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Meibomian Gland Dysfunction

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ISSN 0886-3067 Home (current) Issues OSP Research Grant About The Journal Subscription Submit Article Search Contact Us Volume No 35 Issue No 1 Meibomian Gland Dysfunction 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 sur-face 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 interna-tional 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.
63 Vol. 35, No. 1, Jan Mar, 2019 Pakistan Journal of Ophthalmology
Review Article
Meibomian Gland Dysfunction
Sameera Irfan
Pak J Ophthalmol 2019, Vol. 35, No. 1
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
See end of article for
authors affiliations
Correspondence to:
Sameera Irfan
FRCS, Consultant
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 abnor-
malities 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 prima-
ry cause of dry eye disease worldwide. Previously dry eye disease was consi-
dered 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, blepharos-
he 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 defini-
tion 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 qualita-
tive/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 anatomi-
cally 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 fol-
licles. The term posterior Blepharitis means the in-
flammation 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 seba-
Pakistan Journal of Ophthalmology Vol. 35, No. 1, Jan Mar, 2019 64
ceous 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 parasym-
pathetic nerves (via the V nerve) as supplying the la-
crimal and accessory lacrimal glands, thereby ensuring
an optimal composition of the tear film. There is also a
strong hormonal control mediated by estrogens, an-
drogens, progestins, retinoic acid, growth factors and
The secretion of meibomian glands is called mei-
bum9 which is primarily made up of nonpolar lipids
(about 90%, comprising of wax, sterol-esters and tri-
acylglycerols), while less than 10% are polar amphi-
philic 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 aqueouslipid interface
and acts as a surfactant (essential for the uniform
spreading and stability of the tear film). This is cov-
ered by a thick layer of non-polar lipids that forms the
lipidair 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 re-
lease 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 orbi-
cularis 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
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 thin-
ning and evaporation in-between the blinks, and mak-
ing 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 meibo-
mian 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
vii: The lipids help seal the apposing lid margins dur-
ing sleep.
Pathophysiology of MGD
MGD is a complex disease that is caused by the inter-
play of hormonal, microbial, metabolic and environ-
mental 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 conjunc-
tival 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 sta-
sis 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, de-
creased expression of androgen receptors (hor-
monal 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-
65 Vol. 35, No. 1, Jan Mar, 2019 Pakistan Journal of Ophthalmology
histamines, anti-depressants, hormone replace-
ment 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 fur-
ther decreased secretion of meibum; this makes the
meibum more vicid and enhances further obstruction.
In addition, stasis of meibum inside the ducts pro-
motes the growth of commensal bacteria, which pro-
duce lipases that cause meibum degradation and re-
lease of toxic chemicals. These factors aggravate the
primary hyper-keratinisation and compositional dis-
turbance of meibum and result in a progressive MGD.
Chronic obstruction leads to degeneration of the secre-
tory gland tissue and even if the primary obstruction
is later resolved by therapeutic approaches, the dam-
age 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 sur-
This is due to meibocyte abnormalities seen as re-
sult 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 asso-
ciated 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 hor-
mones (androgen and estrogen) are present within
the meibomian glands while meibocytes (the epi-
thelial cells lining the acini) contain enzymes
which are necessary for the synthesis and metabol-
ism of sex steroids. Androgens stimulate the secre-
tion of meibum by promoting the synthesis of li-
pids 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 produc-
tion 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 meibo-
mian 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 ova-
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 proli-
feration of basal cells of the acini, a high pro-
tein/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 holo-
crine secretion), with subsequent gland atrophy
and hypo-secretion. Exhaustion of the basal cells
leads to the atrophy of acini and meibomian gland
4: Topical Medications19,20: All topical medications
contain preservatives to enhance their shelf life.
The most commonly used preservative is Benzal-
konium 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 morphol-
ogy 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
Pakistan Journal of Ophthalmology Vol. 35, No. 1, Jan Mar, 2019 66
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 organ-
isms on the eyelid margin, in particular Staphylo-
coccus aureus. The bacterial lipases, in turn, break
down the neutral fats and cholesterol esters, re-
leasing glycerides and free fatty acids into the tear
film, destroying the mucin layer and making the
cornea hydrophobic. This makes the tear film un-
stable. 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 humans-
kin and constitutes a part of the normal flora. It
produces disease when its cell population increas-
es 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 fol-
licles, 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 lay-
ing eggs at the base of eyelashes, causing follicular
distention and misdirected lashes. D. brevis me-
chanically 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 drop-
let of oil, sodium fluorescein, peanut oil, or 75% alco-
hol 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
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 in-
flammation. 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 syn-
drome, ectodermal dysplasia with cleft-lip/palate
(ECC syndrome). Rudimentary meibomian glands
maybe visible as yellow streaks on the conjunctiv-
al surface of the tarsal plate.
