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Cover Stories | May 2009

The Incidence and Impact of Blepharitis on Cataract Surgery

Clinical studies are warranted to determine how the pathology occurs and how it can be prevented.

Blepharitis is arguably the most common condition that we ophthalmologists see. Nevertheless, little research has been conducted on the incidence of this pathologic condition. The only prominent study in the literature espouses the expected—that the occurrence of blepharitis increases with advancing age.1 The US military published a survey regarding the incidence of blepharitis among recruits (5.4%) and retirees (71.1%).1 These results confirm other observations of the increasing frequency of blepharitis with advancing age.2

Blepharitis is an ophthalmic term that refers to inflammation of the eyelids, either on the skin or the lid margin. The latter is what usually concerns us. Typically, we ophthalmologists divide lid margin disease into anterior and posterior blepharitis. Cataract surgeons are concerned about blepharitis because of its association of lid margin cultures and endophthalmitis. As pointed out by Mark Speaker, MD, the organism in the lid margin and in the vitreous tap are identical in 82% of cases.3 Therefore, extra care should be taken in patients with severe lid margin disease to help avoid endophthalmitis. In addition, patients with severe blepharitis seem to have more problems after cataract surgery than patients without the disease. Specifically, their eyes tend to be more irritated, inflammation takes longer to respond to medications, and they achieve poorer visual acuity 1 day after surgery. These points strongly argue for a comprehensive preoperative approach to intensive therapy for patients with chronic blepharitis.

Anterior and posterior blepharitis has often been considered a nuisance rather than a serious medical problem. As our understanding of the condition grows, however, it is becoming apparent that blepharitis is more than an annoyance. In isolated cases, it can lead to permanent scarring of the lid margins and other significant problems. Some of the sequelae include common chalazion or internal hordeolum, dry eyes, punctate keratitis, phlyctenular or pannus formation, corneal ulceration, and most dramatically, endophthalmitis.3

Although it can coexist with other forms of blepharitis, anterior blepharitis can be considered a specific entity. It is characterized by inflammation of the anterior lid margin, which includes the adjacent skin, the eyelashes, and the Zeis glands. The condition is often associated with excessive colonization from bacteria. Staphylococcus epidermidis, Propionibacterium acnes, and Corynebacterium species are present in the majority of eyes with anterior blepharitis, and sporadic increases in the amount of these bacteria can lead to clinical disease. Efforts at eradication are useless. Periodic therapy may help but only transiently. Long-term lid hygiene is definitely indicated to reduce the buildup of colonies in the detritus of the lashes.4

Demodex folliculorum, or Demodex brevis, is a common parasite found at the base of the eyelash and is a controversial cause of chronic anterior blepharitis. These mites are found in increasing numbers in eyes with blepharitis, and several researchers feel the mites may have a causative role.5,6 Recently, they have been associated with a series of patients with severe recalcitrant anterior blepharitis that responded to applications of tea tree oil.7

A frequent problem among patients who have anterior blepharitis is that they may develop staphylococcal hypersensitivity. Affected individuals present with red, irritated eyelid margins that exhibit areas of crusting, collarettes (scales that encircle the eyelashes), and focal lash loss (Figure 1). Occasionally, external hordeolum are present. Not infrequently, a phlyctenule or marginal corneal ulceration can be observed. Ironically, although phlyctenule and marginal corneal ulceration may be considered a hypersensitivity response, the corneal inflammation usually improves if the patient is treated with antistaphylococcal agents, which decrease the bacterial colony count. In many of these cases, corticosteroids are unnecessary.

Posterior blepharitis is primarily a disorder of the meibomian glands. The meibum becomes altered, and long-chain fatty acids change to free fatty acids, which combine with inflammation and cause saponification or soap formation, which is accentuated by the action of bacterial lipases. This action further degrades the fatty portion of the tear film and affects the meibum in the glands. As a result, the amount of free fatty acids increases, leading to continued saponification.8

Posterior blepharitis is more common than anterior blepharitis, and the former is extremely difficult to treat. One reason is the lack of a single, specific inciting factor. In other words, posterior blepharitis may be caused by bacterial colonization or changes in the meibum, or it may be nonspecific inflammation due to factors that we have not yet fully elucidated (hormonal, etc.). Ocular allergy and/or dry eye disease may further complicate treatment. Aging also appears to be related to an increased clogging of the meibomian gland's orifices. This obstruction leads to secondary inflammation and additional saponification of the lipid that clinically may be seen as a very rapid tear breakup time. If all of this is left unchecked, evaporative loss increases significantly, resulting in a recalcitrant inferior superficial punctate keratitis. The ultimate result is a moderately severe dry eye, which any associated aqueous tear insufficiency will exacerbate.

