Meibomian Gland Dysfunction: Expert Perspectives

8/1/2014
Disclosures
Meibomian Gland Dysfunction:
Expert Perspectives on Diagnostic and
Therapeutic Considerations of One of the
Most Common Pathologies in Eye Care
Caroline A. Blackie, OD, PhD
Barry Eiden, OD, FAAO
Amber Gaume Giannoni, OD, FAAO
Donald Korb, OD
Walter O. Whitey, OD, MBA, FAAO
Anterior Segment Section Symposium
November 12, 2014
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Interest Continues to Grow:
Dry Eye Studies/Year 2003-2012
1000
900
800
700
600
500
400
300
200
100
0
Meibomian Gland Dysfunction
is One of the
Hottest Topics in Eye Care
Dry Eye Market Overview
• >25 Million Americans suffer from dry eye disease
2003
2004
2005
2006
2007
• $3.8 Billion spent on dry eye symptom relief
annually in the U.S. alone
• Most frequently encountered disease state
by eye care professionals
2008
Opportunity
2009
2010
2011
2012
STUDIES
1 Prevent Blindness America 2013 & Marketscope
2 GlobalData, Inc.
• Caroline Blackie, OD, PhD, FAAO - Co-founder & stockholder
of TearScience Research funding personal and TearScience
• Donald Korb, OD, FAAO - Co-founder & stockholder of
TearScience Research funding personal and TearScience
• Barry Eiden, OD, FAAO • Amber Gaume Giannoni, OD, FAAO – Alcon Advisory Board
• Walter Whitley, OD, MBA, FAAO has received honorarium
or research funding from Alcon (Advisory Board, Research,
Speaker), Allergan (Advisory Board, Research, Speaker),
Bausch and Lomb (Advisory Board, Speaker), Biotissue
(Advisory Board), Nicox (Advisory Board), TearLab (Advisory
Board), Tearscience (Speaker)
Better clinical
outcomes for
patients
Patient Retention
Practice
& Referrals
Growth
Market Scope 2013 Comprehensive Report on the Global Dry Eye Products Market
6
1
8/1/2014
Dry Eye Supplements
Fail to Address the Underlying Cause
Dry Eye Centers Opening Across US
Beard B. Boston Foundation for Sight Survey. Report Back to the Community. Boston Foundation for Sight. July 15, 2010.
www.bostonsight.org.
Why Treat Ocular Surface Disease?
Better Quality of Vision
• Address signs/symptoms
• Provide relief to patients for which there are
limited treatment options
• Improve CL intolerance
• Improve outcomes in surgical procedures
--- 20/20 ---
• Stress of surgery on the visual system and even the
mildest tear film abnormality result in a significant
reduction in quality of vision and patient satisfaction.
• Due to this, proper ocular surface treatment is critical to
outcomes.
• To grow your practice
What is Dry Eye Disease?
Definition:
Dry eye is a multifactorial disease of the tears and
ocular surface that results in symptoms of
discomfort, visual disturbance, and tear film
instability with potential damage to the ocular
surface. It is accompanied by increased osmolarity
of the tear film and inflammation of the ocular
surface.
Dry Eye: Increased Clinical Focus
An Important Opportunity
• Mounting patient awareness
• Progresses with age and lack
of effective treatment
• Driven by tear instability
• Exacerbated by intense,
prolonged visual tasks
• Impacts vision as well as
comfort
DEWS Report, Ocular Surface April 2007 Vol 5 No 2
2
8/1/2014
Growing Awareness of MGD
ESTABLISHING THE PROBLEM
EPIDEMIOLGY OF MGD
Caroline A. Blackie, OD, PhD
Korb Associates, Boston, MA
Senior Scientist TearScience, Inc., Morrisville, NC
Donald R. Korb, OD
Korb Associates, Boston, MA
Co-founder, TearScience, Inc., Morrisville, NC
Anterior Segment Section Symposium
November 12, 2014
DISLOSURE STATEMENT
Founding member of TearScience Inc.
Financial interest in TearScience Inc.
EPIDEMIOLOGY?
• Literally: The study of what is upon the people
• The incidence, distribution, and control of disease in a
population
• The sum of the factors controlling the presence or
absence of a disease
• Prevalence: the percentage of a population that is
affected with a particular disease at a given time
HOW DO WE GATHER THE DATA?
WHY?
We use epidemiological data to:
•
Understand the significance of the MGD within our local, national and
international communities;
•
Assess the ocular surface health states and health needs of our clinical
populations;
•
