to hear this.

But even with zero oil comfortable all day.

I think this is a really important thing for everybody to take note of. Something I've blogged about from time to time is... I think the medical world has kind of encouraged us to obsess about our MGs. But the fact is, what's our goal? To have healthy glands, or to be comfortable and functional? Keep in mind there's a ton of people out there with diseased or even mostly atrophied MGs that are not even symptomatic. The thing that makes us here different is the symptoms. It's not that we want to ignore underlying disease, but I think that letting it be acceptable to have symptom resolution as the goal is also important.

[Guest]

Let me ask you, can you stop the steroids for a while but wear the sclerals til you see Jain? That way you’re not in pain but you can take a break before you get back on. Just a thought..what’s better, let them clog up but protect the eye with a lens and no steroids. Or take steroids and intermittently use sclerals. Just thought of this because it wasn’t an option. Do you think you could use the lotemax less and still keep the MGs functioning while using sclerals for pain management?

[edmunder]

Super. So glad to hear this.



I think this is a really important thing for everybody to take note of. Something I've blogged about from time to time is... I think the medical world has kind of encouraged us to obsess about our MGs. But the fact is, what's our goal? To have healthy glands, or to be comfortable and functional? Keep in mind there's a ton of people out there with diseased or even mostly atrophied MGs that are not even symptomatic. The thing that makes us here different is the symptoms. It's not that we want to ignore underlying disease, but I think that letting it be acceptable to have symptom resolution as the goal is also important.

My main worry is that over time, without oil, my eyes are likely to become damaged. I cant wear the sclerals every waking hour.

Honestly it usually takes me a little while after I get up. Breakfast, hot compress, medication drops like restasis. Then put them in.

Im trying to think long term. Yeah it might be ok for a few weeks or maybe months. Im just terrified if I let the glands die and then I find out I needed them, would be a bad spot.

I have seen people in the big fat scleral group who dont have any glands in one eye or the other. The ones I saw were looking for more comfortable lenses, or has complaints about the comfort in that eye.

There is a guy i chat with from the group whose doctor recommended he do all 4 punctul plugs, get sclerals , etc. He did that with succcess for 4-5 years but now has very intense pain even with sclerals. He has two young children and a wife who depend on his income so we dont get into long talks but he sends a message or two every couple weeks.

Just seems like a bad idea to give up working towards working glands.

There certainly is part of me that wants to plug all 4, travel with the money i have saved and worry about any terrible future outcome later on, if or when.

[edmunder]

Let me ask you, can you stop the steroids for a while but wear the sclerals til you see Jain? That way you’re not in pain but you can take a break before you get back on. Just a thought..what’s better, let them clog up but protect the eye with a lens and no steroids. Or take steroids and intermittently use sclerals. Just thought of this because it wasn’t an option. Do you think you could use the lotemax less and still keep the MGs functioning while using sclerals for pain management?

So far any stops longer than a few days cause total stop of oil.

Im thinking about what is best. So hard to say.

[Guest]

So far any stops longer than a few days cause total stop of oil.

Im thinking about what is best. So hard to say.

Use the minimum amount of lotemax humanly possible to keep the glands flowing so they don’t atrophy. Supplement with sclerals to prevent pain. Seems like the most logical choice right? Which mean lotemax every 3 days correct? When you hit day 4 it stops being effective?

[edmunder]

But without objective data, hard to treat effectively/economically & monitor the progress.

To find a doctor who can perform all necessary tests correctly and
is able to interpret restuls/data is so hard to find.

Erosion is very painful/terrible - be careful and do the night protection.

Hope you will find more relief soon.

MGD1701 I found more data from a different local doctor. I thought you might have found it interesting.

I did osmolarity and inflamadry.

Osmolarity right eye 295, left eye 296.

Inflamadry weak positive. The pink line was barely noticeable.

Doctor said my eye was incredibly foamy so there is still a massive bacteria problem. Suggested i try avenova 3 times a day insteas of occusoft hypochrol. She found a way for me to get it so its not so expensive.

Doctor also gave me a prescription for lotemax gel and 4 refills.

