This live webinar will comprehensively cover various diagnostics in dry eye from simple techniques like slit lamp examination and ocular surface staining to advanced technologies like meibography and tear film osmolarity. It will also elaborate on the stepwise approach to the management of dry eye based on TFOS DEWS II & ASCRS Cornea committee recommendations, as well as simplify the same for day-to-day practice for centers with limited resources. The webinar will also touch upon the recent management options like heated meibum expression and intense pulsed light treatments.
Lecturer: Dr. Madhu Uddaraju, Director, Srikiran Institute of Ophthalmology, Head of Cornea & Refractive Surgery Services, Kakinada, Andhra Pradesh, India
So I’m Dr. Madhu, and I’m from Srikiran Institute of Ophthalmology India. I have no financial disclosures in the talk or in any of the products that I’m going to mention in the presentation. The scope of this talk would start with the pre-test to test the existing knowledge you have in the field. Then I’ll briefly touch upon the definition and classification, we’ll see the pathophysiology, and I’ll simplify the whole dry eye into six simple tasks for you, so that you can easily diagnose and manage this condition. Finally, I’ll touch upon on a deeper way in Meibomian Gland Disease, as most of the participants have asked me to stress upon this disease more, which is part of this dry eye disease. And finally, we’ll end it with the post-test and answer a few questions that the registered delegates have already put in before we go in for the live delegates.
So these are the pre-test questions I have for you. So the first question is, which one of the following is included in the definition of dry eye? ASCRS TFOS DEWS II. It is a multifactorial disease, the patient should have symptoms, hyperosmolarity is part of this definition, or all of the above. Thank you, I’ll go to the next question.
Which one of the following does not cause evaporative kind of dry eye? A Meibomian Gland Disease, B lacrimal gland dysfunction, C improper blinking, D contact lens intolerance. And your time starts now. Thank you.
The third question is, ocular surface staining can be assessed by which of the following? A corneal staining, B lid margin staining, C conjunctival staining, D all of the above. And your time starts now. Thank you for the response.
Which is not a modifiable risk factor in dry eye? Which is not a modifiable risk factor? A contact lens wear, B Meibomian Gland Dysfunction, C computer usage, D medication, this could be ocular or systemic. And your time starts now. Thank you.
Now we’ll go to the final question. Identify the diagnostic test that is being performed in this picture. A MMP 9 detecting device, osmolarity detecting device from Tear Lab, or lipid layer thickness detecting device, both A and C. Thank you.
So that finishes my quiz. Now the answers, the same five questions, we’ll discuss after we finish our topic so that you can gain knowledge out of the coming few slides that I share with you.
So coming to the definition. Let us dissect the definition of dry eye into three steps. The first thing is dry eye is a multifactorial disease of the ocular surface. Two, it is characterized both by an unstable tear film and the patient should have some form of ocular symptoms. And finally, it can be caused by any of these: hyperosmolarity, ocular surface inflammation or damage, and neurosensory abnormalities. So it’s basically a multifactorial disease that can be caused by any of these: hyperosmolarity, ocular surface disease, or neurosensory abnormalities. And it has to have both signs and symptoms. That is the reason you need to document an unstable tear film and also see that the patient has symptoms. Only then it fits into the definition of dry eye.
So when you classify dry eye, it is etiologically-based. Like we see in this picture, this is the lacrimal gland and these are the Meibomian glands. So basically the Aqueous Deficient Dry Eye, it is a deficit in the lacrimal gland function. The tears itself are not produced or produced in a scanty way that leads to this condition called Aqueous Deficient Dry Eye Disease. Whereas in Evaporative Dry Disease, which constitutes to 80% of the cases that we see in our OPD. The problem is not with the lacrimal gland, but these are related to the Meibomian glands that you can appreciate in the lids that are there is the both upper and lower lids here. So the problem with evaporative gland is the problem is mostly related to the Meibomian glands or blink-related problems where the ocular surface is disturbed.
This is a very busy slide, where you can see the pathophysiology of dry eye. So to the left side, you can see all the lacrimal gland-related activity that is taking place and that causes this aqueous deficient dry eye. So in the outer circle here, so these are the things that can cause aqueous deficient dry eye. That can be aging, low androgens, autoimmune diseases, lacrimal obstruction, systemic drugs, but it can be a reflex block because of a surgery, contact lens wear, or anesthesia. Whereas towards your right, whatever you see in the outer circle is related to the Meibomian Gland Disease. Where the cause could be anterior blepharitis, there is an unstable tear film or lipid layer, vitamin deficiency, ocular allergy, preservatives that we use in drops, and all these things come into the evaporative phase and the left side is the low flow. You just cannot separate these two things and look at them in the separate way. In a way at the center, they intermingle with each other and they cause this vicious cycle of one causing the effect on other, and in that way you cannot purely differentiate between these two conditions, but in a way it is a combination of both these things.
