Eyelid lesions

INTRODUCTION — Patients with eyelid abnormalities often present to their primary care practitioner for evaluation and management. Most eyelid lesions are benign. The clinician should be able to identify common etiologies such as hordeola (stye) (picture 1A-B), chalazia (picture 2A-B and figure 1), and xanthelasma (picture 3) and to distinguish them from more serious conditions that require referral to a specialist (table 1).

This topic will discuss the differential diagnosis of non-acute lesions that affect the eyelid. Eyelid lacerations, blepharitis, and evaluation of the red eye are discussed separately. (See "Eyelid lacerations" and "Blepharitis" and "The red eye: Evaluation and management".)

Ligneous conjunctivitis is discussed separately. (See "Plasminogen deficiency", section on 'Ligneous conjunctivitis'.)

EYELID ANATOMY — Eyelids contain the body's thinnest skin, protecting eyes from light, extreme temperature, and trauma. With each blink, the cornea and conjunctiva are swept of debris and relubricated.

The eyelid has five layers (exterior to interior): skin, orbicularis oculi muscle, tarsal plate, levator muscle apparatus, palpebral conjunctiva. The orbicularis oculi muscle helps with both voluntary closure (sleep) and involuntary closure (blink). The muscle also expels tears and debris through the nasolacrimal duct via the two puncta in the upper and lower lids. The tarsal plate is the connective tissue that forms the scaffolding for the lids. The levator muscle apparatus, enervated by cranial nerve III (oculomotor), open the lids. The palpebral conjunctiva is a thin mucous membrane on the inside of each lid.

Tear glands are distributed throughout the eyelid. Meibomian glands are located in the tarsal plate, and secrete the oily, evaporation-prevention portion of tears through their ducts near the posterior eyelid margin. Glands of Moll and Zeiss are associated with each eyelash follicle and secrete sebum to keep the eyelashes soft and flexible. The palpebral conjunctiva contains mucin-producing goblet cells and aqueous-producing Krause and Wolfing glands (figure 2).

COMMON ETIOLOGIES

Hordeolum (stye)

●Clinical presentation – A hordeolum (stye) is an acute inflammation of the eyelid that presents as a localized painful and erythematous swelling or nodule (picture 1A-B and figure 1). It tends to appear rather quickly (in a day or even overnight).

●Pathology – Hordeola can be external or internal. External hordeola arise from glands in the eyelash follicle or lid-margin (gland of Zeis and gland of Moll) (figure 2). Internal hordeola are caused by inflammation of the meibomian gland, resulting in swelling just under the conjunctival side of the eyelid. Staphylococcus aureus is the pathogen implicated in most cases, but hordeola can also be sterile. Patients with underlying skin conditions that affect the eyelids (eg, rosacea and seborrheic dermatitis) are prone to having frequent episodes of hordeolum. Eye makeup, particularly eye makeup contaminated by bacteria, can cause hordeola by clogging and inflaming gland pores. (See "Rosacea: Pathogenesis, clinical features, and diagnosis" and "Seborrheic dermatitis in adolescents and adults".)

●Management – Most hordeola resolve spontaneously over one to two weeks. Management recommendations are largely based on longstanding clinical practices and on case reports more than 20 years old; clinical trial data are lacking [1].

Drainage can be facilitated with warm, moist compresses placed on the affected areas frequently (eg, for 5 to 10 minutes four times a day). Massage and gentle wiping of the affected eyelid after the warm compress can also aid in drainage. Patients should discontinue eye makeup to support healing. If, despite management with warm compresses, the lesion does not reduce in size within two weeks, the patient should be referred to an ophthalmologist for consideration of incision and drainage.

There is little evidence that treatment with topical or systemic antibiotics and/or glucocorticoids promotes healing [2]. However, patients who have frequent hordeola in the setting of rosacea-associated blepharitis and who do not achieve adequate improvement with warm compresses and mechanical removal of lid margin debris may respond to a topical antibiotic/corticosteroid ointment combination. Such patients should be managed by an ophthalmologist because of the potential ocular complications associated with topical glucocorticoid use.

