Review Article
Meibomian Gland Dysfunction
Sameera Irfan
Pak J Ophthalmol 2019, Vol. 35, No. 1
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See end of article for authors affiliations …..……………………….. Correspondence to: Sameera
Irfan FRCS,
Consultant Sam.irfan48@gmail.com |
Dry eyes is a common, chronic condition
that has a prevalence of about 5- 50%.1 According to the Dry Eye
Workshop II report (DEWS II report), published in 2017, the updated
definition of Dry Eye Disease is, “a multifactorial disease of the ocular
surface characterised by a loss of homeostasis of the tear film, and
accompanied by ocular symptoms, in which tear film instability and
hyper-osmolarity, ocular surface inflammation and damage, and neurosensory
abnormalities play etiological roles.” The Tear Film & Ocular Surface
Society (TFOS) released their report on the international work on Meibomian
Gland Dysfunction (MGD)2 in 2011, which defined MGD, classified it
and considered it as the primary cause of dry eye disease worldwide. Previously
dry eye disease was considered as an aqueous deficiency problem, but after
this report by TFOS, there is a paradigm shift towards “not producing enough
lipids to retain the tears that are being produced”. This has led to a huge
impact on the treatment protocols which were previously focused on managing
the sequelae and symptoms of dry eyes rather than targeting directly on the
underlying cause, the MGD. It has now been accepted worldwide that dry eye
occurs when the ocular surface system cannot adequately protect itself from
the desiccating stress due to the lack of a healthy meibomian gland
secretion. This article is mainly focussed on the Meibomian Gland
Dysfunction, discussing the normal anatomy of the glands, how they are
affected by disease, its implications on the ocular surface and finally, the
various treatment strategies. Key words: Blepharitis, Dry
eyes, Meibomian gland dysfunction, blepharospasm. |
The
term meibomian gland dysfunction (MGD) was described for the first time by Korb
and Henriquezin in the early 1980s3. Its prevalence appears to be
much higher in Asian populations4, i.e. greater than 60% while in Caucasians, it spans from 3.5% to 19.9%. There was no firmly
established definition of MGD before 2011 when the International Workshop on
MGD defined it5 as “a
chronic, diffuse abnormality of the meibomian glands, characterised by the
terminal duct obstruction and/or qualitative/quantitative changes in the
glandular secretion. It may result in an alteration of the tear film, symptoms
of ocular irritation, clinically apparent inflammation, and ocular surface
disease”.
MGD
is generally considered by the clinicians as posterior blepharitis6. The term “Blepharitis” means
inflammation of the eyelids. As the eyelid is anatomically made up of two
lamallae, anterior and posterior, the blepharitis is also divided into an
anterior and a posterior variety.
The term “anterior blepharitis” is referred to as the inflammation of lid-margin
anterior to the grey line i.e. of the skin, eyelashes, and lash follicles. The
term “posterior Blepharitis” means the inflammation
of structures posterior to the grey line; that includes the meibomian duct
orifices, meibomian glands, tarsal plate, and the blepharo-conjunctival
junction. Frequently, a mixed variety may be seen as the inflammatory process
spreads from one structure to the next.
Anatomy
& Physiology of Meibomian Glands
The meibomian glands were first described
in detail by Heinrich Meibom7 in 1666.
They are modified sebaceous glands8
with a tubulo-acinar structure. Each gland consists of a cluster of 10-15
secretory acini opening into a long central duct via tiny ductules. There are
30-40 glands in the upper tarsal plate, each gland about 5.5 mm long while
there are 25 glands in the lower tarsal plate, each being 2 mm long. They are
densely innervated by the sympathetic and parasympathetic nerves (via the V
nerve) as supplying the lacrimal and accessory lacrimal glands, thereby ensuring
an optimal composition of the tear film. There is also a strong hormonal
control mediated by estrogens, androgens,
progestins, retinoic acid, growth factors and neurotransmitters.
