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Blepharitis: Diagnosis and Management

Rene Solomon, MD

Ophthalmic Consultants of Long Island Rockville Centre New York, NY

Henry D. Perry, MD

Ophthalmic Consultants of Long Island Rockville Centre, NY

Eric D. Donnenfeld, MD

Ophthalmic Consultants of Long Island Rockville Centre New York, NY

Introduction

Blepharitis, inflammation or infection of the eyelid margins, is one the most common ophthalmological complications as well as
one of the most difficult conditions to treat.1,2 Blepharitis is classified as either related to skin disease or manifesting in the
anterior or posterior eyelid. Blepharitis may also be a combination of these classifications.3

History and Examination

For a patient suspected of having blepharitis, the history and physical examination should include the following details: the
patient should be asked about duration and manifestation of ocular symptoms, unilateral or bilateral presentation, association
with potential exacerbating conditions (e.g., smoke, allergens, wind, contact lenses, low humidity), recent exposure to an
infected individual (e.g., pediculosis), ocular history (e.g., previous ophthalmic surgery and trauma, including radiation and
chemical trauma), systemic history (e.g., dermatological diseases, such as acne, rosacea, eczema, allergies), and use of ocular
medications or retinoids. The examination should include visual acuity, and a careful external examination of facial skin,
eyelids, and eyelashes. Slit lamp biomicroscopy evaluation should focus on the tear film, anterior eyelid margin, eyelashes,
posterior eyelid margin, tarsal conjunctiva, bulbar conjunctiva, and cornea. Tests that may be considered in the work-up
include the use of lissamine green or rose bengal, tear break-up time, Schirmer testing, and Cochet-Bonnet esthesiometry to
check corneal sensation for a unilateral case.

Blepharitis Related to Skin Disease

Blepharitis related to skin disease can be subdivided into the following three categories:

1) Contact dermatitis.
Contact dermatitis develops from type IV hypersensitivity, a T-cell interaction to sensitized allergen that requires 2 weeks
sensitization. Common causes include glaucoma medications, topical anesthetics, antivirals, thimerosal, and cosmetics (Slide 1
and Slide 2). Treatment involves removing the offending allergen and applying topical corticosteroids.
Slide 1. Patient with a nail polish allergy, otherwise known as
eczematoid allergy.

Slide 2. Patient with typical mucous fishing syndrome.

2) Eczematoid blepharitis.
Eczematoid blepharitis is caused by a hypersensitivity reaction to exotoxins and antigens from local flora. Patients usually have
a strong history of atopic disease (i.e., eczema, asthma). These patients often have problems with chronic Staphylococcus
aureus infections. Signs and symptoms include itching of eyelids, burning and irritation, dry, scaly appearance of eyelids with
hyperpigmentation, fissure formation, and lichenification (Slide 3 and Slide 4). It is important to check flexor surfaces of the
body for similar findings. The treatment involves applying topical corticosteroid ointment and avoiding hot compresses and
antibiotics.
Slide 3. Patient with atopic dermatitis of the face.

Slide 4. Close-up of a patient with atopic dermatitis of the face


demonstrating darkening of the lids.

3) Seborrheic blepharitis.
Seborrheic blepharitis is secondary to a dysfunction of the sebaceous glands. It may be caused by Pityrosporum ovale.
Seborrheic blepharitis may occur alone or in combination with posterior blepharitis or staphylococcal blepharitis. Approximately
15% of patients with seborrheic blepharitis develop an associated conjunctivitis or keratitis.4 The keratitis is typified by
punctuate epithelial erosions distributed over the inferior third of the cornea.4 Approximately one third of patients with
seborrheic blepharitis have aqueous tear deficiency.4 Signs and symptoms include burning and irritation of eyelids, yellow,
greasy tenacious scales attached to lid, and erythematous eyelids (Table 1). Sebaceous plaques can be noted in the scalp,
eyelids, nasolabial folds, and retroauricular skin. Treatment includes lid hygiene5 with hot compresses, corticosteroid ointments,
antibiotic ointments, and diluted dandruff shampoo applied to the eyelid margin.
Table 1

Blepharitis Related to Anterior or Posterior Lid Disease

Anterior blepharitis (Slide 5) is usually an infectious blepharitis most commonly due to Staphylococcal infection.3 Signs and
symptoms include morning crusting with foreign body sensation, recurrent hordeola, chalazia (Slide 6), loss of lashes,
conjunctival hyperemia, collarettes scales that encircle the base of the eyelashes and Staphylococcal immune disease
including phlyctenule, inferior conjunctival and corneal punctuate, keratopathy, pannus, and catarrhal infiltrates (Table 1).
Treatment consists of lid hygiene5 with hot compresses, commercial lid scrubs, antibiotic ointment to lid margin (bacitracin,
erythromycin), corticosteroids for persistent inflammation and corneal or conjunctival immune sequelae, and education for the
patients about the chronicity and recurrence of the disease process. Slide 7 demonstrates the lower eyelid of a patient with
anterior blepharitis secondary to Staphylococcal infection. Note the loss of eyelashes, collarettes and crusting around the
remaining eyelashes. Slide 8 demonstrates an eyelid with thinned skin secondary to the chronic use of steroids allowing blood
vessels to show through.
Slide 5. Patient with seborrheic dermatitis.

