Lids, Lashes, and Lacrimal System

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Lids, Lashes, and Lacrimal System

Eyelid Trauma

Eyelid trauma must be evaluated thoroughly, because seemingly trivial trauma may threaten the viability of the globe. Embedded foreign bodies, incomplete eyelid closure, and lacrimal system damage can all have lasting effects beyond any obvious cosmetic consequences. Trauma can be blunt or sharp, with common examples including fist, motor vehicle accidents, or athletic injury. Ominous mechanism of injury, orbital signs, or massive periocular injury may warrant orbital evaluation including computed tomography (CT) scan.


Bruising of eyelid with edema and ecchymosis, usually secondary to blunt injury. Hematomas are often not discrete but infiltrative, involving multiple layers. Unless there is a focal collection of blood, hematomas cannot be effectively evacuated surgically, so the goal of treatment is to reduce further bleeding. Posterior extension into the orbit should be evaluated and, when present, managed accordingly. Ocular involvement is common; traumatic ptosis may occur (mechanical from edema and hematoma, or direct levator injury) and can take up to 6 months to resolve. Usually excellent prognosis if no ocular or bony injuries.

 Cold compresses for up to 45 minutes per hour while awake for 24–48 hours.

 Rule out and treat open globe (see Chapter 4) or other associated ocular trauma.

 Preseptal hematoma (absent orbital signs) is not an indication for canthotomy. Orbital compartment syndrome does not result from preseptal edema /hemorrhage.


Superficial abrasions or mild dermal epithelial abrasions usually heal by secondary intention; rarely require skin grafting.

 Antibiotic ointment (erythromycin or bacitracin) lubrication can be used for superficial wounds. With deeper (full-thickness dermis) defects consider systemic antibiotics.


Tearing or shearing injury to the eyelid resulting in partial or complete severance of eyelid tissue. Surgical repair of eyelid defect depends upon the degree of tissue loss and damage; entirely avulsed remnant should be sought and surgically replaced. Lid-sharing procedures should be avoided in young children owing to the risk of occlusion amblyopia.

When tissue loss is encountered, the approach is individually tailored. Factors such as horizontal eyelid laxity are considered in procedure selection. For example, in an older patient with advanced involutional changes, a defect of up to 30% might be repaired with direct closure, whereas in a younger patient a defect as small as 10% might not be amenable to direct closure without cantholysis. Below are some general treatment guidelines based on defect size.

Upper Lid Defects

 Small (< 33%): Direct closure with or without lateral canthotomy and superior cantholysis.

 Moderate (33–50%): Tenzel semicircular flap advancement, or adjacent tarsoconjunctival flap and full-thickness skin graft.

 Large (> 50%): Lower eyelid bridge flap reconstruction (Cutler–Beard procedure), free tarsoconjunctival graft and skin flap, median forehead flap, or full-thickness lower eyelid switch flap advancement.

Lower Lid Defects

 Small (< 33%): Direct closure with or without lateral canthotomy and inferior cantholysis.

 Moderate (33–50%): Tenzel semicircular flap advancement, or full adjacent tarsoconjunctival flap and full-thickness skin graft.

 Large (> 50%): Upper eyelid tarsoconjunctival pedicle flap with full-thickness skin graft (Hughes procedure), free tarsoconjunctival graft and skin flap, Mustarde’s rotational cheek flap, or anterior lamella reconstruction with retroauricular free skin graft or skin flap advancement.


Cut in the eyelid involving skin and deeper structures (muscle and fat), usually due to penetrating trauma. Lid lacerations are divided into: (1) no lid margin involvement, (2) lid margin involvement, and (3) canthal angle involvement (tendon and lacrimal gland system). Early, clean wounds usually are repaired successfully but can be complicated by lid notching, entropion, ectropion, or cicatrix; dirty wounds are also at risk for infection.

Lacerations involving the canaliculus (tear duct) at the nasal lid margin between the punctum and the medial canthus of either eyelid can result from a number of mechanisms. Penetrating injury such as that occurring with a dog bite may involve the canaliculus directly. Alternately, they often result from shearing at the eyelid’s weakest point. This may occur in conjunction with lacerations located more laterally on the eyelid and due to their relatively small size are often overlooked. They can be identified on slit-lamp examination of the medial eyelid and confirmed with probing and irrigation. Prognosis is good if repaired early over a stent.

