Eyelid Disorders

With aging, many lesions and tumors may appear on the eyelids, often at the nasal aspect. They may be clinically significant (eg, basal or squamous cell carcinomas; see Figure 127-2) or merely cosmetically unattractive (eg, xanthelasma; see Figure 127-3). Because eyelid carcinomas may be aggressive, immediate referral to an ophthalmologist or dermatologist is indicated.

Ectropion

Ectropion is an outward turning of the eyelid margin. It may be classified as congenital, involutional, paralytic, cicatricial, or mechanical. Most cases are involutional, and horizontal eyelid laxity is the primary cause.

Ectropion prevents the punctum from draining tears normally from the conjunctival sac into the lacrimal sac (see Figure 127-4). Thus, patients report excess tearing with tears draining onto the face (epiphora). Also, because action of the orbicular muscles is decreased, the eyelids may not close completely during sleep (called nocturnal lagophthalmos), resulting in corneal drying and secondary abrasion, redness, and irritation (superficial punctate keratitis).

Definitive treatment is surgery to tighten the eyelid. Choice of procedure depends on the degree of laxity and other factors. These procedures usually involve partially excising the tarsal plate and horizontally shortening the eyelid to bring it closer to the eyeball.

Entropion

Entropion is turning in of the eyelid margin, bringing the eyelashes in contact with the eyeball; the eyelashes then rub the eyeball with each blink.

Lower eyelid entropion (usually involutional) is much more common than upper eyelid entropion (usually cicatricial). Entropion may be caused by orbicular muscle spasm after ocular irritation or inflammation. Chronic irritation due to entropion may cause corneal and conjunctival scarring. Surgery is indicated to prevent scarring.

Ptosis

Ptosis (blepharoptosis) is drooping of the upper eyelid. Causes may be primary or secondary. Primary ptosis may be caused by decreased tone in the levator muscle, which decreases the width of the palpebral fissure (distance between the margins of the upper and lower lids). There may be disinsertion of the levator muscle into the apex of the tarsus. Loss of skin turgor with atrophy and loss of elasticity, which may cause the skin of the upper eyelid to hang below the eyelid margin, also decrease the size of the palpebral fissure. Secondary causes include thyroid disorders (which usually cause eyelid retraction), previous eye or eyelid surgery, previous periorbital trauma, and acquired neurologic disorders (eg, 3rd cranial nerve palsy, Horner's syndrome, myasthenia gravis). Marked variability in the degree of ptosis during the day and diplopia suggest ocular myasthenia gravis.

Vision may be impaired, and patients may be concerned about appearance. Many patients with ptosis report difficulty reading because ptosis worsens when they look down. Ptosis decreases the amount of light reaching the macula and therefore can reduce visual acuity, especially at night.

Pseudoptosis (apparent eyelid drooping), which may be caused by disorders such as enophthalmos and contralateral upper eyelid retraction, should be differentiated from true ptosis.

Treatment of primary ptosis is surgical repair if vision is impaired or if patients have cosmetic concerns; treatment of secondary ptosis is managing the underlying disorder. Excess skin of the upper eyelid is excised only if vision is disturbed.

Blepharospasm

Blepharospasm is spasm of muscles around the eye causing involuntary blinking and eye closing.

Blepharospasm affects about 0.03% of the general population. The cause is usually unknown but may be other ocular disorders. It affects more women than men and tends to occur in families. Secondary blepharospasm may result from ocular irritation (eg, trichiasis, corneal foreign body, keratoconjunctivitis sicca) or systemic neurologic disorders that cause spasm (eg, Parkinson's disease). Severe dry eye syndrome, which may result in contracture of the periorbital musculature, may mimic blepharospasm.

Symptoms are involuntary blinking and closing of the eyes; in severe cases, patients cannot open their eyes. Fatigue, bright light, and anxiety may make spasms worse.

Treatment involves injection of botulinum toxin into the eyelid muscles. The effect lasts 3 to 4 mo; then, spasms recur, and reinjection is necessary. The primary adverse effect is ptosis, which develops temporarily in about 20% of patients. Anxiolytics may also help. Surgery to cut the periorbital muscles is effective but, because of potential complications, is considered only if botulinum toxin is ineffective. Sunglasses help decrease the light sensitivity that may cause or accompany blepharospasm.

