This document provides an overview of blepharitis, including its pathogenesis, diagnosis, and treatment. It defines blepharitis as a chronic condition characterized by an intricate relationship between ocular flora and meibomian gland dysfunction leading to lid inflammation. Key factors in blepharitis include abnormal secretions, organisms like staphylococcus, and a dysfunctional tear film. Diagnosis is mainly clinical but can include cultures, gland expression testing, and meibography. Treatment focuses on lid hygiene like warm compresses, scrubs, and massage as well as managing meibomian gland dysfunction and underlying causes like bacteria, Demodex, or rosacea.

1. 177
INTRODUCTION
Blepharitis, first described by Elschnig in 1908,1
is one of the most
commonly encountered ophthalmic conditions. It poses a significant
challenge to the managing clinician due to its chronic nature and avail-
ability of diverse treatment options but lack of scientific evidence for
their use. Nonetheless, given the prevalence of blepharitis, its associa-
tion with dry eye disease (DED), and its vision-threatening sequelae,
better understanding and management of this condition is essential for
reducing ocular discomfort and improving the patient’s quality of life.
PATHOGENESIS
The pathophysiology of blepharitis involves a complex interaction of
various factors, including: abnormal lid-margin secretions, lid-margin
organisms, and a dysfunctional precorneal tear film. There are several
classification systems for blepharitis.1–5
It can be anatomically subdi-
vided into anterior blepharitis (Fig. 4-4-1) that involves inflammation
of the lid margin anterior to the gray line, concentrated around the
eyelashes and follicles; and posterior blepharitis that involves inflam-
mation of the posterior lid margin, which may have different causes,
including meibomian gland dysfunction (MGD) (Fig. 4-4-2). Alterna-
tively, blepharitis can be classified according to the presenting clinical
features into staphylococcal, seborrheic, mixed staphylococcal and seb-
orrheic, and MGD.
Neha Gadaria-Rathod, Karen B. Fernandez, Penny A. Asbell 4.4Blepharitis
SECTION 3 External Diseases
PART 4 CORNEA AND OCULAR SURFACE DISEASES
Definition: Blepharitis is characterized by an intricate relationship
between ocular flora and meibomian gland dysfunction leading to lid
inflammation, corneal and conjunctival changes, and symptoms of
ocular discomfort.
Key features
■ Chronic burning, irritation, foreign body sensation, epiphora
■ Inflammatory changes of the eyelid including thickening,
erythema, hyperkeratinization, vascularization, telangiectasia,
or notching
■ Presence of scurf, collarettes, and sleeves along lashes
■ Minimal meibomian gland secretion with pressure or abnormal
meibum, which is turbid, foamy, or granular in appearance
Associated features
■ Tylosis (thickening and distortion of the lid margin)
■ Poliosis (loss of lash pigmentation)
■ Punctal misdirection and/or scarring
■ Conjunctival hyperemia
■ Perilimbal superficial corneal neovascularization
■ Catarrhal infiltrates
■ Acne rosacea
Fig. 4-4-1 Anterior blepharitis.
Fig. 4-4-2 Meibomian gland dysfunction.
The lid inflammation characteristic of blepharitis is most often due
to a combination of anterior and posterior factors of varying degrees. In
most types of blepharitis, there is some involvement of the meibomian
glands.6
The meibomian glands are tubuloacinar, holocrine glands that
produce and secrete meibum, an oily substance that produces the lipid
layer of the preocular tear film.7
Embedded in the tarsal plates, there are
normally 30–40 meibomian glands in the upper lid and 20–30 glands
in the lower lid. Each meibomian gland consists of a main duct sur-
rounded by grape-like acinar clusters. These ducts open into the lid
margin just anterior to the mucocutaneous junction, delivering
meibum to the tear film. MGD is defined as a chronic, diffuse abnor-
mality of the meibomian glands, commonly characterized by terminal
duct obstruction and/or qualitative/quantitative changes in the glandu-
lar secretion.4
Alterations in the composition of the meibomian secre-
tions occur in patients with chronic blepharitis.7–9
Alteration in
nonpolar lipids raises the melting point of the meibum, leading to

2. 4
178
CORNEAANDOCULARSURFACEDISEASES
rosacea. In ocular rosacea dilated and telangiectatic vessels at the lid
margin, and interpalpebral hyperemia may be seen.
