Flavor of the month CME Series – #18
Dr Agawals Eye Hospital in Chennai
Speaker : Dr Abha Wadhawan
Panelist : Dr Preethi Naveen
Moderator : Dr Indumathy
Education Committee : Dr. Ashvin Agarwal, Dr Preethi S
So once again welcoming everyone all the attendees for the session of Dr diagnostic myself Dr Indi uh from katur Branch I’m a general opthalmologist with Keen interest on refractory surgery counseling and conversions today the speaker is Dr ABA wadan a beauty with brains she’s not only for f refractive surgeon but also a
Certified surgeon from athetics Clinic of India she has done her inters from government Medical College of jamu her DNB and coral Fellowship from HB Desi Hospital Pune she also has to her credit being nabh assessor our panelist for the day needs no introduction one of the rising stars
Of Dr Agarwal a hospital TI Road Center of Excellence queen of pedc and all type of coral transplant surgeries medical director of Dr agarwal’s ibank and academic director of dmbn fellowship program yes none other than a Dr pretty prti nain so today the topic is seems to
Be a simple but it’s a complicated one actually it’s a simple complaint that we see in know day-to-day practice dry eye but which needs a thorough evaluation unless we diagnose the cause correctly we’ll not be able to treat the patient as satisfactory so now I think Dr ABA will take the
Session so over to Dr ABA for your presentation thank you for your kind introduction ma’am and I’m really happy to be here on this to be speaking on the topic of Dr very dear to me so with and thank you very much Dr Ashwin and Dr prti Dr Pras for giving me this
Opportunity today so without any further Ado I’d like to start with the diagnostic and the treatment rational of a dry eye uh my topic would be divided in definition of the dry ey followed by the clinical evaluation and the six steps or the tasks for detecting and treating dry
Eye patient from the beginning till the end and after that the treatment part will be followed up that should be the end of it so starting with the definition of a dry eye we all know it’s a multifactorial disease of corneal ocular surface it’s characterized by an
Unstable film also known as loss of tiar film homeostasis along with that that we have ocular symptoms in which hyperosmolarity ocular surface inflammation and neurosensory abnormalities play eological role but why Dr is so important it is because of the pain and the irritative symptoms that it causes and the decrease of the
Visual performance affecting the uh the productivity of a person at the workplace to around two to three times more the discomfort caused by the dry eyes considers as equivalent to that caused by severe angina or a person undergoing weekly dialysis so we can understand the amount of the global
Economic burden or dry eye causes the various symptoms are as follows as we all know dry iron gritty sensation temporary blurry and foggy visions and uh now we come to the six tasks which have been given by the DU to study which starts from the beginning like so the
First step would be to give offer the patient certain triaging questions these triaging questions are given to find find out and confirm whether the person is actually having dry eye symptoms or is face or we are dealing with a masquerader of the dry eye second would be risk factor analysis
Third would be screening questionnaire fourth is a tiar film homeostasis marker detection and subtype classification with the various diagnostic procedures and the final would be the step-wise management or the treatment part hence these are the six steps in which you’ll be following starting with the very first one that is the triaging questions
The triaging question questions that we have to ask the patient the very first moment the patient turns up to us is how severe is your discomfort do you have mouth dryness which is suggestive of yorran syndrome how long have the symptoms been because it is said that the symptoms increase as the time
Progresses is there a contact lens usage is your vision gets affected or gets clear on blinking because a blinking would improve the vision in a dry eye and deteriorate in allergic conjuntivitis or a masquer and are the symptoms of redness worse in one eye or the or it’s bilateral because dry eyes
Is generally an bilateral disease and do the eyes itch and is there crusting of the lid margins especially in the morning time and if it is such a condition is existing then it could be a lid margin disorder and the patient is having any systemic uh disorder for which he’s
Taking treatment that could be responsible also for causing the dryness in the eye the second is the risk factor analysis it is important because the things that we can control or modify should be modified and things which can’t should be told to the patient that
You have to live with them and but the best we can do for you is the treatment in the following manner so various nonmodifiable risk factors would include aging uh the Aging the gender the race of the person the meibomian gland dysfunction irrespective of having so many treatments still meibomian gland