Preseptal cellulitis is an uncommon complication of hordeolum. It typically presents with unilateral ocular pain, eyelid swelling, and erythema (picture 4). Management consists of antibiotic therapy directed against S. aureus and streptococcus. Diagnosis and management of preseptal cellulitis is discussed separately. (See "Preseptal cellulitis", section on 'Treatment'.)

Chalazion

●Clinical presentation – Chalazion, meaning "hail stone" in Greek, typically presents as a painless localized eyelid swelling (picture 2A). Examination of the inner eyelid reveals a nontender rubbery nodule (picture 2B).

Chalazion is diagnosed based on the typical clinical appearance of the lesion (picture 2A-B). Chalazia and hordeola can have a similar appearance; however, chalazia tend to be painless and are less erythematous and angry-appearing (figure 1). In addition, a chalazion grows slowly, over days to weeks, in contrast to a hordeolum, which appears over a day or so.

Pathology – Chalazia are caused by obstruction of Zeis or meibomian glands (figure 2). Inflammatory conditions like rosacea and meibomianitis thicken gland secretions leading to blockage. Hordeola sometimes transform into chalazia after the inflammation resolves.

Management – Untreated, chalazia may take several weeks to months to resolve. Draining of large chalazia can be facilitated by placing warm compresses on the eyelid for 5 to 10 minutes four times a day. Antibiotics (topical or systemic) are not indicated since chalazion is a granulomatous condition [2]. Patients with lesions that do not resolve over one to two months should be referred to an ophthalmologist for consideration of incision and curettage or glucocorticoid injection [3]. Such persistent or recurring lesions, especially if unilateral, should be assessed histopathologically for possible basal cell, sebaceous cell, or meibomian gland carcinoma. (See 'Malignant lesions' below.)

Xanthelasma

●Clinical presentation – Xanthelasma are soft, yellow plaques that usually appear symmetrically on the medial aspects of the eyelids (picture 3). They occur most often in middle-aged and older adults, tend to be painless, and build gradually over time. Larger xanthelasma may cause discomfort.

●Pathology – Cholesterol-filled xanthelasma are often associated with hypercholesterolemia, and thus we suggest obtaining a lipid profile if the patient has not already undergone screening. Dyslipidemia is present in approximately 50 percent of adult patients with xanthelasma [4,5]. Xanthelasma are a classic feature of primary biliary cholangitis, a condition often associated with marked hypercholesterolemia. (See "Hypercholesterolemia in primary biliary cholangitis (primary biliary cirrhosis)".)

Xanthelasma are common in patients with primary disorders of low-density lipoprotein (LDL) cholesterol metabolism (eg, familial hypercholesterolemia, hyperapobetalipoproteinemia). The finding of xanthelasma in younger individuals, especially children, should prompt consideration of an underlying inherited dyslipidemia [6]. (See "Familial hypercholesterolemia in adults: Overview" and "Inherited disorders of LDL-cholesterol metabolism other than familial hypercholesterolemia" and "Familial hypercholesterolemia in children".)

In patients with a normal lipid profile, the association between xanthelasma and atherosclerosis is not clear. Some studies have found lipoprotein abnormalities other than hypercholesterolemia that may increase the risk of coronary heart disease (eg, low levels of high-density lipoprotein [HDL] cholesterol) in patients with xanthelasma [5,7].

●Management – Xanthelasma lesions themselves generally do not require treatment. Lipid-lowering drug therapy may induce regression of xanthelasma in some patients, but the effect is not consistent [8]. Surgical excision, carbon dioxide laser therapy, or topical trichloroacetic acid (TCA; where available) can be performed for cosmetic reasons, but recurrence is common [9-11]. Treatment of hypercholesterolemia is discussed in detail separately. (See "Low-density lipoprotein cholesterol-lowering therapy in the primary prevention of cardiovascular disease".)