The secretion of meibomian glands is called
meibum9 which is primarily made up of nonpolar lipids (about 90%, comprising
of wax, sterol-esters and triacylglycerols), while less than 10% are polar amphiphilic
lipids (hydroxy fatty acids), and a small amount of proteins and electrolytes.
The tear film lipid is a multilayered structure comprising of a thin layer of
polar lipids that resides at the aqueous–lipid interface and acts as a
surfactant (essential for the uniform spreading and stability of the tear
film). This is covered by a thick layer of non-polar lipids that forms the lipid–air
interface and resists the evaporation of aqueous component of the tear film.
The mode of meibum secretion is Holocrine,
which means that the secretions are produced in the cytoplasm of a cell;
the cell membrane ruptures to release the
secretion into the gland’s lumen while the cell itself is destroyed
in the process. The secretion from multiple acini are poured via tiny ductules
into the central duct that opens at the grey line of the lid margin. A thin
strip of orbicularis muscle fibres, called the Riolan’s
muscle, surrounds the terminal part of the central duct and the few terminal
acini present close to the lid margin.10,11 During a blink, the
pre-tarsal orbicularis muscle generates a uniform compression of the tarsal
plate and of the enclosed meibomian glands, thereby promoting the flow of
secretion towards the duct opening by a milking action. Meibum is
squirted out of the duct openings by the contraction of Riolan muscle.
Meibum is normally liquid at body
temperature and coats the lid margins thus making their movement smooth over
the ocular surface and is delivered to
the tear meniscus. From there it is picked up by the upper lid margin (as it
comes down during a blink and picks up the tear meniscus) and is spread
uniformly over the aqueous layer of the tear-film thus preventing its thinning
and evaporation in-between the blinks, and making the tear film stable. After
an absence of blinking, meibum accumulates within the ducts and is delivered in
increased amounts when a person wakes up in the morning12. This
accounts for the diurnal variation in meibum secretion and the excess amount of
oil in the pre corneal tear film makes the vision misty and blurred in the
morning.
To summarise, the functions of healthy
meibomian lipids are:13
i: To make
the optical surface of the cornea smooth at the air-lipid interface.
ii: They reduce
the evaporation of the tear film.
iii: They
enhance the stability of the tear film.
iv: They allow a
uniform spread of the tear film over the cornea.
v: They
prevent the spillover of tears from the lower meniscus over the lid margin.
vi: They prevent
contamination of the tear film by sebum.
vii: The
lipids help seal the apposing lid margins during sleep.
Pathophysiology of MGD
MGD
is a complex disease that is caused by the interplay of hormonal, microbial,
metabolic and environmental factors14. It is classified according to
the rate of gland secretion:
A: Hypo-secretion of meibum occurs due to:
1: Obstruction of meibomian duct opening by conjunctival scarring
seen in Ocular Pemphigoid, chemical burns, Stevens Johnson’s Syndrome.
2: Duct
obstruction by desquamated epithelial cells, clumped together forming plaques,
due to hyper-keratinisation of the lid margin. This results in stasis of meibum within
the duct; the back pressure produces cystic dilation of the glands, the
pressure compresses the acini and
causes their atrophy. This results in further hypo-secretion.
Hyper-keratinisation is commonly the result of hormonal imbalance as a part of
the ageing process, decreased expression
of androgen receptors (hormonal therapy), blink abnormality, contact lens wear
or medications.
3: Hypo-secretion
with thick, altered meibum may be produced in seborrheic dermatitis, acne
rosacea and as a side-effect of medications (anti-histamines, anti-depressants,
hormone replacement therapy, Isotretinoin for Acne).
It is important to keep in mind the
double vicious cycle14 in which obstruction due to a thick, viscous
meibum or hyper-keratinisation of Meibomian ducts leads to back pressure and
atrophy of acini, with a further decreased secretion of meibum; this makes the
meibum more vicid and enhances further obstruction. In addition, stasis of
meibum inside the ducts promotes the growth of commensal bacteria, which produce
lipases that cause meibum degradation
and release of toxic chemicals. These factors
aggravate the primary hyper-keratinisation and compositional disturbance
of meibum and result in a progressive MGD. Chronic obstruction leads to
degeneration of the secretory gland tissue and even if the primary obstruction
is later resolved by therapeutic approaches, the damage is permanent.