Look at this slide very carefully. This slide will be the entire presentation that I’m going to speak about. For your convenience, this is the slide that is taken from the TFOS DEWS II recommendation. So if you see carefully here, I have divided this slide into six part. The first part is the triaging question. The second part is the risk factor analysis. The third part is the symptomology. The fourth part is the tests that we see for looking at the homeostasis of the tear film and ocular surface. The fifth part is differentiating it from evaporative or aqueous deficient. And the six part, finally, is the management part. So I’ll dissect each one of these part individually for you to make it more simpler.
Just to repeat it for the sake of the audience. So the six tasks that we are going to do in this exercise are, first, triaging questions. This will help us to come from that, we’re looking at dry eye symptoms and not any other eye condition that mimics a dry eye. Second, after you come from that symptoms that are because of dry eye, you go ahead and see what are the risk factors involved in it and know whether they’re modifiable or non-modifiable. Then the third one is this screening questionnaire. Here you try to question the patient for the symptoms they are facing. Depending upon this code and the symptoms, you know the severity of symptoms that the patients are facing. Sorry. Fourth one, we try to do tests like the tear breakup time, that can be invasive or non-invasive, osmolarity, and surface staining. The best part of this test is, you need not do all the tests. The simple thing that all of us have access to is staining. So even if you don’t have an access to non-invasive tear breakup time or osmolarity, nothing to worry. You can still go ahead and do a simple staining, ocular surface staining, to get the tear film and homeostasis marker and get this fourth step done. The fifth thing is, again, some type of classification where you want to know this is because of aqueous deficient or evaporative thing. Where we do some more tests and these tests also you need not depend on high-end equipment. I’ll explain that in detail in the coming slides. And the final step is once you know which kind of dry eye it is, you try to treat it accordingly.
Task one, these are several triaging questions that we have to ask. How severe is the eye discomfort? Is there any associated dryness of the mouth that indicated to Sjogren;s? Are the symptoms continuous in nature or is there a triggering event, was there trauma? Is the patient a contact lens user? Is the vision affected and does it clear with blinking? More toward computer usage syndrome. Are the symptoms worse in one eye than the other? Because usually dry eye is symmetrical or more or less bilateral. So when you see something in one eye, it’s highly more likely that you’re looking at a different condition than dry eye. And the same time to do the eyes itch, are there any swollen, crusty or any other discharge? Are we looking at any lid problems that we have to face because of which this condition has happened? And finally you have to take into account the general health condition of the patient and know are there any other cardiovascular diseases, rheumatoid factors, and all these things. Recent transplants, are all these things when you take into consideration, you’re just finish the first step.
The second step, as I’ve told you, we’ve divided it into two. The modifiable and non-modifiable risk factors. So if you see non-modifiable, aging, as you’re growing age, the prevalence of dry eye inscreases and it is more in female sex when compared to male. And Asians are more prone to dry eye. And in the same way, Meibomian Gland Dysfunction is also, interestingly, it is not modifiable, though we have many treatments for it. It still comes under the non-modifiable part. Next, the systemic conditions like connective tissue disease, graft versus host disease, Sjogren’s Syndrome, rheumatoid arthritis, all these things have non-modifiable. You only treat it symptomatically and try to give relief to the patient, but these are the things that you cannot modify.
Luckily, we have some modifiable things and the risk factors that can be taken care of like. Suppose the patient is having problem with the hormones, like androgen deficiency where you can do an estrogen replacement. Contact lens wear, you can switch from contact lens to glasses, smoking can be stopped, pollution also, you can take sufficient care. Low humidity places, typical sick building syndromes that all our cloth wear companies, where the air is being recirculated in the same building again and again, there is increase in dryness, there is less humidity, this causes dry eye. And in the same, a lot of the drugs that we use, both systemically or topically, most of the antiglaucoma medications, topical anesthetics, or preservatives that are there in the drops. And systemically you can see most of the antipsychotic drugs, anxiolytics, antihistemics, all these things lead to dry eye. And also finally, iatrogenically, it can be caused by surgery that we do, it could be a refractive surgery or a cataract surgery. Or any ocular surface surgery that you’re going to do that will disturb the ocular homeostasis to some extent, leading to dry eye. And it will slowly heal over time with essential treatment.
We have completed task two, let us go to task three. Task three is, again, simple. You don’t invest anything in this. These questionnaires are readily available in the net. The simple questionnaire we follow at our Institute Srikiran is the DEQ. In this question, these are questions about discomfort. If the score is about five or six, we can form that the patient is having symptomatic dry eye. If you want to have a more comprehensive questionnaire, the OSDI questionnaire is better. OSDI questionnaire we only tend to use it when we do research work and we are planning for publication. Even if you don’t have time for any of this questionnaire, it’s not a problem. If the patient is symptomatic, most of the times the non-specific complaints the patient tells. If you go back to the slit lamp, examine properly again, 80% of the time the cause will be dry eye. So that is the reason and the patient is symptomatic, just don’t brush it away. Please go back and see and try to look at the lids, the ocular surface, tear film break, everything in a proper way, so that you give importance to his symptoms and then treat the patient accordingly.
