1. health and fitness
2. disease

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Blepharitis, but not
as you know it
Gillian Bruce MCOptom, DipTP(IP) and Ian Cameron MCOptom, DipCLP, DipTP(IP), FBCLA
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28/02/14 CET
This straight-talking article provides the reader with a clear understanding of how to investigate and diagnose lid
margin disease. It offers useful tips on managing eyelid disease that will save the practitioner time, delight
patients, and provide a welcome boost for business.
Course code: C-35258 | Deadline: March 28, 2014
Learning objectives
To be able to explain to patients about the implications of lid margin disease
(Group 1.2.4)
To be able to recognise the signs and symptoms of lid margin disease and
manage the patient accordingly (Group 6.1.4)
Learning objectives
To be able to explain to patients about the implications of lid margin disease
(Group 1.2.4)
To be able to recognise the signs and symptoms of lid margin disease and manage
the patient accordingly (Group 8.1.1)
Learning objectives
To be able to explain to patients about the implications of lid margin disease
(Group 1.2.4)
Learning objectives
To be able to understand the natural progress of blepharitis and assess its severity
(Group 1.1.1)
To be able to consider the treatment options for blepharitis (Group 2.1.6)
About the authors
Gillian Bruce and Ian Cameron are independent prescriber (IP) optometrists with experience in managing anterior eye conditions. Based in a
leading UK practice, specialising in contact lens and anterior eye conditions, they are responsible for delivering the Lothian hospital contact lens
service. Ms Bruce has lectured nationally on the topic of blepharitis and lid margin disease.
Introduction
Classification of lid disease
The eyelids are inextricably linked with dry
eye, and suffer from a host of inflammatory
conditions and other factors that affect comfort
and vision. The chronic, symptomatic nature
of these conditions means that they are a
persistent problem for patients and an ongoing
challenge for practitioners.
Despite the frequency with which it presents
in practice, blepharitis is still a condition that is
poorly understood. Simply classifying it can be
baffling, with many conflicting and inconsistent
terms in use. The first step to a clearer
knowledge of the murky world of lid disease is
to understand its relationship to anatomy.
Anatomy
The eyelids contain three types of secretory
gland, which are important when considering
lid disease. The meibomian gland and the
Gland of Zeis are both sebaceous types, with
the Gland of Moll, a type of sweat gland, being
the third (see Figure 1). Sebaceous glands are
small, oil-producing glands usually attached to
hair follicles, found in abundance on the face
and scalp. The fatty, oily substance that they
release is called sebum, which acts to lubricate
and waterproof the skin and provide some
protection against bacteria.
It is helpful to consider the eyelid as having
an anterior and posterior portion; anteriorly
consisting of the subcutaneous skin, eyelash
and glands of Zeis and Moll; posteriorly, the
tarsal conjunctiva and the tarsal plate housing
the meibomian glands.
There are approximately 30–40 meibomian
glands in the upper lid and 15–20 in the
lower lid, which are responsible for producing
meibum, a unique type of sebum. Meibum is
composed mainly of lipids along with proteins,
Orbicularis
oculi
Posterior lid
disease
Meibomian
gland
Skin
Gland of moll
Tarsal
conjunctiva
The natural course of
posterior lid disease may be
considered in stages
(see Figure 2):
49
Stages 1–3
Gland of zeiss
Anterior
Posterior
Figure 1 Anatomy of the eyelids
both of which play important roles in the
pre-corneal tear film. The nervous supply
to the meibomian glands are controlled by
the autonomic nervous system and meibum
production is controlled by both neuronal and
hormonal factors.
Meibum, along with lesser contributions
from glands of Zeis and Moll, forms the thin,
outermost lipid layer of the pre-corneal tear
film, the function of which may be summarised
as:
• Providing a smooth optical surface for the
cornea at the air-lipid interface
• Reducing evaporation of the tear film
• Enhancing the stability of the tear film
• Enhancing spreading of the tear film
• Preventing spillover of tears from the lid
margin
• Preventing contamination of the tear film by
sebum
• Sealing the apposing lid margins during
sleep.1
Considered simply, the tear
film can be disrupted by
either low production of
meibum (hyposecretion)
or excessive amounts
of poor quality meibum
(hypersecretion). Hyposecretion can be due to a
physical obstruction of the ducts by keratinised
epithelium or by reduced meibum production
influenced by hormone levels, age, contact
lens wear, and medication including: retinoids
for acne, antidepressants, antihistamines,
along with post-menopausal treatments.1
Hypersecretory changes are commonly linked
to dermatitis, acne rosacea and atopic disease.