B: Hyper-secretion of meibum: is
seen in meibomitis (meibomian gland inflammation) in which excessive amount of
meibum is produced that has an altered chemical composition and is toxic to the
ocular surface.
This is due to meibocyte abnormalities seen as result of ageing, Staph aureus or Demodex folliculorum infection, environmental
factors (hot, dry climate). Moreove nutritional disorders such as generalised
malnutrition, a diet low in omega-3 fatty acids, protein deficiency, vitamin A
deficiency have all been associated with the production of a poor quality
meibum.
Risk Factors for MGD15
1: Ageing
& Hormonal Imbalance: this is the most common cause of MGD.
Receptors for sex hormones (androgen and estrogen) are present within the
meibomian glands while meibocytes (the epithelial cells lining the acini) contain
enzymes which are necessary for the synthesis and metabolism of sex steroids.
Androgens stimulate the secretion of meibum by promoting the synthesis of lipids
and proteins, suppress meibomian gland inflammation and
keratinisation of the ducts, while estrogens reduce/thicken the secretion and
promote inflammation.
With
increasing age, there is a decline in androgen production in both genders.
Similarly in autoimmune disease like rheumatoid arthritis, Sjögren's syndrome
and systemic lupus erythematosus, androgen production is reduced in the body.
In
post-menopausal women, the level of androgen production declines by the ovaries
and adrenal glands causing meibomian glands to atrophy.16
Ageing of the meibomian glands results in a decreased cell renewal and differentiation
of meibocytes, with reduced gland size, and an increased infiltration of
inflammatory cell. These changes lead to generalised atrophy of meibomian
glands and deficiency of meibum. Similar changes in meibomian glands have been
observed in androgen-depleted states in individuals on anti-androgen therapy
for benign prostatic hypertrophy or prostate cancer.
2: Gender: More
common in women17 particularly with oily skin conditions,
post-menopausal state and hormonal imbalance due to polycystic ovaries.
The
key ingredient of many anti-ageing cosmetics that are used for peri-ocular skin
is retinoid acid 18. It suppresses the action of androgens on
meibomian glands leading to their atrophy.
3: Environment:
Hot,
dry environment with low humidity results in structural and functional changes
in meibocytes; there is an excessive proliferation of basal cells of the acini,
a high protein/lipid ratio in the meibum that increases its viscosity and has a
negative impact on the stability of the tear film. Increased production of
meibum causes dilation of ducts as well as depletion of the number of
functioning meibocytes (being a holocrine secretion), with subsequent gland
atrophy and hypo-secretion. Exhaustion of the basal cells leads to the atrophy
of acini and meibomian gland dropout.
4: Topical
Medications19,20: All topical
medications contain preservatives to enhance their shelf life. The most
commonly used preservative is Benzalkonium Chloride, which is most toxic to the
ocular surface. In addition, anti-Glaucoma medications like
beta blockers, prostaglandin analogs, carbonic anhydrase inhibitors result in
an altered morphology of meibomian glands and a decrease in the number of meibocytes.
Chemical formulations containing Adrenaline or phenylephrine promote
keratinisation of the lid margin and blockage of meibomian ducts. Retinoic acid
reduces meibum production and alters its quality.
5: Dietary
Factors:
malnutrition (explained above) alters quality of meibum.
The
use of oral fatty acids improves the quality and expressibility of meibum.
Specifically, the intake of omega-3 fatty acids improves the quality of meibum
with a decrease in the saturated fatty acid content of meibum. It decreases the
ocular surface inflammation. Foods rich in omega-3 fatty acids are flaxseed
oil, and olive oil and oily fish like tuna and cod.
