Seminars in Ophthalmology, 25(3), 7983, 2010 Copyright 2010 Informa UK Ltd.

. ISSN: 0882-0538 print/ 1744-5205 online DOI: 10.3109/08820538.2010.488562

Blepharitis
Taliana Freitas Bernardes, and Adriana Alvim Bonfioli
Oftalmoclnica Rui Marinho, Belo Horizonte, Minas Gerais, Brazil

ABSTRACT Blepharitis is a chronic inflammatory process of the eyelid margin. It is a common eye disorder throughout the world and can affect any age group. It may be associated with several systemic diseases, particularly rosacea and seborrheic dermatitis, and is related to other ocular conditions like dry eye, chalazion, conjunctivitis, and keratitis. Common symptoms associated with blepharitis are burning sensation, irritation, tearing, photophobia, blurred vision, and red eyes. Clinical examination reveals the presence of scurf, telangiectatic vascular changes of the eyelid margin, inspissated meibomian glands, conjuntival hyperemia, punctuate keratopathy, cornea vascularization, and ulceration. Patients with longstanding chronic blepharitis may present hypertrophy of the lid margin, scars, madarosis, trichiasis, and poliosis. Treatment of blepharitis is long and unsatisfactory. Long-term commitment to eyelid hygiene is essential. Other treatment options are discussed.
Keywords: blepharitis; diagnosis; treatment; review

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INTRODUCTION
Blepharitis is a chronic inflammatory process of the eyelid margin. It is a common eye disorder throughout the world and can affect any age group. The disease can result in dry eye, damage to the lids and the cornea. The treatment is prolonged and recurrences are common.

SYSTEMIC ASSOCIATIONS
Blepharitis may be associated with several systemic diseases, particularly rosacea and seborrheic dermatitis (Figure 4). Blepharitis is related to other ocular conditions like dry eye, trichiasis, chalazion ( Figure5), conjunctivitis, and keratitis.

Rosacea

CLASSIFICATION
Blepharitis can be anatomically subdivided into anterior and posterior (Figure 1). Anterior blepharitis is the inflammation of the eyelashes and follicles ( Figure 2), while posterior blepharitis involves the Meibomian glands (Figure 3). Considerable overlap exists between the two types. Anterior blepharitis is usually infectiousbacterial (Staphilococcus), viral (Molluscum contagiosum), and parasitic (phthiriasis)or seborrheic. Posterior blepharitis is commonly metabolic.

Correspondence: Taliana Freitas Bernardes, Av. do Contorno 4747 suite 1705, Belo Horizonte, Minas Gerais, Brazil CEP 30110-090. E-mail: taliana.freitas@gmail.com

Rosacea is a chronic disease characterized by the presence of telangiectasias, erythema, papules, pustules, and hypertrophic sebaceous glands in areas of facial flushing. After a few months it progresses to plaques and phymatous change at the face. The rhinophima is the most advanced stage in the development of rosacea characterized by marked hypertrophic changes at the nose producing firm, reddish or purplish, lobulated masses. Rosacea usually starts around 30 to 40 years old and the signs and symptoms are frequent and occur early in the process of the disease. All suspects should be promptly referred to a dermatologist to confirm the diagnosis and help identify the triggers. Immunoassays tests, using monoclonal antibodies directed against surface antigens and cell receptors, suggest 79

80 T. F. Bernardes and Adriana A. Bonfioli

Figure 4 Blepharitis associated with trichiasis at the inferior margin (courtesy of Alfredo Bonfioli, MD).
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Figure 1 The eyelid margin is subdivided in anterior and posterior portions by the grey line.

Figure 5 Blepharitis associated with chalazion (courtesy of Alfredo Bonfioli, MD).

Figure 2 Anterior Blepharitis.

predisposition, dyspepsia with gastric hypochlorhydria, Helicobacter pylori infection, inflammatory bowel disease, seborrhea, Demodex folliculorum mites, endocrine disorders, vitamin deficiencies, microcirculatory disturbances, liver disease or psychogenic factors.

SEBORRHEIC DERMATITIS
Seborrheic dermatitis is a chronic condition characterized by recurrent erythema, edema, greasy scales, and yellowish crusts, predominantly in areas where there is a greater concentration of sebaceous glands. The etiology is unknown but in predisposed individuals the dermatitis may be triggered or exacerbated by certain factors such as climate change, emotional stress, fatigue, or infections. Seborrheic blepharitis is often associated with seborrheic dermatitis. In these cases it has a chronic and prolonged course and is very difficult to treat. Patients complaints include itchy eyelid and a burning sensation. It is common to observe association with staphylococcal blepharitis and meibomitis. Complications like corneal erosions occur in approximately 15% of cases.