Dysfunction is considered as a non-modifiable risk factor various connective tissue disorders and jogr syndromes these are non-modifiable risk factors certain modifiable factors would be the contact lens where the environment like smoking or the sick building syndrome Androgen deficiency estrogen replacement HRT treatment that the patient is taking these are the risk
Factors which we can modify to the benefit of the patient uh then we have a screening questionnaire now the screening questionnaire by large we use is a dq5 and osdi score the dq5 is a simpler one and the score positive for ocular symptoms would be anything beyond six in
Osdi it would be 13 why is it important because the patient has to have ocular symptoms to be labeled as a dry eyye patient and the uh the scoring is important because we can determine whether the patient is getting better or not with the treatment that we are
Giving and it is also helpful in various research purposes the now looking at the clinical examination before we start with the homeostasis detection homostasis breakdown detection of the T film the very first would be in this gentleman that we are seeing there is presence of brosis there’s presence of dermatosis
There’s orbital fat prolapse in the lower lid margin and there is frontalis overaction now why am i showing this picture is because this patient was being treated as a dry eye patient for since a long time where whereas it is not just the dry eye which is playing
The part in this case because of the lack of opposition of the lower lid margin with the globe because of the orbital fat prolapse this patient is not having the opposition of the punai with the teer lake hence is having epora the dermatochalasis itself is responsible for the excessive uh effort that the
Patient is doing in order to lift his eyelid so by the time it is evening the patient is um not only fatigued because of dry ey probable dry but also because of the lid margin or the lid disorders so we need to evaluate the patient from
Outside to inside in a total so that we know what are we dealing with because every time it’s not going to be dry eye there could be other things also next we come to the clinical examination in which we have to follow the principle of lpp the L would be to
Look what do we have to look at we have to look at the base of the lashes first Mar side to Interior the first would be to detect whether there’s a presence of interior blaris in the patient the lip position is fine or not is it getting
Opposed with the globe what is the tiar meniscus it is reduced or it is there or it is not there is there a presence of conjunctival cesis which is the presence of a conjunctival fold the second would be lifting so when we lift the eyelid we
Up turn we not we need to see look for the papate we need to look for the lid Viper epitheliopathy which picks up the stain on Florine we need to look for uh the Pres of Lal gland prolapse we need to check for whether Lal gland is normal
Shape or is it enlarged or it is at trophied and pulling by pulling we have to pull the upper eyelid margin the upper eyelid to check for whether it is laxed is there for floppy eyelid syndrome and the lower eyelid has to be pulled in order to see whether the
Horizontal axity exists because it will directly affect the lmal pump and the last would be uh to push and in the pushing we are basically pushing the lower lid margin to check for meibomian gland secretions their quantity and their quality so once the outside clinical examination is done one very
Important thing that we need to do is the lmal gland uh uh we can check the Lal glands production or secretion of the Tears by lifting up of the upper eyelid by the procedure called as dats that is dynamic assessment of tear secretion in which we it’s a very simple
Procedure we just uh we just touch the lamal gland with Florine strip and we wait for it just in this similar manner like a cedal test we wait to see whether there is production of the tear Al or not so we we will see for the shape of
The Lal gland we look for the tier flow it should normally be 1.05 microl just by looking we’ll not be able to understand the amount of the secretion but we’ll get an idea the second would be the number of ductules the normal ductules should be at least 3 to five
Per gland and the time lack should be less than one second that mean should be an instant flow which is washing away the uh the Florine that we have touched with the lmal gland uh so here we can see that in a normal uh gland Lal gland
Uh we are having a convex gland which is having a good vasculature and the number of ductules are 3 to five and there’s no subc conjunc fibrosis and the secretion rate is seen to be markedly reduced in a in a jran syndrome as well as an aquous
Deficiency dry eye so this is one of the tests that we can do very simply on the clinical examination on a slit lamp now coming for the tier homeostasis marker the very first would be a invasive tiered breakup time that we can do on the slit lamp this involves touching the