The quantity and quality of the lipids
produced may be observed by expressing the
gland contents. Gentle digital pressure to the
centre of the lower lid for a few seconds during
a routine slit lamp exam should cause an oily
layer of clear or light straw-coloured meibum
to be expressed. If nothing comes out of the
Sub-clinical changes to meibum
Altered tear film
A spectrum condition
It is important to consider lid disease as a
spectrum condition ranging from the mildest
sub-clinical forms, with sequelae leading to
full-blown scarred, inflamed lids. The severity of
symptoms in each case will vary, with patients
presenting to the clinician at any stage of the
disease.
Having classified the lid as having anterior
and posterior portions, lid disease may be
grouped in a similar way with posterior lid
disease, frequently termed meibomian gland
dysfunction (MGD), and anterior lid margin
Signs and/or symptoms of ocular irritation
Clinically apparent inflammation
Structural lid changes
Ocular surface disease
Figure 2 The sequelae of posterior lid margin
disease
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28/02/14 CET
In the good old days of CET, when the multiplechoice questions were the only part of the
article a practitioner read, simply putting
‘blepharitis management’ in the title would be
a guaranteed way to attract attention. Surely
there could not be anything in the article that
you did not know already – a point in the bag.
Think again. CET has been ‘enhanced’ and now
it is time to do the same with the practitioner’s
understanding and management of lid margin
disease.
disease, each of which will be
considered in turn.
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50
glands, you can safely diagnose hyposecretion
of the meibomian glands. In hypersecretion,
the meibum is thicker and opaque with a more
yellow colour. Simple assessment of the tears
can also be a useful diagnostic tool. Reduced
tear break-up time (TBUT) (<10 seconds)
suggests a lack of meibum, while frothy tears
are characteristic of hypersecretory posterior
lid margin disease.
When hypo- or hypersecretion are seen,
the patient has already progressed to Stage
2 posterior lid disease. Left untreated, this
abnormal secretion will deteriorate and
eventually lead to symptoms of ocular
irritation such as foreign body sensation,
epiphora, glare, tired eyes and excessive
blinking, caused by a poor quality tear film.
Stage 4: inflammation
A poor tear film and stagnant lipids provide
an optimum environment for inflammation
and infection. The stagnant material becomes
a growth medium for bacteria that can seep
into the deeper tissue layers of the eyelid,
causing inflammation. A poor tear film and
corresponding dry eye cause inflammation of
the ocular surface and there is some evidence
that changes in lipid composition in the tear
film releases pro-inflammatory mediators.2
At this stage, with inflammation becoming
Figure 3 Staphyloccocal blepharitis
clinically apparent, it may be termed posterior
blepharitis.
Telangiectasia (capillary dilation) of the
posterior lid margin is one of the major
diagnostic signs of inflammation, but the
meibomian glands also begin to be visibly
affected with solidified plugs of opaque
meibum, clogging the openings with waxy
mounds protruding from blocked glands.
Stage 5: structural change
Although the patient may be asymptomatic,
left unchecked, low-grade chronic
inflammation of the posterior lid margin takes
it toll and eventually causes structural change.
Conjunctivalisation is a reliable sign of chronic
inflammation, where the posterior conjunctiva
Symptoms
Signs
Eyelids stuck together on waking
Madarosis (loss of eye lashes)
Itchiness
Trichiasis (misdirected eye lashes)
Glare
Poliosis (white lashes)
Blurred vision
Telangiectasia
Conjunctival injection
Lid margin hypertrophy
Lid scarring
Table 1 Characteristics of anterior lid margin disease
trespasses over the mucocutaneous junction,
causing a fluffy scalloped edge which is
visible at the tear meniscus. Meibomian gland
drop out (ceasing to function) and pitting
or scarring of the lid margin may be seen.
The tarsal plate acts like a skeleton for the
lid so deformity of the meibomian glands
will result in structural change to the lid
and conjunctiva. This undermines the role
of the lid margin in providing support for
the tear meniscus and may allow unwanted
substances to contact
the ocular surface.
Stage 6: ocular surface disease
A poorly performing eyelid eventually
leads to ocular surface disease. Chronic
inflammation and structural changes affect
the integrity of the ocular surface and
serious problems, such as marginal keratitis
and corneal neovascularisation may follow.
Such changes take many years of neglect
to develop, so often patients with more
severe lid problems are elderly and likely to
be referred for cataract and other surgeries.
Devastating surgical outcomes, including
endophthalmitis are associated with lid
disease and a compromised ocular surface.3
Anterior lid margin disease
Anterior lid margin disease originates from
the eyelashes and debris in this area is a
characteristic in the early stages of this
condition. The features of anterior lid margin
disease are summarised in Table 1.