Task four, as I have told you, this is the important test of the basic test we have to perform to confirm whether there is a break in the tear film in homeostasis. As you have seen here, the first box is the non-invasive tear breakup time, which is the preferred one. Because all the recent studies tell that. Fluorescein is not as reliable as the non-invasive tearbreak of time. And in the same way, and again, non-invasive, automotive non-invasive TBUT has a superior discriminative ability in detecting dry eye, according to a study by Mooi JK in “JAMA Ophthalmology.”
So if you see here, it is not a compulsion that you do all the three tests. In the slide, I’m confining myself only to the tear breakup time. If at all you have to do a fluorescein thing, please do the fluorescein test in the last. This is the order in which you have to do the tests. If you don’t have non-invasive tear breakup, forget about it. If you don’t have access to osmolarity, forget about it. The next thing you have to do is, do the conjunctival staining. Once you finish the conjunctival staining, look at the cornea, conjunctiva, and lid margin, and then finally look at the invasive tear breakup with fluorescein. So if you do this singular test, that is good enough for you to know whether the patient has a break in the homeostasis. Now let us look at the automative non-invasive TBUT that we do with the Scheimpflug imaging we have in our institute. This is the Sirius machine, which automatically takes the reading. If you see here, these are all the orange and yellow spots of the dry spots that are happening. So I’ll just play it again for you. So if you see here, when the tear film after the lid is closed, it is green. And once these parts occur, you can see that spots are occurring in the area. And here in the picture down you know exactly in which time those spots have occurred. So the first spot has occurred in the peripheral at 2.9 seconds, followed by 3.4, 4, 6.3, and so on.
This is, again, a test that is homeostasis marker, I don’t think most of you will have access to it, because it’s very expensive. The machine is not only expensive, but the consumables that we use are also expensive in this. So it’s a point of care test. So what happens is here it takes 15 nanoliters of tear from the lower meniscus and we use a single-use test card. The technology is called it’s lab-on-chip technology. That is the reason it is so expensive. And it measures the impedance of this tear films and it gives you a value. So if the osmolarity value is anywhere more than 308, you have to consider it as a dry eye. Or if the inter-eye difference is more than 8, then you also have to consider it as a dry eye.
Now this is the most practical thing that all of us can do. So just a simple conjunctiva stain or corneal staining with fluorescein and sitting under a slit lamp with cobalt flow build up light, you can see this beautiful spots that are seen in the cornea. So any surface that is healthy will not take up stain. That is a simple thing. So when the cornea has a problem, so when you see more than five corneal spots, because of fluorescein, or with lissamine green when you stain the conjunctiva and lid margins, when you see than nine conjunctival spots, and in the lid margin when the lengthwise more than two millimeters is involved and widthwise 25% is involved, these are all signs of dry eye. Just give importance to this treatment. Fluorescein and lissamine green staining in your clinic. So more than five corneal spots of fluorescein, conjunctival spots with lissamine that are more than nine. And in the lid margin, there is more than two mm in length and 25% in width.
The next is going to subclassify whether it is an aqueous deficient or evaporative dry eye. So first we’ll finish up with the aqueous deficient which is not much common. So here, what you have to do is, you have to look at the tear meniscus height, because that is where you know the tear volume. So if you see the tear meniscus height, you can do it in a regular slit lamp that has a good graticule, or you either do it in an OCT, or in most of the tear film devices where we’re able to see the tear meniscus height. So it is the height of the tear meniscus from the lower lid. The tear meniscus height is around .2 millimeters. That is more than 200 microns, it is less less ml, and as it comes down and becomes less than .1 or less than 100 microns, the more severe this disease becomes. There are the cases in which we have to retain the liquid that is already there in the eye by placing some plugs or doing a punctal cautery.
Now let us go to the more common kind of subtype that is the evaporative dry eye and let us go into detail. The Meibomian gland, examination, meibography, blink mechanism and the lipid layer that involved here. So if you see here, Meibomian gland dysfunction is again defined by the International Workshop of MGD, as a chronic, diffuse abnormality of the Meibomian glands, characterized by two things. One, there is a terminal duct obstruction and/or qualitative and quantitative changes in the tears that are being secreted. It can be either of these two or both of them. So the Meibomian Gland Disease, if you see in this vicious circle that happened here. It can be inflammation or blockage in the gland, leading to proliferation of bacteria that releases lipases and esterases, increasing the melting temperature of the meibum, leading to dry eye.
So if you see, the upper lid here has 25 to 40 Meibomian glands that you can appreciate nicely. And the length is around 5.5 millimeters. Whereas in the lower lid, the glands are comparatively less than 20 to 30 and the length is also less, there is only two mm. So this, each gland, again, if you see carefully, they have these dot like things called secretory acini, which secrete the meibum that form the lipid layer of the tears. So this is how the normal upper lid and lower lid looks, the Meibomian glands, and here you can clearly see the Meibomian gland drop open for upper lid then, lower lid.