Slide 6. Patient with acute chalazion of the upper eyelid.


Slide 7. Patient with chronic staphylococcus blepharitis.

Slide 8. Picture demonstrating thinning of eyelids secondary to


corticosteroid use. Note sleeves and scurf.

Posterior blepharitis is most commonly caused by obstruction and inflammation of the meibomian glands (meibomian gland
dysfunction) producing excessively thick inspissated sebaceous secretion.6 Posterior blepharitis may also by caused by atrophic
meibomian glands. Both types of meibomian gland dysfunction are noninfectious and may be idiopathic or associated with acne
rosacea, acne vulgaris, or oral retinoid therapy.7-13 Meibomian gland dysfunction is the most common cause of dry eye.7-13
Patients with meibomian gland dysfunction develop lipid tear deficiency resulting in tear film instability, increased rate of tear
film evaporation, and elevated tear osmolarity.4 Signs and symptoms consist of burning, foreign body sensation with dry eye
symptoms (contact lens intolerance), filmy vision with foam in tear film (soaps and fatty acids), dilated meibomian gland
orifices with plugged "toothpaste"-like material, chalazia, telangiectatic blood vessels, and a thickened lid margin (Table 1).

In a noncontrolled case-cohort study of selected patients with meibomian gland dysfunction, lid hygiene and preservative-free
artificial tears significantly improved tear breakup time and relieved symptoms of the condition.7 Topical cyclosporine A 0.05%
has been evaluated in the treatment of meibomian gland dysfunction and has been demonstrated to decrease the meibomian
gland inclusions in patients with meibomian gland dysfunction.8 Additional treatment involves hot compresses, antibiotic and
corticosteroid ointments, oral tetracycline for chronic or severe disease, especially with facial involvement. Tetracycline has
antibiotic, anticollagenolytic, and anti-inflammatory properties.14-17 Our recommended dose is doxycycline 100 mg twice daily
for 2 weeks, then 100 mg once daily for 1 month. If needed, the dose of doxycycline for chronic therapy is 100 mg every other
day. At the time of taking doxycycline, patients should avoid dairy products, antacids, and calcium pills. Doxycycline is
contraindicated in children under 12 years of age, women who are pregnant, mothers who are nursing, or patients with liver
disease. We have also used lower doses of doxycycline with good results.

Potential adverse reactions from doxycycline are gastrointestinal intolerance, photosensitization of skin, or Candida vaginitis
(these adverse reactions are minimized with the lower dose schedule). Other options to treat posterior blepharitis are high-dose
cod liver oil eicosapentaenoic and dodocapentaeneil polyunsaturated fatty acids, flax seed oil,18 omega-3 (n-3) and omega-6
(n-6) polyunsaturated fatty acids.

The meibomian glands in the eyelid use essential fatty acids to manufacture the oil layer of the tear film. High performance
liquid chromatography mass spectrometry studies have shown that the polar lipid profiles of meibomian gland secretions in
female patients with Sjgrens syndrome are controlled by the dietary intake of omega-3 essential fatty acids. Patients with
high intakes of omega-3 show single-prominent-peak polar lipid pattern, whereas patients with low dietary intakes show
multiple smaller peaks.19 It seems reasonable to infer that dietary omega-3 is being used in the production of meibomian
secretions and is contributing to and augmenting the tear film oil layer. Clinical reports have observed clearer and thinner oils
with omega-3 treatment.20 With an improved supply of omega-3, the oils produced by the meibomian glands flow better and,
as a result, may create a better oil layer covering for the tear film. The improvement of the oil layer often will provide dry-eye
relief for patients with meibomian gland dysfunction.21

Unusual causes of chronic blepharoconjunctivitis (Table 2) that should be considered in the differential diagnosis include
molluscum, pediculosis (Slide 9), canaliculitis, masquerade syndrome, and angular blepharitis. Angular blepharitis is classically
due to Moraxella lacunata, presenting as a chronic angular blepharoconjunctivitis with crusting and ulceration of the skin in the
lateral canthal angle and papillary or follicular reaction on the tarsal conjunctiva. M lacunata angular blepharoconjunctivitis is
frequently associated with concomitant S aureus blepharoconjunctivitis.4

Table 2

Patients with atypical eyelid disease or inflammation that is not responsive to medical therapy should be carefully re-evaluated.
The presence of features such as a nodular mass, ulceration, extensive scarring, localized crusting, and scaling of the dermis,
or yellow conjunctival nodules surrounded by intense inflammation, may suggest the presence of an eyelid tumor. Basal cell
carcinoma and squamous cell carcinoma are the most frequently encountered malignant tumors involving the eyelids.
Melanoma and sebaceous gland carcinoma are the next most frequently diagnosed malignant tumors of the eyelid.22,23
Sebaceous gland carcinoma may present as an ulcerative blepharitis mimicking basal cell carcinoma and because of a typically
multicentric origin may also induce severe conjunctival inflammation due to pagetoid spread all of which add to the difficulties
in making in accurate diagnosis.22,24
Slide 9. Patient with Pthirus pubis with critters on eyelashes.