Blepharitis

Blepharitis is acute or chronic inflammation of the eyelid margins. Acute blepharitis may be ulcerative or nonulcerative. Symptoms and signs include itching and burning of the eyelid margins, redness, and edema. Diagnosis is by history and slit-lamp examination. Acute ulcerative blepharitis is usually treated with topical antibiotics; systemic antivirals are given if herpes is suspected. Acute nonulcerative blepharitis is occasionally treated with topical corticosteroids. Treatment of chronic blepharitis (seborrheic blepharitis and meibomian gland dysfunction) includes eyelid hygiene, warm compresses, and antibiotic ointments.

Etiology

Blepharitis may be acute (ulcerative or nonulcerative) or chronic (seborrheic blepharitis or meibomian gland dysfunction). Acute ulcerative blepharitis is typically caused by bacterial (usually staphylococcal) infection of the eyelid margin at the origins of the eyelashes and affects the lash follicles and meibomian glands. This form may also be caused by a virus (eg, herpes simplex, varicella zoster). Acute nonulcerative blepharitis is usually caused by an allergic reaction (eg, atopic blepharodermatitis, seasonal allergic blepharoconjunctivitis, contact sensitivity dermatoconjunctivitis) and affects the same area.

Chronic blepharitis is noninfectious inflammation of unknown cause. Seborrheic blepharitis often accompanies seborrheic dermatitis of the face and scalp. Secondary bacterial colonization often occurs on the scales that develop on the eyelid margin.

Normally, meibomian glands in the eyelid produce lipids (meibum) that stabilize tears by forming a lipid layer on top of the aqueous tear layer, thus reducing evaporation. In meibomian gland dysfunction, lipid composition is abnormal, and gland ducts and orifices become inspissated with hard, waxy plugs; in most patients, tear evaporation increases and keratoconjunctivitis sicca develops. The disorder often occurs in patients with rosacea, a history of recurrent hordeola or chalazia, or both.

Symptoms and Signs

Symptoms common to all forms include itching and burning of the eyelid margins, conjunctival irritation, lacrimation, and photophobia.

In acute ulcerative blepharitis, small pustules develop in eyelash follicles and eventually break down to form shallow marginal ulcers. Removal of tenacious, adherent crusts leaves a bleeding surface. Eyelids become glued together by dried secretions during sleep. Recurrent ulcerative blepharitis can cause eyelid scarring and loss of eyelashes.

In acute nonulcerative blepharitis, eyelid margins become edematous and erythematous; eyelashes may become crusted with dried serous fluid.

In seborrheic blepharitis, greasy, easily removable scales develop on eyelid margins. In meibomian gland dysfunction, gland orifices are dilated and inspissated; with pressure, they exude a waxy, thick, yellowish secretion. Most patients with seborrheic blepharitis and meibomian gland dysfunction have secondary keratoconjunctivitis sicca, which causes a foreign-body or gritty sensation, eye strain and fatigue, and blurring with prolonged visual effort.

Diagnosis

Diagnosis is usually by slit-lamp examination. Chronic unilateral blepharitis that does not respond to treatment requires biopsy to exclude eyelid tumors that can simulate the disorder.

Treatment

Acute ulcerative blepharitis is treated with an antibiotic ointment (eg, bacitracin/polymyxin B or gentamicin 0.3% qid for 7 to 10 days). Acute viral ulcerative blepharitis is treated with systemic antivirals (eg, for herpes simplex, acyclovir 400 mg po tid for 7 days; for varicella zoster, famciclovir 500 mg po tid for 7 days, although acyclovir 800 mg po 5 times/day for 7 days is also effective and is safe for patients with adequate renal function). The topical antiviral eye drop trifluridine 1% is also effective for viral blepharitis.

Treatment of acute nonulcerative blepharitis begins with avoiding the offending action (eg, rubbing) or substance (eg, new eye drops). Cold compresses over the closed eyelid may speed resolution. If swelling persists > 24 h, topical corticosteroids (eg, fluorometholone ophthalmic ointment 0.1% tid for 7 days) can be used temporarily. Using corticosteroids for > 1 wk is not recommended because continued use can elevate intraocular pressure and lead to glaucoma.