Figure 3 Posterior Blepharitis (courtesy of Alfredo Bonfioli, MD).

that inflammation of the eyelids and ocular surface in rosacea is due to the presence of inflammatory mediators in the tear film and antigenic stimuli from the eyelid margins. The exact etiology of rosacea is still unknown and believed to be multifactorial. Over the years many causes have been suspected and not confirmed like genetic

FREQUENCY
Blepharitis and associated ocular conditions are very commom. Hom et al. found that 38.9% of randomly
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Blepharitis 81 selected patients presented some degree of lipid secretion disfunction.1 Studying 1148 patients with ocular discomfort Venturino etal. found that 12% had anterior blepharitis, 24% had posterior blepharitis, and 21% had dry eye.2 are 30 to 40 glands at the upper lid tarsus and 20 to 25 at the lower lid tarsus. They form lobules that center around main tubules in the upper and lower tarsus. The lipids manufactured in these glands are expressed through the meibomian openings located between the epithelial skin and the gray line inside the tarsus and will form the lipid layer of the tear film. They prevent tear evaporation and tear outflow, prevent contamination and decrease evaporation of the tear film, help forming a regular optical surface at the cornea and act as a barrier against any particulates. McCulley etal.8 reported that among patients with meibomian gland dysfunction, the amount of tear production is often decreased. In addition, Zengin etal.12 reported that tear break-up time decreases in these patients because the tear film has become destabilized, thus increasing tear evaporation.

ETIOLOGY
The cause of blepharitis is unknown and probably multifactorial. Bacteria have been implicated in playing a significant role in the pathogenesis of blepharitis.3,4 The conjunctival flora in patients with blepharitis has been reported to have a greater number of bacteria than normal individuals.5,6 Bacterial lipase changes the secretion of the meibomian glands, increasing cholesterol concentration and favoring bacterial growth and proliferation.7,8 Toxic residues from bacteria, direct tissue invasion, and immune mediated damage play an important role in the development of the disease (Figure6). Dermodex folliculorum are small parasitic mites that live in hair follicles, sebaceous glands and meibomian glands. It is commonly seen at the face, neck, axillary and pubic regions. First seen by Henle e Berguer in 1841 and described in detail by Simon in 1842,9 it was related to chronic blepharitis. It is still controversial and some authors believe D. folliculorum to be innocuous.10

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CLINICAL PICTURE
Common symptoms associated with blepharitis are burning sensation, irritation, tearing, photophobia, blurred vision, and red eyes. They are usually worse in the morning, because during sleep the inflamed lids are in close contact with the ocular surface. Also, without blinking, the lipid content of the tear film builds up, achieving a concentration 50% higher than in the rest of the day. During the night there is a decrease in tear production which, associated with the constant liberation of inflammatory mediators, adds to the corneal damage. Clinical examination (Figure 7) reveals the presence of scurf, telangiectatic vascular changes of the eyelid margin, inspissated meibomian glands, conjuntival hyperemia, punctuate keratopathy, cornea vascularizaA B

PATHOPHYSIOLOGY
Blepharitis is usually secondary to dysfunction or structural changes on the meibomian glands. There

Figure 6 Dermodex folliculorum. 2010 Informa UK Ltd.

Figure 7 Clinical examination; (A) and (B) eyelid margin hyperemia, telangiectasy and ulceration, localized trichiasis and madarosis. (B) and (C)Associated seborrheic dermatitis.

82 T. F. Bernardes and Adriana A. Bonfioli tion and ulceration (Figure 8). Hard crusts around the base of the cilia (collarets) are typical of staphylococcal blepharitis. Seborrheic blepharitis is characterized by hyperemia, lipid secretion and soft crusts at the lid margin and eyelashes. Patients with longstanding chronic blepharitis may present hypertrophy of the lid margin, scars, madarosis, trichiasis and poliosis. Posterior blepharitis has more pronounced symptoms with less clinical signs. Meibomian gland orifices have small drops of lipid secretion. Pressure on the tarsus releases a thick lipid secretion. Tear film is oily and foamy. Chronic blepharitis may result in the obstruction of the gland ducts and structural changes. In such cases there is a secondary Meibomian gland dysfunction that presents as a second peak of symptoms late in the day, caused by excessive evaporation of the tear film and hyperosmolality. At the final stages, there is fibrosis and obliteration of the glands and reduction of the inflammation. The morning symptoms disappear and the evaporative symptoms late at the day tend to intensify. 15 may be confused with less aggressive lesions. Meibomian gland carcinoma infiltrates the dermis and results in eyelid margin thickening. Sclerosing basal cell carcinoma (BAC) also infiltrates the dermis and may be mistaken for localized chronic blepharitis.19 Determining the clinical margins of the tumor is very difficult.

