and/or the isolation of staphylococcal species other than S aureus does not exclude the diagnosis, particularly if a predominant manifestation of the disease is punctate epithelial keratopathy, marginal infiltrates, or phlyctenulosis. Susceptibility testing may be useful in guiding treatment in cases that have been refractory to empiric antibiotic therapy.
MANAGEMENT Effective treatment addresses both the infection and the associated inflammation. Eyelid hygiene, with either commercially available eyelid scrub kits or warm water with diluted baby shampoo, may help reduce bacterial colonization and the accumulation of sebaceous secretions. With these treatments, patients should focus their attention on the base of the lashes, where colonization and seborrhea are the greatest. Topical bacitracin, erythromycin, and azithromycin may be applied to the eyelid margin to reduce both the bacterial load and inflammation. Concomitant ATD and/or lipidinduced tear-film instability may also occur and should be treated to improve comfort.
Cases with prominent infectious conjunctivitis should be treated with an antibiotic solution. Since treatment of staphylococcal blepharitis is likely to be prolonged and repeated, special attention to minimizing drug toxicity and resistance is necessary. A well-tolerated, narrow-spectrum antimicrobial agent effective against the majority of staphylococci should be selected, used at therapeutic doses, and discontinued as soon as feasible.
Anti-inflammatory therapy consists of limited and judicious use of mild doses of topical corticosteroids in selected cases. Patients with routine staphylococcal blepharitis or blepharoconjunctivitis obtain more rapid symptomatic relief with the use of adjunct topical corticosteroids, but their use should be weighed against the risk of side effects and, less likely, further proliferation of the pathogen. Routine use should be discouraged.
Although corticosteroids provide little therapeutic benefit for toxic-related punctate epithelial keratopathy, marginal infiltrates and phlyctenulosis have a strong immunologic component and thus respond promptly to topical corticosteroid therapy. In the case of phlyctenulosis, corticosteroids are usually necessary early in the course of treatment. Eyelid hygiene and antibiotic therapy alone may be sufficient in cases of marginal infiltrates, but corticosteroids may be introduced earlier if the diagnosis is certain. If epithelial defects are noted over the infiltrates, diagnostic cultures should be considered before corticosteroid treatment is begun. Long-term or indiscriminate use of corticosteroids should always be avoided.
Hordeola and Chalazia
CLINICAL PRESENTATION Hordeola present as painful, tender, red nodular masses near the eyelid margin (Fig 3-20). Those occurring on the anterior eyelid in the glands of Zeis or lash follicles are called external hordeola, or styes. Hordeola occurring on the posterior eyelid from meibomian gland inspissation are termed internal hordeola. Both types are associated with a localized purulent abscess, usually caused by S aureus. They may rupture, producing a purulent drainage. Hordeola are generally self-limited, improving spontaneously over the course of 1–2 weeks.
Figure 3-20 Hordeolum. (Courtesy of Vincent P. deLuise, MD.)
Internal hordeola occasionally evolve into chalazia, which are chronic lipogranulomatous nodules involving either the meibomian glands or the glands of Zeis. The lesion disappears in weeks to months, when the sebaceous contents drain either externally through the eyelid skin or internally through the tarsus or when the extruded lipid is phagocytosed and the granuloma dissipates. A small amount of scar tissue may remain. Occasionally, patients with a chalazion experience blurred vision secondary to astigmatism induced by its pressure on the globe. It should be noted that basal cell, squamous cell, and sebaceous cell carcinoma can masquerade as chalazia or chronic blepharitis. The histologic examination of persistent, recurrent, or atypical chalazia is therefore important.
MANAGEMENT Cultures are not indicated for isolated, uncomplicated cases of hordeolum or chalazion. Warm compresses with light massage over the lesion can facilitate drainage. Topically applied antibiotics are generally not effective and, therefore, are not indicated unless an accompanying infectious blepharoconjunctivitis is present. Systemic antibiotics are generally indicated only in rare cases of secondary eyelid cellulitis; however, if the patient has a prominent and chronic accompanying meibomitis, oral doxycycline may be necessary.
If the hordeolum evolves into a chalazion that fails to respond to warm compresses and eyelid hygiene, then intralesional injection of a corticosteroid (eg, 0.1–0.2 mL of triamcinolone 40 mg/mL), incision and drainage, or both may be necessary. In general, intralesional corticosteroid injection works best with small chalazia, chalazia on the eyelid margin, and multiple chalazia. Intralesional corticosteroid injection in patients with dark skin may lead to depigmentation of the overlying eyelid skin and thus should be used with caution.