Implement and evaluate interventions that are designed to treat MGD;
•
Efficiently and effectively provide screening and treatment for MGD to all
members of our population in a way that is consistent with our policy and
health resource values.
•
Make decisions regarding reimbursement and other policy recommendations
for the management of MGD.
HOW DO WE GATHER THE DATA?
EPIDEMIOLOGICAL STUDIES
COHORT STUDIES
CASE STUDIES
RETROSPECTIVE
EPIDEMIOLOGICAL STUDIES
EXPERIMENTAL
OBSERVATIONAL
PROSPECTIVE
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RANDOMIZED CONTROLLED
TRIAL
EXPERIMENTAL
OBSERVATIONAL
COHORT STUDIES
CASE STUDIES
RETROSPECTIVE
RANDOMIZED CONTROLLED
TRIAL
PROSPECTIVE
Challenge:
1. Clear Definition
2. Metrics to gather high quality data
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8/1/2014
MEIBOMIAN GLAND DYSFUNCTION
Do we know what it is?
PRE 1977, 80: INFECTED/INFLAMED, HYPERSECRETORY STATE
TWO LANDMARK PAPERS
MEIBOMIAN GLAND DYSFUNCTION
The MGD workshop executive summary (2011):
•
•
“MGD may well be the leading cause of Dry Eye through out the world”
“Although this condition affects the health and well-being of millions of people, there is no
global consensus on the definition, classification, diagnosis, or therapy for MGD.”
McCulley and Sciallis, 1977:
Identified ‘Meibomian Dysfunction’ that resulted in:
–
–
–
–
–
Stagnation of the gland secretions
Minimal signs lid inflammation
Ocular surface inflammation (SPK)
Tear film instability due to a compromised lipid layer
Symptoms of discomfort
Korb and Henriquez 1980:
DEFINITION
•
Meibomian gland dysfunction (MGD) is a chronic, diffuse abnormality of the
meibomian glands, commonly characterized by terminal duct obstruction and/or
qualitative/quantitative changes in the glandular secretion.
It may result in alteration of
•
–
–
–
–
Introduced the term ‘Meibomian Gland Dysfunction’.
–
–
–
–
–
Gland obstruction: Unexplained contact lens discomfort
Dry eye symptoms
Reduced MG secretion
Pathophysiological evidence for obstruction
Consequences of obstruction: Duct dilation, atrophy, drop out
the tear film,
symptoms of eye irritation,
clinically apparent inflammation,
and ocular surface disease.
RISK FACTORS
•
Systemic:
–
•
• Aqueous Deficiency Dry Eye
Aging, Hypertension, Menopause, Complexion, Rosacea, Atopy,
Androgen deficiency, Prostate hyperplasia, Lupus, Parkinson’s,
Polycystic ovary syndrome, Sjögren’s, etc.
• Contact Lens Wear
• Glaucoma Medications
Medications:
–
•
OPHTHALMIC RISK FACTORS
• Other Lid Margin Disease
Anti-depressants, Antihistamines, Acne (Isortretinoin Tx),
Antiandrogens, Prostate Medications, etc.
– Anterior blepharitis
Environment:
– Rosacea
–
– Demodex
Humidity, Visual task, Geography, Temperature, etc.
AQUEOUS DEFICIENT DRY EYE & MGD
CONTACT LENS WEAR & MGD
The mere presence of a contact lens on the eye induces evaporative stress.
• MGD Workshop report on Epidemiology 2011:
– MGD is more likely to be present with ADDE and with
Sjögrens syndrome compared to controls
• Bron et al. 2009:
– The phenotypes of ADDE and EDE can be difficult to separate
particularly in advanced disease
• Suhalim et al. 2014:
– Evaporative stress results in MGD (even when the
evaporative stress does not originate with the glands)
•
Korb et al. 1986:
•
Suhalim et al. 2014:
•
Korb and Henriquez 1980:
•
Ong and Larke 1990:
–
–
–
–
This alteration of the normal tear film results in abnormal, unstable (or, in some cases, undetectable)
lipid layer and increased rates of evaporation
Any form of evaporative stress results in MGD
Contact lens wearers with unexplainable reduced wearing time had very high likelihood of MGD
After 6 months of CL wear 30% of wearers showed increase in MGD where as only 20% on controls did.
CL wear accelerates MGD
•
Paugh et al. 1990:
•
Arita et al. 2009:
–
–
Treatment for MGD (lid margin scrubs and lid massage) was effective in improving tear film stability and
reducing ocular surface inflammation in contact lens wearers with MGD
Contact lens wearers (mean age ~30) demonstrated the same degree of MGD and drop out as the 60+
age group of normals. CL wear accelerates MGD
