Eyelid Infections

Introduction

Eyelid infections comprise a heterogeneous group of anatomic substrates and etiologic agents. Clinical findings and treatments vary according to the substrate and agent. The complex anatomy of the eyelid contributes to the diversity of infectious presentations. Eyelid components that can be involved in infectious processes include keratinized and conjunctival epithelium, lash follicles, multiple sebaceous and eccrine glands, ducts, and the loose subdermal connective tissue. Eyelid infections can thus be categorized as follows:

• Marginal blepharitis
• Angular blepharitis
• Meibomianitis
• Internal and external hordeola and chalazia
• Canaliculitis
• Localized ulcerative, vesicular, and papular blepharitis
• Infectious dermatitis and preseptal cellulitis

Clinical Findings

Marginal Blepharitis
A staphylococcal infection of the eyelid margin is possibly the most common ocular infection presenting to the ophthalmologist. Often, the course of these infections is chronic and smoldering with pathologic changes associated as much with the chronic inflammatory response as with the infectious process itself. Symptoms may be as mild as nonspecific irritation, or patients may be asymptomatic. More severe manifestations include pruritus, burning, crusting, redness, and lash loss. Signs include pathognomonic lash collarettes - fibrin crusts that remain impaled on lashes as the lashes grow out from the lid margin - erythema of the lid margin, madarosis, and poliosis. Accompanying signs include papillary conjunctivitis, punctate keratopathy of the inferior cornea, peripheral corneal infiltrates, superficial corneal neovascularization, and phlyctenulosis.^1,2

Staphylococcal blepharitis must be distinguished from other processes that cause lid margin irritation and lash debris. Infestation of the lash follicles with the parasite Demodex folliculorum results in typical keratin sleeves or turtlenecks around the lash bases, thought to be due to reactive hyperkeratosis of the follicle. Infestation with Phthirus pubis lice is diagnosed by visualization of the lice themselves or their egg cases (nits) attached to the lashes. Seborrheic blepharitis is marked by greasy skin flakes, or scurf, in the lashes.¹

Rarely, enteric gram-negative bacteria such as Pseudomonas, Proteus, or Escherichia coli can cause an ulcerative, necrotizing marginal blepharitis. The lesion may start as a vesicle, which quickly progresses to ulceration and eschar formation. Usually, these infections occur in an immunocompromised host, but have been reported in immunocompetent patients as well. A culture is needed to differentiate these pathogens from more common staphylococcal infections.¹

Angular Blepharitis
Angular blepharitis, inflammation of the skin of the outer and inner canthi, is often heralded by sharp eye pain. Redness and crusting of the skin creases of the canthi, sometimes associated with inflammation of the contiguous bulbar conjunctiva, are the main signs. In temperate climates, staphylococci are the most common pathogens, although in more equatorial climates Moraxella species are frequently pathogenic. Herpes simplex has been implicated in rare cases.¹

Meibomianitis
A chronic staphylococcal infection of the meibomian glands is thought to be a significant factor in most cases of meibomianitis, although primary meibomian gland dysfunction appears to play an equally important role. Other bacteria, fungi, and parasites have also been implicated in the pathogenesis of some cases. Symptoms include dry eye symptoms, pruritus, and lash crusting, often most noticeable upon waking. Clinical signs include early tear break-up, vascular injection and rounding of the posterior lid margin, inspissated secretions at the meibomian orifices, and thickened or frothy secretions expressed with digital pressure on the glands. Meibomianitis is often associated with acne rosacea, and treatment of the rosacea can result in improvement of the meibomianitis.^1-3

Hordeola and Chalazia
A hordeolum is an acute infection of a sebaceous gland of the lid. External hordeola involve Zeis glands and internal hordeola involve meibomian glands. Patients present with sudden onset pain and a nodular swelling of the affected lid. External hordeola are centered on an eyelash and often point through the overlying skin. Internal hordeola produce dilation or clogging of the affected meibomian gland orifice. Purulent material can often be expressed through that orifice with digital pressure. The conjunctiva lining, an internal hordeolum, is characteristically deep red and velvety. Chronic obstruction of the meibomian glands after resolution of an acute internal hordeolum can result in a chalazion, a chronic inflammatory response to sebaceous material released into surrounding tissue upon rupture of the gland. Association with chronic staphylococcal blepharitis implicates this bacterium in the pathogenesis of hordeola and chalazia.¹