TREATMENT
Basic treatment for blepharitis includes a long-term commitment to eyelid hygiene. The process begins with the application of warm compresses to promote evacuation and cleansing of the gland secretory passages. The margin is then washed using mild shampoo (baby shampoo) diluted in water or commercial formulations. A cotton swab dipped in the solution is used to rub the base of the eyelashes, removing the crusts. Finally, an antibiotic-corticosteroid ointment is applied to the margin. This combination should only be used for short periods of time. If there is papillary conjunctivitis or marginal keratitis secondary to hypersensitivity to bacterial toxins mild steroid drops, 3 to 4 times a day, for a short period, are recommended. Lubricants are indicated if there is tear film instability. Increasing the intake of Omega-3 and 6 fatty acids (flaxseed olil supplements) is considered an adjunctive therapy for several forms of tear deficiencies. They have an anti-inflammatory effect and improve lubrication.20 Refractory cases often respond to oral antibiotics. The authors use doxycycline 100mg, once a day for 10days, followed by 50mg once a day for 6 to 12weeks. Other options include tetracycline, minocycline, erythromycin, and azythromycin. Aguilar etal. suggest that the blepharitis caused by Dermodex folicullorum should be treated by rubbing cotton swabs dipped in ether.21

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DIFFERENTIAL
Most cases of discoid lupus affecting the eyelids present as blepharitis, with small infiltrated discoid plaques, edema, infiltration and inflammation of the margin (Figure 9).16,17 Early sebaceous gland carcinoma presents only subtle signs of malignancy and

RECENT STUDIES
Figure 8 Blepharitis associated with corneal ulceration.
A B

Figure 9 Discoid lupus.

Topical azythromycin is a promising agent for blepharitis treatment. It was demonstrated that it effectively reduces the symptoms and signs.22 However, due to the chronic course of the disease and the chance of bacterial resistance, there could be serious consequences to its indiscriminate use. Topical levofloxacin 0,5% is effective in eradicating bacteria in patients with blepharoconjunctivitis.23 Further studies are necessary to clarify the role of bacteria in the pathophysiology of blepharitis in order to develop an effective treatment.
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REFERENCES
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[13] Gilbard JP, Cohen GR, Baum J. Decrease tear osmolarity and absence of the inferior marginal tear strip after sleep. Cornea. 1992; 11:231233. [14] Shimazaki J, Sakata M, Tsubota K. Ocular surface changes and discomfort in patients with meibomian gland disfunction. Arch Ophthalmol. 1995; 113:12661270. [15] Gilbard JP. Dry eye in deph. In: Proceedings of the New Orleans Academy of Ophthalmology, 1997. Available from: http://www. theratears.com/New%20Orleans%20Dry%20Eye.html [16] Feldman G, Papa A, Baroni E, Amoros N, Giavarini A, Bergero A, etal. Lupus eritematoso crnico de localizacin palpebral: respuesta a la talidomida en un caso. Arch Argent Dermatol. 1995; 45(3):101103. [17] Gloor P, Kim M, McNiff JM, Wolfley D. Discoid lupus erythematosus presenting as asymmetric posterior blepharitis. Am J Ophthalmol. 1997; 124(5):707709. [18] Skare TL. Reumatologia: Princpios e Prtica, Guanabara Koogan, Rio de Janeiro, BR, 2007. [19] Kanski JJ. Oftalmologia Clinica (5th edn.). Windsor, UK: Butterworth-Heinemannn; 2003:912. [20] Pinheiro JR, Neuzimar M, et al. Uso oral do leo de linhaa (Linum usitatissimum) no tratamento do olhoseco de pacientesportadores da sndrome de Sjgren. Arq. Bras. Oftalmol 2007; 70 (4):649655. [21] Aguilar AJ, Berra A. Blefaritis crnica/Chronic blepharitis. Arch. Alerg. Inmunol. Clin. 2001; 32(3):98100. [22] Luchs J. Efficacy of topical azithromycin ophthalmic solution 1% in the treatment of posterior blepharitis. Adv Ther. 2008; 25(9):858870. [23] Yactayo-Miranda Y, Ta CN, He L, Kreutzer TC, Nentwich MM, Kampik A, Mino de Kaspar H. A prospective study determining the efficacy of topical 0.5% levofloxacin on bacterial flora of patients with chronic blepharoconjunctivitis. Graefes Arch Clin Exp Ophthalmol. 2009; 247(7):993998.

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