DIAGNOSIS AND ANCILLARY TESTING
Blepharitis is mainly a clinical diagnosis. However, ancillary testing
may be considered in those who have chronic disease or are unrespon-
sive to therapy, to monitor treatment effect, and for research
purposes.
Cultures taken from the eyelid margins may grow the typical
bacteria associated with blepharitis, as well as viruses, such as herpes
simplex, herpes zoster, and molluscum contagiosum. Microscopic
examination of the epilated lashes may show demodex eggs, and
adult mites.17
Meibomian gland secretion can be analyzed by its quality and
expressibility. This can be done by digital pressure or with the use of a
device that applies a standard pressure that is equivalent to the pressure
exerted on the lids during a normal blink.22
This device is supposed to
target a standard area of one-third of the total number of glands (8–10
glands). Expressibility is graded according to the number of glands that
express fluid, and decreased expressibility indicates disease. Although
it sounds simple, a marked variability exists between individuals, hence
a definite cut-off cannot be defined. Also, the location of the glands
along the lid margin has influence in their expressibility. It was found
that nasal glands tend to express most actively, followed by central
glands, and then temporal glands.22
There is also evidence of diurnal
fluctuation of meibomian gland expression that may affect diagnosis
using this method.23
Quality of glandular secretion can be evaluated in
terms of appearance. It can be graded according to how cloudy or vis-
cous the secretion is. It can be classified as clear, cloudy opaque, vis-
cous, or toothpaste-like using various grading schemes.17,24
Changes in meibomian gland morphology and gland dropout can be
assessed using meiboscopy. This is done by transillumination through
the skin and observing the glandular silhouette through the everted
mucosal side. Photodocumentation of the same is called meibogra-
phy.17
Disadvantage of the transillumination method is that it may be
tedious and time-consuming. Non-contact meibography applies the
same principle but is easier and more rapid than transillumination. It
uses an infrared transmitting filter attached to a slit lamp and video
camera.25
Photographs are taken and meibomian gland morphology
and dropout are then analyzed. In vivo laser scanning confocal micros-
copy can be used to examine the microstructure of meibomian gland
acinar units and measure their size. These serve as new parameters
that significantly correlate with the clinical ocular surface and tear
function findings of MGD.26
TREATMENT
Treatment strategies include a combination of lid hygiene, manage-
ment of MGD, reducing bacterial colonization of the lids, suppression
of inflammation, and restoring tear function.27
It is crucial to educate
patients about the chronic, recurrent nature of the disease and the need
for long-term intervention. Despite the availability of diverse treatment
options, very few treatments have been extensively evaluated for safety
and efficacy in randomized controlled trials, and most are typically not
FDA approved for use in blepharitis specifically. Treatment recommen-
dations are largely dependent on clinical experience and published case
reports.
Lid hygiene, the mainstay of treatment for blepharitis, consists of
warm compresses, lid massage, lid scrubs, and avoidance of excessive
eye make-up. Treatment with warm compresses involves the placement
of a warm washcloth on closed lids daily for 5–10 minutes. Alternative
sources of heat for warm compresses include eye warmer devices with
infrared irradiation and moist air or eye warmer masks.27–29
The goals
of heat therapy are to soften and loosen encrustations, liquefy the
solidified and stagnant secretions and to dilate the ducts. This is fol-
lowed by lid massage. The eyelid is held taut at the outer corner with
one hand while the index finger of the other hand sweeps from the
inner corner of the lid toward the ear while applying pressure. This is
repeated several times to express the meibomian gland contents, which
have melted during the warm compresses step. Cleansing with lid
scrubs is usually done once or twice daily initially. Commercially avail-
able scrubs or a cotton-tipped applicator soaked with a weak solution
of baby shampoo can be used to rub along the lid margin to remove
deposits and the abnormal oily secretions from the lids. Patients should
