Cheeks
OVERVIEW
The cheeks constitute the largest area of the face and may be affected by various conditions that are often signs of underlying infections or systemic diseases (e.g., the “slapped cheeks” of erythema infectiosum and the “butterfly rash” of systemic lupus erythematosus; both are discussed in Chapters 21 and 22). Also, various benign, premalignant, and malignant lesions are found on this sun-exposed location.
In infants, atopic dermatitis and acne occur on the cheeks and often appear at less than 1 year of age. Teenage acne (acne vulgaris), adult-onset acne, and rosacea, as well as pigmentary disorders e.g., vitiligo, pityriasis alba, and melasma, also are seen on the cheeks. Infections such as impetigo and tinea commonly arise on the cheeks and paranasal regions.
NEONATES, INFANTS, AND CHILDREN
Atopic Dermatitis (Atopic Eczema)
Atopic dermatitis (AD) is the most common inflammatory skin condition in children. Atopic dermatitis, “atopic eczema,” and “eczematous dermatitis” are terms that are often used interchangeably. AD can present in various clinical forms and can be quite confusing for patients and their nondermatologic health care providers. Terminological confusion also may arise if the word “dermatitis”—a more generalized, often vague designation that refers to inflammation of skin—is used synonymously with eczema or is coupled with it. In general, it is acceptable to use eczema and dermatitis interchangeably. Eczematous dermatitis, therefore, is somewhat redundant, although some might argue that the term is more inclusive than either word alone.
The word eczema was coined by the Ancient Greeks to mean “a boiling out or over” and it accurately describes both the microscopic and clinical appearances of acute eczema in which the epidermal keratinocytes are swollen and “boil over” creating epidermal vesicles. Currently, the term eczema is more widely applied to a heterogeneous group of inflammatory skin eruptions that share clinical (pruritus, erythema, and scale) and histologic (spongiosis) hallmarks. For simplification, the term “atopic dermatitis” or AD will be used in most of this book.
Atopic Dermatitis
Atopic dermatitis (AD) often starts in infancy (from 2 months to 2 years) and may present as a generalized facial, scalp, and truncal rash. In many cases, AD first manifests with seborrheic dermatitis (“cradle cap”) (see Fig. 2-1) with features of AD becoming prominent after the seborrheic dermatitis subsides. The following three phases of AD are not always clearly distinct, and any or all manifestations (i.e., acute, subacute, or chronic) of AD may exist in a single patient (see also Scalp, Eyelids and Periorbital Area, Lips and Perioral Area, Arms, and Hands and Fingers).
Infantile Phase
Distinguishing Features
The face and/or scalp is involved in almost all affected infants
Skin lesions present with varying amounts of ill-defined, scaly, erythematous, edematous, papules and plaques on the cheeks, forehead, and scalp
Lesions are bilaterally symmetric with classic red, glazed, scaly cheeks (Fig. 7-1)
Oozing and secondary infection (impetiginization) with Staphylococcus aureus is common. Impetiginization of eczema is characterized by yellow or varnish-colored crusting overlying the eczema lesions (Fig. 7-2)
Sleep is disturbed due to associated pruritus
The infant is often irritable and itchy as indicated by rubbing the scalp and head on crib bedding, by pinching, scratching, or tapping the skin
Diagnosis
Clinical
Eczematous lesions are often present elsewhere on the body
Atopic predisposition such as asthma, seasonal allergies, chronic rhinitis, or atopic dermatitis in the patient’s family
 Figure 7-1 Infantile atopic dermatitis. Acute red, glazed, scaly eczematous plaques on the cheeks and chin of an infant. |
 Figure 7-2 Infantile atopic dermatitis, impetiginized. This infant’s cheek is infected (impetiginized) with S. aureus. |
Management
Despite popular belief to the contrary, patients with AD, especially children, should be bathed daily
The benefits of bathing include removal of excess dirt, potential irritants, allergens, and surface microbes. Bathing also hydrates the skin and allows for better delivery of topical corticosteroids and moisturizers
Baths should be short—no longer than 10 minutes—with tepid water. “Bleach baths” can be helpful in cases of recurrent infection. This is done by adding 1/4 to 1/2 cup of Clorox Bleach to a full adult bathtub
Directions
Use of mild, moisturizing soaps such as Dove or Baby Dove or nonsoap cleansers such as Cetaphil
Gentle Cleanser
Pat dry followed immediately by the application of a topical corticosteroid to areas of active dermatitis
Suggested ointments: Vaseline Petroleum Jelly, Aquaphor
Suggested creams: CeraVe cream, Cetaphil cream
Treatment
Topical steroids: A low-potency topical corticosteroid (TCS) such as 1% hydrocortisone cream or ointment (Cortaid) is often recommended to begin therapy; however, using such a low-potency agent may prove to afford little relief and may eventually prolong therapy, especially if the eruption is severe. Therefore, short-term use of a mid-strength TCS such as hydrocortisone butyrate 0.1% (Locoid cream) to a higher-strength TCS such as triamcinolone 0.1% (Kenalog) or even clobetasol 0.05% ointment can be used to initiate therapy for a day or two (“strong, but not long”).