Ocular surface with a Florine strip now TI film breakup patterns this was given by the Asian dry eye uh Society this is having five different patterns in which the tier film can break up the first one is the area break the area break where there is no
Movement at all of the tier film that is suggestive of a severe aquous deficiency dry eye the second is a spot break the spot break and The dimple break the spot break is something that occurs even before the lid margin or uh uh the entire opening of the eye takes place
Even before that this formation of small oval spots generally on the Superior part of the cornea this is suggestive of decreased wetability the line break is suggestive of a mild moderate Aquis deficiency and a dimple break would be seen as uh straight straight streaky lines in the center of the cornea
Suggestive of moderate decrease of wetability of the tier film and a random break would be like the moment the tier film is formed after a blink there is a quick break and the random spots appear all over the Cora this could be because of reduced wetability also and by large
Because of the evaporative dry eye the second homeostasis marker would be uh the film osmolarity checkup that is done with the help of a tier lab uh test in this uh the instrument is used to pick up the tier the tier film and it tells you about the smity present in the tiers
Normally it should be less than 308 mosmos anything more than that or an inter between the two eyes any variation Beyond it M Osmos will be considered as a positive marker for a dryer the third homostasis marker is the ocular surface stain in which we are having Coral it
Will be considered positive if there is presence of more than five corneal spots of the staining and more than nine spots on Thea and the lid margin stain pick up at least 2 mm in the length and more than 25% of the width of the lid margin getting stained with taking up the
Stained with the Florine so this is the manner in which we can classify the ocular staining divide the eye and uh we can measure the amount of per quadrant staining so that when we treat the patient we can not only detect or tell the level of the staining severity but
Also help in checking whether the patient is getting better with the ocular surface stain so the pathophysiology of a dryer involves neurosensory abnormalities tiar film instability tiar film hyperosmolarity and ocular surface inflammation so in the similar manner we’ll be detecting and going for diagnostic tests also so the tier film detection with the
Diagnostic test first homeostasis marker as explained is a non-invasive breakup time this can be done with the Oculus keratograph or it also can be done by ocular surface analyzer in which the appearance of the dry spot is noted the time at which it is appearing is noted
And that can help us in detecting the stability of the tier film so this is about Oculus keratograph Oculus keratograph 5m it not only tells us about the topography which is Placo base but it also talks about the redness score so we can also detect the congestion levels or the redness levels
And compare it with the slides that we have it tells us about the non-invasive breakup time also it also tells us about the non-invasive breakup time the tier meniscus height the mography and certain conal stating staining images can also be picked up the Oculus surface analyzer is the latest and very very
Comprehensive uh diagnostic modality which helps us in not only detecting the lipid layer thickness the tier meniscus height the noninvasive breakup time meograph redness score also gives idea about the pupilometry and Osa plus which is the latest would also give us about tell us about the blink ratees and
Whether they are complete or partial blink blinks and it also gives a three dimensional meibography picture of the glands and also detects tier meniscus height at multiple points of a blink so this is a idra ocular surface Osa report this as we can see it’s just like a
Traffic signal the green yellow and the red so anything which is going in the danger zone will be shown in a Red Zone anything which is on the body line will be shown by the yellow and by the green we can see the normal values so in one
Go we can detect what exactly the problem is existing with the patient St film and we will be able to diagnose whether he’s having aquous deficiency or evaporative or a mixture of the two this is a lip view obl liy scan which not only helps in detecting the uh the llt
That is a lipid layer thickness normally it should be 100 nanometer and above anything between 65 to 100 is still moderate deficiency anything below 65 nanometer would be considered as a lipid deficiency or evaporative dry eye besides this it not it also gives us an idea about the blinks the first 20
Seconds how many blinks are taking place and how many of those blinks are partial and how many of those blinks are complete why is it important we’ll be discussing that in a while um now detecting the tiar film volume tiar film volume can be easily detected by the