Molluscum contagiosum

●Clinical presentation – The typical appearance of Molluscum contagiosum is that of multiple or single small, flesh-colored papules with central umbilication (picture 5A-B). While generally painless, they can potentially become inflamed and swollen. Chronic conjunctivitis may occur with lesions located on the lid margin. It is commonly seen in children but can also occur in adults. Immunocompromised patients are at risk for extensive and persistent disease. The diagnosis is based on clinical appearance; biopsy is rarely necessary.

●Pathology – Molluscum contagiosum is a poxvirus that causes localized skin infections.

●Management – Molluscum contagiosum infection is usually self-limited in immunocompetent individuals. The lesions typically resolve within two months with complete clearing by 6 to 12 months. When treatment is desired, options include cryotherapy, curettage, and desiccation.

Molluscum contagiosum is discussed in greater detail separately. (See "Molluscum contagiosum".)

Seborrheic keratosis

●Clinical presentation – Most commonly occurring after age 50, seborrheic keratosis appears typically as a well-demarcated, round or oval "stuck-on" lesion with a dull, verrucous surface (picture 6). Lesions are usually painless. The diagnosis is usually clinically based on the appearance of the lesion; biopsy generally isn't necessary. However, lesions with atypical clinical features (eg, large lesions, history of rapid change or growth, ulcerated lesions) should be biopsied.

●Pathology – Seborrheic keratoses are common epidermal tumors consisting of a benign proliferation of immature keratinocytes.

●Management – Seborrheic keratoses are benign and slow-growing lesions and thus treatment is generally not required. However, lesions that are symptomatic or that cause cosmetic concerns can be removed with cryotherapy or curettage. Seborrheic keratosis is discussed in greater detail separately. (See "Overview of benign lesions of the skin", section on 'Seborrheic keratosis'.)

Actinic keratosis

●Clinical presentation – Actinic keratosis consists of common cutaneous lesions that are usually dry, scaly, and flat with an erythematous base (picture 7). The diagnosis can be made clinically; however, biopsy may be warranted to distinguish actinic keratosis from squamous cell carcinoma (SCC). (See "Actinic keratosis: Epidemiology, clinical features, and diagnosis", section on 'Diagnosis' and "Actinic keratosis: Epidemiology, clinical features, and diagnosis", section on 'Progression to skin cancer'.)

●Pathology – Actinic keratoses result from the proliferation of atypical epidermal keratinocytes. Unlike seborrheic keratosis, actinic keratosis may transform into SCC. The risk of progression to SCC appears to be low; however, the exact rate is uncertain. (See "Actinic keratosis: Epidemiology, clinical features, and diagnosis", section on 'Progression to skin cancer'.)

●Management – Treatment options for actinic keratosis include surgery, cryotherapy, dermabrasion, topical medications, and photodynamic therapy. Treatment of actinic keratosis is discussed separately. (See "Treatment of actinic keratosis".)

Squamous papilloma — Squamous papilloma is the most common benign tumor of the eyelid. (See "Human papillomavirus infections: Epidemiology and disease associations".)

●Clinical presentation – Squamous papilloma presents as a frond-like (skin tag) or lobular projection of skin that contains a central vascular core (picture 8). Diagnosis is made by clinical appearance of the lesion. Biopsy is only required if there are unusual features that raise concern for possible malignancy. (See 'Malignant lesions' below.)

●Pathology – Squamous papilloma is caused by the human papillomavirus (HPV).

●Management – If treatment is desired (eg, for cosmetic reasons), options include surgical excision or cryotherapy, both of which are curative.

Benign nevi — Benign pigmented skin lesions and melanocytic nevi (moles) sometimes occur on the eyelid. Within this category, acquired melanocytic nevi are the most common.

●Clinical presentation – Benign nevi typically present in adolescence or early adulthood as hyperpigmented macular or papular lesions (picture 9). They tend to be small (≤6 mm in diameter) and symmetric with a homogeneous surface, even pigmentation, regular outline, and sharply demarcated border. The risk of malignant transformation is low. (See "Acquired melanocytic nevi (moles)".)