 Tetanus booster (tetanus toxoid 0.5 mL IM) if necessary for tetanus prophylaxis (> 10 years since last tetanus shot or if status is unknown); consider rabies with animal bites.

 Fat prolapse into wound suggests orbital septum violation.

 For dirty wounds, systemic antibiotic (dicloxacillin 250–500 mg po qid or cephalexin 250–500 mg po qid for 7–10 days; consider penicillin V 500 mg po qid for animal or human bites).

 Surgical repair of eyelid laceration not involving lid margin: The area around the wound is infiltrated with 2% lidocaine with epinephrine 1 : 100,000. The area is prepped and draped using povidone-iodine (Betadine) solution. The wound is inspected carefully for the presence of foreign bodies. Deep portions are probed to the base of the wound and any septal penetration noted. (Wounds involving levator muscle or levator aponeurosis require layered closure, usually with an extended incision along the major lid crease, and external repair.) Copiously irrigate with saline or bacitracin solution. All tissue should be preserved if possible; only severely necrotic tissue must be excised. Horizontal or arcuate wounds oriented along orbicularis typically are closed in a single layer that includes skin only; gaping wounds or wounds that are oriented transverse to orbicularis are closed in two layers. 6-0 polyglactin interrupted, buried sutures are used to close orbicularis; skin can be closed separately. Some advocate interrupted sutures, whereas others prefer a running stitch. If permanent sutures are used, such as a 6-0 prolene or nylon, they should be removed 5 or 6 days later. Alternatively, an absorbable suture (6-0 fast-absorbing gut) can be used. This is particularly advantageous in children in whom suture removal is challenging or in patients felt unlikely to reliably return for suture removal. Topical and, in most cases of trauma, systemic antibiotics should be prescribed.

 Surgical repair of eyelid laceration involving lid margin, sparing canaliculus: The area around the wound is infiltrated with 2% lidocaine with epinephrine 1 : 100,000. The area is prepped and draped using povidone-iodine (Betadine) solution. The wound is inspected carefully for the presence of foreign bodies. Canalicular involvement is assessed via lacrimal probing and irrigation. All tissue should be preserved, if possible; only severely necrotic tissue must be excised. The lid margin is reapproximated using two to three interrupted 6-0 nylon or 7-0 Vicryl sutures. The initial suture is passed through the meibomian gland orifices, usually in a vertical mattress fashion, to align the tarsus, with one to two additional interrupted sutures to align the lash line. For each suture, it is important that the bites on the two sides are equidistant from the wound margin. It is important to cinch the tarsal suture tightly to evert the reapproximated wound edges slightly; otherwise as the wound heals and stretches a notch may form at the lid margin. These sutures are left long. The margin sutures can be placed untied on Steri-Strips temporarily to allow better exposure for tarsal closure. The remaining tarsus is closed using interrupted lamellar 6-0 polyglactin sutures with the knot on the anterior tarsal surface to avoid erosion to the ocular surface. Attention must be paid to the distance from the lid margin each suture is placed to ensure even reapproximation of the tarsus. In the upper lid it is important to avoid full-thickness bites onto the conjunctival surface, although this is safely tolerated in the lower eyelid. If they were left untied, the lid margin sutures are now tied. Orbicularis is closed using interrupted, buried 6-0 polyglactin sutures. Skin is closed using interrupted 6-0 nylon or fast-absorbing gut sutures. The long ends of the lid margin sutures are incorporated into a skin suture to keep them away from the cornea. The wound is dressed with antibiotic ointment. Skin sutures can be removed in 7–10 days, but the lid margin sutures should remain for 10–14 days to avoid dehiscence of the margin with resultant notching.