Her idea is: my eyes look good. I have meibomian gland loss but its just shoterning of glands. No total losses.

Osmolarity is good. Very little inflammation. But lots of bacteria so i need to find a way to kill it. Use avenova 3-4 times per day. Try to kill the bacteria. Use lotemax to keep the glands open and working. Continue IPL.

EDIT ADD —- Doctor also wanted me to stop restasis and xiidra to see what happens. I will try that. Ive been on restasis for 4 months.


I will go see Jain as well.

[farmgirl]

I would continue with the IPL, I did 4 and it has helped but I still don't think my oils are thin enough yet not to clog again. I am going to do 2 more soon as i believe it to have been very worthwhile. It can take some time to kick start the process. I assume you take a quality oil like PRK, not just your run of the mill omegas, and are you drinking lots of water. I know that if I get slack my eyes get worse.

Regarding steroids there are non preserved steroids and I would not use preserved type, actually I couldn't because my reaction to BAK is so immediate and severe. Try Bausch and Lomb minims. There is enough in each vial for a couple of days even though it says to throw it out after one use.

Have you tried Xiidra yet for inflammation? I started it recently and am having good results, much better than with Restasis....stay strong

[Guest]

MGD1701 I found more data from a different local doctor. I thought you might have found it interesting.

I did osmolarity and inflamadry.

Osmolarity right eye 295, left eye 296.

Inflamadry weak positive. The pink line was barely noticeable.

Doctor said my eye was incredibly foamy so there is still a massive bacteria problem. Suggested i try avenova 3 times a day insteas of occusoft hypochrol. She found a way for me to get it so its not so expensive.

Doctor also gave me a prescription for lotemax gel and 4 refills.

Her idea is: my eyes look good. I have meibomian gland loss but its just shoterning of glands. No total losses.

Osmolarity is good. Very little inflammation. But lots of bacteria so i need to find a way to kill it. Use avenova 3-4 times per day. Try to kill the bacteria. Use lotemax to keep the glands open and working. Continue IPL.

EDIT ADD —- Doctor also wanted me to stop restasis and xiidra to see what happens. I will try that. Ive been on restasis for 4 months.


I will go see Jain as well.

What’s odd is this...she saw very little inflammation, inflammadry weak positive. Then the next statement, steroids are the only thing keeping the glands open. That’s odd. Makes me wonder what’s going on here. Maybe MMP9 isn’t your biggest cause of inflammation. Osmolarity is normal so I’m assuming the lacrimal gland isn’t too stressed. It’s clearly eyelid related. What’s the cause though? I wonder if it could be fhat lax upper lid. You made a comment a long time ago your lower lid is super tight and the upper is loose. Am I remembering that correctly?

[Milo007]

MGD1701 I found more data from a different local doctor. I thought you might have found it interesting.

I did osmolarity and inflamadry.

Osmolarity right eye 295, left eye 296.

Inflamadry weak positive. The pink line was barely noticeable.

Doctor said my eye was incredibly foamy so there is still a massive bacteria problem. Suggested i try avenova 3 times a day insteas of occusoft hypochrol. She found a way for me to get it so its not so expensive.

Doctor also gave me a prescription for lotemax gel and 4 refills.

Her idea is: my eyes look good. I have meibomian gland loss but its just shoterning of glands. No total losses.

Osmolarity is good. Very little inflammation. But lots of bacteria so i need to find a way to kill it. Use avenova 3-4 times per day. Try to kill the bacteria. Use lotemax to keep the glands open and working. Continue IPL.

EDIT ADD —- Doctor also wanted me to stop restasis and xiidra to see what happens. I will try that. Ive been on restasis for 4 months.


I will go see Jain as well.

edmunder

You are not addressing the cause of inflammation by using steroids. Steroids are doing a palliative job.

The little theory behind saponification of lipids is bacterial conversion of long chain lipids into highly irritating free fatty acids and simultaneous release of exotoxins that trigger a chain reaction of inflammatory mediators which further cause inflammation and affect the meibocytes to synthesize altered composition of lipids that have abnormal freezing and melting points unlike normal meibum (19-40°C).