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ROSACEA, ANTERIOR BLEPHARITIS, DEMODEX &
MGD
GLAUCOMA MEDICATION & MGD
ALL STRONGLY ASSOCIATED WITH MGD
•
Arita et al. 2012a and b, Bahtra et al. 2012, Cunniffe et al. 2011:
•
- Glaucoma medications significantly elevate the risk and progression of MGD.
-
– 87% of patients with anterior blepharitis evidenced abnormal gland secretions compared to
6% of controls
The preservatives in glaucoma medications are known to destabilize the tear film, cause
evaporative stress and result in dry eye.
•
• Suhalim et al. 2014:
-
McCann and Tomlinson 2009:
– 80% of patients with anterior blepharitis evidenced meibomian gland drop out compared to
30% of controls
• Baudouin et al. 2004 and 2008:
MGD Workshop Epidemiology Report 2011:
– 74% of patients with mixed blepharitis evidenced MG drop out compared to only 20% in
controls
Evaporative stress has been shown to cause MGD through a cascade of events starting
with up-regulation of the glands, depletion of meibocyte stem cells and early aging of the
glands. This results in gland obstruction, gland atrophy and drop out.
•
Soboleskwa et al. 2014:
•
Bahtia and Del Rosso 2006:
•
Liu et al. 2010:
– One of the most common ocular findings with rosacea is MGD
Glaucoma patients are at very high risk
– Demodex is more prevalent and more active in patients with rosacea
for developing MGD and dry eye due to the glaucoma therapy itself.
– Demodex causes meibomian gland dysfunction
GENERAL PREVALENCE DATA
BURDEN ON SOCIETY
THE DATA IS ALL OVER THE MAP (3.5-70%)
No consistent metrics, varying definitions
Society is causing the problem and we are paying the price
Impossible to answer due to poor prevalence data.
• The Shihpai Eye Study 2003:
DE in general (this means a symptomatic mixed population):
– 61.7% of the symptomatic population had MGD
• Ong 1996:
– 49% of contact lens wearers and 43% of general population
•
Miljanovic et al 2012, Tong et al 2010:
•
Yu et al 2011:
•
Galor et al 2012:
•
Wadhuthantri et al 2012:
– Patients struggle with everyday tasks (reading, working, etc.)
• Ong and Larke 1991:
– 39% of general population
– Direct healthcare costs ~ $3.84 billion (~$783 per patient per year)
• Beijing study 2009:
– 4 X increase in expenditure on DE between 2001 and 2006
– 69.3% of general population
• Foulks et al 2012:
– Per patient expenditure on pharmaceuticals including OTC drops and ointments was up by ~
7% from 2008-2009
– True prevalence of MGD is not known: studies show 20-60%
GOING FORWARD
WHAT NOW?
METRICS FOR:
DEFINITION
• Meibomian gland dysfunction (MGD) is a chronic, diffuse
abnormality of the meibomian glands, commonly
characterized by terminal duct obstruction and/or
qualitative/ quantitative changes in the glandular
secretion.
• It may result in alteration of
–
–
–
–
the tear film,
symptoms of eye irritation,
clinically apparent inflammation,
and ocular surface disease.
•
Functional
State of the
Glands
Sequelae
DRY EYE
MGD is MUCH bigger than the symptomatic dry eye population.
Screen everyone for MGD.
Secretion quality
-
Currently a qualitative measure. Assign a number to the appearance. Quantify pressure.
-
Functional volume (what is expressed with blinking)
-
MGE (developed by TS)
•
Gland structure
•
Secretion volume
-
Gland imaging: Meibography/ Transillumination)
-
Assess for gland truncation/ or drop out and duct dilation.
-
Typically a qualitative measure. Assign a number for the estimated volume. Quantify pressure.
-
Meibometry
-
Interferometry
-
Qualitative e.g. TearScope
-
Quantitative e.g. LipiView (cut off value diagnostic for MGD)
SCREEN FOR MGD NOT DRY EYE
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FUTURE is PREVENTION
Thank you!
Stop only looking for Dry Eye.
START LOOKING FOR MGD.
•
Learn to how to identify and diagnose MGD to
-
Establish true prevalence data
-
Educate clinics and patients about MGD
-
Embrace a culture of prevention by offering cutting edge
treatments and ongoing lid margin health maintenance
Pathophysiology Defined
Webster Medical Dictionary, 2014
PATHOPHYSIOLOGY OF
MEIBOMIAN GLAND
DYSFUNCTION
The physiology of abnormal states,
Donald R. Korb, OD
Korb Associates, Boston, MA