 Surgical repair of eyelid laceration involving lid margin and canaliculus: The area around the wound is infiltrated with 2% lidocaine with epinephrine 1 : 100,000. The area is prepped and draped using povidone-iodine (Betadine) solution and inspected carefully with minimal manipulation. Small (0.3 mm) forceps and cotton-tipped applicators are helpful in locating the nasal end of the transected canaliculus. The punctum of the involved canaliculus is dilated and then intubated with a silicone stent with nasolacrimal probes on each end. The first probe is passed through the puncta and the lateral portion of the lacerated canaliculus. It is then inserted into the medial portion of the canaliculus and advanced into the nasolacrimal sac to a hard stop against the lacrimal sac fossa. The nasolacrimal duct is then intubated by slowly rotating the probe in a superior–inferior orientation with slight downward pressure until a path of low resistance is found, which will be the probe passing through the opening of the nasolacrimal duct. The probe is then retrieved from under the inferior turbinate in the nose by using a straight hemostat, groove director, or hook inserted through the naris. The second arm of the tube is advanced through the opposite puncta and retrieved in the same manner, and the tubes are secured at the external naris. The canalicular tear is closed using two to three interrupted 7-0- polyglactin sutures, which are passed through the canalicular walls. Pericanalicular sutures are added as needed. The lid margin is repaired as described above except that there is no tarsus medial to the puncta. The stent is removed after 3 months.

Eyelid Infections

Blepharitis and Meibomitis


Inflammation of the eyelid margins (blepharitis) and inspissation of the oil-producing sebaceous glands of the lids (meibomitis, meibomian gland dysfunction [MGD]); often occur together. Blepharitis is classified by location (anterior [infectious], posterior [meibomitis, MGD], angular [at lateral canthus]) or etiology.


Chronic Staphylococcus or Demodex infection, seborrhea (alone, with staphylococcal superinfection, with meibomian seborrhea, with secondary meibomitis), primary meibomitis, atopic dermatitis, psoriasis, and fungal; angular blepharitis is associated with Moraxella infection. A change in the composition of meibomian gland secretions causes obstruction of the glands, inflammation, and altered tear film. Ocular surface disease results from disruption of the tear film (from bacterial lipolytic exoenzymes and abnormal meibum), epithelial cell death, and inflammation.


Very common in adult population, prevalence estimated at 12% for anterior blepharitis and 24% for posterior blepharitis; often coexists with dry eye disease (see Chapter 4); also associated with staphylococcal marginal keratitis (see Chapter 5) and acne rosacea (see below).


Itching, red eye, burning, tearing, mild pain, foreign body sensation, filmy vision; often worse on awakening and late in the day.

Anterior Blepharitis

Crusting /scales along eyelashes (“scurf” [scale fragments] and “collarettes” [scales that encircle base of lash]), loss of eyelashes (madarosis), lid margin redness, conjunctival injection; may develop pannus, phlyctenules, corneal infiltrates, and ulceration.


Thickened and erythematous eyelid margins with telangiectatic blood vessels; atrophic, swollen, pitted, or blocked meibomian glands; turbid, thickened meibum (may have “toothpaste sign”: gentle pressure on lids expresses columns of thick, white sebaceous material; the quality of meibomian gland secretions can be graded on a 0 to 3 scale [i.e., 0 = clear; 1 = cloudy; 2 = granular; 3 = toothpaste]); may have meibomian gland inclusions (visible under the tarsal conjunctiva as yellow bumps), decreased tear break-up time, tear film debris and foam, conjunctival injection, corneal staining (typically inferiorly); may also develop recurrent chalazia /hordeola.

Differential Diagnosis

Dry eye disease, primary herpes simplex virus infection, allergic or infectious conjunctivitis, corneal foreign body, sebaceous cell carcinoma, squamous or basal cell carcinoma, discoid lupus, medicamentosa, ocular cicatricial pemphigoid.


 Complete history with attention to history of skin cancer, sexually transmitted diseases, cold sores, allergies, eye medications, and chronic recurrent disease; unilateral, chronic, or refractory symptoms suggest malignancy.

 Complete eye exam with attention to facial skin, lids, meibomian gland orifices, lashes, tear film, conjunctiva, and cornea.

 Biopsy if lesions are suspicious for malignancy (ulcerated, yellow, chronic, scarred, or unilateral lid lesions, often with concomitant corneal pathology).

 Lab tests: Chlamydia cultures (if there is associated chronic follicular conjunctivitis or suspicion of sexually transmitted disease).



 Lid hygiene: Daily application of hot compresses to the eyelids followed by massage and cleansing of the lid margins with commercial lid scrub pads, or face cloth or cotton-tipped applicator soaked in dilute baby shampoo or tea tree oil shampoo solution. In addition, consider weekly application of 50% tea tree oil followed by topical steroid drop tid for 2 days.