Shas which tells us about the T of formation within five minutes as we all know the minimum possible reading should be 10 mm and above and but this is not a very sensitive it Sensi but not a very specific test so the other test available would be anterior segmentos as
Shown on the left side this helps in detecting the tier meniscus height and we also have the tier strip menisc this will give us an idea about the tier of volume and this directly correlates the tmh directly correlates with the probability of having Aquis deficiency dryi this can be incorporated in a slit
Lamp examination very easy this is tier lab we’ve already discussed it will tell us about the hyperosmolarity levels of the T as it is very important part of the definition of the dued to study given by the dryi so if we can incorporate it in our OPD it will be really helpful this
Is the mmp9 test or the rpr detection this helps in detecting the presence of mmp9 this is the Matrix Metallo proteinase enzyme and it’s generally seen in said to be raised in the tier uh inflammation so whether there whenever there will be an inflammation in the tear film
Detection we we can start the patient with tropical steroids or with cyclosporin or with tacas so this is helpful in making our diagnosis and treatment easier this is uh the normal picture of a picture of a normal meibomian glands where the upper eyelid is having around roughly around
25 to 40 the length is around 5.5 mm the lower Lids are having 20 to 30 glands which are around 22 mm in the length and any abnormality in the structure can be detected by the meibography uh this is a picture ma’am uh besides just having a meibography in
Case if you don’t have we can look at the structural abnormalities of the Moman glands with the help of Auto refractometer also NCT I will Master a fundus camera or a specular microscopy also helps us in detecting the glands uh by retroillumination this is a uh Osa plus that we discussed
Earlier this is giving a three-dimensional model appearance of the mography so it will help us in detecting not only the atrophy of the glands but collapse of the glands and and any kind of an obstruction of the glands also this is a MOS scale which
Helps in it’s a very easy thing we can see the the type of glands that we are seeing on the diagnostic modality we’re using and we can compare it with the pictures given and hence Define what degree of the Moman gland loss is there the these are the various morphological patterns in
Which the meibomian glands can undergo destruction which is a normal uh meibomian gland which should be like the keys of a piano so whenever they are hooked or they’re overlapping and they’re extremely short and thick and some dropouts of the glands are seen these will be suggestive of a Moman
Gland dysfunction this is important because we need to know how many glands are available for us because if we don’t have any glands at all no matter whatever expression no matter whatever leapy flow whatever we do it’s not going to make any difference to the patient because there’s no Factory for the
Production of the oil GL so once we have gotten enough information through our clinical examination and diagnostic procedures this is the chart that we can follow where Shas is normal lipid is normal teer breakup is normal diagnosis is normal we need not treat this patient a patient is having
Normal uh tear breakup time and Shas is decreased lipid layer is normal this would be a preclinical add that is Aquis deficiency dry eye and so and so forth so a tier breakup time is most important thing if the tier breakup time is normal it is always be considered as a p
Preclinical and the treatment would be dependent on the presence or the absence of certain symptoms are the signs whereas if we have tier breakup time which is shorter and which is generally seen in allergic conjunctivitis or in the younger patient there the treatment modality would be different now coming
To the treatment rational now when we talk in the same pattern the tier film stability will be seen first tier film stability is lost whenever we are having any one of the components of the tier film not being not being present in the right quantity either in excess or in
Less so whenever we have an increased evaporation which can be seen because of the lack of lipid layer we need to give the patient certain liposomal sprays and oils in order to thicken up the lipid lay besides that doing leapy flow and hot fermentation and other Omega fatty acid supplementations if there’s aquous
Deficiency and mucco Aquis deficiency in those cases as we have already seen by the clinical examination by the various patterns of breakup and by the tier miniscus height and by the the various lacrimal gland morphology we should be able to give them certain viscosity enhancing agent which not only increases
The retention time of the lubricant on the ocular surface but also prevents the friction between the lid margin and the ocular surface now we have we need osmoprotectants as well and we’ll be explaining coming to that in a while why the osmoprotectants are required so that the the epithelial