thickening of the meibum and stagnation. Decreased amounts of polar
lipids result in uneven spreading of tears.10
This leads to instability of
the tear film and hyperosmolarity, increased bacterial growth, evapora-
tive dry eye, and ocular surface inflammation, including keratinization,
scarring, and retraction of the gland orifices, thus further exacerbating
MGD. Several factors can aggravate MGD such as increasing age, con-
tact lens wear, and hormonal imbalance.5,6,9
Several bacteria, fungi (Pitysporum), and parasites (Demodex) have
also been implicated. A phenomenon called Quorum sensing causes
normally innocuous ocular flora to acquire increased virulence and
become pathogenic.11,12
The most common organisms isolated from
patients with chronic blepharitis include Staphylococcus epidermidis,
Propionibacterium acnes, corynebacteria, and Staphylococcus
aureus.13,14
S. epidermidis and S. aureus produce lipolytic enzymes such
as triglyceride lipase, cholesterol esterase, and wax esterase, which
hydrolyze wax and sterol esters with the release of highly irritating free
fatty acids, resulting in the disruption of the tear film integrity.7
In
seborrheic blepharitis, the increased amount of low viscosity meibum
favors the growth of bacteria and leads to inflammation of the lids.9
Blepharitis is also frequently associated with acne rosacea, seborrheic
dermatitis, psoriasis, and atopy.13
Acne rosacea is a relatively common
chronic skin disease characterized by persistent erythema, telangiecta-
sis, papules, pustules, and sebaceous gland hypertrophy, predominantly
affecting the forehead, cheeks, and nose. Though the pathogenesis is
still unclear, recent studies suggest that it is primarily due to an altered
innate immune response in those with a genetic predisposition. Cer-
tain reactive oxygen species and infectious agents such as Demodex
folliculorum and H. pylori have also been implicated.15
OCULAR MANIFESTATIONS
Typical symptoms of blepharitis include redness, itching, burning,
crusting along the lid margin, loss of lashes, stickiness of lashes,
and tearing. Furthermore, as MGD has been suggested to be the
leading cause of DED,16
symptoms such as dryness, ocular irritation
and fluctuating vision may also point a clinician to examine the lid
margin. These symptoms are chronic, usually waxing and waning,
and may be exacerbated by some environmental factors, such as
wind, smoke, dust, cosmetic products, etc. Symptoms are usually
bilateral, but may be asymmetrical. The presence of predominantly
unilateral symptomatology should alert the clinician to consider other
diagnoses that may masquerade as chronic unilateral blepharitis,
such as sebaceous cell carcinoma.
External examination using slit-lamp biomicroscopy is essential in
establishing diagnosis and determining the type of blepharitis. Staphylo-
coccal anterior blepharitis is more common in the younger population
with female preponderance. Findings include vascularization and ery-
thema of the lid margin, telangiectasia, eyelid edema, loss or misdirec-
tion of lashes, collarettes around the base of the lashes, and crusting or
hyperkeratosis. Chronic findings of ulceration, punctal misdirection,
and scar formation may also be seen. There can be subtle signs of cor-
neal involvement in severe cases, presenting with phlyctenulosis, cor-
neal neovascularization, thinning, or marginal ulceration. Seborrheic
blepharitis is more common in the older age group. It presents with
scurfs, which is a term used for the scales, oily debris, and greasy mate-
rial that collects along the lash shaft as a result of hypersecretion from
the meibomian glands.17
In blepharitis associated with Demodex sp.
infestation, the most commonly seen finding is coating of the lash with
cylindrical dandruff-like material (sleeves).18
Clinical signs of MGD may include rounding, thickening, and
irregularity of the eyelid margin; changes in the lid vascularity and pres-
ence of telangiectasia; pouting, plugging, and narrowing of the gland
orifices; reduction in volume and number of glands secreting liquid;
and changes in gland secretion quality, clarity, and viscosity with
greater pressure required to express secretions.18,19
‘Nonobvious MGD’
is a common form of obstructive MGD that shows no obvious signs of
inflammation, hypersecretion, or purulent secretion of the glands.20
In
chronic MGD, there may be cicatricial changes along the lid margin,
and the mucocutaneous junction may migrate anterior to the meibo-