6: Microbial
infection: Cholesterol esters present in meibum promote the growth
of commensal organisms on the eyelid margin, in particular Staphylococcus
aureus. The bacterial lipases, in turn, break down the neutral fats and
cholesterol esters, releasing glycerides and free fatty acids into the tear
film, destroying the mucin layer and making the cornea hydrophobic. This makes
the tear film unstable. The free fatty acids also stimulate
hyper-keratinisation of the lid margins, with keratin plugs adding to the
blockage of meibomian ducts.
7: Infestation
with the Demodex mite: Demodex mite is a
microscopic ectoparasite of the humanskin and constitutes a part of the normal
flora. It produces disease when its cell population increases which has been
detected in about 46.8% of MGD patients.21,22. It is of two distinct
varieties: demodex folliculorum that infests the eyelash follicles, and demodex brevis that burrows deep into the sebaceous and
meibomian glands. It causes a direct mechanical damage to the epithelial cells
of eyelash follicles (by feeding on them), and by laying eggs at the base of
eyelashes, causing follicular distention and misdirected lashes. D. brevis mechanically
blocks the orifice of meibomian ducts and produces a granulomatous reaction
inside the glands resulting in a chlazion.23 Therefore, it should be
considered in the differential diagnosis of every ocular surface disease.
Diagnosis
can be made by random epilation of nonadjacent eyelashes placed on a glass
slide, mounted with a coverslip with the addition of a droplet of oil, sodium
fluorescein, peanut oil, or 75% alcohol which helps release embedded Demodex in
the hair follicles.
8: Contact
Lens Wear 24: The
pre-corneal tear film is approximately 3 microns thick; the average central
thickness of a contact lens is 30 microns. When the contact lens is worn, the
tear film is split both above and below the lens, its thickness is altered
resulting in excessive evaporation and further thinning.
Contact lenses cause a direct mechanical trauma to the lid margin by
constant rubbing, desquamating the epithelium, plugging
the meibomian duct orifices
resulting in gland atrophy.
Also,
chronic ocular surface inflammation affects the gland morphology and function,
with secretion of altered meibum that adds to the ocular surface inflammation.
All these changes worsen as the duration of contact lens wear increases.
9: Congenital
anomalies of meibomian glands: A reduction in the number or
complete absence of meibomian glands maybe seen in Turner syndrome, ectodermal
dysplasia with cleft-lip/palate (ECC syndrome). Rudimentary meibomian glands
maybe visible as yellow streaks on the conjunctival surface of the tarsal
plate.
Dystichiasis (aberrant row of eyelashes) maybe
present at birth in which meibomian glands are replaced by an extra row of
eyelashes at the grey line. The misdirected eye lashes cause ocular surface trauma
as well as meibum deficiency. Dystichiasis can also occur secondary to repeated rubbing of eyelids that occurs in VKC,
chronic allergic conjunctivitis or in the autosomal dominant lymphoedema.
Rubbing induces metaplasia of meibocytes to form eyelash follicles.
Clinical Presentation of MGD
MGD, in its early stages, is asymptomatic
and may remain undiagnosed. It only becomes symptomatic when it has worsened
enough to cause tear-film instability or eyelid inflammation. Its symptoms and
signs are varied and include changes due to:
a: Altered
morphology of the lid margin, altered meibum secretion, bacterial overgrowth
and gland dropout.
b: Tear
film instability.
c: Ocular surface inflammation
Symptoms & Signs
The most common symptom is visual
fluctuation that occurs during visual tasks associated with decreased blinking,
such as driving, reading, staring at a computer screen or watching television.
This results in blurred vision, reduced focusing ability, and diplopia. Despite
the presence of a dry eye, a foreign body sensation and paradoxical reflex
tearing may occur (as the lacrimal gland function is normal and dry spots on
cornea stimulate the reflex), particularly when patients are
exposed to low environmental humidity and blowing air.
Chronic lid margin inflammation is
manifested by symptoms of lid discomfort, pain, redness and irritation.
