Learning from failures – My top 3 dry eye treatment mishaps

Having practiced for over 10 years now, I’ve had the most success and most impact on my dry eye patients in the last 2 years.  I just celebrated a milestone of having helped 200 patients achieve a level of clinical stability and symptomatic relief of their chronic dry eye disease.  I attribute that success to the breadth of clinical knowledge and research that I’ve put into building the dry eye clinic in addition to the dramatic increased volume of peer reviewed science directed towards the study of dry eye disease and its causes. More than anything else, however I attribute my patients success to the cases that failed initial treatment.  A good scientist’s successes are shouldered by his or her failures.

In this brief article I want to share from my dry eye cases that responded poorly or not at all to therapy.  It’s funny but 3 specific cases always come to mind when I think about this subject.  One case involves Lyme disease, another was a male with ‘borderline-normal’ testosterone and the last was a case of ‘he said she said’.

1) Patient S.A. had been battling a diagnosis of Lyme disease when she presented to my office and all clinical signs pointed to MGD.  Meibography showed mild truncation but nothing more than I had seen in my most successful cases, and they certainly had viable expression on forced palpation.  Despite effective clearing of obstruction using LipiFlow (confirmed on post meibography) and improved ocular surface staining, she remained with mild improvement in meibum expression.  Her symptoms, as often observed with dry eye disease failed to match the improved clinical picture.   Systemically she was also not improving which I attributed to her lack of improvement.  However on closer inspection corneal sensitivity pre-treatment and 6 months later had increased.  I had assumed that initial testing was basal and normal, however it was more likely that this patient had experienced hypoaesthesia on presentation and treatment resulted in increased surface threshold sensitivity – a return to normal feeling if you will.  Lesson:  Longstanding cases of DED with and without systemic involvement will at some point undergo neural upregulation (or dysregulation) which can and will confuse the clinical picture.  I’ve learned from this that staying the course in the interest of decreasing inflammation is prudent, despite a failing symptomatic picture.  Sometimes feeling anything is better then feeling nothing at all!

2) Patient M.H.  had been to 3 corneal specialists in the previous 5 years.  He had been on various doses of doxycycline, restasis, all artificial tears, plugs with little improvement and even less hope.  The lid margin was hyperkeratinized and expression was low volume but clear.  Without staining these lids, I could see why my 3 colleagues before me were frustrated.  I proceeded with lid margin debridmenet/scaling technique by Maharaj Triad technique.  Patient had mild relief lasting 3 days and symptoms returned to similar levels as previous.  The brief improvement validated my approach so we proceeded twice more 1 month apart each.  Each time relief was lasting longer but failing to provide any sustained comfort.  Finally he mentioned how depressed this was getting him and how he had experienced sexual dysfunction that had been worsening over the last few years (he was late 30’s).  On further questioning his energy had reduced greatly and he had been on and off anti-depressants.  I promptly requested getting his testosterone measured by his family physician.  This was the missing link and it proved to be a turning point in this patient’s disease state.  Lesson:  Men with dry eye disease with limited clinical signs should be screened for androgen insufficiency.  Increasing this patient’s zinc intake and making some lifestyle changes had a significant impact on the ocular surface and meibum volume.

3) Patient TS.  presented with severe symptoms and clinical signs of chronic mixed aqueous/evaporative DED.  Meibography showed a unique pattern of atrophy, however the majority of the ductule and acini were intact.  She insisted on not having undergone any treatment other than some at home efforts with warm compresses and all the artificial tears on the market with little help from anything.  Although the atrophy was atypical, I proceeded to clear the meibomian gland obstructions using LipiFlow in addition to lid margin debridement/scaling.  All metrics showed that she should have overwhelming success.  She did not.  At month 1 her glands had not improved and there appeared to be increased keratinization at the margin accompanied by further atrophy and cicatricial changes.  The patient had no history of viral conjunctivitis and I was officially stumped.  She consistently returned to my clinic enthusiastic but always reserved and mixed up on her use medicines and on chronology of her appointments.   I smelled deception.  By probing further and being honest about my disappointment in her lack of success, she volunteered that she had undergone meibomian gland probing 2 weeks after having had LipiFlow with me.  This explained everything.  Lesson:  Honesty is the best policy, but shouldn’t always be assumed.  Patients can be deceptive for reasons of guilt, lack of understanding, overconfidence, or just plain confusion.  When the clinical picture doesn’t fit for your dry eye patient, probe and question further.  History is still the gold standard in choosing a path of treatment for these patients!

Other tips:

1) Don’t wait to offer more than artificial tears and prescribed drops.   These aren’t restorative treatments but are palliative in nature.  Almost every patient I’ve treated has said, “I only wish I had this done sooner.”  The average patient has been seen by 3 doctors prior to showing up at the dry eye clinic.

2) Follow through – what patients don’t tell you is that it’s just not working or that they’ve lost confidence in the ‘same old approach.’  Like the contact lens patient that has been fitted in monthly CL’s for years from their optometrist, they will leave if offered a more comfortable 1 day disposable by the nearest competitor and they won’t tell you about it.  Tell your patients about new options for dry eye disease and give them a chance to say no.