Canaliculitis
As the lacrimal canaliculi are components of the lacrimal system, canaliculitis is usually considered with tearing disorders, not infectious blepharitis. However, as the clinical appearance of canaliculitis can be confused with blepharitis, it will be mentioned here. Canaliculitis is usually caused by Actinomyces israelii, a filamentous, gram-positive rod, although a number of bacteria, viruses, and fungi have been implicated. As with blepharitis, the lid margin can appear erythematous with an associated follicular conjunctivitis, but the predominant symptom is tearing secondary to the canalicular obstruction. In addition, examination is significant for a pouting punctum and a grating sound upon canalicular probing due to the concretions formed by A. israelii casts in the canaliculus. Sometimes these casts can be expressed with digital pressure.⁴

Localized Ulcerative, Vesicular, and Papular Blepharitis
Several viruses commonly infect the eyelids, causing a papulovesicular blepharitis. The eyelids can be involved in chickenpox, the manifestation of a primary infection with varicella-zoster virus. Maculopapular lesions develop into vesicles, then open and crust over. However, more often varicella-zoster virus presents to the ophthalmologist as herpes zoster ophthalmicus, the reactivation of latent virus years after the primary infection. A similar rash appears, but in the dermatomal distribution of the ophthalmic division of the fifth cranial nerve. The rash is often preceded by 1 to 2 days of intense pain in the same distribution. The skin of the tip of the nose can be involved if the nasociliary nerve is infected, portending that the cornea, supplied by this same nerve, may also be affected.

The papulovesicles of herpes simplex blepharitis can look similar to those of herpes zoster, but do not follow the V1 distribution, and are not generally preceded by pain or paresthesia. Sometimes the papulovesicles accompany eruptions elsewhere on the body, or are accompanied by typical herpes simplex keratitis dendrites, helping to differentiate this infection from herpes zoster.

Molluscum contagiosum virus can infect the eyelid, appearing as an umbilicated nodule or cluster of nodules. Release of viral particles from the umbilicated center of nodules at the lid margin can cause an associated conjunctivitis and keratitis. Infection is often chronic or recurrent, and fairly benign. The lesion must be differentiated from the umbilicated nodule of keratoacanthoma, which is generally larger, faster growing, and associated with greater inflammation, and that of squamous cell carcinoma, which can be slow growing but generally progresses to a larger size than molluscum nodules.

Papillomavirus can infect the lid, stimulating verrucae vulgaris. These warts can appear sessile or pedunculated, and are typically lobular or multifronded. The lesions are often slow growing, and usually do not cause lash loss or an inflammatory response.¹

Infectious Dermatitis and Preseptal Cellulitis
Immune reaction to staphylococcal antigens can cause an eczematoid dermatitis of the eyelid similar in mechanism to phlyctenulosis or staphylococcal marginal keratitis. The thin eyelid skin predisposes to penetration of staphylococcal toxins and fastens to the subepithelial tissues, where these antigens can stimulate the immune system to cause a hypersensitivity reaction.

Impetigo and erysipelas can involve the eyelids. Impetigo is a superficial, typically bullous dermatitis caused by group A streptococci and staphylococci. Diphtheria involvement of the lids may initially resemble impetigo, but progresses to a membranous ulceration. Erysipelas is a superficial cellulitis usually caused by group A streptococci. It appears as a raised, well-demarcated area of bright red, indurated skin.

Preseptal cellulitis is an infection of the deeper subdermal tissues of the eyelids. It, too, is typically caused by gram-positive cocci, but is less well demarcated than erysipelas. Lid edema and erythema are prominent, but pain with eye movement, proptosis, decreased visual acuity, and pupil defects are absent. The latter signs suggest spread of the infection posterior to the orbital septum (i.e., an orbital cellulitis). An orbital computed tomography (CT) scan can aid in identifying an orbital cellulitis.¹