So before we go into meibography again here a simple LLPP testing, to look at the lids and Meibomian glands can be done in a slit lamp. So look at the base of the lashes, lid position, whether the position is good or not. How is the blink? Look at the tear meniscus, conjunctiva and cornea, look for any inflammatory signs. Next, lift the upper lid, look for superior corneal lesions, any conjunctival anomalies like papulae or foreign bodies and rule out superior limbic keratitis. Pull the upper lid again to look for laxity and floppiness. And finally push the lower lid to express the meibum, see for the meibum what is the quality and quantity that you’re expressing out of it.
LLPP, again, is a very classical clinical examination that all of us can do without any fancy equipment in our routine OPDs. So LLPP should be performed for all the cases where you’re suspecting MG disease and dry eye.
Now let us go into meibography. When I tell meibography, most of you may be thinking that it’s an advanced thing where you need to invest again in a new equipment, but you’ll be surprised to know that most of your existing equipment will be helpful for you to highlight these Meibomian glands. In fact, you’re not having that also you can do a simple do-it-yourself thing that I’ll share it. Next, I’ll catch up the dedicated/advanced things and also for economic interest, I’ll touch up on the confocal microscope.
If you see here, with regular white light illumination, you only see the blood vessels that are here. So once that is illuminated with infrared, this is how beautifully you can see the Meibomian glands with the slit lamp. This is already, this kind of infrared illumination would be there in most of the autorefs. So if you see here, thise are the pictures taken with autoref. Again, these are the pictures taken with NCT, however the central part is dark in NCT. Then IOL Master 500, again, you have access to it, you can see these things beautifully. Any fundus camera with infrared camera, again, you can see these things. And if you have access to specular microscopy also, you can highlight this too.
If you have any of this equipment already in your clinic, try to invert the lids and just see through the screen. Most of the times you’ll be able, however, you’ll not be able to document it, but you’ll be able to appreciate any drop out straight away.
Suppose you don’t have access to any of these, even then it is fine. You can just buy an infrared light source that is hardly $100 online. The specification should be that it should be an 850 nanometer light source. And the camera should not have an infrared filter. So most of the Samsung cameras, or slit lamps with automating systems will not have this IR filter. So once you shine this light, this is how you can get those images beautifully taken with a simple torch light illumination and a camera with infrared lighting without a filter.
So coming to the standard meibographers, as I have told you, we are using this Sirius meibography. Where we use the infrared illumination here to see the thing. But there is something called more advanced, like the lipiscan. Where it highlights and crosses even transillumination to have a better look at the, also as an individual unit. So next model is auto detection and 3D modeling that is available from SBM IDRA, where you can see this image that it has actually 3D modelled the entire Meibomian glands that are there in this area. It auto detects them and then creates a 3D model for you to know exactly where the cell loss is there.
And whatever meibography you use, you can use this Meiboscale to see the degree of loss depending on the area of drop out, it becomes degree zero to degree four, starting from 0, 25, 25 to 50, 50 to 75, and more than 75. And it is different both for lower lid and upper lid, as we have seen that both of them have different glands and different lengths.
This is just for economic purposes. If you want to go ahead and histologically classify the type of dry eye. This is how a normal Meibomian glands look like, the lumens are very clear and the walls are nice. Grade one, lumen obstruction with minimal inflammation is seen. You can see also the oval shape here and some inflammation with cells. The grade two, there is intraepithelial inflammation and there is loss of the complete lumen. Finally, there is fibrosis and epithelial destruction. So these are the in vivo confocal microscopy images of the lids.
Next, coming to the important part, the lipid layer thickness of non-invasive TBUT, non-invasive TBUT we have already covered previously. So this is more regarding the lipid layer thickness. There is an equipment called LipiView, again, which sees this lipid layer thickness specifically. And anything that is above 100 nanometers is considered to be normal. It gives a report like this, where you can see the average LLT is below 100 and there is also a dropout. So you can correlate both LLT and MGD and you can come to a comprehensive conclusion with help of this equipment. Here if you see this eyelids here, these are the areas in which the blink has occurred. And when the blink has occurred, still after a blink, the lipid layer thickness did not go up 100, which is normal. It still continued to be below 50, which is very far below normal. So you can also correlate between the blink and the lipid layer thickness here in this picture.
The final task here is to treat these diseases depending whether it is aqueous deficient or evaporative diseases. The first line of treatment is education, environmental modification, lubricants, lid hygiene, and warm compresses. The second line is preservative-free lubricants, temperature-controlled massage, punctal occlusion, LipiFlow or intense pulsed light, which I’ll show you a few videos. And then you can add eye pulsed steroids, doxycycline, and cyclosporine, or punctal plugs in this stage.