Other variants include the divided or kissing nevus, which involves both the upper and lower eyelids (picture 10); congenital blue nevus, which is flat and smooth; and the Nevus of Ota, a large diffuse nevus of the periocular area seen in Black or Asian individuals (picture 11). Nevus of Ota is associated with scleral involvement in two-thirds of cases, which confers a higher risk of glaucoma [12]. (See "Congenital melanocytic nevi" and "Benign pigmented skin lesions other than melanocytic nevi (moles)", section on 'Nevus of Ota'.)

●Pathology and management – Indications for biopsy are discussed separately. (See "Acquired melanocytic nevi (moles)", section on 'Principles of diagnosis and indications for biopsy'.)

Milia

●Clinical presentation – Milia are pinpoint, multiple, firm, white lesions that usually occur on both the upper and lower eyelids (picture 12). Milia are common lesions; they occur at all ages and are a common finding in newborns. (See "Skin lesions in the newborn and infant", section on 'Milia'.)

●Pathology – Milia are caused by the plugging of hair follicles (pilosebaceous units) by keratin.

●Management – As milia are benign lesions, treatment is generally not necessary. If the lesions are bothersome to the patient, they can be managed by puncturing the lesions with a pin and expressing the contents. To prevent clogged hair follicles, patients should be advised to exfoliate and wash the face regularly while avoiding heavy facial creams and cosmetics. (See "Overview of benign lesions of the skin", section on 'Milium'.)

LESS COMMON ETIOLOGIES

Benign lesions

Epidermal inclusion cyst — Epidermal inclusion cysts are solitary, slow-growing, firm, mobile, subcutaneous nodules most commonly found on the upper eyelid (picture 13). They can form after trauma or surgery, or may be congenital. Diagnosis is made clinically based upon the characteristic appearance of a discrete cyst or nodule, often with a central punctum. They are usually painless unless they become infected or rupture, causing an inflammatory reaction. Uninfected epidermoid cysts may resolve spontaneously without therapy, although they tend to recur.

Treatment is not necessary unless desired by the patient. If surgical excision is undertaken, the entire cyst, including its wall, should be removed to prevent recurrence. (See "Overview of benign lesions of the skin", section on 'Epidermoid cyst'.)

Dermoid cyst — Dermoid cysts are usually recognized in infancy and often grow during puberty. They are firm, mobile, subcutaneous cysts found most commonly in the lateral brow or upper eyelid region (picture 14). Attachment to the frontozygomatic skull suture is often present and can extend far back into the orbit. (See "Skin nodules in newborns and infants", section on 'Dermoid cysts and sinuses'.)

Port wine birthmark (nevus flammeus) — Port wine birthmarks (also called nevus flammeus or capillary malformations) are congenital low-flow vascular malformations. The characteristic clinical features include blanchable pink to red patches typically with a unilateral or segmental distribution that respects the midline (picture 15A-B). On the face, capillary malformations tend to follow the distribution of the trigeminal nerve branches (figure 3). Port wine birthmark is a feature of Sturge-Weber syndrome and other rare congenital syndromes. It can also be associated with ocular and leptomeningeal vascular hamartomas, glaucoma, and retinal detachment.

Diagnosis and management of port wines birthmarks are discussed separately. (See "Capillary malformations (port wine birthmarks) and associated syndromes".)

Infantile hemangioma — Infantile hemangiomas are vascular tumors that present in early infancy. Most are not clinically evident at birth but become apparent within the first days to months of life.

Most lesions are solitary but multiple lesions can occur. They appear as a bright-red papule, nodule, or plaque (picture 16). They range in size from a few millimeters to many centimeters in diameter. They may be superficial, deep, or combined. Hemangiomas characteristically undergo a growth phase that is most rapid for the first several months, followed by a spontaneous involution phase that typically begins after one year and lasts a variable number of years.

Diagnosis and management of infantile hemangioma are discussed in greater detail separately. (See "Infantile hemangiomas: Epidemiology, pathogenesis, clinical features, and complications" and "Infantile hemangiomas: Management".)

