with sutures. When surgery is performed under local anesthesia, the patient should be raised to a sitting position to assess the lid height and contour.

●With fair levator function (5 to 7 mm), a large external levator resection (up to Whitnall’s ligament in many cases) may be necessary to achieve the desired result. The procedure is similar to the external approach for levator repair. Resection of the superior tarsus is an additional technique for maximal elevation of the eyelid.

●Ptosis with poor levator function (4 mm or less) generally requires frontalis suspension. This can be performed either transcutaneously or transconjunctivally, utilizing autogenous or banked fascia lata or synthetic materials such as silicone rods. These materials are used to suspend the eyelid directly from the frontalis muscle to allow the brow to efficiently raise the eyelid. When the ptosis is unilateral, some advocate disinsertion of the (normal) contralateral levator aponeurosis combined with bilateral frontalis suspension to further stimulate frontalis use and to achieve symmetry on downgaze. The decision to modify a normal eyelid is controversial and requires thorough preoperative discussion.

●In patients with mild ptosis, excellent levator function, and a positive phenylephrine test, a conjunctiva-Möller’s resection via an internal approach is effective. The lid is everted, and a segment of conjunctiva and Müller’s muscle is resected using a Putterman clamp. The cut edges of the incision are sutured with 6-0 plain suture.

●For patients in whom surgery is not an option, ptosis crutches may be attached to the upper posterior rim of eyeglasses and used to mechanically elevate the lid. The lid may not close properly, however, and the patient could develop exposure keratopathy.

COMPLICATIONS

The complications of surgical ptosis management may be divided into the categories of overcorrection, undercorrection, improper suture placement, and tissue reaction.

●In general, overcorrection causes exposure keratitis and therefore necessitates early adjustment. The external levator approach allows loosening or removal of the sutures in the levator aponeurosis, and this adjustment can easily be performed in the outpatient clinic under local anesthesia during the early postoperative period. Overcorrection after any method of ptosis repair may cause severe exposure keratopathy and should especially be avoided in patients with poor Bell’s phenomenon and weak orbicularis function, as occurs with chronic progressive external ophthalmoplegia, dystrophies, and congenital fibrosis syndrome. Occasionally, the lid must be lowered to a less functional and cosmetically appealing height to prevent keratopathy.

●Undercorrection is common in congenital ptosis and may necessitate repeat surgery depending on the needs and expectations of the patient and family.

●If the sutures attaching the frontalis sling or levator aponeurosis to the tarsus are placed too high or too low, entropion or ectropion may result. Careful attention to incorporation of levator aponeurosis within lid crease fixation sutures may also avoid lid malpositions.

●With large levator resections, conjunctival prolapse may result and can be treated with patching, suturing of the palpebral conjunctiva up into the fornix, or excision of the redundant tissue.

●In patients with frontalis slings, there may be exposure of silicone rods or early reabsorption of banked fascia lata, necessitating repeat surgery.

●Patients with concomitant strabismus should have their extraocular muscle surgery first because changes in extraocular muscle placement may affect lid position. In addition, if the strabismus cannot be satisfactorily treated in adults, intractable diplopia may result from elevation of the lid to a normal height.

COMMENTS

Ptosis is a complex and challenging disorder, requiring careful evaluation of the causative mechanism and surgical options to devise the most appropriate treatment strategy for each patient.

REFERENCES

Anderson RL: Aponeurotic ptosis surgery. Arch Ophthalmol 97:1123, 1979.

Callahan M, Beard C: Ptosis. 4th edn. Birmingham, Aesculapius, 1990.

Frueh BR: The mechanistic classification of ptosis. Ophthalmology 87:1019, 1980.

Wobig JL, Dailey RA: Oculofacial plastic surgery. New York, Thieme, 2004.

252 SEBORRHEIC BLEPHARITIS

372.20

Peter B. Marsh, MD

Portland, Oregon

ETIOLOGY

Seborrheic blepharitis is a common cause of eyelid inflammation which may affect the anterior or posterior lamella of the eyelids, or both, and cause significant ocular discomfort. It is frequently seen in patients with seborrheic dermatitis. Seborrheic blepharitis alone presents with inflammation of the anterior lid margin with greasy sebum secretions near the eyelashes. Posteriorly, involvement of the meibomian glands is one cause of meibomian gland dysfunction. In contrast to seborrheic blepharitis alone, this may lead to patchy inflammation of the meibomian glands which in turn can cause blockage of the glands with inspissated secretions and significant periods of exacerbation of symptoms. The exact etiology is not known. However, an altered meibum composition may be responsible, along with increased Staphylococcus aureus colonization of the eyelid. Although usually a chronic condition, treatment can improve symptoms, especially during times of exacerbation.