As with posterior disease, anterior
conditions have a spectrum of severity
where chronic inflammation will result in
structural changes and eventually ocular
surface disease. Given their proximity,
chronic inflammation of either the anterior or
posterior lid margin will ‘spill over’ and begin
to affect the fellow margin. The characteristics
of the lash debris are a key differentiator in
identifying the cause.
Staphylococcus are part of the commensal
flora of the eyelid about 75% of the time,
becoming problematic only if a there is a
hypersensitivity reaction to either the bacteria
itself, or its toxins, waste products and
enzymes. Staphylococcal debris and white
blood cells form yellow, brittle fibrinous scales
at the lash base (see Figure 3). They may form
into distinctive rings or pyramids of debris
around the lash base, called collarettes.
Figure 4 Demodex mite infestation
Demodex mite infestation
Demodex mites are found on the human body
in or near hair follicles, including the eyelids
(see Figure 4). They feed on skin cells, oils and
hormones and exist in two forms, Demodex
folliculorum at the lashes and Demodex brevis
in the meibomian glands.4 The prevalence of
the mites increases with age and poor hygiene
and are strongly associated with symptoms
of ocular discomfort. Demodex infestation
forms a distinctive ‘greasy sleeve’-type collar
around the lashes. A demodex mite is about
half the diameter of a grain of table salt and is,
therefore, extremely difficult to see even at the
slit lamp.4
Seborrhoea
Certain dermatological conditions, such as
seborrhoeic dermatitis, rosacea and eczema
carry an increased risk of anterior lid margin
disease. Seborrhoea (a skin condition caused
by excess production of sebum) is present in
around 5% of the population. Scaly and greasy
material collects along the lashes and sticks
the lashes together in greasy clumps (see
Figure 5). The skin around the eyelashes often
looks greasy.
disconnect between practitioner and patient in
terms of stressing the importance of managing
the condition. Even the most enthusiastic
practitioner can become jaded with lid disease
but the chronic nature of the condition is of
utmost concern to the long-suffering patient
who may be blighted by symptoms of irritation
and visual impairment, leading to frustration
and even depression. Failure to manage lid
disease appropriately can result in cessation
of contact lens wear, delays to ocular surgery,
avoidable referrals into secondary care and
patients can become disillusioned with the
care from their eye care practitioner. Needless
to say, a more complete approach to eyelid
health is required:
Screening
To allow for early intervention, patients should
be screened. Taking a thorough history bearing
in mind risk factors and looking for external
clues from the patient’s appearance. Risk
factors include duration of contact lens wear,
dry eye disease, hormonal conditions, acne
rosacea, psoriasis, seborrhoeic dermatitis,
atopic history and hypertension.5
Management
Treatment
Expert consensus universally recommends
lid hygiene as the management of choice,
but if the treatment is so simple, why is lid
disease so poorly managed? The fundamental
reason is poor patient compliance. Lid
disease is poorly understood by patients, ill
communicated by the optometrist and the
commonly recommended treatments (sodium
bicarbonate, salt water, baby shampoo,
flannels) are laborious and long-term. Further,
the burden of maintaining treatment falls to
the patient and there can be a fundamental
Omega-3 essential fatty acids (EFA) directly
improve the lipid composition of the meibum
as well as having anti-inflammatory properties,
unlike omega-6, which is pro inflammatory.
Omega-3 and 6 compete for the same
conversion sites in the body; therefore,
improving the ratio of 3:6 is the aim. The
omega-3 EFAs critical for wellness and disease
prevention in humans are eicosapentanoic acid
(EPA) and docosahexanoic acid (DHA). These
are found in fish oils and are converted more
effectively by the body than alphalinolenic
acid (ALA), found in flaxseed oil, nuts, seeds
and dark leafy vegetables.
In general, patients will be more compliant
with therapies that are easily managed in
daily life. However, it is important to realise
that the presentation and content of the
advice may infer the seriousness of the
condition. With this in mind, recommending
kitchen cupboard ingredients as the
therapeutic agent of choice is, perhaps,
not the required approach. There is scant
evidence to suggest pre-made products have
superior efficacy to homemade remedies
and any form of lid hygiene is better than no
lid hygiene, although anecdotally, patients
respond well to using purpose-designed
products to treat lid disease.
Warm compress therapy
Warming the lash debris will ease removal,
while warming the meibomian glands will
aid expression. The meibum from normal
subjects becomes liquid at 28–32°C, but the
melting point is approximately 35°C for MGD
patients. This means that warm compress
therapy needs to be at a precise and constant
temperature,6 something not easily done
with a warm flannel at home. Custom-made
devices such as Eyebags are simple to use,
safe, effective and affordably priced. A novel
moist heat, lid-warming device, Blephasteam,
is also available for home use.