The symptoms related to ocular surface
inflamma-tion are burning, itching, frequent blinking and photophobia which
gradually worsens to severe blepharospasm.25 In a study, MGD and dry
eyes were the most common causative factors for blepharospasm.26 The
symptoms of ocular irritation tend be worse in the morning because of prolonged
exposure of the ocular surface to toxic meibum and hyper-osmolar tears (due to
poor clearance of the tear film) during sleep. These symptoms also get worsened
after the insertion of punctal plugs due to poor tear clearance. The most
troublesome symptom is chronic burning with or without associated photophobia. This
is presumably attributable to the presence of inflammatory mediators or to
increased tear osmolarity in the pre-corneal tear film. Itching of eyelids is
more commonly present in atopic patients.
Morphological
changes should be assessed on slit lamp examination
and documented27.
i: Lid
margin:
thickening, hyperaemia, telangiectasia, keratinisation, foaminess or frothing
at the canthal angles and along the lid margin. Presence of scales along
eyelash follicles should be noted (keeping in mind Demodex infestation).
ii: Meibomian
duct orifice: plugging with thick meibum, notching (indicating
lost/atrophic glands), distichiasis.
iii: Meibum quality is assessed by gently pressing the
lid margin with a finger or a cotton-tipped applicator, and noting the ease
with which meibum is expressed and its texture.
Meibomian
gland expressibility (MGE) is a clinical score28 that helps in
assessing the severity of disease at initial presentation, and how it improves
with treatment. This is calculated by finding the number of glands that can be
expressed with mild pressure either with a cotton-tipped swab or a commercially
available device that is specifically formulated for this purpose. Five glands
in the nasal, middle, and lateral thirds of the lower eyelid (total 15 glands)
are expressed and scored at each visit. A score of zero indicates a complete
blockage of ducts and total absence of meibum. A score of 15 indicates that the
glands are expressible throughout the lower eyelid. Patients with MGE score 0-5
are always symptomatic, and those with a score of 7 or more, are usually
asymptomatic. The quality of secretion
is noted whether clear, opaque, vicid, cheesy.
MGD is graded accordingly:29
Grade 0: Normal, clear
meibum is seen squirting out of the duct orifices with each blink and can be
easily
expressed by lightly touching the lid margin.
Grade 1 MGD: meibum looking
opaque, viscous and needs pressure on the lid
margin to be expressed. Patient is asymptomatic at this stage and has no corneal
staining. MGE score is more than 7.
Grade 2 MGD: meibum becomes
more thick, cheese like, expressed with difficulty; frothing may be noted at
the lid margins (indicates lipid breakdown by bacterial lipases). Patient may
be asymptomatic or may have slight discomfort of lid margins, mild conjunctival
hyperaemia, mild corneal staining detected by fluorescein at the inferior
limbus and an MGE score of 7.
Grade 3 MGD: plugging of ducts
with thick meibum that cannot be expressed by pressure. MGE score is 3-7. Excessive
frothing at the canthal angles or the lid margins is noted. Patient is
moderately symptomatic with irritable lid margins, injected, watery eyes with
inferior corneal and conjunctival staining.
Grade 4 MGD: Meibomian gland
dropout is detected by the presence of notching at the grey line and by transillumination
with a pen-light through everted eyelids or by infrared photography. MGE score
0-3. At this stage patient presents with severe dry eye symptoms and corneal
staining.
iv: Ocular Surface Signs: Damage
to the ocular surface can result from avariety of closely linked factors like
increased tear-film evaporation that causes hyperosmolar tears and mediates the
release of pro-inflammatory mediators in the tear-film like cytokines,
leukotriens, as well as decreased lubrication of the conjunctival surface of
the eyelids prevent their smooth excursion over the eyeball. These result in an
irritable eye and the symptoms overlap with the dry eye disease. MGD is considered
as themain contributor to an evaporative dry eye disease, but an increased tear
production (measured with Schirmer’s test)
may be noted in patients with MGD. This is due to a compensatory reflex tearing
due to ocular surface abnormalities and discomfort.