Using steroids help in your case because they halt the development of inflammatory mediators temporarily as long as they are being administered and your meibocytes get some relief from inflammation to partially get back to normal production of the correct composition of lipids even though the conversion of those lipids into free fatty acids continue in the background by bacterial colonies. So while on steroids you do get "better quality" of flowing lipids but "some" solidification due to bacterial conversion that isn't too evident at times.

But that's not addressing the root cause of your problem which is bacterial overgrowth that continues to be there despite steroid use. Steroids are only providing a temporarily bail out at the cost of an even better playing ground for the bacteria due to decreased immune response locally. So in the long run it's making things worse if you are counting only on steroids. When I was on steroids for months it only got worse when I needed more and more instillations of daily steroids to get relief but that back fired within hours. Azithromycin and doxycycline brought me out of the sink hole.

My advice would be to switch back to topical azithromycin and another potent combination of broad spectrum topical antibiotic such as chloramphenicol and polymyxin B as was advised by my doctor after a one month application of azithromycin. And you should continue this with oral doxycycline and topical steroids as usual.

The motto of your treatment should be aggressive control of bacterial overgrowth and simultaneous addressal of inflammation to break through the cycle of "eternity".

Lid hygiene is perhaps more important for you than anything else. Use of Avenova and a tea tree oil based eyelid cleanser could be very beneficial. You can also try rubbing pure TTO on closed eyelids and eyelash margins at night. This will cover the potential threat of demodex as well. Remember demodex is a vector for staphylococcus aureus and they work in partnership.

I would also suggest you to kick start your treatment with an oral antibiotic that works specifically well for staphylococcus strains of bacteria.

You have perhaps tried too many things "together" in the past but they may have been lacking cohesiveness. You must base your treatment upon careful observations, analysis and a definite diagnosis even if that might be hypothetical. More importantly you must wait to see the response and results of a particular approach before trying out too many other things altogether. This makes it difficult to distinguish among what's working and what's not and based upon that experience what's the cause of the problem in your case and what's not.

Hope this helps.

[Meibum Ian]

Milo007 amazing post! I'll be re reading that a couple of times as some may apply to me. Please continue to share your knowledge where possible!

[Milo007]

Milo007 amazing post! I'll be re reading that a couple of times as some may apply to me. Please continue to share your knowledge where possible!

Glad to help in whatever way I can!

[hopeful_hiker]

Milo007 Interesting read. Thanks for sharing. Where did you get the information from? I've glanced through the TFOW DEWS II report but did not find description of this mechanism. I am curious to learn more. Did you read it in the Workshop on MDG report? Excerpt below:

"At present, obstructive MGD is thought to be caused by hyperkeratinization of the excretory duct and orifice, dependent on several endogenous and exogenous factors as explained earlier. Secreted meibomian lipids can be altered by bacterial enzymes (e.g., lipases and esterases), which are produced by commensal bacteria.^41,353 The bacteria are located on the lid margin⁴² but are also cultivated from freshly expressed meibum³⁵³ in normal subjects and in patients with blepharitis.⁴² These bacterial enzymes lead to the release of lipid breakdown products, such as free fatty acids, that cause irritation of the epithelia and stimulate more keratinization, as is thought to be the case on the lid margin⁴¹ and has been shown for the skin.³⁸⁶ Altered lipid composition may also increase the melting point, leading to a lipid of high viscosity that mixes with desquamated epithelial cells and causes obstructive MGD.

On the other hand, it is possible that changes in the lipid profile, such as those in hormonal disturbances,^223,257,259 also occur because of alterations in lipid synthesis within acinar epithelial cells of the meibomian gland. The extent to which such changes contribute to meibomian gland obstruction remains to be determined."