Co-founder, TearScience, Inc., Morrisville, NC
Affiliated Clinical Professor
School of Optometry, University of CA, Berkeley
Anterior Segment Section Symposium
November 12, 2014
DISCLOSURE STATEMENT
Co-founder & stockholder of TearScience
Research funding personal and TearScience
Please silence all mobile
devices. Unauthorized
recording of this session
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Pathophysiology Defined
Webster Medical Dictionary, 2014
What is MGD ?
Classical Ophthalmology = Infective ̶ inflammation
The physiology of abnormal states,
and specifically: the functional changes that accompany a particular syndrome or disease
Meibomitis ̶ Meibomianitis
Inflammation of the meibomian
(tarsal) glands
Can discuss anatomy without function,
but not function without anatomy
Dorland’s Illustrated Medical Dictionary, 2011
MGD ̶ Term coined in1980
Korb and Henriquez
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8/1/2014
MGD Defined
2011 International Workshop on MGD
MGD is the leading cause of dry eye
"Meibomian gland dysfunction is a chronic, diffuse abnormality
of the meibomian glands, commonly characterized by
NOT aqueous deficiency
terminal duct obstruction and/or
qualitative/quantitative changes in the glandular secretion.
This may result in alteration of the tear film,
symptoms of eye irritation,
clinically apparent inflammation, and ocular surface disease.”
Contemporary Understanding of MGD ̶ 2014
Contemporary Understanding of MGD ̶ 2014
Obstruction
of duct
Meibomitis ̶ Meibomianitis
• Not a primary bacterial disease
• Often associated with blepharitis
Dilation
of duct
Autoimmune
• RA
• Sjögrens
• Lupus
FUNCTION and STRUCTURE
Obstruction
of duct
McCulley 1977
• Stagnant MG secretions
and sequelae
Dilation
of duct
Korb and Henriquez 1980
• Obstruction of duct
• Pathophysiology – obstruction
Jester 1982
• MG obstruction = duct
• Dilation and cystic changes
Meibomian Gland Dysfunction
• Obstructive
• Obvious
• Non Obvious
Obvious MGD
Normal appearing lids
(Does not rule out non-obvious MGD)
Pathophysiology of Ductal Obstruction
Obvious MGD
Norn 1987
• Active or inactive glands
Blackie and Korb 2006 - 2014
• Developed function
• Non obvious MGD
• Morphology-function – no
correlation
Normal appearing lids
(Does not rule out non-obvious MGD)
Pathophysiology of Ductal Obstruction
Korb and Henriquez – 1980 (humans)
Korb and Henriquez – 1980 (humans)
Obstruction of the Meibomian
gland orifices by desquamated
epithelial cells in keratotic clusters
Obstruction of the Meibomian
gland orifices by desquamated
epithelial cells in keratotic clusters
Jester – 1982 (rabbits)
• Used epinephrine to block orifices
• Led to duct dilation and cystic changes
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Pathophysiology of Ductal Obstruction
Korb and Henriquez – 1980 (humans)
Obstruction of the Meibomian
gland orifices by desquamated
epithelial cells in keratotic clusters
Pathophysiology of Ductal Obstruction
2014 – Irrefutable Conclusion
Obstruction of the Meibomian glands leads to:
• Loss of function
Jester – 1982 (rabbits)
• Used epinephrine to block orifices
• Led to duct dilation and cystic changes
Nichols et al – 2014 (mice)
• Cauterized orifices
• At 12 weeks morphological changes
• Atrophy and gland drop out
• Morphological changes
• Atrophy
• Gland drop out
Treatment must deal with obstruction
Etiology ̶ Evaporative Stress
Etiology ̶ Evaporative Stress
Effect of desiccating stress on mouse meibomian gland function
Effect of desiccating stress on mouse meibomian gland function
Suhalim JL, Jester JV. Ocul Surf, 2014
Suhalim JL, Jester JV. Ocul Surf, 2014
Mice placed in low humidity
Mice placed in low humidity
Evaporative stress
Evaporative stress
Increased meibocyte production – oil production
Increased meibocyte production – oil production
Dilation of ducts extensive and possible obstruction
Dilation of ducts extensive and possible obstruction
Short maturation time = increase in protein/lipid ratio
Short maturation time = increase in protein/lipid ratio
Tear film stability impaired = > evaporative stress
Tear film stability impaired = > evaporative stress