Diagnostic tests:30
1: Administer
a symptoms questionnaire, Ocular
surface Disease Index (OSDI).31 This questionnaire assesses symptoms of photophobia, ocular/ eyelid pain,
blurring of vision, problems with reading/driving/watching TV.
2: Measure
blink rate and blink interval: Blinking normally occurs once
every 3-4 seconds (15-20 times /minute) in most people.
However, during reading or staring at a computer/cellphone screen, the blink
rate slows to 4.5 per minute, or once every 13.5 seconds. Blinking has a
significant role in the secretion of meibum into the tear film, as already
explained. If the blink rate is slowed or blinks are incomplete (the upper lid
fails to close onto the lower lid), the lipid layer will build up at the lid
margin and meibomian glands will be used less over time. This could lead to
meibomian gland atrophy if unidentified.
3: Measure
lower tear meniscus height and its clarity. Normal lower tear meniscus
is 1.00-2.00 mm. It can simply be measured by narrowing the vertical beam of a
slit lamp or by Meniscometry: an instrument measures the tear meniscus height,
its radius and cross-sectional area.
4: MGE
score: Expressibility of meibum, noting its quality and grading the
MGD.
5: Measure
tear osmolarity:32 (measuring the concentration of solutes/salts).
As the aqueous component of the tear-film evaporates, the concentration of
solutes (mainly salts) increases. This test has become a critical part of dry
eye management. It requires only a microlitre sample of tears (0.2 μL)
collected by a micro-pen from the lateral canthal tear meniscus. It is placed
in an instrument, called the osmometer, which gives the reading in a minute.
The disadvantages are the need for an expensive equipment and its constant maintenance.
The
osmolarity of both eyes is measured; a difference of 8 mOsm/L or more in the
tear osmolarity between the two eyes is considered abnormal.
The
osmolarity score of 300 mOsm/L or greater in the higher scoring eye is
considered abnormal. From 300-320 mOsm/L, is graded
as mild; from 320-340 mOsm/L, is graded as
moderate; and greater than 340 mOsm/L, is graded
as a severe dry eye disease.
6: Ocular
surface staining by Fluorescein: It stains the corneal stroma under the
desquamated epithelium but does not stain a
dry spot (it becomes hydrophobic after losing its mucin coating), and appears
as a blue spot in the uniform green fluorescence of the tear film. Fluorescein pools in the
areas of epithelial erosions/thinning. The area of ocular surface stained
should be noted as an interpalpebral staining is due to excess evaporation of
aqueous while an inferior limbal staining is due to
a toxic meibum production.
Rose
bengal and lissamine green stain dead / devitalised epithelial cells and
healthy cells that have lost their mucin coating. The
conjunctiva is more intensely stained than the cornea. Therefore, early or mild
cases of dry eye disease can be detected more easily with these dyes.
7: Tear-film
Break up time (TFBUT): It is assessed by instilling a drop of
fluorescein stain in the conjunctival sac and using a slit lamp with cobalt
blue illumination. Time is noted between the last blink and the appearance of a
black island in the normal green fluorescence of the tear film, or the first
dry spot on the cornea. The test is performed prior to the instillation of
anaesthetic eye drops (as they are toxic to the corneal epithelium and produce
dry spots). Normal TFBUT is 15-45 seconds. If it is
> 5 seconds, the patient is usually
asymptomatic, but when it becomes less than 2 seconds,
the patients are almost invariably symptomatic.
8: Blink
dynamics need to be noted: The examiner evaluates, by inspection on a
slit-lamp, whether the upper lid closes on to the lower lid with a blink, the
frequency of partial and complete blinks, the area of ocular surface (cornea
and conjunctiva) that remains exposed with each complete blink.
9: Schirmer’s test:33 It is
of two types: Schirmer I performed without the topical anaesthesia and Schirmer
I performed after topical anaesthesia.