 Topical antibiotic ointment (bacitracin or erythromycin qhs for 2–4 weeks).

 Nutritional supplements (i.e., oral flaxseed /fish oils [omega-3 fatty acids]).

 Consider short course (1–2 weeks) of topical antibiotic-steroid (Tobradex drops qid or ointment bid).

 Hot compresses and lid massage.

 Consider oral antibiotic (doxycycline 50 mg po bid or minocycline 50 mg po qd for 2 weeks, then doxycyline 20–50 mg po qd) for recalcitrant or rosacea-associated cases. Tetracycline 250 mg is also effective but requires more frequent dosing and is associated with more frequent gastrointestinal side effects. These agents are not offered to women in their childbearing years or to children with deciduous dentition. Alternatively, erythromycin 250 mg po bid then qd may be used.

 Consider azithromycin (Azasite) bid for 2 days, then qd for 2–4 weeks.

 Consider topical cyclosporine 0.05% (Restasis) bid for 3 months.

 Consider LipiFlow treatment, intense pulsed light (IPL) therapy, and/or intraductal Meibomian gland probing.

 Treat associated pathology such as rosacea and dry eye.


Good; flare-ups and remissions are common; maintenance treatment often required indefinitely.

Herpes Simplex Virus

Primary infection due to herpes simplex virus; often mild and unrecognized. Patients may note pain, itching, and redness. Appears as small crops of seropurulent vesicles on the eyelid that eventually rupture and crust over; marginal ulcerative blepharitis, follicular conjunctivitis, punctate or dendritic keratitis, and preauricular lymphadenopathy may also occur.

 Cold compresses bid to qid to affected skin area.

 Systemic antiviral (acyclovir [Zovirax] 400 mg po 5 times /day or famciclovir [Famvir] 500 mg po or valacyclovir [Valtrex] 1 g po tid for 7–10 days).

 Topical antiviral (ganciclovir gel 0.15% [Zirgan] 5 times/day, trifluridine 1% [Viroptic] 9 times /day, or vidarabine 3% [Vira-A] 5 times /day for 1–2 weeks) for patients with blepharoconjunctivitis or corneal involvement.

Herpes Zoster Virus

Reactivation of latent varicella zoster virus in the first division of cranial nerve V (herpes zoster ophthalmicus, HZO) usually involving the upper eyelid. Herpes zoster affects 20–30% of the population and increases in incidence and severity with age > 60 years (50% in 85-year-olds), 10–20% of these patients have HZO. Appears as an acute, painful, unilateral, dermatomal maculopapular skin eruption, followed by vesicular ulceration and crusting; new lesions develop for up to 1 week and then resolve in 2–6 weeks. Patients have a prodrome of fever, headache, malaise, and pain (tingling, paresthesias, itching, burning) over the affected cranial nerve V1 dermatome, which may occur without the rash (zoster sine herpete); involvement of the tip or side of the nose (Hutchinson’s sign) is an indicator of ocular involvement (nasociliary branch of the ophthalmic nerve). Ocular involvement occurs in 50% if no antiviral treatment is given; lid scarring may result with entropion, ectropion, trichiasis, lash loss (madarosis), canalicular and punctal stenosis, necrosis, and lid retraction with lagophthalmos and exposure keratitis. Fifty percent develop complications; most common is postherpetic neuralgia (PHN), a neuropathic pain syndrome that continues or occurs after resolution of the rash. PHN also increases in incidence and severity with increasing age (37% in those > 60 years old, 48% in those > 70 years old); other risk factors include severity of pain (prodromal and acute), severity of rash, and ocular involvement.

 Cool saline or aluminum sulfate-calcium acetate (Domeboro) compresses bid to tid.

 Topical antibiotic ointment (erythromycin or bacitracin bid to tid) to affected skin.