Chronic exposure to evaporative stress depletes the
meibocyte stem cells resulting in early aging of the
glands, gland atrophy and drop out
Etiology of MG Obstruction
Evaporative stress
Blinking inhibition
Age
Drugs
Epithelial overgrowth
Hormones
Eczema
Lipid Profiles
Seborrhea
Surfactants - Phospholipids
Dry Eye Cascade
Korb & Blackie - 2008
Stasis – Obstruction

Decrease in lipid secretions and LLT

Evaporation increases – 4 - 16 x

Decrease in aqueous layer thickness

Unstable tear film and evaporative stress
Stare Test
Is inflammation the cause or a sequelae ?
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Pathophysiology MGD
Obstruction – many causes
including evaporative stress
SYMPTOMS
START

Loss of MG function

Evaporative stress ̶ tear film compromise

Lubricity
compromised
LWE

Ocular surface
compromise
Atrophy
Gland dropout

Anatomical
changes
Notching
Line of Marx

Inflammation

Corneal hyperalgesia

Fulminant Disease
Definition: Coming on suddenly with great severity
S
Y
M
P
T
O
M
S
I
N
C
R
E
A
S
E
• Occurs, but rarely
• Triggers not known
• Many anecdotes suggest an acute situation
triggers neuropathic pain
Neuropathic pain
Summary – Pathogenesis of MGD
Summary – Pathogenesis of MGD
• Evaporative stress results in a broad spectrum of sequelae,
and is the single most frequent cause of MGD
• Evaporative stress results in a broad spectrum of sequelae,
and is the single most frequent cause of MGD
Contact lens considerations
Contact lens considerations
• Blink inhibition and partial blinking also result in MGD
Summary – Pathogenesis of MGD
Summary – Pathogenesis of MGD
• Evaporative stress results in a broad spectrum of sequelae,
and is the single most frequent cause of MGD
• Evaporative stress results in a broad spectrum of sequelae,
and is the single most frequent cause of MGD
• Blink inhibition and partial blinking also result in MGD
• Blink inhibition and partial blinking also result in MGD
• Terminal duct obstruction is the mechanism which
initiates the pathophysiology of MGD
• Terminal duct obstruction is the mechanism which initiates
the pathophysiology of MGD
Contact lens considerations
Contact lens considerations
• The cascade results in ocular surface compromise, lack
of lubricity, lid changes, MG atrophy and drop out,
inflammation, corneal hyperalgesia and neuropathic
pain.
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Summary – Pathogenesis of MGD
Thank you to the over 400
• Evaporative stress results in a broad spectrum of sequelae,
and is the single most frequent cause of MGD
Contact lens considerations
Scientists
• Blink inhibition and partial blinking also result in MGD
Optometrists
Ophthalmologists
• Terminal duct obstruction is the mechanism which initiates
the pathophysiology of MGD
Residents & Fellows
And all those in industry
• The cascade results in ocular surface compromise, lack of
lubricity, lid changes, MG atrophy and drop out,
inflammation, corneal hyperalgesia and neuropathic pain.
Who have taught me unselfishly
• Treatment must be directed to the prevention and
resolution of MG obstruction
& worked with me
for the past 40 years
Disclosures:
AAO Anterior Section Symposium
• Paid Advisory Board Member for Alcon
Meibomian Gland Dysfunction:
Clinical Diagnosis and Technology
Amber Gaume Giannoni, OD, FAAO, Diplomate (ABO)
agaume@optometry.uh.edu
Goals:
After this lecture, the attendee will:
• Be able to identify lid margin, gland and
meibum changes associated with MGD
• Understand the latest tools, techniques and
technology in diagnosing MGD
• Become familiar with MGD classification
I do not have any financial or proprietary interests
relative to this presentation
Outline:
I. Who should you assess?
 Why is it important?
 Identifying patients
II. Clinical Assessment and New Technology in MGD:





Tear film quality and blink assessment
TBUT and staining
Lid margin changes and inflammation
Meibum quantity and quality
Meibomian gland imaging
III. Staging/Classification of MGD
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Why Is It Important?
Ocular surface wellness is imperative for:




Successful surgical outcomes
Minimizing post-surgical complications
Successful contact lens wear (any type)
Quality of Life
Identifying patients:
Who should we evaluate?
 Symptomatic
 Screening failures:
 OSDI, SPEED, other questionnaire
 Point-of-care diagnostic tests (i.e. TearLab, InflammaDry etc.)
 Every pre-CL fit
 Dry-eye inducing systemic disease
 Dry-eye inducing medications
Clinical Assessment:
Tear Stability/TBUT:
Tear-Film:
General Appearance:





Clinical Assessment:
Debris?
Oily?
Foamy (saponification)?
Meniscus height?
Blink assessment (partial blinks)?
Stability:
 Interferometry
 Tear break-up time (TBUT)
 NaFl BUT:
 > 2ul of NaFl destabilizes the tear film*
 No volume control with conventional strip
 Micropipette?
 Dry Eye Test (DET) strip: <1ul of NaFl
 Non-invasive BUT:
 Manual keratometer, placido topography, keratograph
 How many readings?
* Marquardt et. al., 1986
NEW TECHNOLOGY:
NEW TECHNOLOGY:
Keratograph 5M (Oculus, Inc) with Dry Eye Suite
Keratograph 5M (Oculus, Inc) with Dry Eye Suite
Computerized Non-Invasive Keratograph Break Up Time (NIKBUT)
• Tear meniscus height
• Computerized redness classification
• Qualitative tear interferometry
•
•
•
•
Placido disk topography
Anterior segment photography/video
Noninvasive break-up (NIK-BUT)
Infrared meibography
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Clinical Assessment:
Lid Margin Evaluation:
Tear Film
Photo/Video Discussion