And finally, then you can add autologous serum eye drops, bandaged contact lens, oral secretagogues. And now we also have mucin secretagogues like the Rebamipide from Reversed. And finally, we can go for longer steroid use, amniotic membrane graft, tarsorrhaphy, and permanent punctal occlusion. However, salivary gland transplantation that is rarely deployed. This is stepwise direction that we’ve taken this.
Coming broadly in the medical management of Meibomian Gland Disease, antibiotics play a very important role because these antibiotics, especially doxycycline, is known for its anti-MMP activity. So usually an MGD we give 100mg BID for two to three weeks, MGD is really bad, there is no harm in prolonging this treatment for one to two months. Along with this, we also give azithromycin 1% eye ointment at nighttime for two weeks. And if there is inflammation still that is persisting, you can add eye azithromycin/dexamethasone eye drops that are available BID/TID for two weeks, depending upon the severity. So it’s about the systemic and topical antibiotics that are prefered for MGD. When it comes to anti-inflammatory, we should always prefer steroids pairing drugs like cyclosporine or tacrolimus. Rarely even they’re not controlled with these drugs, you can use dexamethasone, prednisolone, or loteprednol, closely monitoring the IOP and titrating the drugs according to it.
In the western countries, they also use Lifitegrast and Interleukins that are not available in our country. Essential fatty acids is a controversial topic that DREAM study tells that it doesn’t have a role. But if you see the recent ASCRS Cornea Clinical Committee, 80% of this committee have recommended the role as an adjunctive therapy. Omega 3 fatty acids, there’s no harm in using. I still prefer to use them for most of my patients. Especially that I’m doing a refractive procedure, cataract, or a refractive surgery. We can use them for three to six months. And if the patient has an associated blepharitis or Demodex, we have to give them lid scrubs and tea tree oil.
If you see, this is simple after asking the patient to do heat compression for a few weeks, you can manually express the meibum with help of this meibum expressors that are easily available in most of the companies. You just go sectionally, one by one, and sequentially you can beautifully open up those Meibomian glands. You can apply some topical anesthesia so that the patient will not feel the pain. You can do it as an OPD procedure. You can do two lids at a time, give a break, and do the second lid again.
And this is the LipiFlow. And in this, the device is not shown here, but the advantage with this thing is, the device gives pulsations from the inner part of the lid. It actually gives pulsations like this and clears the blocks that are there in the acini glands and lets out the meibum. But if you see the pulsations, along with heat, work in a very nice way. That will help to clog out all the material that is there. If you carefully see here, that is the applicator. It goes and sits on the sclera, it doesn’t touch the cornea. It goes and sits on the sclera and its posterior surface is just on the inner side of the lower and upper lid that starts to give a pulsation.
Finally, this is again a very simple technique, that is iLux. It captures the eye lid, both from inside and outside and it raises its temperature to 42 degrees and keeps it to 40 or 50 seconds. And after that, you manually press the button to express out the meibum. This is a very handy device and it’s not very expensive. But still not available in India, but widely used in western countries. And finally we have limited experience with this intense pulsed light. That in which intense regulated pulse lights are given in the lower lid and left lateral canthal area, which stimulates the parasympathetic nerves, leading to opening of the clogged fluids. All these things they don’t work in isolation, sometimes you’ll need to combine each of these things and see which works best for the patient, along with your regular medication. You have to be more aggressive if the patient is going for a refractive surgery.
All said and done in a lighter vein, what we have learned from this MGD therapy is, in a way MGD is like your spouse, you presume to control it, but in reality the control is only transient. As all of you remember in the initial slides I have told you, MGD is still a non-modifiable risk factor. Whatever you’re going to do, is going to be there only for six months or one year. You need to repeat this treatment and just plan the next treatments accordingly.
Now let us go to the post test answers that we have finished our session now. We’ll go back to the five questions that I’ve asked you in the starting of this session.
Which one of the following is included in the definition of dry eye? Multifactorial disease, ocular symptoms, hyperosmolarity, all of the above. Thank you. That’s a 94% correct answer, so happy for that, thank you. All of the above is the right answer.
Which one of the following does not cause evaporative dry eye? MGD, lacrimal gland dysfunction, improper blinking, contact lens intolerance. Thank you. That’s a decent enough. Lacrimal gland dysfunction is the right answer. And 70% of you have answered it right.
Next, ocular surface staining can be assessed by? Corneal staining, lid margin staining, conjunctival staining, all of the above. I expect a very good answer for this, I think we have spent sufficient time on this slide. Excellent, that’s a 95% correct answer. It’s all of the above is the answer.
Next, which is not a modifiable risk factor in dry eye? Contact lens wear, MGD, computer usage, medications. Thank you. Again, it’s an 80% correct answer. As I’ve told you, Meibomian Gland Disease is not a modifiable disease, good.
Final question. Identify the diagnostic test in the picture. MMP 9 detecting device, Tear Lab osmolarity testing, lipid layer thickness detecting device, both A and C. Osmolarity is the correct answer. Right. So we’ve finished this post test now.
Thank you all for your kind attention.