Source: Knop et al. (2011)

"These findings do not mean that human meibomian glands cannot become inflamed or infected. A single meibomian gland, for instance, may develop a chalazion (i.e. inflammation associated with a blocked gland), that may become secondarily infected. Further, LPS can induce leukotriene B4 secretion from human meibomian gland epithelial cells [60], and isotretinoin can induce the expression of some inflammatory mediators in these cells [45]. However, neither inflammation nor infection is a characteristic of obstructive MGD, which affects multiple glands [36,506]."
Source: TFOS DEWS II report (2018)

So to summarize in layman's terms: bacteria is not in the glands, it is on the lid margin (and somehow in the oil). Their activity leads to the meibum hardening once it is close to the margin. Everyone has bacteria but MDG folks may have more hence the obstruction problem. Is that right?

Some new interesting stuff:

"Both aerobic and anaerobic bacteria can be isolated from the ocular surface of healthy subjects. Patients with MGD demonstrate significantly higher culture positivity and more complex bacterial profiles than the controls. Bacterial related cytotoxicity and/or inflammation may contribute to the pathological process of MGD."
Source: Zhang et al. (2017)

[Milo007]

Milo007 Interesting read. Thanks for sharing. Where did you get the information from? I've glanced through the TFOW DEWS II report but did not find description of this mechanism. I am curious to learn more. Did you read it in the Workshop on MDG report? Excerpt below:

"At present, obstructive MGD is thought to be caused by hyperkeratinization of the excretory duct and orifice, dependent on several endogenous and exogenous factors as explained earlier. Secreted meibomian lipids can be altered by bacterial enzymes (e.g., lipases and esterases), which are produced by commensal bacteria.^41,353 The bacteria are located on the lid margin⁴² but are also cultivated from freshly expressed meibum³⁵³ in normal subjects and in patients with blepharitis.⁴² These bacterial enzymes lead to the release of lipid breakdown products, such as free fatty acids, that cause irritation of the epithelia and stimulate more keratinization, as is thought to be the case on the lid margin⁴¹ and has been shown for the skin.³⁸⁶ Altered lipid composition may also increase the melting point, leading to a lipid of high viscosity that mixes with desquamated epithelial cells and causes obstructive MGD.

On the other hand, it is possible that changes in the lipid profile, such as those in hormonal disturbances,^223,257,259 also occur because of alterations in lipid synthesis within acinar epithelial cells of the meibomian gland. The extent to which such changes contribute to meibomian gland obstruction remains to be determined."

Source: Knop et al. (2011)

"These findings do not mean that human meibomian glands cannot become inflamed or infected. A single meibomian gland, for instance, may develop a chalazion (i.e. inflammation associated with a blocked gland), that may become secondarily infected. Further, LPS can induce leukotriene B4 secretion from human meibomian gland epithelial cells [60], and isotretinoin can induce the expression of some inflammatory mediators in these cells [45]. However, neither inflammation nor infection is a characteristic of obstructive MGD, which affects multiple glands [36,506]."
Source: TFOS DEWS II report (2018)

So to summarize in layman's terms: bacteria is not in the glands, it is on the lid margin (and somehow in the oil). Their activity leads to the meibum hardening once it is close to the margin. Everyone has bacteria but MDG folks may have more hence the obstruction problem. Is that right?

Some new interesting stuff:

"Both aerobic and anaerobic bacteria can be isolated from the ocular surface of healthy subjects. Patients with MGD demonstrate significantly higher culture positivity and more complex bacterial profiles than the controls. Bacterial related cytotoxicity and/or inflammation may contribute to the pathological process of MGD."
Source: Zhang et al. (2017)

I have been browsing through so many journals and case studies in the internet. Can't remember exactly which website I got the info from but it was probably from an article in "optometrytimes.com" and similar info was independently published in one of the research gate papers if I remember correctly. The problem is I don't keep a bookmark of the websites I go through in an indexed manner. So far I have bookmarked around 200+ weblinks in my email (I share the link of the website I go through via email to my MAIL account.... LOL). I will copy paste the exact content if I come across it again.

But it was not from the TFOS DEWS reports as I never went through TFOS DEWS reports. I do Google searches with random keywords like "meibomian gland capping", "lid margin hyperkeratinization", "low meibum volume" etc. in order to find related content and go through independent case studies and research findings from various sources. You know what I mean. You have to put in the relevant combination of keywords to find new content. TFOS DEWS might be the single most comprehensive source of information but it doesn't include all independent research findings happening across the globe or even new findings that has taken place after the publication of TFOS DEWS II report. So I rely on more dynamic sources of information.