Increased thickness?
Posterior lid margin redness?
Telangiectasia?
Scalloping/serration?
Epithelial ridging?
Conjunctivalization?
Lid wiper epitheliopathy?
Clinical Assessment:
Meibomian Gland Evaluation:
General Appearance:
 Caps?
 Focal injection?
 Distended or pouting gland orifices?
 Migration of gland line?
 Narrowing of ducts/loss of cuffing?
 Opaque glands/scarring?
Lid and Meibomian Gland
Photo/Video Discussion
Clinical Assessment:
Diagnostic expression should evaluate:
What if the lids and glands look normal?
Are we done?
MUST express to properly assess!
1. Ease of expression:
• Mimic normal blink force
2. Secretion quality:
• Thin and clear vs. turbid, thickened or none
3. Number of expressible glands:
• 20-70% of glands are expressible at any given time*
* Norn. Acta Ophthal. 1987; Blackie, Korb. Cornea, 2009
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Clinical Assessment:
Meibomian Gland Evaluation:
Diagnostic Gland Expression
Photo/Video Discussion
 Imaging:
 Contact transillumination
 Infrared meibography (great for patient education!)
 What do I look for?
 Gland distention
 Partial glands
 Missing glands
GRADE
PARTIAL GLANDS
1
No partial glands
2
<25% partial glands
3
25%-75% partial glands
4
>75% partial glands
GRADE
GLAND DROPOUT
0
No dropout
1
<25%
2
< 50%
3
>75%
4
< 100%
Staging/Classification of MGD:
Importance of Disease Staging:
Meibography
Photo/Video Discussion
 Foundation for diagnosis, especially if
unfamiliar with MGD
 Monitor response to treatment, especially
when symptoms aren’t improving
 Foundation for stepped therapy instead of
“shooting in-the-dark”
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Staging and of MGD
(Outlined from the MGD Workshop Staging Chart)
STAGE
DRY EYE
SYMPTOMS
1
None
•Oil quality score: >2 to <4
•Expressibility score:1
•No lid changes or gland dropout
2
Mild
•Oil quality score: Grade <4 to <8
•Expressibility score: 1
•Mild lid changes, no gland dropout
3
Moderate
4
Severe
CLINICAL SIGNS OF MGD
CORNEAL/CONJ
STAINING
None
None to mild
•Oil quality score: >8 to < 13
•Expressibility score: 2
•Moderate lid changes, plugging,
vascularity
Mild to Moderate
conjunctiva and
periph cornea
•Oil quality score: >13
•Expressibility score: 3
•Severe lid changes, dropout,
displacement, inflammation
Severe
conjunctiva, periph
and central cornea
GRADE
MEIBUM
QUALITY*
MEIBUM
EXPRESSIBILITY
(central 8 glands)
(central 8 glands)
0
Clear fluid
All expressible
1
Cloudy fluid
3-4 expressible
2
Particulate fluid
1-2 expressible
3
Toothpaste
None express
*Each expressed gland is assigned a grade
for a cumulative meibum quality score
OK, we diagnosed MGD,
Now what do we do about it???
S.Barry Eiden, OD, FAAO
North Suburban Vision Consultants, Ltd.
Keratoconus Specialists of Illinois
Assistant Clinical Professor, University of Illinois
Medical Center, Dpt. of Ophthalmology
Adjunct Faculty: Indiana, Illinois, Salus and UMSL
Colleges of Optometry
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8/1/2014
General Dry Eye Therapy…
it should be based on the cause
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Is it due to exogenous causes?
Is it due to anatomical issues?
Is it assoc. w/ blepharitis / MGD?
Is there an inflammatory component?
Is there an aqueous deficiency (ADDE)?
Is there a lipid deficiency – evaporative
component (EDE)?
Key: Target your therapy
Therapeutic Approaches for MGD &
Evaporative Dry Eye
• OTC, Mechanical and Adjunctive Therapy
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Heat application
Tear film “stabilizers” (reduce evaporation)
Lid Hygiene
MG Expression
MG orifice exfoliation
MG Probing
• Medical Therapy
– Topical (anti-inflammatory, combination agents)
– Oral (Omega-3, Doxy)
• Advanced Therapeutic Technologies
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LipiFlow
MiBo Thermaflow
ILP
BlephEx
Heat Application to MGs
Lid Hygiene
• M.O.A.:
Liquification and loosening of the meibum
• Traditional Approaches:
• Home Remedy: “Baby Shampoo Systems”
• Heat Masks:
• Prepared Tx: “Medicated Lid Wipes”
– Warm/hot washcloth compresses
– Heated “Rice Baggy”
– Others
– Bruder Heat Mask
– TranquilEyes
– Others
Tear Film “Stabilizers”
• Use range: BID to QID
• Purpose: to reduce tear film evaporation by
stabilizing the lipid layer
• Egs:
– Systane Balance
– Oasis Tears (+)
– Liposome Spray
– Ocusoft Retaine MGD
– Others
– Wash cloths
– Q-Tips
– Others
– Types (pads, foam, “+” w/antibacterial
preservative )
– Compliance based on perception
Therapeutic Approaches
& EDE
for MGD
“Tear Film Stabilizers”
–Blink Tears line: low to high viscocity (tears, tearsPF,