Dystichiasis (aberrant row of eyelashes) maybe
present at birth in which meibomian glands are re-
placed by an extra row of eyelashes at the grey line.
The misdirected eye lashes cause ocular surface trau-
ma 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 insta-
bility 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
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 com-
puter screen or watching television. This results in
blurred vision, reduced focusing ability, and diplopia.
Despite the presence of a dry eye, a foreign body sen-
sation 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 blow-
ing air.
Chronic lid margin inflammation is manifested by
67 Vol. 35, No. 1, Jan Mar, 2019 Pakistan Journal of Ophthalmology
symptoms of lid discomfort, pain, redness and irrita-
The symptoms related to ocular surface inflamma-
tion are burning, itching, frequent blinking and pho-
tophobia which gradually worsens to severe blepha-
rospasm.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, telangiecta-
sia, 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 appli-
cator, 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 treat-
ment. 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 com-
plete 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. Pa-
tient 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 bac-
terial lipases). Patient may be asymptomatic or may
have slight discomfort of lid margins, mild conjunctiv-
al hyperaemia, mild corneal staining detected by fluo-
rescein 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 symp-
toms and corneal staining.
iv: Ocular Surface Signs: Damage to the ocular sur-
face can result from avariety of closely linked factors
like increased tear-film evaporation that causes hyper-
osmolar 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 contribu-
tor to an evaporative dry eye disease, but an increased
tear production (measured with Schirmers test) may
be noted in patients with MGD. This is due to a com-
pensatory reflex tearing due to ocular surface abnor-
malities and discomfort.
Diagnostic tests:30
1: Administer a symptoms questionnaire, Ocular
surface Disease Index (OSDI).31 This question-
naire assesses symptoms of photophobia, ocular/
eyelid pain, blurring of vision, problems with
reading/driving/watching TV.
Pakistan Journal of Ophthalmology Vol. 35, No. 1, Jan Mar, 2019 68
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 al-
ready 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 in-
strument 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 concen-
tration of solutes/salts). As the aqueous component
of the tear-film evaporates, the concentration of
solutes (mainly salts) increases. This test has be-
come a critical part of dry eye management. It re-
quires 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 ex-
pensive equipment and its constant maintenance.
The osmolarity of both eyes is measured; a differ-
ence of 8 mOsm/L or more in the tear osmolarity be-
tween 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 epithe-
lium but does not stain a dry spot (it becomes hy-
drophobic after losing its mucin coating), and ap-
pears as a blue spot in the uniform green fluores-
cence of the tear film. Fluorescein pools in the
areas of epithelial erosions/thinning. The area of
ocular surface stained should be noted as an inter-
palpebral 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 / de-
vitalised 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 conjunc-
tival sac and using a slit lamp with cobalt blue il-
lumination. 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 pa-
tients 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 con-
junctiva) that remains exposed with each complete
9: Schirmer’s test:33 It is of two types: Schirmer I per-
formed 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 fil-
ter 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 pro-
duction. 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 secre-
tion 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 anaes-
thesia. The nasal mucosa is stimulated by a cotton
69 Vol. 35, No. 1, Jan Mar, 2019 Pakistan Journal of Ophthalmology
wisp or a pungent odour and the amount of tear pro-
duction (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 mei-
bomian gland count in upper and lower lids by in-
fra-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 dis-
ease. In disease of intermediate duration/ mod-
erate severity, the gland dropout increases with
loss of identifiable gland architecture. In pro-
longed / 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 ef-
fects 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 micro-
bial load.
iii: Warm compresses or application of heat is the
mainstay of therapy. Normal meibum is liquid at
body temperature, but denatured meibum be-
comes thick, dry and hard. It blocks the duct open-
ing as well as the whole lumen of the ducts. Heat
therapy dissolves the thick meibum, and to be ef-
fective, the glands have to be consistently heated
to at least 45°C (113°F). This can be done with ap-
plication 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 devic-
es (Lipi Flow Thermal Pulsation System, MiBo
Thermaflow)35 that helps the liquefaction of mei-
bum and massages it upwards towards the ducts
from where it can be easily expressed.