 Systemic antiviral (acyclovir [Zovirax] 800 mg po 5 times /day for 7–10 days, or famciclovir [Famvir] 500 mg po or valacyclovir [Valtrex] 1 g po tid for 7 days). If immunocompromised, acyclovir 10–12 mg / kg /day IV, divided q8h for 10–14 days; resistant strains are treated with systemic vidarabine or foscarnet. Antiviral treatment within 72 hours of the rash decreases virus shedding, severity and duration of the rash, acute pain, and incidence of ocular involvement. Treatment with either famciclovir or valacyclovir is preferred to acyclovir because the former two medications reduce the incidence, duration, and severity of PHN.

 Rule out ocular involvement (see Chapters 5 and 6).

 Treatment of PHN consists of one or more of the following agents: tricyclic antidepressants (amitriptyline, doxepin, nortriptyline, or desipramine 25–100 mg po qd), gabapentin (Neurontin 600 mg po 2–6 times a day), pregabalin (Lyrica 300–600 mg po qd), opioids (oxycodone 10–30 mg po bid), topical analgesics (lidocaine 5% ointment, lidocaine-prilocaine cream, or lidoderm 5% patch q4–6h; capsaicin 0.025% [Zostrix] cream is poorly tolerated), and oral steroids (prednisone 60 mg po for 1 week, then 30 mg for 1 week, then 15 mg for 1 week); consider diphenhydramine (Benadryl 25–50 mg po qhs) for postherpetic itching. May rarely require nerve block or botulinum map injections.

 Vaccination in individuals ≥ 60 years old. Safety and efficacy demonstrated in the Shingles Prevention Study (SPS); vaccination reduces the incidence of herpes zoster by 51%, the incidence of PHN by 67%, and the severity and duration if shingles does occur; however, the efficacy of the vaccine decreases with increasing patient age.

Molluscum Contagiosum

DNA poxvirus infection, typically occurs in children and is spread by direct contact. Usually asymptomatic; appears as shiny dome-shaped waxy papules with central umbilication on the lid or lid margin; papules may appear anywhere on the body. May be associated with chronic follicular conjunctivitis, superficial pannus, and superficial punctate keratitis. Although disease is self-limited, resolution may take years; disseminated disease occurs in patients with acquired immunodeficiency syndrome (AIDS).

 Treatment is by curettage, cryotherapy, or cautery of one or more lesions with the intention of stimulating the immune system to eliminate satellite lesions. Suggested protocol includes excisional biopsy of one lesion with curettage of at least one additional lesion.


Parasitic hair follicle infection with Demodex folliculorum or D. brevis; associated with blepharitis. Very common infestation but usually asymptomatic; may incite hordeolum formation. Examination of epilated hair follicles reveals sleeves of thin, semitransparent crusting at the base of the lashes.

 Lid scrubs may be effective: Commercial preparations are available; alternatively, a warm solution of baby shampoo and water (50 : 50 mixture) may be applied rigorously to the lids and lashes using cotton, a face cloth, or cotton-tipped applicator. Tea tree oil shampoo can also be considered.

Phthiriasis or Pediculosis

Infestation of eyelashes with lice (Phthirus pubis); usually sexually transmitted or from very close contact with an infected individual. Patients note itching and burning; signs include small, pearly, white nits (eggs) attached to lashes, adult lice, preauricular lymphadenopathy, blood-tinged lids and lashes, blepharoconjunctivitis, conjunctival follicles, and conjunctival injection.

 Mechanical removal of lice and nits with fine forceps.

 Topical ointment (erythromycin or Lacrilube tid for 14 days) to suffocate lice.

 Physostigmine 0.25% ointment × 1, repeat in 1 week, or fluorescein 20% 1–2 drops to lid margins plus delousing creams and shampoo (not for ocular use): permethrin cream rinse 1% (Nix), lindane 1%, γ-benzene hexachloride (Kwell), or pyrethrins liquid with piperonyl butoxide (RID, A-200 Pyrinate liquid). (Warning: Kwell and RID not recommended for pregnant women and children.)

 Discard or thoroughly wash in hot cycle all bedding, linens, and clothing.

 Treat sexual partner.


Chronic infectious disease caused by Mycobacterium leprae, a pleomorphic, acid-fast bacillus. Of the four variants, tuberculoid and lepromatous leprosy can have eyelid involvement, including loss of eyelashes and eyebrows (madarosis), trichiasis, paralytic ectropion, lagophthalmos with exposure keratitis, and reduced blink rate; may develop corneal ulceration and perforation.