I think very rarely in life you see people who believe in this philosophy that we are here to add what we can to life and not to get what we can from it. And I’m so fortunate that I have been able to meet three people who believe in this thing and have taught me all that I have learned here. One is my teacher, Dr. Venkatesh Prajna from Aravind Eye Hospital in Madurai. One is our chairman, Dr. Chandrasekhar from Srikiran Institute of Ophthalmology, Kakinda. And my father, Dr. Udry Uddaraju from Bhimavaram. And I thank my family and cornea team, especially my fellows, for helping me to put this presentation for you.
Now, without much delay, let us first answer the questions that are raised by the delegates who have registered. So they have asked me to elaborate about punctal plugs and cautery. So if you see punctal plugs and cautery, we use it in moderate dry eye conditions and there are presently three options that are available for you. One is the collagen plugs that are short-term and dissolvable. It can be used like a therapeutic trial. But the problem with these plugs is, once they start to dissolve, they go into the canal layer and it is difficult for you to remove if there’s any inflammatory or infectious condition that is involved.
The most common plugs that we use in practice are the silicone plugs. Because they are permanent plugs, they come in multiple sizes, you have better sizing options. And there’s also a probe that comes with this injection, an injector. And the advantage of it, it also has closed and open head. If you see here, it is an open head. Because sometimes we need to use drugs like cyclosporine, Rebamipide, or steroids. So these drugs they may not stay in the eye for longer time, but at the same time, when it is done, they get drained off easily and you can still use lubricants when you use these open headed silicone plugs.
Intracanalicular plugs are very rarely used in our part because actually, they’re longer lasting but they’re more associated with complications. And the advantage with them is, there’s less a foreign body sensation.
If you don’t have access to any of these plugs, not an issue at all. You have an access to cautery. A simple punctal cautery will do the job. So when you cauterize the lower punctum properly, a lot of tear film can be retained. The advantage of this is when you do it under a microscope, you are 100% sure of the closure. And you can give good result to the patient even if you don’t have access to punctal plugs.
Next, somebody asked me about the association between dry eye and vitamin D deficiency. I think it’s a very recent study published by Watts et al in IJO. If you see, vitamin D deficiency in India is somewhere between 40 to 80% and vitamin D deficiency is also associated with diabetes, CVD, and atopy, again, which is a risk factor for dry eye. And vitamin D deficiency has a very important role in estrogen biosynthesis and signaling. And especially in post-menopausal women when estrogen comes down, the dry eye becomes more evident, this can be attributed to it. I just trying to find out from my endocrinologist friends that all that we can give vitamin D supplementation orally, like vitamin D3 1000 IU capsules once daily for a month or two months. And injections, single dose of IM 50,000 as an injection. But you have to monitor the blood levels of D3 and D2 and then titrate the medications accordingly. So there is definitely a relation between vitamin D and diet that is now recently coming up, but it still is in an evolving stage.
Next is the question about diabetes. Diabetes, again, 15 to 30% of the diabetes have dry eye. After diabetic retinopathy in diabetics, the most common eye condition is dry eye with most of us undertreat. And especially this increases to 50% with age. So any individual 65 years of age is 50% chance. Every one person in two, elderly, diabetic patients is more likely to suffer from dry eye. And it has a very positive correlation with glycosylated hemoglobin and we should treat this condition judiciously. This is a simple artifactorial way in which diabetes can cause dry eye, by decreasing the density of neuronal fibers, impairment of epithelium, epithelial wound healing, increase osmolarity, development of inflammation, and dysfunction of tear film. But this leads to structural and micro-environmental changes disturbing the ocular surface. And effects of hyperglycemia can directly affect the lacrimal gland leading to dysfunction. And from that affects the aqueous deficient side and this is from the evaporative side.
Finally this is one more question most of the participants have asked me to tell about pediatric dry eye disease that we try to underestimate into as well. It has become very prominent so after this COVID situation, because most of our children are attending these classes on online platforms. So several studies, even before this pandemic, showed that dry eye disease was there in seven to 25% of the cases. The causes are similar to adults like congenital anomalies, autoimmune diseases, allergy, increased screen time that is there in today’s scenario, iatrogenic causes, and vitamin A deficiency.
How do we prevent this dry eye, was one of the questions I was asked. The main thing for prevention is patient education and telling the patient that this problem is chronic. So first he has to do certain environmental modifications to prevent dryness. To avoid direct blow air that is going into his eye, manage his screen time in a sufficient way to avoid over exposure to digital screens. And use artificial tears and omega 3 fatty acid supplements in proper way. And apart from that, keep a good lid hygiene, and make sure that the lids and ocular surface are always healthy.
Next question is dry eye in Sjogren’s syndrome. This is, again, aqueous deficient kind of dry eye in which omega 3 fatty acids have been very beneficial effort. The differentiating factor here is that the patient also has a dry mouth where the exocrine gland dysfunction is seen. Here, corticosteroids that can be used both orally and topically. Special RBP lenses can be used, cyclosporin, autologous serum, punctal plugs with cautery, filaments debridement with N-acetylcysteine drops can be used. Environmental modification and the similar management as we do in from rheumatoid arthritis and cardiovascular disease.