Cells do not undergo damage because of hyperosmolarity and then we have ocular surface apotosis which is a part of the inflammation and because of excessive mechanical friction this can be taken care of by providing topical vitamin A uh ointments and by giving PRP ey drops or autologous serum ey drops and certain
Sodium uronate and carboxy cellulose derivative as supplements ocular surface inflammation can be detected either by congestion of the teil uh congestion in the conjuntiva or by the presence of mmp9 positive in these cases we we are treating them with steroids and other cyclosporin imun modulation so the
Second is the Hy popularity in the pathophys iology pattern what exactly happens is that whenever the hyperosmolarity is there it leads to osmotic pull now the the fluid from the epithelial cells will go out into the extra cellular environment causing uh crenation of the cells once the crenation takes place the cell starts
Becoming a leaky body when the Leaky body is take become it becomes a leaky body it becomes more behaves more like a antigen and once the epithelial cells turn into into antigens they become the source of inflammation and the inflammation starts the imuno immunopathological cycle so whether it
Is hyponic out ECF or hypotonic it will cause the cell to swell up and ultimately will cause apotosis to the cell hence there is a requirement of the presence of osmoprotectants in various lubricants now the natural bio protectors like the tral loel cartine all these will help in stabilizing the
Lipid membrane and preventing the osmotic pressure inside and outside this epithelial cell in order to avoid the crenation of the cell and prevent the exposure to designation stress these are other osmoprotectants available like the sorbitol elol lcarnitine now once the Leaky body has formed which becomes the
Antigen for the ocular surface now there are two Pathways involved in immunopathogenesis of a dry eye one is innate and the other is adaptive we need to know this because we need to know why why are we putting an ey drop and what is the reason for doing it so as soon as
The antigen is produced we have a non-specific cytosine storm on the ocular surface in which various pro-inflammatory cyto kindes are released these pro-inflammatory cyto kindes which are interin one inin 6 Tor necrosis Factor Alpha and the production of Matrix metalloproteinase 9 all these lead to the immature antigen presenting
Cells which are already present on the ocular surface to come and engulf the antigen so once the antigen is engulfed it starts processing that in the immature antigen presenting cells it picks a part of the antigen puts it out on the cell surface becomes a MHC Class
2 uh complex and once the MHC Class 2 complex is present it attracts further cyto kindes to come and help in its maturation once the antigen presenting cell becomes completely mature it leaves the ocular surface and enters into the afferent pathway of the Adaptive uh response by utilizing ccr7 once it
Enters into the aeren pathway of the lymphatic cells there is upregulation I cam intercellular molecules through which this molecule is able to attach and reach into the lymph node in the lymph node it recruits and converts th0 the hel cells into th1 and th17 they get back to the ocular surface
Where they release various interin interlukin interferon gamma and they also release Matrix metalloproteinases so once it this entire cycle is established it becomes a constant vious cycle which the dry ey has to be dry eye keeps increasing because it gets involved in the Vicious Cycle so we need
To step in and any of the places like it could be innate or the Adaptive in whichever medical modality we have in order to stop it from getting uh into further apotosis and breakdown of the epithelial cell barriers so this is is a mechanism of action of imuno modulatory
Eye drops where the first phase is the initiation the second is amplification third Recruitment and damage in cell so the steroids cortico steroids to cut it short the Coro steroids is what will help in preventing the formation of pro-inflammatory cyto kindes the very first St the first very first stage the
Second is the amplification where uh the zedra or the the lii grasp molecule will act it does not mature antigen presenting cells to attach itself with the IAM expressed by the endothelial cells in the vasculature so it does not allow the the mature antigen presenting cells to get into the lymph node and
Within the lymph node it does not allow it to produce uh further recruitment of th1 and th uh 17 helper T cells so this is how it acts so it acts on the aant as well as ephant pathway of the adapter immunity the cyclosporin has a intracellular mechanism through which it
Doesn’t allow the amplification of the te- cells and production of the cyto by the t- cells therefore we always require a corticosteroid along with any of these immunomodulators because once the t- cell has been activated it cannot be switched off so whatever is on will will