DIAGNOSIS

Clinical signs and symptoms

Patients with seborrheic blepharitis present with symptoms of ocular irritation, including burning, itching, redness, and mildly decreased vision. Meibomian keratoconjunctivitis is

252 CHAPTERBlepharitis Seborrheic •

Eyelids • 21 SECTION

distinguished from other types of seborrheic blepharitis by a shorter duration of symptoms at the time of presentation and a more pronounced inflammation of the eyelids. The anterior aspects of the lids frequently are only minimally involved with deposition of an oily scurf. The prominent feature is diffuse inflammation around the meibomian glands, which are dilated with retained meibum that is not easily expressed. The orifices of the glands are obstructed and pout with these secretions. There is a marked inflammation around the meibomian glands and the orifices. Tear breakup time is frequently shortened due to the abnormal composition of the lipid tear layer.

In addition to the lid findings, an important associated condition found in these patients is aqueous tear deficiency (ATD). The symptoms of ATD are similar to those in (and may be masked by the complaints of) patients whose predominant problems are related to blepharitis. Patients with chronic blepharitis, however, have been shown to have changes in the composition of meibum, which may lead to alterations in the tear film, thereby predisposing these patients to associated ocular surface problems related to an unstable tear film. Studies have documented concurrent ATD in a high percentage of patients with chronic blepharitis. It is important to look for an accompanying dry-eye state in these patients and to treat it when present.

Laboratory findings

Although diagnosis is usually made clinically without laboratory testing, research has shown alterations in bacterial colonization and composition of meibum in patients with this condition. Aerobic and anaerobic culturing of healthy control patients and patients with each form of chronic blepharitis has revealed a significantly greater incidence of colonization, with Staphylococcus aureus only in the seborrheic subgroups. There was no significant difference in the incidence of coagulase negative Staphylococcus (C-NS), Propionibacterium acnes, or any other bacteria isolated in any of the various patient subgroups compared with control patients. The cultures of meibum revealed no evidence to support its role as a reservoir for bacterial colonization in any form of chronic blepharitis.

The possible role of bacterial lipases in modifying the composition of meibum and differences in the biochemical composition of meibum in the various subgroups of chronic blepharitis have also been examined by McCulley et al. Studies have shown that there is a higher percentage of C-NS species capable of de-esterifying fatty waxes and cholesteryl esters in the types of chronic blepharitis with meibomian gland involvement.

The exact role of these various meibum components has not been fully defined, but they may provide new avenues for more definitive therapeutic intervention.

TREATMENT

Systemic

When meibomian gland dysfunction is present in patients with seborrheic blepharitis, systemic treatment with tetracycline may be indicated. Usual dosage is tetracycline 250 mg PO q. i.d., doxycycline 50 mg PO b.i.d., or minocycline 50 mg PO b.i.d. These medications may improve this condition by decreasing bacterial flora on the eyelid or by decreasing bacterial lipase activity, thereby altering the composition of meibum.

Nutritional supplementation with omega-3 fatty acids (fish oil or flax seed oil) may be helpful in decreasing the inflammatory component of blepharitis and meibomitis.

Ocular

Warm compresses to the eyelids for 5 to 10 minutes b.i.d. This may be done with a warm wet washcloth or with 1 cup of dry rice in a clean sock heated in a microwave for approximately 45 seconds.

Eyelid scrubs with dilute baby shampoo or a commercial lid scrub b.i.d.

Bacitracin or erythromycin ointment applied to the lid margins after lid scrubs and to the cul-de-sac at bedtime.

Rarely, short-term topical steroids.

Topical cyclosporin A drops have been shown to decrease objective signs of meibomitis.

Preservative-free artificial tears, and punctal occlusion for associated keratoconjunctivitis sicca.

Dermatologic consultation for manifestations of seborrheic dermatitis.

COMPLICATIONS

Tetracycline or doxycycline should not be administered to children because of the effect on dental enamel; in addition, it is contraindicated in pregnant women and lactating mothers. Tetracycline should be taken on an empty stomach, such as 1 hour before or 2 hours after meals. If associated gastrointestinal irritation presents as a side effect, 100 mg of doxycycline b.i.d., which may be taken with food, can be substituted. When tetracycline is contraindicated, erythromycin is a suitable alternative.

COMMENTS

Seborrheic blepharitis is usually a chronic disease, which may have bothersome exacerbations especially if associated with meibomian gland inflammation. However, with proper diagnosis and treatment, patients can usually experience significant improvement in their symptoms. Nevertheless, the chronic nature of the disease needs to be explained to patients initially so false expections are not created. Careful examination for coexisting conditions such as dry eye and other eyelid conditions is important so that specific treatment may be initiated.

REFERENCES

Dougherty JM, McCulley JP, Silvany RE, Meyer DR: The role of tetracycline in chronic blepharitis. Invest Ophthalmol Vis Sci 32:2970–29075, 1991.

McCulley JP, Dougherty JM: Bacterial aspects of chronic blepharitis. Trans Ophthalmol Soc UK 105:314–318, 1986.

McCulley JP, Dougherty JM, Deneau DG: Classification of chronic blepharitis. Ophthalmology 189:1173–1180, 1983.

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 25(2):171–175, 2006.

Ta CN, Shine WE, McCulley JP, et al: Effects of minocycline on the ocular flora of patients with acne rosacea or seborrheic blepharitis. Cornea 22(6):545–548, 2003.