gel tears), contains “HA” but low MW.
• Systane Balance: combination elements
of Systane Ultra and Soothe XP, the “guar”
complex – anionic phospholipids acts like
velcro and attaches the aqueous layer to the
lipid layer.
– Designed for MGD and EDE
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HA*: Eye’s Natural Lubricant
General Properties of HA:
• One of the body’s natural lubricants:
found in synovial fluid in the joints
and in the eye
Therapeutic Approaches
MGD & EDE
for
“Tear Film Stabilizer”
• Oasis Tears / Tears Plus
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– naturally occurring glycosaminoglycan
(a mucopolysaccharide)1
– shown to have anti-inflammatory properties,2 play a role in wound
healing,3 and have a protective effect against
oxidative damage 4
• Each molecule can hold up to 1000x its
weight in water
1,5
• Stabilizes pre-corneal tear film
HA
HA
6 H 2O
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*Hyaluronan is the salt form of hyaluronic acid.
Figure reproduced from Winter WT, Arnott S. J Mol Biol. 1977;117:761-784.
1. Lapcik L Jr et al. Chem Rev. 1998;98:2663. 2. Pauloin T et al. Mol Vis. 2009;15:577. 3. Lerner L et al. Exp
Eye Res. 1998;67:481. 4. Presti D, Scott JE. Cell Biochem Func. 1994;12:281. 5. Winter WT, Arnott S. J Mol
Biol. 1997;117:761.
Oasis Tears / Tears Plus
• Hyaluronic Acid (HA) High M.W.
• Glycerin (holds water molecules to the ocular
surface)
• Prolonged activity (8+hrs.)
• Preservative free
• One re-capable vial per day
*Aragona A, et al, BJO 2002 86: 181-184.
OCUSOFT RETAINE MGD
Delivers phospholipids
to the tear film via the
LIPOSOME SPRAY
surface of closed
eyelids.
Single-Dose. Light Mineral Oil 0.5%, Mineral Oil 0.5%
- Provides long-lasting relief for moderate to severe dry eyes
utilizing Novasorb, a proprietary cationic oil emulsion technology
(microemulsification)
Patented liposome
technology to deliver
water, lipids and
vitamins A, C and E
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8/1/2014
Meibomian Gland Expression
Meibomian Orifice Exfoliation
Devitalized epithelial cells accumulate on the lid margin,
over the meibomian gland orifices. Significant accrual of
this material can obscure the MG orifices and significantly
impact MG function
Mastrota
Meibomian Paddle
Tx: application of 1 drop topical anesthetic followed by
mechanical debridement of the keratinized lower lid
margin.
MG Expressor
Gulden, inc.
Korb DR, Blackie CA Debridement-scaling: a new procedure that increases Meibomian gland function and reduces dry eye
symptoms Cornea 2013 Dec;32(12):1554-7
CONCLUSIONS:
The debridement-scaling of the LOM and lower lid margin provides statistically
significant symptom relief and improvement in the MG function. The novel
procedure should be considered in the management of MGD and evaporative dry
eye
Collins dual side MG Expressor
***Pre-MGE - Lid heating
Maskin MG Probing Procedure
• 2 & 4mm MG probes developed by
distributed by Rhein Medical
Steven Maksin, MD,
• http://www.rheinmedical.com/search/index.php?method=details&id=1546&cl
ass_id=
Maskin Procedure –
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Therapeutic Approaches
MGD & EDE
Modified
Method by D. Seibel, OD, FAAO
1. Perform baseline Tear Osmolarity and then instill Proparacaine
2. Insert soft bandage contact lens
3. Apply topical ointment to lashes & lid margin - C-Lidocane 8%, 25% Jojoba Oil in petroleum
base order in 45 GM quantity from Leiter's pharmacy 800-292-6773 - Ask for "Maskin Oinment".
4. After a few minutes wipe off ointment with tissue or gauze pads.
5. Glove up
6. Express meibomian glands with Qtip or Mastrota paddle
7. Use Maskin Aluminum Handle (Ref 91-1004 from Rhein Medical) and load Maskin 2mm probe
(Ref 07-6040-2 from Rhein Medical - 800-637-4346 or www.RheinMedical.com).
8. Use Qtip or gauze pad in fingertips to slightly evert upper eyelid and expose MGs some
hopefully pouted but not open and insert probe parallel to ductal tract until you feel a
"pop". Some MGs are too atrophied to pop. Attempt to fully insert 2mm probe even in partially
open ducts. Some small bleeding is normal but pt will not notice but will notice some
discomfort. If probe bends you can bend in back straight with your finger no more than 4 times
before it breaks off. I can usually get one probe to last for both upper lids.
9. Re-express MG with Qtip or Mastrota Paddle on upper lid.
10. Repeat Steps 6,8 & 9 on opposite upper lid.
11. Remove Bandage CLs, apply topical antibiotic sol and Pred Forte sol in-office. Tell pt that lids
maybe puffy & red for 1 or 2 days.