Malignant lesions — Primary carcinomas of the eyelid include basal cell carcinoma (BCC), squamous cell carcinoma (SCC), keratoacanthoma, and sebaceous carcinoma. These should be managed by an ophthalmologist and oncologist who have familiarity with these conditions. They are staged according to the tumor, node, metastasis (TNM) staging system of the Union for International Cancer Control (UICC) and the American Joint Committee on Cancer (AJCC) [13]. This system is summarized in the table (table 2). Melanoma, Kaposi sarcoma, and Merkel cell carcinoma (MCC) can also affect the eyelids.

Cutaneous horn — Cutaneous horns are not malignant lesions per se, but they usually overlie an area of malignancy (BCC or SCC). Cutaneous horns are dark keratinized protrusions on the surface of the skin (picture 17). Biopsy of the horn and underlying skin is performed to establish the diagnosis [14].

Basal cell carcinoma — BCC is the most common malignant tumor of the eyelid, accounting for 85 to 90 percent of all such malignancies [15,16]. It usually arises in fair-skinned individuals with a history of prolonged sun exposure. It may be associated with basal cell nevus syndrome (Gorlin-Goltz Syndrome) or xeroderma pigmentosum, particularly in younger patients. (See "Nevoid basal cell carcinoma syndrome (Gorlin syndrome)".)

●Clinical presentation – BCCs are slow-growing, firm, painless, pearly, indurated lesions (picture 18). There may be associated telangiectasia. Sometimes there is a loss of lashes associated with the lesions. Morpheaform tumors are less common but more aggressive: these nodules are firm, raised, plaquelike, and often show ulceration. Up to two-thirds of BCCs involve the lower eyelid margin [17]. They can also occur in the medial canthus, upper eyelid, and lateral canthus [16].

●Pathology – BCCs are locally invasive but only rarely metastasize. However, neglected tumors can grow to large size and invade as deeply as bone. (See "Basal cell carcinoma: Epidemiology, pathogenesis, clinical features, and diagnosis".)

Diagnosis, which is suspected by clinical appearance of the lesion, should be confirmed by incisional biopsy with histopathological analysis.

●Management – Diagnosis and treatment of BCC, including periocular BCCs, are discussed in greater detail separately. (See "Basal cell carcinoma: Epidemiology, pathogenesis, clinical features, and diagnosis".)

Squamous cell carcinoma — SCC of the eyelid is much less common than BCC but is faster growing and more likely to metastasize. SCC can arise de novo or from preexisting actinic keratosis. (See 'Actinic keratosis' above.)

●Clinical presentation – Most eyelid SCCs are found on the lower lid, with a propensity for the lid margin [16,18]. Similar to BCC, prolonged sun exposure is a risk factor for this malignancy. SCCs present as slow-growing crusted nodules or plaques with everted edges (picture 19). Unlike BCCs, SCCs do not show surface telangiectasia.

Diagnosis, which is suspected by clinical appearance of the lesion, should be confirmed by incisional biopsy with histopathological analysis.

●Pathology and management – Diagnosis and treatment of SCC are discussed in greater detail separately. (See "Cutaneous squamous cell carcinoma (cSCC): Clinical features and diagnosis" and "Treatment and prognosis of low-risk cutaneous squamous cell carcinoma (cSCC)".)

Keratoacanthoma — Keratoacanthoma is a rapidly growing cutaneous tumor that most commonly occurs in middle-aged and older adults with fair skin.

●Clinical presentation – It is classically described as a dome-shaped 1 to 2 cm papule with a central keratinous plug (picture 20A-B); however, the appearance varies with the stage of lesion. Keratoacanthomas grow to considerable size over the course of three to six weeks. By contrast, SCCs typically grow slowly over months to years. Controversy exists over whether keratoacanthoma represents a distinct disease entity or a variant of SCC. Incisional biopsy is helpful in making the diagnosis.

●Pathology – Histopathologic findings alone cannot definitively differentiate keratoacanthoma from SCC. Diagnosis is based on combined assessment of the clinical and histopathologic findings.

●Management – Although the tumor has potential for spontaneous resolution, most advocate for treatment. Diagnosis and treatment of keratoacanthoma are discussed in greater detail separately. (See "Keratoacanthoma: Epidemiology, risk factors, and diagnosis" and "Keratoacanthoma: Management and prognosis".)