Large chalazia are best treated with surgical drainage and curettage. Internal chalazia require vertical incisions through the tarsal conjunctiva along the meibomian gland to facilitate drainage and avoid horizontal scarring of the tarsal plates. Surgical drainage usually requires perilesional anesthesia. Recurrent chalazia should be biopsied to rule out meibomian gland carcinoma.
See also BCSC Section 7, Orbit, Eyelids, and Lacrimal System, for further discussion of chalazion.
Structural and Exogenous Disorders Associated With Ocular
Surface Disorders
Exposure Keratopathy
PATHOGENESIS Exposure keratopathy can result from any disease process that limits eyelid closure. Lagophthalmos can be caused by the following:
neurogenic diseases such as seventh nerve palsy degenerative neurologic conditions such as Parkinson disease cicatricial or restrictive eyelid diseases such as ectropion drug abuse
blepharoplasty
skin disorders such as Stevens-Johnson syndrome and xeroderma pigmentosum
Proptosis caused by thyroid eye disease or other inflammatory or infiltrative orbital diseases can also result in exposure keratopathy.
CLINICAL PRESENTATION Exposure keratopathy is characterized by a punctate epithelial keratopathy that usually involves the inferior one-third of the cornea; however, the entire corneal surface can be involved in severe cases. Large, coalescent epithelial defects may result, which may lead to ulceration, melting, and perforation. Symptoms are similar to those associated with dry eye, including foreign-body sensation, photophobia, and tearing, unless an associated neurotrophic component results in corneal anesthesia.
MANAGEMENT Therapy is similar to that for severe dry eye. In the earliest stages, nonpreserved artificial tears during the day and ointment at bedtime may suffice. Taping the eyelid shut at bedtime can help if the problem is primarily one of nocturnal exposure. The use of bandage contact lenses can be hazardous in patients with exposure keratopathy because of a high incidence of desiccation and infection. For cases in which the problem is likely to be temporary or self-limited, temporary tarsorrhaphy using tissue adhesive or sutures should be performed. However, if the problem is likely to be long-standing, definitive surgical therapy to correct the eyelid position is mandatory. Correction of any associated eyelid abnormalities, such as ectropion and/or trichiasis, is also indicated.
Most commonly, surgical management consists of permanent lateral and/or medial tarsorrhaphy. Insertion of gold or platinum weights into the upper eyelid is also an effective, more cosmetic approach to promote eyelid closure. Reported complications of gold weight implants include infection, shifting, extrusion, induced astigmatism, unacceptable ptosis, and noninfectious inflammatory response to the gold. The weights remain stable when exposed to magnetic resonance imaging. In cases of paralytic ectropion of the lower eyelid, a horizontal tightening procedure may
also be beneficial in correcting the flaccid lower eyelid.
See BCSC Section 7, Orbit, Eyelids, and Lacrimal System, for further discussion of thyroid eye disease, lagophthalmos, and proptosis.
Floppy Eyelid Syndrome
Floppy eyelid syndrome usually occurs in obese individuals, who often have obstructive sleep apnea, and consists of chronic ocular irritation and inflammation. Patients have a flimsy, lax upper tarsus that everts with minimal upward force applied to the upper eyelid. Clinical findings include small to large papillae on the upper palpebral conjunctiva, mucus discharge, and corneal involvement ranging from mild punctate epitheliopathy to superficial vascularization (Fig 3-21). Keratoconus has also been reported in patients with floppy eyelid syndrome. The problem may result from spontaneous eversion of the upper eyelid when it comes into contact with the pillow or other bed linens during sleep. Direct contact of the upper eyelid with bed linens may traumatize the upper tarsal conjunctiva, inducing inflammation and chronic irritation. The condition may be unilateral if the patient always sleeps in the same position. Treatment consists of covering the affected eyes with a metal shield, taping the eyelids closed at night, or performing surgical eyelid-tightening procedures. Differential diagnosis includes vernal conjunctivitis, giant papillary conjunctivitis, atopic keratoconjunctivitis, bacterial conjunctivitis, and toxic keratopathy. See also BCSC Section 7, Orbit, Eyelids, and Lacrimal System.
Pham TT, Perry JD. Floppy eyelid syndrome. Curr Opin Ophthalmol. 2007;18(5):430–433.