iii: Gentle massage: after the application of heat, up-
per 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 de-
vice 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 infec-
tions: 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 res-
toring healthy meibum secretion. Azithromycin
250 mg once daily is also affective in patients al-
lergic to doxycycline.
vi: Topical Cyclosporin eyedrops (0.5%)36 or Tacro-
limus 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 af-
fects but without the side-effects of prolonged ste-
roid 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 quali-
ty 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 Manage-
ment involves reduction in the number of Demo-
dex 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 eye-
lids twice daily with baby shampoo diluted with
water to yield a 50% dilution and applying an an-
tibiotic ointment at night until resolution of symp-
toms) 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 an-
Pakistan Journal of Ophthalmology Vol. 35, No. 1, Jan Mar, 2019 70
tiseptic 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 an-
timicrobial, antifungal, and antiseptic properties.
There are many commercially available products
that contain tea tree oil like shampoo, soap, oint-
ment, 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 pre-
viously 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), inflam-
mation, lid congestion with improvement of
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
The International Workshop on MGD recom-
mended a Staged Treatment Algorithm, depending
upon the grade of MGD.
Grade 1:
i: Patient education regarding MGD, diet, environ-
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 (Top-
ical Cyclosporin 0.5%, Tacrolimus 0.03%)40,41
ii: Ductal probing.
Grade 4: All of Grade 3 therapy.
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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... 4 Posterior Blepharitis and Meibomian gland disease contribute around 60% of the disease burden in Asian countries. 5,6 An estimated 16.4 million individuals in America face dry eye conditions and MGD, with the burden of the disease being 9.3% among adults. 7 However, long-term treatments lead to complications. ...
Objectives: to compare the efficacy of warm compresses to add-on therapy with Loteprednol-Tobramycin in patients withposterior Blepharitis. Study Design: Quasi-experimental study. Place and Duration of Study: Armed Forces Institute of Ophthalmology, Rawalpindi Pakistan, from Jun 2020 to Jul 2021. Methodology: Pre-diagnosed posterior blepharitis patients using warm compresses (Group-A) and add-on antibiotic steroid therapy (Group-B) were included in the study. A detailed history and ophthalmic examination evaluated tear breakup time, tear film height, intra-ocular pressure measurement, meibomian gland function, structure, and meibum appearance. In addition, the patient's symptoms were noted through the ocular surface disease index questionnaire. Results: The study sample had seventy-one males (56%) and 55 females (43.6%) with mean age of 35.33±12.24 years. The clinical parameters in the two groups were almost alike at enrollment. There was a significant improvement in the clinical parameters in both groups. With slightly better improvement among Group-B (using Loteprednol-Tobramycin), Only two individuals did not report an increase in IOP at six weeks of treatment in Group-B. (p=0.53). Conclusion: Lid hygiene with warm compresses is an effective alternative with no side effects, provided if appropriately practised; however, add-on therapies may further improve MGD and Blepharitis.Keywords: Blepharitis, Meibomian gland dysfunction, Warm compresses.
... The wearers of eye cosmetics, particularly oil-based products, tend to present higher rates of demodex mites. 90 This common parasitosis within eyelash follicles is responsible for duct blockage. 51 These mites are highly prevalent in the older population with dry eye and specifically manifest symptoms of itching and cylindrical dandruff. ...
Full-text available
Dry eye disease (DED), a multifactorial condition of the tear film and ocular surface, is one of the leading reasons for patients seeking eye care. Despite the multiple toxic ingredients of eye make-up products and their long-term application close to the ocular surface, few studies have analyzed their role in initiating and worsening DED. Females and the elderly experience the highest prevalence of DED and may be particularly vulnerable to the effects of eye make-up. The multifactorial nature of DED and common mechanisms behind several ocular surface diseases make it difficult to link a particular ingredient-driven mechanism to DED. Therefore, here, we list potential responses to eye cosmetics that may be involved in DED development. The first part of this review introduces the anatomy of the eye and DED, the second section explains the classification of eye cosmetic products, and the final part discusses the undesired effects under physical, pathogenic, and chemical insults.