12. Rx Doxycycline 100 mg p.o. BID x 2 wks
13, RTO in 2 wks and re-express upper MD and ductal probe lower MGs with another 2 wk round
of Doxy. RTO 2 wks
14. Perform Tear Osmolarity to compare and then re-express all 4 lids. Usually find an
approximately 15 point improvement in Tear Osmolarity after Tx.
for
Medical Therapy (anti-inflammatory):
– Azithromycin topical (Azasite) – off label use
– Topical steroids (Loteprednol – Lotemax ung) or
Combo agents (Tobradex gtts vs. ung)
– Cyclosporine (Restasis) – off label use
– Oral Doxy ( maint. low dose – 20 to 50 mg)
– Omega – 3 Fatty Acids (2g/day)
Tobradex ST
• Tx of acute posterior blepharitis:
apply directly to lid margins
BID for
1 to 2 weeks
• Lower Dexamethasone concentration vs.
Tobradex
(0.05% vs. 0.1%) yet:
• “Bioequivalent” due to increased
retention time on the ocular surface
(Xanthan Gum vehicle)
• Alternative: Tobradex ung to lid margins
BID
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8/1/2014
Azithromycin (Azasite – Akorn)
AzaSite®
(azithromycin 1%
solution) Treatment of blepharitis(off label use)
• Both antibiotic and
anti-inflammatory activity
• High tissue penetration into lids
• Extended duration w/ “DuraSite”
vehicle
• R’xd: 1 gtt QHS for 1 month
for treatment of blepharitis
• PM application to lids or drop
• Duration & Frequency of Tx for
chronic condition?
– Recently: “new bottle!”
2wk Tx effect on lid redness
(apply as drop or directly to lid margins)
IN DEVELOPMENT:
“AzaSite Plus”
1% azithromycin
+
0.1% dexamethasone
Durasite vehicle
Doxycycline Issues:
• GI issues, photosensitivity
• Cost Issues – Eg low dose tx:
– Periostat (20mg tabs): 100 tabs apx. $110.
– Orecea (40mg SR caps): 30 capsults apx. $400!
– Generic Doxy. (50mg tabs can be “pill cut” to
25mg): 60 tabs apx. $13!
a
2wk Tx effect on MG plugging
Luchs J,
Advanced Ocular Care
May/June 2010
Oral Management of
Blepharitis and MGD
• Doxyclycline
– dosed 100 mg. BID 1mo, 50mg BID 1mo,
50 mg. QD 1mo
– reduced to a maintenance dose of 25 mg. QD
(cut 50mg tab)
– Other lower doses:
(Alodox kit 20mg/Periostat 20mg/Oracea
40 mg SR)
• Omega 3 “Nutraceuticals”
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HydroEyes
TheraTears Nutrition
PRN Omega
EZ Tear
Desire 2gm/day dose
How to Minimize Stomach Problems with
Tetracycline
1. Do not take the second pill (bid) before
going to bed
2. Do not take pills with acidic beverages
3. Take pills with food (except a high dairy
meal)
4. Prescribe the lowest dose available
Courtesy Paul Karpecki, OD, FAAO
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8/1/2014
Advanced Therapeutic Technologies
for Tx of MGD/EDE
LipiFlow®
(Tear
Thermal
Science)
Pulsation System
• LipiFlo (Tear Science)
• MiBo Thermaflow (Pain Point)
• Intense Light Pulse Tx
• BlephEx (Rysurg)
LipiFlow Thermal Pulsation
by TearScience, Inc.
Intense Pulsed Light Treatment
(IPL) *dev. by R. Toyos, MD – Memphis, Tn.
LipiFlow safely and effectively treats Meibomian
Gland Obstruction in both upper and lower eyelids
simultaneously, in an in-office procedure, taking
only 12 minutes per eye
MiBo Thermaflow
(Pain Point Medical)
Intense Pulsed Light Treatment
(IPL)
• Originally developed for Dermatology (Rosacea Tx)
• Short bursts of wavelength specific light
(500-800nm)
• Treat “ear to ear” (better effect vs. only lid tx)
• + Effect via:
– Increase in temperature (“worlds best hot compress!”) –
should express glands after tx
– Direct closure of superficial vessels reduces release of
inflammatory mediators assoc. w/ MGD
– Anti infective : kills pathogenic flora
(bacteria and demodex)
• Year 1: 3-4 Tx’s monthly then
maintenance Tx Q 6-12mo.
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8/1/2014
BlephEx Treatment
Eiden’s Tx Protocols
for MGD/EDE:
• Mild Cases: Tear film stabilizers 3-4/d (pre & w/
CL if wearers), heat mask 2/d 2weeks then QD
ongoing, Omega-3, lid wipes2/d 2 weeks then QD
• Moderate Cases: above + In office Txs (MGE,
Exfoliation, MTF / LipiFlow) + consider oral Doxy
therapy
• Obvious Inflammation Cases: above +
Topical Tobradex ST BID to lids 2 weeks, Azasite
QHS 1 mo.
Practitioner Survey Outcomes
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Do you use tear stabilizer OTC agents?
Do you use Omega 3’s?
Do you use heat treatment?
Do you express MGs?
Do you exfoliate MG orifices?
Do you probe MGs?
Do you use topical Rx Tx?
Do you use oral Rx Tx?
Do you use any advanced technology Tx?
(Survey being taken from a group of 14 prominent
anterior seg/CL specialty OD practices – will have results
prior to AAO)
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