Your post mentions of lid margin hyperkeratinization leading to obstructive MGD which is interestingly the exact problem I am facing. I can see tiny little cappings on my gland openings that look like lipid filled globules protruding out. I initially thought of them as hardened meibum but later realized they are fluid filled "sacs" as I call them. And I get them mostly on my lower lid margins. I do a lid margin debridement with a dry q-tip to remove them or puncture the bigger ones with a sterile needle. But they reform as quickly as in 7-8 hours. Another thing I have noticed is more vigorous rubbing of my lid margin with the dry q-tip will result in more cappings the next day and even bigger ones with bumps on my lid margins. So removing the epithelial covering by abrasion will only invite more epithelial formation and gland capping. I don't repeat the procedure too often as repeated injury to lid margin can result in scar tissue formation which is what I am afraid of most.


You seem not to carefully read the content you have published. It says bacteria is present in the the lid margin but is also cultivated in freshly expressed meibum in normal patients and patients with blepharitis. It's a misconception that bacteria is not present in the glands normally. There are thousands of strains of bacteria and other microorganisms present inside the glands in normal patients (even in sebaceous glands). You are doubting bacterial presence whereas even demodex mites which are much more bigger in size are present inside the glands in normal patients. It's a symbiotic balance of microorganisms that exist in our tissues. Then why do some people get MGD if everyone has bacteria in their glands? Well it's not the presence of bacteria that's the critical factor but their "overgrowth" and "over population" as a result of some "abnormal" conditions that help them to multiply in such large colonies and manifest their presence creating "abnormal" biochemical changes after sometime. More precisely, in patients with MGD the bacteria cause problems because they have the ideal conditions for overgrowth which is stagnant or very slowly moving meibum due to low blink rate initially. So they can facilitate the conversion of normal lipids into free fatty acids. The conversion won't be possible in normal patients because normal patients blink frequently and the meibum is constantly flowing out so there's not enough time for stagnation and the solidification to take place. Chronic stagnation in patients with low blink rate provides the bacteria an opportunity to facilitate the conversion which then kick starts a cascade of inflammatory reactions that cause hyperkeratinization and create a blockage in the the form of "cappings" as your post mentions. Then once the cappings block the glands externally it provides even a better environment for the bacteria (anaerobic) to breed and release exotoxins that cause even more inflammation and hardening of the lipids. The patient realizes this when 70% of the glands are already blocked and it is already late. You must be knowing inflammatory mediators damage the meibocytes inside the acini and this results in loss of the meibocytes ability to secrete the correct composition of lipids. So apart from bacterial conversion of lipids to free fatty acids the inflammation inside the glands also act as a secondary factor to damage the meibocytes which could be even permanent. This is why you notice some glands don't secrete too much oil even if they have more number of acini visible through a lipiscan. That's because the meibocytes have been partially or fully damaged by chronic inflammation.

Your assumption is totally wrong when you assume that meibum hardening takes place once it reaches the lid margin. Meibum hardening takes place inside the glands and that's why you need warm compresses to melt it internally. Watch the animation of the lipiflow procedure to get an idea of what I have said.

To summarize low blink rate is initially the key reason of all problems in MGD development followed by bacterial conversion of lipids that are irritating to the epithelial cells of the lid margin and the duct surfaces which is combined with simultaneous release of bacterial exotoxins that invites more inflammatory mediators. The inflammatory mediators act on the epithelial lining of the lid margins to create hyperkeratinization and blockages in the form of cappings. This provides ideal environment for the bacteria to breed and cause more conversion of stagnant meibum with subsequent hardening and inter glandular inflammation. Left untreated meibomian glands die out of "disuse atrophy" and inter glandular inflammation which leads to scarring internally. Only way to avoid this is to act quickly and remove the blockage followed by clearance of stagnant meibum followed by control of bacteria and inflammation simultaneously to break out of the endless cycle of inflammation and blockage.