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Steven J Dell Dell Laser Consultants, Austin, TX, USA Abstract: There is a clear association between dry eye disease (DED) and skin inflammatory diseases occurring in close proximity to the eyelids, such as facial skin rosacea. Intense pulsed light (IPL) is widely accepted as a treatment for skin rosacea. A number of recent studies demonstrated that, in patients suffering from meibomian gland dysfunction (MGD), IPL therapy also reduces signs and symptoms of DED. Despite these encouraging results, in the context of DED and MGD, the mechanisms of action of IPL are not well understood. The purpose of this review was to raise the potential mechanisms of action and to discuss their plausibility. Keywords: intense pulsed light, dry eye disease, meibomian gland dysfunction, skin rosacea
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Purpose: The aim of the study was to understand natural changes of meibomian glands (MG) that occur with aging in the absence of any ocular pathology or ocular discomfort symptoms, to differentiate between "age normal" and pathologic or dysfunctional changes of the MG. Methods: A total of 185 subjects (109 females) with no pre-existing ocular and systemic abnormalities were recruited and divided into four age groups: 25 to 34, 35 to 44, 45 to 54, and 55 to 66 years. At a single visit, the following MG measures were collected: meibum quality (MQ) and MG expressibility (MGE) of the lower lid, and MG drop-out score (meiboscale) using infrared meibography of the upper and lower lids. Assessments of anterior eye, tear function variables, noninvasive and invasive tear breakup time (TBUT), corneal integrity, and lid wiper epitheliopathy were also performed during the visit. An Ocular Surface Disease Index (OSDI) questionnaire was used to record dry eye symptoms. Meibum lipids samples were collected and analyzed. Results: A majority of the study population (61%) was asymptomatic. There was a significant worsening in the MQ (P< 0.048), MGE (P < 0.03), and meiboscale (P < 0.01) with increasing age. Significant increase was observed in anterior blepharitis (P < 0.001) and telangiectasia (P< 0.02) with aging. Interestingly, tear osmolarity decreased significantly (P < 0.001), while tear meniscus height (P < 0.001) and invasive TBUT (P = 0.02) increased with increase in age. There was no significant association between MG variables and sex, ocular discomfort symptoms, or meibum lipids classes. Conclusions: Progressive MG loss occurs normally with age accompanied by reduced quality and quantity of the meibum produced. However, clinical presentation of ocular discomfort symptoms is stalled without corresponding disruption to tear function.
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Meibomian gland dysfunction (MGD) is the most frequent cause of dry eye disease (DED). Eyelid inflammation, microbial growth, associated skin disorders as well as potentially severe corneal complications culminate to make MGD a complex multifactorial disorder. It is probable that MGD is a heterogeneous condition arising from any combination of the following five separate pathophysiological mechanisms: eyelid inflammation, conjunctival inflammation, corneal damage, microbiological changes and DED resulting from tear film instability. The pathogenesis of both MGD and DED can be described in terms of a ‘vicious circle’: the underlying pathophysiological mechanisms of DED and MGD interact, resulting in a double vicious circle. The MGD vicious circle is self-stimulated by microbiological changes, which results in increased melting temperature of meibum and subsequent meibomian gland blockage, reinforcing the vicious circle of MGD. Meibomian gland blockage, dropout and inflammation directly link the two vicious circles. MGD-associated tear film instability provides an entry point into the vicious circle of DED and leads to hyperosmolarity and inflammation, which are both a cause and consequence of DED. Here we propose a new pathophysiological scheme for MGD in order to better identify the pathological mechanisms involved and to allow more efficient targeting of therapeutics. Through better understanding of this scheme, MGD may gain true disease status rather than being viewed as a mere dysfunction.
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Introduction: A new technique of minimally invasive orbicularis myectomy is described. A study is presented to show its efficacy in relieving spasms in benign essential blepharospasm and to note any complications resulting from it. Materials and Methods: In a prospective clinical, interventional study conducted at oculoplastics department of a tertiary care center, 25 consecutive cases (50 eyes) of benign essential blepharospasm were included, from January 2012 to December 2014. The patients consisted of 19 women and 6 men between the ages 28 and 66 years (mean age, 52 years). After a thorough history, a complete ophthalmological examination, and assessment of functional disability, they received appropriate therapy for triggering factors such as dry eyes, meibomitis, blepharitis, and trachoma for 1 month, after which a minimal orbicularis myectomy of both the upper and lower lids was performed simultaneously under local anesthesia by a single surgeon. The cases were followed up after 1 week, 1 month, 3 months, 6 months, and 1 year. Results: Six cases (24%) needed simultaneous brow suspension; 4 cases (16%) had blepharoplasty for dermatochalasis. Postoperatively, ecchymosis of lids was noted in 13 cases (52%) and lid swelling in 3 cases (12%). No lad lag, lid asymmetry, or corneal exposure was seen in any case. Three cases needed frontalis suspension for apraxia of upper lids, which was done 1 month postoperatively. Patient satisfaction was 100%, with improved functional disability. Conclusion: Minimal orbicularis myectomy was found to be effective in providing a long-term relief of spasms and was not associated with any com plications. However, proper patient selection is mandatory.