253 CHAPTER Trichiasis •

Eyelids • 21 SECTION

Eyelid margin rotation procedures, e.g. the Lagleyze or Weis procedures, can be considered for trichiasis associated with cicatricial entropion.

Lid-splitting procedures (at the gray line) with or without insertion of a mucus membrane or amniotic membrane graft are alternatives for trichiasis associated with cicatricial entropion.

COMMENTS

For trichiasis treatment to be effective, it is important to recognize and treat any underlying pathology. The extent of the abnormal eyelashes and the underlying cause generally dictate the treatment modality. Several abnormal eyelashes may be treated with laser ablation or cryosurgery. Cryosurgery is more effective for larger eyelashes as compared with fine lanugo hair. Larger patches of eyelashes may require cryosurgery or surgery. Extensive trichiasis, with ongoing cicatricial disease, is best treated with excision and mucous membrane grafting. Timely delivery of treatment provides the best outcome for the patient and decreases the risk of corneal vascularization, scarring, and visual loss.

REFERENCES

Bearden W, Anderson R: Trichiasis associated with prostaglandin analog use. Ophthalmic Plast Reconstr Surg 20:320–322, 2004.

Berry J: Recurrent trichiasis: treatment with laser photocoagulation. Ophthalmic Surg 10:36–38, 1979.

Gossman MD, Brightwell JR, Huntington AC, et al: Experimental comparison of laser and cryosurgical cilia destruction. Ophthalmic Surg 23:179–182, 1992.

Johnson RLC, Collin JRO: Treatment of trichiasis with a lid cryoprobe. Br J Ophthalmol 69:267–270, 1985.

Rosner M, Bourla N, Rosen N: Eyelid splitting and extirpation of hair follicles using a radiosurgical technique for treatment of trichiasis. Ophthal Lasers Imaging 35:116, 2004.

254 XANTHELASMA 374.51

(Xanthelasma Palpebrarum)

Geoffrey Gladstone, MD, FAACS

Southfield, Michigan

Shoib Myint, DO, FAACS

Royal Oak, Michigan

ETIOLOGY/INCIDENCE

Xanthelasma palpebrarum, or simply xanthelasma, is a raised, soft, yellow, plaque-like, velvety lesion most commonly occurring in the medial canthal area of the eyelid. Erasmus Wilson originally described the term xanthelasma 100 years ago. It is derived from the Greek xanthos, meaning ‘yellow,’ and elasma, meaning ‘beaten metal plate.’ These lesions will rarely enlarge so as to obstruct vision.

Xanthelasma was considered at one time to be a degenerative phenomenon, which involved the subcutaneous and muscular tissue. Histologic studies, however, have shown it to be a pathologic change confined to the skin. Most agree that this condition commonly occurs as an isolated disorder. It has not been

associated with aging or hormonal changes. The age of onset ranges from 15 to 73 years old, with the peak in the fourth and fifth decades. One-third of patients have a family history of this condition. Xanthelasma has been known to occur as a result of hyperlipemia, hypercholesteremia, obesity, and cardiovascular changes. Approximately 33% of men and 40% of women with xanthelasma have elevated cholesterol levels. Obesity was found in 26% (in women more than in men), and vascular changes were found in 18% of adults. One study, which involved 8000 healthy men and women, found xanthelasma in 1.1% of women and 0.3% of men with hyperlipidemia. It has also been associated with familial hyperlipoproteinemia type 2 and, rarely, type 3. It may be seen with xanthoma tuberosum or eruptive xanthomatoses. Patients with normal levels of serum lipids have been known to have xanthoma disseminatum. It has also been described in histiocytosis X, most commonly the Hand-Schöller–Christian type. Association with other xanthomas elsewhere is usually less than 2%.

COURSE/PROGNOSIS

With excision, the 1-year recurrence rate is 26%. The younger patients had an earlier recurrence. If all four lids are involved, the recurrence rate with excision is approximately 70% to 80%. Once plaques are established, they will remain static or increase in size.

Patients with first-time excision should be advised of a 40% to 50% success rate. Higher recurrence rates are associated with systemic hyperlipemia, the involvement of all four eyelids, and more than one recurrence after surgery.

DIAGNOSIS

Types

●Xanthelasma with lipemia, acquired or inherited.

●Hypercholesteremia, frequent.

●Hyperneutrolipemia, rare.

●Xanthelasma with normolipemia.

●Local.

●Generalized.

●Xanthoma disseminatum.

●Histiocytosis X.

●Reticulohistiocytoma cutis.

Laboratory findings

Xanthomas are foam cells with lipid found in the superficial reticular dermis. Occasionally, multinucleated giant cells (toutan cells) and fibrosis are observed. A tumor of epidermal origin is possible.

Differential diagnosis

●Myxedema.

●Cirrhosis.

●Diabetes mellitus.

●Plasma protein abnormalities.

●Amyloidosis.

TREATMENT

●Various treatment methods include dietary, medical, dermatologic, surgical, and laser.

254 CHAPTERXanthelasma •