Cause the damage there comes the role of aquatic steroids then imuno modulation can also be brought out by autolus serums and platelet rich plasma why is it helpful because of the presence of certain growth factors which are epitheliotropic they help in anti- apototic they have anti- apototic nature the production of various
Immunoglobulins also have anti- apototic activity fibronectin which gets stepped up whenever there is a apotosis it helps in forming a scaffold for the cell migration and certain cyto and soses have anti-inflammatory action and certain vitamins are also present which help in maturation of the epithelium so
What we have right now are the steroid ey drop cyclosporin a liity grast and blood Biologicals for topical immunomodulation whereas the newer drugs around the corner are these I would just want to touch them in brief the first is ar1 15512 this works on the cold thermoreceptor so when whenever we are
In cold there’s excessive production of mucin in the eye so this kind of activates this receptor for better production of the T film RGN 259 these are all molecule names this helping prom in cell migration and prevents the apotosis visomitin it is an anti-aging type of H drop which prevents the
Oxidative stress on the lmal gland hence it would be it’s still in the clinical trials it will help in preventing the development of dry eye a rmd will be a kattic Opthalmic solution which can be used for prevention of obstructive type of MGD laep is lacritin and this will be
This lactin is generally having prosecretory properties so it will help in increase production by the Lal gland GLK 301 as pyo carpin as we know it helps in improving secretion tener necept would be a tumor necrosis Factor Alpha inhibitor hence it will prevent the inflammation and cerine is something
Which will help in neurotrophic atitis by improving the formation uh the improving the nerve structure and preventing the formation of various we have IPL intense pul light therapy for ban gland dysfunction it works by two mechanism the first part which involves exposure of the ocular surface to 500 to
1200 nanometer light is basically to have an anti-inflammatory activity so it it uh it is absorbed by the hemoglobin in the tel incaic vessels where it causes the clotting of the blood and breakdown of the blood vessels hence the inflammatory mediators are not able to reach the ocular surface so this is the
First mechanism also it leads to upregulation of collagen synthesis and kills the Demodex if present it also causes suppression of Matrix Metallo proteines in this manner it acts on the innate immunity pathway the second mechanism is generally uh which is brought about by the N trinal nerve
Stimulation in this op that is Optimum light the therapy which is given this helps in stimulating the trigeminal nerves the Opthalmic and the max axillary division which get into the midbrain and from there they bring about impulses for better secretion through the Lal gland as well as the meibomian
Gland hence in my opinion the IPL is not only helpful in evaporative dry eye but it is of certain help in Aquis deficiency dryer as well these are the diagram or the pictures of certain types of ipls that we are having like Optima the iight by the topcor and the EI by
The East Wind this is the leapy flow uh this is basically working on the vector thermal pulsations it is generally used for obstructive kind of Moman gland dysfunction where a heat is produced and there’s a mechanical milking action through which the meibomian gland secretion comes out onto the ocular
Surface and hence the obstruction is open and the normal secretion from the muin gland start uh now we also have neurosensory abnormalities as the eological part of the dry eye in this we are having reduction in the sub basal bman plexus of the nerve this can be
Improved by various neurot ne ne nerve growth factors that are available in the autous serum does any patient who is having decrease in the caral sensitivity or neurotropic atitis that can be helped by giving PRP ey drops or autologous serum it is seen that at the end of four
To six months there is an improvement of the density of the nerve fibers various alternative therapies uh for for the treatment of the dry ey would be Lal gland hypofunction in which we can inject the Lal gland with PRP with certain stem cells and we can also have transcutaneous nerve stimulation which
Improves the secretion from the lmal gland and we also have Improvement in the secretion by the lamal gland through trans cranial PMS trans cranial magnetic stimulation and the nerve injury if caused can if there’s a type of a neuropathic pain besides giving patient Gabapentin we can also diagnose whether
It’s a central or a peripheral and treat them accordingly if it is a peripheral neuropathic pain it can be treated with amniotic membrane and if it is a central certain nerve blocks and botl inum Toxin and transcutaneous nerve stimulations can be done Moman gland dysfunction we are giving uh eyelid massages and IPL
And topical antibiotics interestingly Manuka Honey is also something which can be tried and the ocular surface inflammation can be prevented with Ral in IPL thank you