Full-text available
To summarize recent advances on ocular Demodex infestation. Demodex infestation is a potential cause of ocular surface inflammation. The pathogenesis of Demodex in eliciting ocular surface inflammation has been further clarified. Cliradex is currently the treatment of choice, it comprises the most active ingredient of tea tree oil, that is terpinen-4-ol, which helps eradicate Demodex mites and reduce ocular surface inflammation. Ocular demodicosis is a common but overlooked eye disease that manifests a number of morbidities. Demodex folliculorum causes chronic anterior blepharitis whereas Demodex brevis causes posterior blepharitis, meibomian gland dysfunction, recurrent chalazia, and refractory keratoconjunctivitis. The lash sampling and microscopic counting method and in-vivo confocal microscopy are key diagnostic methods. Cliradex shows promising potential to reduce Demodex counts with additional antibacterial, antifungal, and anti-inflammatory actions.
Aims: To report the clinical characteristics and correlation between meibomian gland dysfunction (MGD) and keratitis in young patients with ocular demodicosis. Methods: Observational case series of 60 patients younger than 35 years with ocular demodicosis, of which the diagnosis was based on microscopic counting of Demodex folliculorum and D. brevis of epilated lashes. Severity of keratitis and MGD was graded by photography and meibography, respectively, in a masked fashion. Results: MGD was detected in 54/60 (90%) patients with the loss of meibomian gland in the upper lid more than the lower lid (p<0.001). Blepharoconjunctivitis and a variety of corneal pathologies were noted in 47/60 (78.3%) and 39/60 (65%) patients, respectively. For a total of 120 eyes, normal cornea was noted in 53 (44.2%) eyes, superficial punctate keratitis or limbitis was noted in 17 (14.2%), while corneal stromal infiltration was found in 50 (41.7%) eyes. Both univariate and multivariate analyses showed that the severity of meibomian gland loss was significantly correlated with higher D. brevis count and more severe keratitis (all p<0.05). Rapid resolution of keratitis and blepharoconjunctivitis was accompanied by significant reduction of the Demodex count in 48 patients receiving lid scrub directed to kill mites. Conclusions: There is a significant correlation between MGD and keratitis in young patients with ocular demodicosis especially inflicted by D. brevis.
The members of the Management and Therapy Subcommittee undertook an evidence-based review of current dry eye therapies and management options. Management options reviewed in detail included treatments for tear insufficiency and lid abnormalities, as well as anti-inflammatory medications, surgical approaches, dietary modifications, environmental considerations and complementary therapies. Following this extensive review it became clear that many of the treatments available for the management of dry eye disease lack the necessary Level 1 evidence to support their recommendation, often due to a lack of appropriate masking, randomization or controls and in some cases due to issues with selection bias or inadequate sample size.
Background/aims To assess the efficacy and safety of oral azithromycin compared with oral doxycycline in patients with meibomian gland dysfunction (MGD) who had failed to respond to prior conservative management. Methods 110 patients (>12 years old) with MGD were randomly assigned to receive either oral 5-day azithromycin (500 mg on day 1 and then 250 mg/day) or 1-month doxycycline (200 mg/day). They also continued eyelid warming/cleaning and artificial tears. A score comprising five symptoms and seven signs (primary outcome) was recorded prior to treatment and at 1 week, and 1 and 2 months after treatment. Total score was the sum of both scores at each follow-up. Side effects were recorded and overall clinical improvement was categorised as excellent, good, fair or poor based on the percentage of change in the total score. Results Symptoms and signs improved significantly in both groups (p=0.001). While improvement of symptoms was not different between the groups, bulbar conjunctival redness (p=0.004) and ocular surface staining (p=0.01) were significantly better in the azithromycin group. The azithromycin group showed a significantly better overall clinical response (p=0.01). Mild gastrointestinal side effects were not significantly different between the groups except for the second visit, when the doxycycline group had significantly more side effects (p=0.002). Conclusions Although both oral azithromycin and doxycycline improved the symptoms of MGD, 5-day oral azithromycin is recommended for its better effect on improving the signs, better overall clinical response and shorter duration of treatment. Trial registration number NCT01783860.