S
I test performed after topical anaesthesia measures only the basal
lacrimal secretion. It is highly
specific and sensitive for a dry eye disease due to aqueous deficiency. After
instilling a topical anaesthetic, a thin strip of filter paper (5 x 35 mm) is
placed in the inferior cul-de-sac in the lateral canthus. The excess tears
should be wiped off prior to measuring the basal aqueous production. This
distinguishes a dry eye due to less aqueous production from the one due to
excess aqueous evaporation (due to MGD).
S
I test can be performed without the anaesthesia: this measures the
basal tear secretion (which is from the accessory lacrimal glands) as well as
the reflex secretion from the main lacrimal gland which is stimulated by the
irritating nature of the filter paper. Less than 10 mm of wetting after 5
minutes is diagnostic of ATD. The test is relatively specific, but it is poorly
sensitive.
Schirmer
II test is performed without the anaesthesia. The nasal mucosa is stimulated by
a cotton wisp or a pungent odour and the amount of tear production (both reflex
and basal) are noted. This should only be performed in patients in whom
Schirmer I test fails to demonstrate tear production (in KCS).
10: Meibography: Document
morphology and meibomian gland count in upper and lower lids by infra-red
camera, confocal microscopy, spectral-domain optical coherence tomography.
Normal meibomian glands are long, vertical, extending from the lid margin to
the end of tarsal plate. They become dilated and tortuous in early/mild disease.
In disease of intermediate duration/ moderate severity, the
gland dropout increases with loss of identifiable gland architecture. In prolonged
/ severe disease, all glands are markedly shortened or absent.
Management and Treatment of MGD34
i: Patient
education: this is the most important part of treatment in order
to ensure compliance to therapy. Patients need to be educated regarding the
chronic nature MGD, its prolonged therapy, affect of diet (flaxseed oil, fish
oil, and olive oil), environment dryness/humidity and the drying effects of
topical or systemic medications.
ii: Lid
hygiene: lids
should be scrubbed gently with diluted baby shampoo applied on cotton-tipped
applicator, and rinsed with lukewarm water. This removes toxic foamy meibum and
reduces microbial load.
iii: Warm compresses or application of
heat is the mainstay of therapy. Normal meibum is liquid at body temperature,
but denatured meibum becomes thick, dry and hard. It blocks the duct opening as
well as the whole lumen of the ducts. Heat therapy dissolves the thick meibum,
and to be effective, the glands have to be consistently heated to at least 45°C
(113°F). This can be done with application of a warm wet towel or cotton pads,
soaked in hot (not boiling) water; with the eyes closed, the hot towelis held onto the
eyelids for 2 minutes. It is made wet again with hot water and the process
repeated five times, so that total heat application is for 10 minutes. This
needs to be done daily for at least a month. It can also be done with commercially
available heat masks, or devices (Lipi Flow Thermal Pulsation System, MiBo
Thermaflow)35 that helps the liquefaction of meibum and massages it
upwards towards the ducts from where it can be easily expressed.
iii: Gentle
massage:
after the application of heat, upper eyelid should be massaged downwards with
the fingers, while the lower lid massaged upwards to establish meibum flow out
of the glands.
iv: Blinking
exercises: they help improve meibum flow and tear-film spread over
the ocular surface by contraction of pre-tarsal orbicularis and Riolan muscle.
Patients should be advised to do 10 good blinks at a
time; the eyes should be fully closed for 2 seconds, then squeezed for another
2 seconds. This should be done for every hour of
digital device use.
iv: Topical
lubricants: They help to relieve ocular surface irritation by replenishing
the tear film. Preservative-free
preparations should be preferred to prevent further damage to the ocular
surface.
v: Topical or
systemic antibiotics to control infections: low-dose oral
doxycycline (50-100 mg/day for 6 weeks) helps to reduce inflammation in the
eyelid tissue, it is anti-angiogenic and helps in restoring healthy meibum
secretion. Azithromycin 250 mg once daily is also affective in patients allergic
to doxycycline.
vi: Topical
Cyclosporin eyedrops (0.5%)36 or Tacrolimus ointment
/ skin cream 0.03%: Cyclosporine as well as Tacrolimus are highly specific
immuno-modulator drugs that primarily affects T-lymphocytes. They are used as
steroid-sparing agents as they have all the anti-inflammatory affects but
without the side-effects of prolonged steroid use. They increase the production
of aqueous, improve goblet cell count and reduce meibomian gland inflammation.