In unusual cases, additional diagnostic tests may be considered. Cultures may be indicated for patients with recurrent anterior
blepharitis with severe inflammation as well as for patients who are not responding to therapy. Biopsy of the eyelid excludes
the possibility of carcinoma and may be indicated in cases of marked asymmetry, resistance to therapy, or unifocal recurrent
chalazion.

References

1. Smith RE, Flowers CW. Chronic blepharitis: A review. CLAO J. 1995;21:200-207.


2. O'Day DM. Classification of chronic blepharitis (Discussion). Ophthalmology. 1982;89:1180.
3. McCulley JP, Dougherty JM, Deneau DG. Classification of chronic blepharitis. Ophthalmology. 1982;89:1173-1180.
4. American Academy of Ophthalmology: External disease and cornea. In: Basic and Clinical Science Course. Vol 8.
American Academy of Ophthalmology; 1995: 65-67, 69-70, 153-154.
5. Key JE. A comparative study of eyelid cleaning regimens in chronic blepharitis. CLAO J. 1996;22:209-212.
6. McCulley JP, Shine WE. Meibomian secretions in chronic blepharitis. Adv Exp Med Biol. 1998;438:319-326.
7. Romero JM, Biser SA, Perry HD, et al. Conservative treatment of meibomian gland dysfunction. Eye Contact Lens.
2004;30:14-19.
8. Perry HD, Doshi S, Donnenfeld ED, et al. Double masked randomized controlled study evaluating topical 0.05%
cyclosporine A in the treatment of meibomian gland dysfunction (posterior blepharitis). Invest Ophthalmolol Vis Sci.
2003;44:E. Abstract 1395.
9. Gilbard JP. Dry eye, blepharitis and chronic eye irritation: Divide and conquer. J Ophthalmic Nurs Technol.
1999;18:109-115.
10. Shimazaki J, Sakata M, Tsubota K. Ocular surface changes and discomfort in patients with meibomian gland
dysfunction. Arch Ophthalmol. 1995;113:1266-1270.
11. Driver PJ, Lemp MA. Meibomian gland dysfunction. Surv Ophthalmol. 1996;40:343-367.
12. Bron AJ, Benjamin L, Snibson GR. Meibomian gland disease. Classification and grading of lid changes. Eye.
1991;5:395-411.
13. Mathers WD, Shields WJ, Sachdev MS, et al. Meibomian gland dysfunction in chronic blepharitis. Cornea. 1991;10:277-
285.
14. Frucht-Pery J, Sagi E, Hemo I, Ever-Hadani P. Efficacy of doxycycline and tetracycline in ocular rosacea. Am J
Ophthalmol. 1993;116:88-92.
15. Zengin N, Tol H, Gunduz K, et al. Meibomian gland dysfunction and tear film abnormalities in rosacea. Cornea.
1995;14:144-146.
16. Dougherty JM, McCulley JP, Silvany RE, Meyer DR. The role of tetracycline in chronic blepharitis. Inhibition of lipase
production in staphylococci. Invest Ophthalmol Vis Sci. 1991;32:2970-2975.
17. Perry HD, Hodes LW, Seedor JA, et al. Effects of doxycycline hyclate on corneal epithelial wound healing in the rabbit
alkali burn model. Cornea. 1993;12:379-382.
18. Sullivan BD, Cermak JM, Sullivan RM, et al. Correlations between nutrient intake and the polar lipid profiles of
meibomian gland secretions in women with Sjgren's syndrome. Adv Exp Med Biol. 2002;506:441-447.
19. Sullivan RM. Correlations between nutrient intake and the polar lipid profiles of meibomian gland secretions in women
with Sjgren's Syndrome. Presented at the Third International Conference on the Lacirmal Gland, Tear Film and Dry
Eye Syndromes: Basic Science and Clinical Relevance. Maui, Hawaii; November 15-18, 2000.
20. Boerner CF. Dry eye successfully treated with oral flaxseed oil. Ocular Surgery News. 2000;10:147-148.
21. Mathers WD, Lane JA. Meibomian gland lipids, evaporation, and tear film stability. Adv Exp Med Biol. 1998;438:349-
360.
22. American Academy of Ophthalmology, Preferred Practice Patterns Committee, Cornea/External Disease Panel. Dry eye
syndrome. Preferred Practice Pattern. San Francisco, CA: American Academy of Ophthalmology; 1998.
23. Margo CE, Mulla ZD. Malignant tumors of the eyelid: A population-based study of non-basal cell and non-squamous cell
malignant neoplasms. Arch Ophthalmol. 1998;116:195-198.
24. Cavanagh HD, Green WR, Goldberg HK. Multicentric sebaceous adenocarcinoma of the meibomian gland. Am J
Ophthalmol. 1974;77:326-332.

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