3) Don’t let a patient become refractory to treatment!  A 50+ female wearing makeup and  reusable contact lenses with a history of eczema is (or will soon become) already a  DED patient.  A suspicious optic nerve get’s a glaucoma work-up, so why does the dry eye patient deserve anything less?  Tear film analysis and meibography are critical to staging the disease…and like glaucoma, the symptoms can be silent!

There it is -Some (certainly not all) of my learnings after spending over 600 clinical hours in the last 2 years at the dry eye clinc treating this challenging condition and the patients that live with it.  Confidence in understanding the physiology of dry eye disease allows the lessons of the failure of one patient to be the success of the next.  

In good health,

Dr. Richard Maharaj OD, FAAO

Cinical Director,

eyeLABS Optometry and Center for Ocular Surface Disease

www.eyelabs.ca

twitter: @eyelabsinc

info@eyelabs.ca

Do you suffer from acne? Bumps on your eyelids can be a sign

Do you suffer with zits or chronic acne on your face or elsewhere on your body?  Are you obsessed with having and maintaining clear skin?  If you don’t already know, a zit or a pimple on your skin happens when the oils in your pores are trapped, built up and harden.  Your ‘pores’ on your skin are actually called sebaceous glands and are oil producing glands that give your skin the glowing complexion.  Irregular production and secretion of these oils can be caused by dirt from your hands and makeup and lack of proper cleaning of your skin from dead tissue or built up debris.  When these glands, or pores, become obstructed the skin tissue becomes inflamed turning red swollen and sometimes painful.  This inflammation is the body’s response to local trauma.  Now this isn’t the trauma caused from a hit or a poke, but microtrauma induced by the trapped oil and debris pushing on the surrounding wall of the gland and skin.  Some people with certain skin types have a strong inflammatory response which in biology is known as the triple response (of Lewis) which consists of:

1. Red spot: due to small capillary dilatation
2. Flare: redness in the surrounding area due to arteriolar dilatation
3. Wheal: due to leakage of fluid from capillaries and venules

Those with a stronger response will be more likely to have stubborn acne that has limited responses to commercial products.  These cases usually require a skin specialist (dermatologist) to treat it medically.  People with eczema, asthma, psoriasis and rosacea (to name a few) are known to have a hypersensitive triple response.

Now that you understand what causes a pimple, you should also know that those sebaceous glands found on your skin are also found in your eyelid and are slightly modified to secrete oils for the eye’s surface.  Each eyelid contains 20-40 of these glands and have a very specialized function.  These glands are called meibomian glands and react the same way the pores on your skin react to debris, dirt, bacteria and general trauma.  What’s different about this area of the body however is that your eyelid is constantly moving and wiping away environmental debris from the ocular surface.  If you are a contact lens wearer, then it is also rubbing the plastic of the contact as well causing friction on the inner eyelid.  Considering what we know about trauma and what it does to our glands, imagine that this microtrauma happens every time you blink, every time you apply make up, every time you wear a contact lens and every time your eye is exposed to environmental debris.  That is pretty much every minute of every day!   The average human blinks seven to ten thousand times a day and for those people that have a heightened inflammatory response are more susceptible to the meibomian glands becoming obstructed which can lead to an eyelid pimple otherwise known as a stye.  These styes can get very large if untreated and become chalazion or an eyelid cyst which can in some cases require surgery.  Interestingly, a stye only happens when the blockage has gotten large enough to become visible to the human eye.  The blockage usually starts long before it becomes visible externally.

Unfortunately though, these meibomian glands are few and once blocked or inflamed can quickly become dysfunctional and die off.  The eyelid surface is uniquely situated close to the eyelash follicles.  Naturally occurring bacteria often accumulate in high numbers in this area due to built up dead skin, makeup and environmental debris.  This surface cannot be cleaned by commercial products with the precision required without causing harm to the eye (cleanser in the eye, removal pads can abrade the cornea, etc.).  Also the inner eyelid tissue known as the wiper is too sensitive to touch or use retail cleaning agents on without causing pain and or damage.  Basically this tissue is never really cleaned and these glands are under constant burden.

Your eyelid glands are just like your skin glands and need clinical attention to keep them functional and prevent meibomian gland dysfunction which causes up to 86% of dry eye disease patients.  In many cases it is a preventable condition, but only recently has clinical periocular hygiene emerged as a new effective maintenance treatment.  Using special dyes and instruments, the eyelid surface and glands can be treated comfortably in your eye doctor’s office.   New advances in this area allow even the most hardened blockages to be melted using prescribed heat and pressure simultaneously (LipiFlow thermal pulsation) in non-surgical painless procedure.

Bumps on your eyelid are exactly the same as pimples on your face, however the consequence of not treating it or preventing it are potentially vision threatening.  If left untreated eventual gland death can occur decreasing the stability and vitality of your tearfilm.  This puts the entire surface of the eye at risk for infection, chronic inflammation and even scarring of the conjunctiva or cornea.