One more question I was asked was graft versus host disease. Ocular GVHD affects the ocular surface and mucins. So it typically follows an allogenic hematopoietic stem cell transplant and it usually happens between one month to one year postoperatively. What happens is the donor immune system from the stem cell attacks the healthy recipient cells. So if you see here, that is why there is vascularization that comes into the cornea and this lipid deposits that you can see on the cornea. So here there is a promising role of mucin secretagogues like Rebamipide 2% that can be used two times, continuously, along with all the armamentarium of drugs we have. And all the treatment protocols you can follow similarly.
One more interesting question I had was the association between dry eye and refractive errors. There is a negative correlation with hyperopia and a positive correlation with myopia. Non-invasive TBUT correlates, the tear meniscus height does not correlate. This is what we got to study again from IJO Aldawesh et al.
Dry eye and keratoconus, this is one more important question where we see there is a decreased mucin production and greater tear instability sequentially because of it. And the contact lens wear can also aggravate dry eye. So in this case scleral contact lens can give better vision and wetting of ocular surface.
There are several drugs that have asked me the relation between drugs and dry eye. All your glaucoma drugs can cause dry eye. All your anti-allergics can cause dry eye. Decongestants like naphazoline can cause dry eye, antivirals can cause dry eye, preservatives like BKC can cause dry eye. Your dilating drops and anesthetic drops also, when abused, can cause dry eye. When coming to systemic drugs, mostly antipsychotic drugs and antihistamines are the most common. Followed by sedatives and drugs that have secreted in tears like clofazimine and hydroxychloroquine.
So next important question I was asked was dry eye and cataract surgery. I think this is very relevant in today’s scenario where our patients are demanding for refractive outcomes in cataract surgery. So it’s very important that when the patient comes for a preoperative visit, it’s better to have a contact lens holiday or no drops within two hour prior to examination. So all the non-invasive refractive preop measurements like keratometry, topography, biometry, aberrometry have to be done after you don’t use drops for two hours. That is the protocol given by ASCRS. So next you go to the OSD screening. You can use the questionnaires I have given or I’ll show you a separate ASCRS questionnaire that is there for it. And signs, again, you can see through osmolarity or conjunctival staining. Negative screen, OSD unlikely, you just do LLPP and go ahead with surgery. If it is positive, go again for optional non-invasive test with meibography, non-invasive TBUT time and that.
Then, this is the first part of the questionnaire, again, this is mostly about symptoms. The second part is more about the lid conditions and the symptoms that the patient are having during day and night. So depending upon the score, if the scoring is around 28, the more number of red boxes the patient ticks, we have to be careful. And the last line is most important thing, whether the patient is easy going or perfectionist. Anything beyond this line, just forget about refractive cataract surgery. Just offer him a simple monofocal surgery here.
The next question was about which artificial tears and when? Practically speaking, all of them work very well. It’s an individual choice that you can make. But commonly, we try to start off with CMC or HPMC. And then if the patient is not happy with it, we go to liquid polyols like PVA, PEG, and glycerin, and all this come in. There’s a lot of choices that are available, but you have to remember that the value or the action of this is very limited and transient. I prefer to give any CMC in the daytime and nighttime I try to give a preservative-free eye ointment. Always try to go in for a preservative-free drug because BKC can sometimes tend to trigger a dry eye situation.
Dry eye and refractive surgery was one more question that was asked. In dry eye and refractive surgery, these are the five steps you have to follow. Because in refractive surgery, again, if you don’t treat the patient preoperatively it can affect the topography and it can affect your refractive outcomes. So PRK has lesser dry eye when compared to Femto and Femto has lesser dry eye when compared to LASIK. LASIK has the highest number of dry eye according to larger studies. And the first point is look for dry eye preoperatively and don’t miss dry eye. Treat it and only then proceed for surgery. Educate the patient that the dry eye symptoms may aggravate post surgery, and he need to use drops for a certain amount of time like six month or one year also in certain cases. Increase the aggressiveness of treatment with all the armamentarium we are having now, depending upon the symptoms of the patient. It’s simple, but the patient’s refractive outcomes are involved here, we just have to be more aggressive in both diagnosis and treatment.
And the final question which was very interesting, was dry eye and allergy, how do we differentiate? Actually we can’t differentiate it per se, because it’s a broad overlap of interaction. That is because you can’t really differentiate, I’ll just highlight some points. Like in dry eye, the tear breakup time is shorter, whereas an allergic conjunctivitis is less likely to be affected. The conjunctival morphology, again, in dry eye will be normal, but when you life the upper lid here you can papulae. Again, ocular symptoms with dry eye improves with blinking, here it worsens if the papulae is there. The dry eye is worse in the evening. As the day progresses, the dryness increases. Whereas in allergy, morning time it’s worse when compared to the evening.