Massage
Thirty seconds of massage should be used
to physically express the contents of the
glands after warming them. Applying gentle
pressure from the root of the gland to the
duct, repeating the process a number of
times and advising patients that it is normal
to experience a smearing effect on vision.
Meibum expression is a sign of progress that
the glands are expelling unhealthy secretions.
Cleaning
In addition to removing secretions,
cleaning can provide antibacterial and antiinflammatory cover. Making a homemade
cleaning solution is time-consuming and
involves appropriate dilution to be safe. There
are a number of convenient products now
available in the form of solutions, gels and
impregnated cleaning pads.
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Staphyloccocal infection
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Tea tree is highly effective in the removal
of demodex mites. Guidelines suggest that
demodex can be killed by daily lid scrub with
50% tea tree oil (50% mineral oil is commonly
called ‘liquid paraffin’ in the UK) but this
should be undertaken only by experienced
practitioners as such preparations are toxic
to the ocular surface.7 Preparations such as
Cliradex and Ocusoft treatment kits for direct
use on the lashes are not readily available in
the UK, with lack of evidence to support the
efficacy of the lower concentrations of tea
tree oil in these products. Local herbalists
may be able to provide a safe preparation of
tea tree that can be used on the lashes. Tea
tree shampoos and facial soaps for the face
and scalp are widely available and readily
recommended by some ophthalmologists but
the low concentrations of tea tree oil in these
products means their efficacy is no better than
a basic lid hygiene regime.
Lubrication
After cleaning it is beneficial to restore
the tear film by instilling an artificial tear.
A non-preserved formulation should be
recommended for safe long-term use.
Figure 5 Seborrhoeic blepharitis
potent anti-inflammatories that inhibit the
production of bacterial lipases and alter the
consistency of meibomian oils. Oral antibiotics
can be prescribed by independent prescribing
optometrists or in conjunction with a GP for
the treatment of more significant disease,
pre-surgically, or in systemic conditions such
as acne rosacea. Such treatment needs to be
continued for a number of months and topical
applications can be used for more significant
inflammation. In seborrhoeic conditions,
medicated shampoos are recommended.
Lid hygiene should be performed twicedaily for the ‘treatment period’ (usually a
fortnight) and then may be reduced to daily
or less frequently for maintenance, under
supervision of the optometrist.
Medication
If staphylococcal infection is present then
a topical antibiotic ointment such as 1%
Chloramphenicol can be used on the lid
margin. Systemic tetracycline antibiotics, for
example, Oxytetracycline or Doxycycline, are
Communication
The key to success with all treatment is
good communication with the patient.
Other members of staff, trained in lid
hygiene procedures, can reinforce verbal
communication from the optometrist. Written
information consolidates the advice given in
the consulting room and hopefully prevents
patients straying to friends or the internet for
their information.
Information leaflets can be obtained from
the College of Optometrists, or can be written
by practitioners to reflect their choice of
treatment regimes. It is helpful to issue
patients with a ‘lid management care plan’, to
clarify the diagnosis to the patient, allowing
them to understand the cause of their
symptoms and engage in treatment. It details
each stage of the cleaning regime and the
required frequency of treatment and follow up.
Asking the patient to grade symptoms over a
number of months of treatment, reaffirms the
long-term nature of the regime.
Lid care/pre-surgery packs of products can
be put together with relevant information to
further reduce complications for the patient
and encourage repeat sales of cleaning and
lubricating products for the practice. These
packs can be recommended to every patient
prior to referral for cataract surgery.
Conclusion
The ageing population will only continue to
deliver more lid disease and with that more
potential for loyal patients who will need
and value continued care from the dedicated
practitioner. Treating lid disease is clinically
interesting, of lasting benefit to patients and
provides a revenue stream for the practice.
MORE INFORMATION
References Visit www.optometry.co.uk/clinical, click on the article title and then on ‘references’ to download.
Exam questions Under the new enhanced CET rules of the GOC, MCQs for this exam appear online at www.optometry.co.uk/cet/exams.
Please complete online by midnight on March 28, 2014. You will be unable to submit exams after this date. Answers will be published on
www.optometry.co.uk/cet/exam-archive and CET points will be uploaded to the GOC every two weeks. You will then need to log into your CET
portfolio by clicking on ‘MyGOC’ on the GOC website (www.optical.org) to confirm your points.
Reflective learning Having completed this CET exam, consider whether you feel more confident in your clinical skills – how will you change the way you
practice? How will you use this information to improve your work for patient benefit?