Sebaceous carcinoma — Sebaceous carcinoma is a rare aggressive tumor that predominantly affects adults over age 50 and is often mistaken for recurrent chalazion or blepharoconjunctivitis [19].

●Clinical presentation – The typical presentation is that of a painless, rounded nodule, most often located on the upper eyelid (picture 21), less commonly on the lower lid (picture 22B). Occasionally, the lesion can be inflamed and painful. The nodule may resemble a chalazion initially, but with progression there is subsequent loss of lashes and destruction of the meibomian gland orifices (picture 22A).

●Pathology – These tumors arise from meibomian or Zeis, both sebaceous glands (figure 2). Diagnosis, which is suspected by clinical appearance of the lesion, should be confirmed by either full-thickness incisional biopsy or excisional biopsy with histopathological analysis.

●Management – Diagnosis and treatment of sebaceous carcinoma are discussed in greater detail separately. (See "Sebaceous carcinoma".)

Melanoma — Malignant melanoma accounts for about 1 percent of all eyelid malignancies but about two-thirds of tumor-related deaths from eyelid malignancies [20]. Excessive sun exposure, genetic factors, light skin pigmentation, and changing skin nevi are important risk factors for this disease. (See "Melanoma: Epidemiology and risk factors".)

●Clinical presentation – The appearance of melanomas varies considerably and four distinct subtypes have been described (superficial spreading melanoma, nodular melanoma, lentigo maligna melanoma, and acral lentiginous melanomas). In one study, nodular melanoma was the most common subtype among patients with eyelid melanoma [21]. (See "Pathologic characteristics of melanoma".)

Lentigo maligna presents as a flat melanotic lesion with irregular borders (picture 23A). The superficial spreading melanoma lesion is usually smaller with elevation (picture 23B). Both of these forms typically have a long phase of superficial growth before invasion into deeper tissues. Nodular melanoma is more aggressive and may present as a pigmented or amelanotic nodule that grows rapidly and may bleed (picture 23C). Early signs of melanoma include asymmetry, irregular borders, variegated color, diameter ≥6 mm, changing appearance, and/or enlarging over time. (See "Melanoma: Clinical features and diagnosis".)

●Pathology – Diagnosis, which may be suspected by clinical appearance, should be confirmed by incisional biopsy with histopathological analysis.

●Management – Diagnosis and management of melanoma are discussed in detail separately. (See "Melanoma: Clinical features and diagnosis" and "Surgical management of primary cutaneous melanoma or melanoma at other unusual sites".)

Merkel cell carcinoma — MCC is a rare but aggressive neuroendocrine malignancy occurring mainly in White individuals, starting over age 50 and peaking in the 70s.

●Clinical presentation – Lesions appear on the eyelid or periocular region (as well as head and neck) as solitary pink, red, or violet nodules, often with overlying ulcer or telangiectasia (picture 24). The upper eyelid margin nodules with eyelash loss remain most common.

●Pathology – The nodules are associated with a history of sun exposure, infection with polyomavirus, and immunosuppression. MCC often has poor prognosis due to late diagnosis, with lesions over 2 cm associated with positive sentinel lymph nodes and high rate of metastases.

●Management – Treatment can include surgical excision (including Mohs) with sentinel lymph node biopsy, radiotherapy, and chemotherapy. Spontaneous complete regression has been recorded in a tiny number of cases.

Kaposi sarcoma — Kaposi sarcoma is seen most often in patients with AIDS [22]. It can also be seen rarely in older adult men from the Mediterranean region.

●Clinical presentation – Kaposi sarcoma is a vascular lesion that appears red or purplish (picture 25).

●Pathology – Kaposi sarcoma is caused by human herpesvirus, type 8 (HHV-8).

Diagnosis, which may be suspected by clinical appearance, should be confirmed with incisional biopsy.