And if you go into tests, the prick test for allergens will be positive in allergic conjunctivitis and histamine levels will be more than 50, which is pathogramic of allergy conjunctivitis.
Now I’ll take the questions that are there in the Q&A sections. I think we still have some time.
May I have your opinion about warm compresses and eye lid scrub? What is your technique and do the scrub? This is a simple thing. I think it’s best to ask them to come by with their bathing routine. Strokes both from the upper lid and lower lid 10 times after warm compresses. Then they can do the lid scrubs with baby shampoo. So if you ask them to do without the bathing routine, they will try to skip it. So you can ask them to do it twice a day, morning and evening, so that it makes it more practical.
Dry eye in children, I think I’ve already covered that slide. Testing changing? Yes, the testing changes when the child as we go only for non-invasive tests first, and then rarely use the invasive tests. Play important all in dryness? Yes, I have told you, scleral contact has a very good role in this thing. Harika, our old student, has asked what is the name of the instrument used to? That is called the iLux, it is available from Alcom.
What is the antibiotic? And when to do for LipiFlow? All these I have told you. LipiFlow and IPO treatments, we usually for them before the patient is opting for a refractor outcome, especially cataract surgery or monofocal surgery or refractive LASIK. We want to make sure that the ocular surface is healthy prior and post to have a good refract outcome. That is where we treat it aggressively. If the patient is not having much symptoms, that is when we don’t go for these procedures.
iLUX massage does help in dry eye. Right time to start topical cyclosporine? Topical cyclosporine you can start right from the moderate dry eye. When the symptoms are there in a moderate condition itself. We prefer to use cyclosporine before steroids because it’s a steroid sparing drugs and you can avoid all the complications because of steroids.
What if the patients are intolerant to doxycycline? That’s a good question, I don’t have an answer, but you can still try the topical medication like azithromycin that I have told you. Azithromycin and dexamethasone combination also works well. Probably you can also try roxithromycin if it’s not with doxy.
Yeah, there is again a question that foreign body sensation after cataract surgery. Yeah, this is again because all these patients I have told you, our diabetic patients, especially if they’re undergoing cataract surgery, the symptoms are not overt, they’ll be subclinical. But your surgery will break this homeostasis and they’ll becoming clinical and they’ll start to attribute the foreign body sensation to your surgery. That is the reason that you have to do a very meticulous ocular surface examination before you go ahead.
I think, again, my very close friend, Dr. Sujid Visfers from Bangladesh has raised a very good question. Do you think dry eye evolving as a public health problem? I do agree with you, dry eye is slowly becoming a pandemic after COVID. And as ophthalmologists, it’s our duty to educate the public, especially younger children now who are more becoming addicted to digital screens. And I think dry eye cases are going to increase and I told you in the start, dry eye by itself is going to become a subspecialty in ophthalmology.
In a low case, what should be an entry point of care for dry eye? I think the simple lid scrubs that we have discussed should do. Lid massages and artificial tears. Filamentary keratopathy is very easy to treat. Filamentary keratopathy, you just moisten the bed with a topical anesthetic and you debride the bed under slit lamp, and place a BCL and put the patient on N-acetylcysteine. N-acetylcysteine is not available as drops form, so they’re available as injections that they use for patients with respiratory problems. These things you can just double dilute it so you can get N-acetylcysteine in drops form, store them in the fridge, and use it three to four times a day.
What is the rate of punctal opening determined? That’s a very good question. I think 20% of them try to open partially, 10% of them will open back again normally. But again, if you do it meticulously under a microscope, this reopening becomes less problematic.
Caster oil treatment for dry eye? I don’t have a personal experience with it, sir. But I have to check for the literature to see it.
Yes, cyclosporine can be used as a first line therapy moderately, not for mild diseases. You just keep it for moderate dry eye disease.
Yes, viral conjunctivitis leads to, yes, viral conjunctivitis leads to decreased this thing. And any correlation with COVID? Yeah, I think now that is a hot topic now. But we are yet to analyze the data that is going to come out.
What is your protocol for omega 3 prescriptions, all in moderate dry eyes opposed to refractive surgery? We give omega 3 fatty acids from one month to three months.
MG probing? I don’t believe in probing, but the expression I have showed you, that is a better way to do it. Because probing, I don’t think you can practically do each and every gland. So instead of that you ask the patient to use hard compresses in the home for one or two weeks and then with help of this meibum expressors, you can easily remove all the things that you have had.
I think, yeah, I have answered most of the questions. We just have one more minute and I would like to thank Lawrence, once again, for being in the background and supporting me to give this wonderful lecture today. Thank you, Lawrence, thank you once again.
April 16, 2021
6 thoughts on “Lecture: Dry Eye: Evolving Diagnostics and Care”
It was wonderful session
Thank you. Very useful and up-to-date information.
Great presentation All the best
Very nice informative presentation on dry eye, common disorder in present time…. thanks
thank you very much