mian gland line.21
Subtle signs, such as frothy quality of the tear menis-
cus, and decreased Schirmer’s scores and tear break-up time, may be
found. Other ocular conditions, such as recurrent chalazia, trichiasis,
and keratoconjunctivitis sicca, may also be seen. External examination
of the face and skin may reveal associated dermatologic problems, such
as seborrheic dermatitis, atopy, herpes zoster ophthalmicus, and acne

3. Blepharitis
4.4
179
can help improve both MGD and DED. Treatment options include
minimally or nonpreserved tears, gels, and ointments, environmental
control, and moisture goggles. A newer class of tear substitutes involv-
ing the use of lipid-containing eye drops, liposomal sprays, emulsion-
type eye drops, and ointments may be more effective than artificial
tears in DED associated with MGD.36,37
Dietary supplementation with
omega-3 fatty acids has been shown to be effective in improving signs
and symptoms of DED and MGD by reducing ocular surface inflamma-
tion and improving the lipid composition of meibum.6
There are several additional methods of treatment that have been
found to be helpful when used in conjunction with the core interven-
tions mentioned above. Antiseborrheic shampoos such as those con-
taining selenium sulfide or tar may be helpful when seborrheic
dermatitis is significant. Weekly lid scrubs with 50% tea tree oil and
daily lid scrubs with tea tree shampoo are effective in eradicating demo-
dex infestation of the lids.38
As MGD may be related to androgen defi-
ciency or receptor dysfunction, topical androgens are being evaluated as
a possible therapeutic option for patients with MGD.39
A new approach
for surgically treating MGD is currently being evaluated. It involves
insertion of small stainless-steel probes in the meibomian orifices and
ducts to remove obstruction and thus improve symptoms.40
Thus, a
combination of interventions, including environmental, dietary, phar-
macological, and surgical, may provide a more effective approach in
future to prevent and treat this chronic disease.
KEY REFERENCES
Geerling G, Tauber J, Baudouin C, et al. The international workshop on meibomian gland
dysfunction: report of the subcommittee on management and treatment of meibomian
gland dysfunction. Invest Ophthalmol Vis Sci 2011;52:2050–64.
Graham JE, Moore JE, Jiru X, et al. Ocular pathogen or commensal: a PCR-based study of surface
bacterial flora in normal and dry eyes. Invest Ophthalmol Vis Sci 2007;48:5616–23.
Ibrahim OMA, Matsumoto Y, Dogru M, et al. The efficacy, sensitivity, and specificity of in vivo laser
confocal microscopy in the diagnosis of meibomian gland dysfunction. Ophthalmology
2010;117:665–72.
Knop E, Knop N, Millar T, et al. The international workshop on meibomian gland dysfunction:
report of the subcommittee on anatomy, physiology, and pathophysiology of the
meibomian gland. Invest Ophthalmol Vis Sci 2011;52:1938–78.
Korb DR, Blackie CA. Meibomian gland diagnostic expressibility: Correlation with dry eye
symptoms and gland location. Cornea 2008;27:1142–7.
Lane SS, Dubiner HB, Epstein RJ, et al. A new system, the LipiFlow, for the treatment of
meibomian gland dysfunction. Cornea 2012;31:396–404.
Macsai MS. The role of omega-3 dietary supplementation in blepharitis and meibomian gland
dysfunction (an AOS thesis). Trans Am Ophthalmol Soc 2008;106:336–56.
Maskin SL. Intraductal meibomian gland probing relieves symptoms of obstructive meibomian
gland dysfunction. Cornea 2010;29:1145–52.
Meadows JF, Ramamoorthy P, Nichols JJ, et al. Development of the 4-3-2-1 meibum expressibility
scale. Eye Contact Lens 2012;38:86–92.
Nelson JD, Shimazaki J, Benitez-del-Castillo JM, et al. The international workshop on meibomian
gland dysfunction: report of the definition and classification subcommittee. Invest
Ophthalmol Vis Sci 2011;52:1930–7.
Pult H, Riede-Pult BH. Non-contact meibography in diagnosis and treatment of non-obvious
meibomian gland dysfunction. J Optom 2012;5:2–5.
Rubin M, Rao SN. Efficacy of topical cyclosporin 0.05% in the treatment of posterior blepharitis.
J Ocul Pharmacol Ther 2006;22:47–53.
Scaffidi RC, Korb DR. Comparison of the efficacy of two lipid emulsion eyedrops in increasing tear
film lipid layer thickness. Eye Contact Lens 2007;33:38–44.
Tomlison A, Bron AJ, Korb DR, et al. The International Workshop on Meibomian Gland
Dysfunction: Report of the Diagnosis Subcommittee. Invest Ophthalmol Vis Sci 2011;52:
2006–49.