 Systemic multidrug treatment with dapsone (100 mg po qd) and rifampin (600 mg po qd); consider adding clofazimine (100 mg po qd).

 Reduce corneal exposure with temporary or permanent tarsorrhaphy.

Eyelid Inflammations

Chalazion or Hordeolum (Stye)


Obstruction and inflammation of meibomian gland with leakage of sebum into surrounding tissue and resultant lipogranuloma formation; often evolving from an internal hordeolum; associated with meibomitis and rosacea.


Acute bacterial infection of sebaceous eyelid gland; most commonly meibomian gland (internal hordeolum) or gland of Zeis or Moll (external hordeolum); associated with Staphylococcus aureus.


Painful, hot, swollen, red eyelid lump; chronic chalazia become nontender.


Erythematous subcutaneous nodule, sometimes tender with visible pointing or drainage; usually solitary, but can be multiple or bilateral; occasionally, severe swelling prevents visualization or palpation of a discrete nodule; may have signs of blepharitis, meibomitis and rosacea; may develop super-infection with associated cellulitis.


Figure 3-12 Chalazion of the upper eyelid.

Differential Diagnosis

Preseptal cellulitis, sebaceous cell carcinoma, pyogenic granuloma.


 Complete ophthalmic history and eye exam with attention to previous episodes, fever, facial skin, lids, meibomian gland orifices, eyelid eversion, lashes, motility, and cornea.


 Warm compresses with gentle massage for 10 minutes qid.

 Topical antibiotic ointment (erythromycin or bacitracin bid to tid) in the inferior fornix if lesion is draining.

 Consider short course (1–2 weeks) of topical antibiotic-steroid ointment (Tobradex bid).

 Consider incision and curettage after 1 month if no improvement.

 Consider intralesional steroid injection (triamcinolone acetate 10 or 40 mg / mL; inject 0.5 mL with 30-gauge needle) for chalazia near lacrimal system or if only partially responsive to incision and curettage.

 Recurrent lesion must be evaluated by biopsy to rule out malignancy.

 Treat underlying meibomitis and rosacea.

 Multiple and recurrent chalazia may respond to oral antibiotic (doxycycline 50 mg po or minocycline 25 mg po bid). Tetracycline 250 mg is also effective but requires more frequent dosing and is associated with more frequent gastrointestinal side effects. These agents are not offered to women in their childbearing years or to children with deciduous dentition. Alternatively, erythromycin 250 mg po bid may be used.


Good; may take weeks to months to resolve fully; recurrence is common (especially in blepharitis or acne rosacea); conservative treatment is recommended; surgical drainage through a posterior incision with curettage and excision of the lipogranulomatous material can lead to scarring and further episodes; steroid injection may produce hypopigmentation or local fat atrophy.

Contact Dermatitis


Acute skin inflammation resulting from chemical or mechanical irritants, or from immunologic hypersensitivity to an allergic stimulus.


Swelling, redness, itching, tearing, foreign body sensation, and ocular and eyelid discomfort.


Erythematous, flaking, or crusting rash accompanied by edema; may have vesicular or weeping lesions; lichenified plaques suggest chronic exposure to irritant.

Differential Diagnosis

Herpes simplex, herpes zoster, preseptal cellulitis; chemical, ultraviolet, or thermal burns.


 Complete history with attention to exposure to irritants such as soaps, fragrances, cosmetics, hairspray, nail polish, jewelry, medications, poison ivy; and chemical, ultraviolet, or thermal exposure.

 Complete eye exam with attention to facial skin, lids, conjunctiva, and cornea.

 Consider dermatology consultation.


 A stepwise approach is required given the wide range of severity that can occur in eyelid dermatitis. Periocular steroids should not be used for more than 2 weeks without ophthalmic supervision.

 Identify and remove inciting agent(s); may require allergic patch testing to determine causative allergens.

 Cold compresses.

 Topical antibiotic ointment (erythromycin or bacitracin bid) to crusted or weeping lesions.

 Consider mild steroid cream (< 1% hydrocortisone cream bid to tid for 7–10 days) on eyelids; avoid lid margins and ocular exposure (for this reason, it is safer to use an ophthalmic preparation, e.g., fluorometholone [FML] ointment).