Not unexpectedly, anterior and posterior blepharitis can coexist. In such cases, inflammation may occur in the anterior and posterior lid margins and often presents with signs of acute infection due to bacterial contamination, requiring management with an antibiotic. The residual inflammation after treatment with an antibiotic may require short courses of corticosteroid therapy. The dangers of a patient's dependence on corticosteroids cannot be overemphasized and have recently led to the use of alternate therapy with topical cyclosporine with some success.9,10

The diagnosis of posterior and anterior blepharitis is based essentially on the clinical examination, with the associated symptoms of ocular surface disease. Since both anterior and posterior blepharitis can cause red, irritated eyes, the defining signs of anterior blepharitis are usually the presence of crusting on the eyelid margins, the appearance of lid debris, and a worsening of symptoms upon waking. The clinical examination reveals collarettes and further flaking or dandruff-like debris on the lashes themselves and on the lid margin as seen in Figure 1. Conversely, posterior blepharitis causes pouting or obstruction of the meibomian glands, which is associated with neovascularization of the lid margin, and obscuration of the glands as the disease progresses (Figure 2). It should be noted that the secretion of the meibum changes with increasing severity in posterior blepharitis. The fluid can become opaque and, in severe cases, may come to resemble toothpaste (Figure 2 to 4). If untreated, the disease may completely obstruct the meibomian glands and cause a severe dry eye that is difficult to treat.11

Clinically, one of the hallmarks of patients with significant meibomian gland disease is a foamy tear film (Figure 5). Also, patients with posterior blepharitis frequently complain of ocular burning, irritation, and dryness upon waking. Patients with dry eye disease have similar symptoms, but they are worse at the end of the day. This is a subtle differentiation, because many patients with dry eye disease also have posterior blepharitis. It is not uncommon for these individuals to have prominent symptoms upon waking that improve for a few hours but worsen again by the end of the day.

Understanding the pathophysiology of blepharitis is helpful in framing treatment plans to care for our patients. A balanced approach of lid hygiene and the judicious use of antibiotics and anti-inflammatories will probably lead to better clinical outcomes and thus lessen or avoid the complications engendered by chronic blepharitis in patients undergoing cataract surgery.

Henry D. Perry, MD, is senior founding partner of Ophthalmic Consultants of Long Island in Rockville Centre in New York. Dr. Perry may be reached at (516) 766-2519; hankcornea@aol.com.

  1. Stanek S. Meibomian gland status comparison between active duty personnel and US veterans. Mil Med. 2000;165(8):591-593.
  2. Carcia CA, Pinheiro FI, Montenegro DA, et al. Prevalence of biomicroscopic findings in the anterior segment and ocular adnexa among school children in Natal/Brazil. Arg Bras Oftalmol. 2005;68(2):167-170.
  3. Speaker MG, Milach FA, Shah MK, et al. Role of external bacterial flora in the pathogenesis of acute postoperative endophthalmitis. Ophthalmology. 1991;98(5):639-649.
  4. McCulley JP, Shine WE. Meibomian gland function and the tear lipid layer. Ocul Surf. 2003;1(3):97-106.
  5. Aylesworth R, Vance JC. Demodex folliculorum and Demodex brevis in cutaneous biopsies. J Am Acad Dermatol. 1982:7:583-590.
  6. Czepita D, Kuzna-Grygiel W, Czepita M, Grobelny A. Demodex folliculorum and Demodex brevis as a cause of chronic marginal blepharitis. Ann Acad Med Stetin. 2007;53(1):63-67.
  7. Kheirkhah A, Casas V, Li W, et al. Corneal manifestations of ocular Demodex infestation. Am J Ophthalmol. 2007;143(5):743-749.
  8. Shine WE, McCulley JP. Meibomiam gland triglyceride fatty acid differences in chronic blepharitis patients. Cornea. 1996;15(4):340-346.
  9. Rubin M, Rao SN. Efficacy of topical cyclosporine 0.05% in the treatment of posterior blepharitis. J Ocul Pharmacol Ther. 2006;22(1):47-53.
  10. Perry HD, Doshi-Carnevale S, Donnenfeld ED, et al. Efficacy of commercially available topical cyclosporine A 0.05% in the treatment of meibomian gland dysfunction. Cornea. 2006;25(2):171-175.
  11. Dougherty JM, McCulley JP. Analysis of the free fatty acid component of meibomian secretions in chronic blepharitis. Invest Ophthalmol Vis Sci. 1986;27(1):52-56.
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