In addition, Tacrolimus cream applied to the lid margin reduces vascular
congestion, telengiactasia, and improves the quality of meibum produced. To
have these affects, therapy has to be continued for 2-4 months. The tear-film
break-up time has shown to improve with this therapy.
vi: Treating
Demodex mite infestation:37 Management involves reduction in the number of Demodex mites;
total eradication is not required as it is a part of the normal skin flora. This
can be achieved by a combination of lid scrubs (scrubbing the eyelids twice daily
with baby shampoo diluted with water to yield a 50% dilution and applying an antibiotic
ointment at night until resolution of symptoms) and removal of the eyelash
collarettes with the use of a cotton-tipped applicator and lid foam. Demodex
mites are resistant to a wide range of antiseptic agents including 10%
povidone-iodine, 75% alcohol and erythromycin. The most effective and commonly
used treatment is tea tree oil. Chemically, it is Terpinen-4-oil –a terpene
with antimicrobial, antifungal, and antiseptic properties. There are many commercially
available products that contain tea tree oil like shampoo, soap, ointment, skin
cream. Hypochlorous acid and mercury oxide 1% ointment is also effective.
Patients should be instructed to avoid oil-based cleansers and greasy makeup as
they can provide further "food" for the mites. They should discard
the previously used make-up, use hot water to wash their clothes, and a hot
dryer to dry them.
vii: Intra-ductal
Probing:
it clears the obstruction of the ducts and allows the meibum to flow thereby
reducing the intra-ductal pressure (IDP), inflammation, lid congestion with
improvement of symptoms.
viii: Intense
pulsed light (IPL): this also liquifies the meibum and
improves its drainage by delivering a
combination of heat and gentle pressure to the eyelids. It is an in-office
therapy and requires 1-2 sessions.
The
International Workshop on MGD recommended a Staged Treatment Algorithm,
depending upon the grade of MGD.
Grade
1:
i: Patient
education regarding MGD, diet, environment.
ii: Lid hygiene.
iii: Warm compresses.
Grade
2:
i: Advise
patient to use humidifiers in air-conditioned rooms, and increase dietary
intake of Omega 3 fatty acids, or use dietary supplements containing linoleic
acid (vegetables, fruits, nuts, grains and seeds; linseed oil) or
docosahexaenoic acid (DHA) 1000 mg daily.
ii: Warm compresses followed by firm lid massage
.
iii: Blinking exercises.
iv: Topical Lubricants.
v: Topical
tetracycline / azithromycin eye ointment massaged to lid margin38.
VI: Oral tetracycline,
50-100 mg or azithromycin, 250 mg daily for a month39.
Grade
3: All in Grade 2 plus:
i: Add
anti-inflammatory therapy for dry eyes (Topical Cyclosporin 0.5%, Tacrolimus
0.03%)40,41
ii: Ductal probing.
Grade
4: All of Grade 3 therapy.
CONCLUSION
MGD
is an extremely common clinical entity and is the leading cause of an
evaporative dry eye. It should be specifically looked for and treated in its
early stages even in an asymptomatic patient; if untreated, it progresses to
meibomian gland atrophy and drop out which is an irreversible stage. The goal
of therapy is to improve the flow and the quality of meibum so as to restore
the stability of the tear film. Since the therapy has to be continued for 2-3
months, patient education is mandatory to ensure compliance.
Author’s Affiliation
Dr.
Sameera Irfan
FRCS,
Consultant
Author’s Contribution
Dr.
Sameera Irfan
Literature
review, Manuscript writing & review.
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