Treatment

Treatment of eyelid infections varies with the clinical presentation. Staphylococcal marginal and angular blepharitis and meibomianitis must be recognized as chronic conditions requiring long-term management rather than a short-term, definitive cure. Lid margin hygiene is the mainstay of treatment. Warm compresses are used to unclog oil glands at the lash follicle and meibomian glands. Massage during the compress can help express retained secretions, thus reducing the bacterial load. Scrubbing the lid margin with specifically designed eyelid wipes or a simple lather of non-irritating baby shampoo removes accumulated secretions, again reducing the bacterial load and keeping the meibomian orifices open.^1,5 Topical antibiotics, especially in ointment formulation which remains longer in the lashes, can be effective for acute exacerbations, but chronic use should be avoided due to the development of resistance. Topical corticosteroids can also help by reducing the inflammatory response, but again, long-term use should be avoided. Systemic tetracycline is used long-term (over several months) to control chronic meibomianitis. This may exert its effect by altering the consistency of the sebaceous secretions, as treatment appears to improve the condition even in cases where the microorganism is tetracycline-resistant in culture.6 When culture reveals a bacterial pathogen other than staphylococcus, antibiotic treatment should be guided by culture sensitivities.

As hordeola are often sequelae of staphylococcal blepharitis, treatment includes the measures listed above, with the addition of surgical drainage, when appropriate. Often, the pustules will drain spontaneously with warm compresses only. However, failure of this treatment or patient discomfort may necessitate incisional or aspirational drainage. Once a lesion develops into a sterile inflammatory chalazion, it is unlikely that conservative measures will suffice. Intralesional injection of corticosteroids is often effective, but surgical excision or curettage may be necessary. Vertical incisions into the conjunctival surface of the tarsus are used to incise a chalazion with minimal disruption to adjacent glands. This can be combined with a horizontal incision of the skin to maximize surgical exposure. Warm compresses are used postoperatively to facilitate further drainage.¹

Staphylococcal eczematoid dermatitis is treated with topical antibiotics and a steroid cream to control the inflammatory reaction. Lid hygiene is also used to reduce the antigenic load. Systemic antibiotic treatment is required for impetigo, erysipelas, and preseptal cellulitis. It is imperative to differentiate preseptal from orbital cellulitis, and to treat each appropriately. Preseptal cellulitis can sometimes be handled in an outpatient setting with parenteral antibiotics, but care must be taken to monitor possible progression to orbital cellulitis. If the septum is breached, intravenous antibiotics in a hospital setting are generally required.

Canaliculitis is treated with antibiotics appropriate for the pathogen cultured and surgical opening of the canaliculus by curettage and/or canaliculotomy. Herpetic dermatitis due to either herpes simplex or zoster can be treated with systemic antiviral agents if diagnosed early. This treatment can speed the healing of the dermatitis and, importantly, can prevent the occurrence of herpetic keratitis. Prophylaxis against secondary bacterial infection of herpetic skin ulcers can be accomplished with topical antibiotics. Molluscum contagiosum lesions are treated surgically with excision, curettage, or cauterization, to stimulate blood flow to the infected tissue. Verrucae are treated with excision if necessary, but this can stimulate more vigorous recurrence. Cryotherapy for conjunctival-based lesions and cautery to the base of pedunculated verrucae have been advocated.¹

References

1. Starr MB. Infections and hypersensitivity of the eyelids. In: Nesi FA, Lisman RD, Levine MA, Brazzo BG, Gladsone GJ, eds. Smith's Ophthalmic Plastic and Reconstructive Surgery, 2nd ed. St Louis, MO: CV Mosby; 1998:485-530.
   
   
2. Smith RE, Flowers CW Jr. Chronic blepharitis: A review. CLAO Journal. 1995;21:200-207.
   
   
3. Barnhorst DA Jr, Foster JA, Chern KC, Meisler DM. The efficacy of topical metronidazole in the treatment of ocular rosacea. Ophthalmology. 1996;103:1880-1883.
   
   
4. Bartley GB. Acquired lacrimal drainage obstruction: An etiologic classification system, case reports, and a review of the literature, parts 1-3. Ophthalmic Plast Reconstr Surg. 1992;8:237-249 and 1993;9:11-26.
   
   
5. Key JE. A comparative study of eyelid cleaning regimens in chronic blepharitis. CLAO Journal. 1996;22:209-212.
   
   
6. Dougherty JM, McCulley JP, Sivany RE, Meyer DR. The role of tetracycline in chronic blepharitis. Inhibition of lipase production in staphylococci. Invest Ophthalmol Vis Sci. 1991;32:2970-2975.