 Alternatively, ophthalmic steroid solution may be massaged onto affected eyelids bid.

 Tacrolimus 0.1% (Protopic), a nonsteroidal ointment, is very effective in the treatment of eyelid dermatitis and can be considered a first-line medication in advance of topical steroids.

 Oral antihistamine (diphenhydramine 25–50 mg po tid to qid) for severe or widespread lesions or excessive itching.

 Consider short-term oral steroids (prednisone 40–80 mg po qd tapered over 10–14 days) for severe cases; check PPD and controls, blood glucose, and chest radiographs before starting systemic steroids.

 Add H2-blocker (Zantac 150 mg po bid) or proton pump inhibitor when administering systemic steroids.


Usually good; resolution occurs 1–2 weeks after removal of inciting agent; rebound can occur if steroids tapered too rapidly.


Idiopathic, recurrent episodes of painless edema of the upper eyelids with or without redness and itching. Over time, repeated episodes may result in atrophy and laxity of the upper eyelid tissues, causing premature wrinkling of the skin, ptosis, deep superior sulci from fat atrophy, and lacrimal gland prolapse. Typically occurs in young females, first episode usually occurs before the age of 20. Inflammation may be treated acutely with topical steroid ointment; there is no treatment to prevent or shorten the episodes. Blepharoplasty may be helpful in addressing the long-term sequelae of multiple inflammatory episodes.



Local or diffuse loss of eyelashes or eyebrows or both.


Chronic blepharitis, eyelid neoplasm (basal cell, squamous cell, or sebaceous cell carcinoma), burn, trauma, trichotillomania, eyelid infection (zoster, varicella, vaccinia, syphilis, tuberculosis, fungal).


Endocrine (hypothyroidism, pituitary insufficiency), dermatologic (psoriasis, seborrheic dermatitis, alopecia syndromes, acne vulgaris, neurodermatitis, ichthyosis, impetigo, lichen planus), medications (topical epinephrine, gold, arsenic, barbiturates, propylthiouracil (PTU), quinine, chemotherapeutic agents), connective tissue disease (systemic lupus erythematosus), chronic malnutrition.


Asymptomatic; may have redness, itching.


Madarosis; may have lid or skin lesions.


 Complete ophthalmic history and eye exam with attention to facial skin, scalp, eyebrows, lids, and lashes. High suspicion for neoplasm, especially with focal areas of madarosis.

 Evaluation for underlying hormonal or nutritional deficits.

 Consider medical or dermatology consultation.


 Treat underlying etiology.

 May require eyelid biopsy.

 Consider en bloc eyelash transplantation.


Depends on underlying etiology.

Vitiligo and Poliosis

Total absence of melanin in hair follicles of the eyelashes or eyebrows (poliosis) and in skin (vitiligo), leading to focal patches of white hair or skin; associated with severe dermatitis, Vogt–Koyanagi–Harada syndrome, tuberous sclerosis, localized irradiation, sympathetic ophthalmia, and Waardenburg’s syndrome (autosomal dominant [AD], white forelock, congenital poliosis, nasal root abnormalities, synophrys [hypertrophy and fusion of the eyebrows], congenital deafness, iris heterochromia, and hypertelorism.)

 Treat underlying medical condition.

Acne Rosacea


Chronic inflammatory disorder of the midline facial skin and eyelids.


Rosacea is caused by inherent defects in the body’s immune system and vasoregulatory processes and may result from degenerative changes in perivascular collagen resulting in blood vessel dilation and leakage of inflammatory substances into the skin. There is a genetic predilection and it is more common in certain ethnic backgrounds (e.g., Northern European ancestry); more common in women (2–3 ×). Ocular signs and symptoms may occur prior to cutaneous manifestations in 20% of patients; approximately 5% manifest corneal disease. It has also been suggested that the pathophysiology may include an inflammatory response to D. folliculorum or H. pylori. Facial flushing is associated with triggers such as alcohol, spicy foods, caffeine, extreme temperatures, and prolonged sunlight exposure.


Facial flushing, tearing, dry eye, and foreign body sensation.


Acne, facial and eyelid telangiectasia, flushing most predominantly involving the nose and malar skin, persistent facial erythema, rhinophyma, blepharitis, recurrent chalazia / hordeola, conjunctivitis, keratitis, pannus, decreased tear break-up time, tear film debris and foam.