Experts from around the world have now recognized meibomian gland dysfunction as being perhaps the most pervasive cause of dry eye disease around the planet.  These tiny delicate pores have a huge impact on our visual health.  Talk to your eye doctor about your glands and be proactive.  Having dedicated my career to the ocular surface and spending the last 2 years specifically developing treatments in this area, my advice is:  don’t let the symptoms start!

In good health,

Dr. Richard Maharaj OD, FAAO

Cinical Director,

eyeLABS Optometry and Center for Ocular Surface Disease

www.eyelabs.ca

twitter: @eyelabsinc

info@eyelabs.ca

Revitalizing the Eye Waterfront: Treating Lid Disease

Managing patients with dry eye disease (DED) over this past year has transformed the foundation for my clinical decisions with regard to the ocular surface.  Going back to basics has  had a profound impact on my patients with ocular surface disease (OSD).  In November 2012, I wrote a piece on eyelid plaque and its role in OSD which spread to eye physicians globally, all asking about how and why this hasn’t been done before and if I have any examples that I could share.

The answer as to why Line of Marx (LOM) debridement technique isn’t well documented lies in the fact that LOM isn’t robustly described in scientific literature nor has significant emphasis been put on this area in academic institutions or research arenas.  Well if it is not trickling down to clinicians yet, it soon will.  Already, the 2012 American Academy of Optometry meeting in Phoenix featured a lecture being leading experts Dr. Kelly Nicols and Dr. Caroline Blackie in which Dr. Blackie mentioned LOM debridement as an effective adjunct for MGD patients.  In a recent article in the Review of Optometry, a Lifetime of Dry Eye, Dr. Cheryl Murphy mentions this technique while quoting Dr. Blackie.  I would keep your eyes and ears open at CE and research meetings in 2013 for works related to LOM as a source of chronic  DED.

In the mean time I will share an example of a recent case of a longstanding chronic DED patient.  This female patient in her late 30’s underwent LipiFlow Thermal Pulsation 7 months ago and has been relatively asymptomatic since that time.   She uses oil emulsified drops once daily.  Prior to her therapy, she presented with mg atrophy and notching L>R, but symptoms were always greater on her left side which happened to be the side with more mg notching and atrophy.  She has poor lid apposition (lid seal) and is a partial blinker – which is exacerbated at night by exposure.  On Friday’s presentation she reported significant burning OS of gradual onset throughout the week.  Clinically she presented with moderate to severe superficial nasal and temporal keratitis.  Her LOM was anteriorly displaced (no progression since LipiFlow) and had moderate devitalized epithelial accumulation.  I performed LOM debridement and meibomian gland expression to her left eye and advised to increase lubrication to twice a day (vs. once daily).  Historically she responded well to this, however if this was an initial presentation on a new patient, I would add topical antibiotic for coverage and add an overnight ointment.

The patient returned 3 days later for follow-up and as can be seen in her slit lamp image with fluorescein staining, the keratitis was vastly improved and symptoms were resolved.  And so it goes with many of my dry eye patients.   A burdened cornea needs less burden which is why I did not add copious lubrication, and therefore copious preservatives, to the regimen.  This technique offers a management alternative to loading the ocular surface with agents that may mask the true etiology of the problem.  Ideally this patient should do well with a preservative-free option, however she hasn’t found relief in this in the past and was using PF drops 10-15 times a day with limited relief.  With lid therapy we managed to lighten the financial burden as well

This is a chronic patient, and by no means am I or is she expecting a cure-all of her OSD.   The ‘after’ is still not perfect, but it is a safer cornea.   We will continue to work together to as doctor and patient to customize her therapy all while maintaining her lid surface regularly.

When I originally read Bron’s work (Ocul Surface, April 2011) about  the solute gradient created in hyperosmolar tears and how it relates to LOM and MG damage, it was hypothetical at best to me and I had a hard time picturing it.  In this picture, the process comes to life as you can visualize the LOM with little ‘teeth’ straying periodically toward individual MG orifices.  This is the path to damage and helps to explain why a notched lid has that v-shaped appearance – it is not unlike a high speed river creating a pathway clearing anything in its way to get to the drain, which in this case is the meibomian gland.  Once this pathway is created, the gland is now at the mercy of inflammatory factors and the solute gradient created at the base of the tear film.

Clearing this devitalized epithelium from this pathway may serve to disrupt the cycle and slow the progression of lid disease.  With research and new drugs being aimed at reducing ocular surface inflammatory mediators, eye care providers can make a difference by monitoring this tissue closely and revitalizing it periodically.

SideNote:  All the clinical images were taken with a smartphone through a slit lamp.  This is a simple yet effective way to monitor the anterior segment and can be done with relative ease.  There are a number of smart phone adapters available, however none that are universal.  The variations in eye piece diameter make this difficult, however I managed to align these images manually.  

 

 

 

Dr. Richard Maharaj OD, FAAO

Director of Optometry,

eyeLABS Inc.

www.eyelabs.ca

twitter: @eyelabsinc

rmaharaj@eyelabs.ca

Got Dry Eye ?

100 million people globally suffer with dry eye. Lid disease has been shown to be a major culprit behind dry eye.