Initially, treatment of seborrheic blepharitis or meibomian gland dysfunction is eyelid hygiene: gentle cleaning of the eyelid margin twice/day with a cotton swab dipped in a dilute solution of baby shampoo (2 to 3 drops in ½ cup of warm water), warm compresses 4 times/day to melt the waxy plugs, and occasionally eyelid massage to extrude trapped secretions. A topical antibiotic ointment (bacitracin/polymyxin B, erythromycin ophthalmic ointment, or sulfacetamide 10% at bedtime for up to 3 mo) may be added if patients are unresponsive after weeks of eyelid hygiene. Tetracycline (eg, doxycycline 100 mg po bid for several weeks and then tapered over 3 to 4 mo or 50 to 100 mg once/day used indefinitely) may also be effective.

Chalazia and Hordeola

Chalazia and hordeola are localized swellings of the eyelid that appear suddenly. A chalazion is caused by noninfectious meibomian gland occlusion; a hordeolum is caused by infection. Both disorders initially cause eyelid hyperemia, edema, swelling, and pain. With time, a chalazion becomes a small, nontender nodule in the center of the eyelid; a hordeolum remains painful and localizes to an eyelid margin. Diagnosis is clinical. Treatment is with warm compresses. Both disorders resolve spontaneously, but incision or, for chalazia, intralesional corticosteroids may be used to hasten resolution.

A chalazion is a noninfectious occlusion of a meibomian gland causing extravasation of irritating lipid material in soft tissues of the eyelid and a focal inflammatory response. This common disorder often occurs in patients with rosacea, chronic meibomian gland dysfunction, or both. Occasionally, a chalazion is confused with a malignant tumor. Initial features are eyelid hyperemia, edema, swelling, and pain. After 1 to 2 days, a chalazion centers in the body of the eyelid, forming a small, nontender nodule or lump that points toward the inner surface of the eyelid or, rarely, toward the outer surface. A chalazion usually drains or absorbs spontaneously over 2 to 8 wk but can persist longer.

A hordeolum is an acute, localized, pyogenic (usually staphylococcal) infection or abscess of the eyelid that may be external (stye) or internal.

External hordeola result from infection and obstruction of an eyelash follicle and the adjacent gland of Zeis or Moll's gland. They frequently develop in patients with blepharitis. Symptoms are pain, redness, and tenderness of the eyelid margin, occasionally with tearing, photophobia, and a foreign-body sensation. Signs are tenderness and a small yellowish spot (pointing) at the base of the eyelashes, indicating suppuration; the spot is surrounded by hyperemia, induration, and diffuse edema. Orbital cellulitis may develop. Within 2 to 4 days, the lesion ruptures, discharging pus and relieving pain.

Internal hordeola, which are much rarer, result from meibomian gland infection. Symptoms are the same as those of chalazia, with pain, redness, and edema localized to the posterior tarsal conjunctival surface. A small elevation or yellow area can be seen on the tarsal conjunctivae near the affected gland. Later, an abscess forms, pointing on the conjunctival side of the eyelid; it sometimes points through the skin. Spontaneous rupture is rare, and recurrence is common.

Initially, chalazia and hordeola are clinically indistinguishable, causing the same symptoms and signs. They can be distinguished after 1 to 2 days, when an external hordeolum localizes to the eyelid margin, but a chalazion localizes to the center of the eyelid.

Diagnosis of chalazion and both kinds of hordeola is clinical. If a chalazion or hordeolum lies near the inner canthus of the lower eyelid, it must be differentiated from dacryocystitis (see Figure 127-5), usually by noting the location of maximum induration and tenderness (eg, eyelid for a chalazion, side of the nose for dacryocystitis). Also, successful lacrimal duct irrigation rules out dacryocystitis. Chronic chalazia that do not respond to treatment require biopsy to exclude tumor of the eyelid.

Most chalazia disappear gradually after 1 to 2 mo, and most external hordeola rupture on their own after 2 to 4 days. Hot compresses for 5 to 10 min 2 or 3 times/day can be used to hasten resolution. An external hordeolum can also be incised with a sharp, fine-tipped blade as soon as pointing occurs. If chalazia are large and unsightly and persist for more than several weeks despite conservative therapy, incision and curettage or intralesional corticosteroid therapy (0.05 to 0.2 mL triamcinolone 25 mg/mL) may be indicated. Antibiotics (eg, dicloxacillin or erythromycin 250 mg po qid) are indicated when preseptal cellulitis accompanies a hordeolum; orbital cellulitis usually requires IV antibiotics.

For internal hordeola, treatment is oral antibiotics (usually dicloxacillin 250 mg po qid or erythromycin 250 mg po qid) and, if needed, incision and drainage. Topical antibiotics are usually ineffective.

This topic was last updated May 2006.