●Management – For many patients with AIDS-related Kaposi sarcoma, antiretroviral therapy (ART) may be sufficient to induce regression of the lesion(s). Others may require ART plus local or systemic chemotherapy. Diagnosis and treatment of Kaposi sarcoma are discussed in greater detail separately. (See "AIDS-related Kaposi sarcoma: Staging and treatment".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5^th to 6^th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10^th to 12^th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

●Basics topics (see "Patient education: Stye (The Basics)" and "Patient education: Chalazion (The Basics)" and "Patient education: Seborrheic keratosis (The Basics)")

SUMMARY AND RECOMMENDATIONS

●Common benign lesions – Most eyelid lesions are benign. The clinician should be able to identify common etiologies such as hordeola (stye) (picture 1A-B), chalazia (picture 2A-B), and xanthelasma (picture 3) and to distinguish them from more serious conditions that require referral to a specialist (table 1). (See 'Introduction' above.)

•Hordeolum – Acute eyelid inflammation that presents with localized pain, erythema, and edema, often developing within one day or overnight (picture 1A-B and figure 1). Most hordeola resolve spontaneously over one to two weeks and do not require specific intervention.

-We suggest use of warm, moist compresses on the affected areas (for 5 to 10 minutes four times a day) to facilitate drainage (Grade 2C). Gentle eyelid massage may also facilitate drainage. (See 'Hordeolum (stye)' above.)

-Topical or systemic antibiotics are unlikely to improve outcomes and are not indicated. Infrequently, hordeola present with preseptal cellulitis, necessitating systemic antibiotics. (See "Preseptal cellulitis", section on 'Treatment'.)

-If the hordeolum does not reduce in size within two weeks, we advise referral to an ophthalmologist for potential incision and drainage. Patients who have frequent hordeola in the setting of rosacea-associated blepharitis should also be managed by an ophthalmologist for consideration of treatment with a combination topical antibiotic/corticosteroid. (See 'Hordeolum (stye)' above.)

•Chalazion – Painless nodule caused by obstruction of the eyelid glands. Presents with localized eyelid swelling, usually developing over days to weeks (picture 2A and figure 1). Examination of the inner eyelid reveals a nontender rubbery nodule (picture 2B).

Small chalazia often resolve without intervention over several weeks to months. For larger lesions, we suggest use of warm, moist compresses on the affected areas (for 5 to 10 minutes four times a day) to facilitate drainage (Grade 2C). (See 'Chalazion' above.)

Patients with lesions that do not resolve over one to two months should be referred to an ophthalmologist for consideration of incision and curettage or glucocorticoid injection. Such persistent or recurring lesions, especially if unilateral, should be assessed histopathologically for possible basal cell, sebaceous cell, or meibomian gland carcinoma. (See 'Malignant lesions' above.)

•Xanthelasma – Xanthelasma are cholesterol-filled, soft, yellow plaques that usually appear on the medial aspects of the eyelids (picture 3). They most often occur in middle-aged and older adults. Xanthelasma are often associated with hypercholesterolemia, and, thus, we suggest obtaining a lipid profile if the patient has not already undergone screening. (See 'Xanthelasma' above.)

•Other – Other common eyelid lesions include molluscum contagiosum (picture 5A-B), seborrheic keratoses (picture 6), actinic keratosis (picture 7), squamous papilloma (picture 8), benign nevi (moles) (picture 9), and milia (picture 12). (See 'Common etiologies' above.)

●Less common lesions – Less common benign lesions of the eyelid include epidermal inclusion cyst (picture 13), dermoid cyst (picture 14), port wine birthmark (nevus flammeus) (picture 15A-B), and infantile hemangioma (picture 16). (See 'Benign lesions' above.)

●Malignant lesions – Malignant lesions that can occur on the eyelid include cutaneous horn (this lesion is not malignant per se but it typically overlies a malignancy) (picture 17), basal cell carcinoma (picture 18), squamous cell carcinoma (picture 19), keratoacanthoma (picture 20A-B), sebaceous carcinoma (picture 22A-B), melanoma (picture 23A-C), Kaposi sarcoma (picture 25), and Merkel cell carcinoma (picture 24). (See 'Malignant lesions' above.)