Veldman P, Colby K. Current evidence for topical azithromycin 1% ophthalmic solution in the
treatment of blepharitis and blepharitis-associated ocular dryness. Int Ophthalmol Clin
2011;51:43–52.
be instructed to avoid excessive scrubbing and massage, as it can lead
to ocular irritation. Besides self-care, therapeutic meibomian gland
expression as an in-office procedure performed by the clinician can help
relieve MGD. However, therapeutic expression may be painful to the
patient. Conventional heat and massage techniques are frequently inef-
fective in delivering heat to the meibomian glands. Recently, a new
thermopulsation device has been developed, which allows heat to be
applied to the palpebral surfaces of the lids directly over the meibomian
glands while simultaneously applying graded pulsatile pressure to the
outer eyelid surfaces, thereby gently expressing the meibomian glands
during heating.30
Topical antibiotics are added when underlying bacterial infection is
suspected. Bacitracin and erythromycin ophthalmic ointments are
effective agents for anterior blepharitis. Generally, ointments are
applied directly to the lid margins to avoid toxicity to the ocular sur-
face. Fluoroquinolone eye drops have minimal ocular toxicity with a
wide coverage of organisms. However, emergence of resistant organ-
isms has limited their use. Topical fusidic acid has shown efficacy in
patients with ocular rosacea blepharitis. Though not yet FDA approved,
topical metronidazole gel 0.75–1.0% also may be effective when used
on the lid margin for treatment of ocular rosacea.27
Systemic antibiotics
like cloxacillin may be added for treatment of persistent or recurrent
staphylococcal blepharitis. Oral tetracyclines are commonly used in the
management of rosacea and MGD. They are mainly used for their anti-
inflammatory and lipid-regulating properties, rather than for their
antimicrobial effects. They decrease the production of bacterial lipases,
thus reducing the concentration of free fatty acids and their deleterious
effects on lipid composition.31
They exert anti-inflammatory effects due
to inhibition of matrix metalloproteinases (MMPs), cytokines, lym-
phocyte and neutrophil activation, and chemotaxis. They also have
anti-angiogenic and anti-apoptotic properties.32
They are usually used
in doses ranging between 250 mg once to four times a day (tetracycline
and oxytetracycline) and 50–100 mg once or twice a day (doxycycline
and minocycline). Low doses of doxycycline 20 mg may be used when
long-term therapy is required. A 40 mg/day slow release dose of doxy-
cycline is approved for treatment of rosacea and is used by some clini-
cians. Tetracycline use is limited by its common side-effects, which
include sun sensitivity and gastrointestinal upset and known contrain-
dications to use in pregnant women and children. Oral macrolide anti-
biotics, like erythromycin and azithromycin, are safer and also have
immunomodulatory and anti-inflammatory effects similar to tetracy-
clines. Recently, the use of a topical azithromycin (1%) was suggested
as an effective treatment of posterior blepharitis, with a significant
improvement in meibomian gland secretion quality, eyelid redness, tear
quality, and overall symptomatic relief, but results from studies regard-
ing efficacy are mixed.33
In cases with more severe lid margin inflammation, a short-term
course of topical steroids or antibiotic–steroid combinations may be
utilized. However, long-term use of steroids is limited by their serious
side-effects such as cataracts, glaucoma, superinfection, and corneal
thinning. Topical immunomodulators like cyclosporine A 0.05%, a
calcineurin inhibitor, have been shown to be beneficial in the treatment
of MGD in conjunction with rosacea and/or DED, with a significant
improvement in lid margin inflammation and signs of DED.34
Tac-
rolimus, a potent immunosuppressive agent that inhibits the transcrip-
tion of interleukin-2, may be an effective alternative for blepharitis that
is refractory to traditional treatments;35
however, evidence for the same
is very limited.
As change in tear composition and tear film stability is a key con-
tributor to lid margin inflammation, supplementation of the tear film
Access the complete reference list online at

4. Blepharitis
4.4
179.e1
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blepharitis. J Ocul Pharmacol Ther 2006;22:47–53.
35. Joseph MA, Kaufman HE, Insler M. Topical tacrolimus ointment for treatment of refractory
anterior segment inflammatory disorders. Cornea 2005;24:417–20.
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increasing tear film lipid layer thickness. Eye Contact Lens 2007;33:38–44.
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Ophthalmol 2006;142:264–70.
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meibomian gland dysfunction. Cornea 2010;29:1145–52.