 Complete ophthalmic history and eye exam with attention to facial skin, lids, tear film, conjunctiva, and cornea.



 Oral antibiotic (doxycycline 100 mg po or minocycline 50 mg po bid for 3 weeks, followed by qd for 3–4 months). Tetracycline 250 mg is also effective but requires more frequent dosing and is associated with more frequent gastrointestinal side effects. These agents are not offered to women in their childbearing years or to children with deciduous dentition. Alternatively, erythromycin 250 mg po bid then qd may be used.

 Topical agents: metronidazole 0.75% (MetroGel, MetroCream) bid for 2–4 weeks; also, azeleic acid 20% (Azelex, Finevin), clindamycin 1% (Cleocin-T), or permethrin 5% (Elimite) cream.

 Consider topical tea tree oil.

 Avoidance of triggers of flushing.

 Telangiectasis can be treated with green-tinted cosmetics, pulsed dye laser, or IPL therapy.

 Advanced rhinophyma can be treated with carbon dioxide laser, incisional surgery, or electrocauterization.


 Oral antibiotic (see above).

 Lid hygiene: Daily application of hot compresses to the eyelids followed by massage and cleansing of the lid margins with commercial lid scrub pads, or face cloth or cotton-tipped applicator soaked in dilute baby shampoo or tea tree shampoo solution.

 Consider topical azithromycin (Azasite bid for 2 days, then qd for 2–4 weeks).

 Consider short course of topical antibiotic-steroid (see Blepharitis section) or compounded metronidazole 0.75% ointment for refractory cases.

 Consider LipiFlow treatment, IPL therapy, and/or intraductal Meibomian gland probing.


Clinical course is variable; depends on severity of disease and response to treatment.

Eyelid Malpositions



Drooping of the upper eyelid(s).

Aponeurotic (Involutional)

Disinsertion, central dehiscence, or attenuation of the levator aponeurosis causing lowering of the upper eyelid. Most common form of ptosis, often associated with advanced age, eye surgery, ocular trauma, pregnancy, chronic eyelid swelling, and blepharochalasis; good levator function.


Poor upper eyelid elevation due to mass effect of tumors, or to tethering of the eyelid by scarring (cicatricial ptosis); good levator function.


Inherent weakness of levator palpebrae superioris due to muscular disorders including chronic progressive external ophthalmoplegia, myotonic dystrophy, and oculopharyngeal dystrophy; extremely poor levator function.


Defects in innervation to cranial nerve III (oculomotor palsy) or sympathetic input to Müller’s muscle (Horner’s syndrome) or generalized dysfunction of neuromuscular junction such as myasthenia gravis; variable levator function depending on etiology.


Poor levator function from birth; usually unilateral, nonhereditary, and myogenic with fibrosis and fat infiltration of levator muscle; rarely results from aponeurosis dehiscence (possibly birth trauma), in which case good levator function would be expected. Congenital Horner’s syndrome (ptosis, miosis, anhidrosis, iris hypopigmentation) with poor Müller’s muscle function from decreased sympathetic tone, or congenital neurogenic with Marcus Gunn jaw-winking syndrome from aberrant connections between cranial nerve V (innervating the pterygoid muscles) and the levator muscle.


Figure 3-20 Congenital ptosis of the right eye in a child.


Figure 3-21 Same patient as Figure 3-20, demonstrating poor levator function with upgaze of the right eye. Note reduced levator excursion.


Superior visual field defect, brow ache, loss of depth perception; may have decreased vision (congenital cases with deprivation amblyopia).


Drooping of upper eyelid(s) with impaired elevation on upgaze, recruitment of brow muscles with brow furrows, higher lid crease and apparently smaller eye on ptotic side, abnormally high contralateral eyelid (Hering’s law); in downgaze, affected lid may be higher than contralateral lid in congenital ptosis (lid lag) and lower in acquired cases; may have decreased visual acuity when visual axis obscured or head tilt with chin-up position when bilateral; other associated abnormalities in congenital ptosis include lagophthalmos, decreased superior rectus function, high astigmatism, anisometropia, strabismus, amblyopia, epicanthus, and blepharophimosis.

Differential Diagnosis
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