For Longer-Term Use and Maintenance
Nonsteroidal immunomodulators: tacrolimus (Protopic ointment) 0.03% or 0.1 % ointments and pimecrolimus cream (Elidel) may be alternated with topical steroids.
Alternatively, crisaborole 2% ointment (Eucrisa), a phosphodiesterase-4 inhibitor, is also a nonsteroidal agent. It is approved for the treatment of eczema in children >3 months of age. If the child’s skin is very inflamed, crisaborole may sting.
Childhood Phase
Distinguishing Features
The childhood phase of AD follows the infantile phase beginning at around 2 years of age and continues through puberty. Lesions, which often continue to involve the face, also begin to localize to the flexural aspects of the elbows and knees (antecubital and popliteal fossae), the wrists, ankles, and the posterior neck in a symmetric distribution. Lesions may also occur on the lips, scalp, and behind the ears.
Figure 7-3 Kaposi varicelliform eruption (eczema herpeticum).
Multiple intact and hemorrhagic vesicles, as well as hemorrhagic crusts are evident in this 14-year-old boy. Lesions resolved with minimal scarring after oral antiviral treatment.
Itchy, scaly, erythematous plaques appear on the face
Frequently become infected (impetiginized) with S. aureus
The secretion of toxins (superantigens) by S. aureus may trigger relapses of AD; also herpes simplex virus may attack the relatively defenseless eczematous skin and result in Kaposi varicelliform eruption (eczema herpeticum) (Fig. 7-3) which requires treatment with oral or systemic antiviral medications, such as acyclovir or valcyclovir
Management
Similar to that of the infantile phase described above
Adolescent Phase
Distinguishing Features
There are few areas of the skin that are ignored by eczema. The predominant areas of involvement continue to be the flexural surfaces (see Figs. 13-9, 13-10, 13-11); in addition, the dorsal aspect of the hands and feet are also commonly affected. Lesions also may appear in other extensor locations such as the shins, ankles, feet, and the nape of the neck. Sometimes lesions are limited to the lips (atopic cheilitis), eyelids, vulvar or scrotal areas
Management
For mild-to-moderate involvement, topical steroids and nonsteroidal immunomodulators (as described above) may be adequate to control disease
For moderate-to-severe disease that is recalcitrant to topical therapy, dupilumab (Dupixent), a targeted biologic therapy that inhibits signaling of interleukin-4 and interleukin-13, key proteins that may play a role in the inflammation underlying atopic dermatitis, is FDA approved for patients over the age of 6 years. Dupilumab is administered by subcutaneous injection. Dupixent is effective and side effects have been mostly minimal; an important side effect that must be discussed with patients is conjunctivitis
Port Wine Stain (Nevus Flammeus)
A port wine stain (PWS) or nevus flammeus is a congenital capillary malformation that typically presents as a deep pink to reddish-purple discoloration of the skin on the head and/or neck. Most of the time a PWS is an isolated lesion but when it appears on the face, particularly in the V1(±V2 and V3) distribution, it can be seen as sign of Sturge-Weber syndrome, which may involve various complications such as neurological abnormalities and glaucoma.
Distinguishing Features
A PWS presents at birth as a flat, well-demarcated, pink to dark red (“port-wine” color) blanchable patch, most commonly noted on the face (Fig. 7-4)
PWSs are usually unilateral but can be bilateral
Figure 7-4 Port wine stain (nevus flammeus).
Port-wine stain in the typical location on the face. Note the sharp midline demarcation. (Image courtesy of Robert I. Rudolph, MD.)
Lesions darken progressively and can become thickened over time. Some develop secondary proliferative nodules on their surface
Diagnosis
The diagnosis is made clinically. Workup for an underlying association such as Sturge-Weber syndrome is based on the location of the PWS, especially when a child is born with a facial cutaneous vascular malformation covering a portion of the upper or the lower eyelids
Management
A complete physical examination should be performed to assess for any other congenital defects. If a PWS in a high-risk location is identified, an appropriate workup and referrals should be made
Once a potential syndrome association has been ruled out, the PWS can be approached as a cosmetic issue and treated (especially facial PWS) with various lasers, if desired
An infantile hemangioma (IH) appearing in the central face can lead to permanent cosmetic disfigurement. When it arises in certain vital locations such as near the eyes or mouth, an IH can potentially interfere with vision (Fig. 7-5) or impair breathing and therefore must be treated more aggressively.
 Figure 7-5 Infantile hemangioma. Infantile hemangioma on the eyelid. Had this lesion not been treated, it might eventually interfere with this child’s visual development. (Image courtesy of Robert I. Rudolph, MD.) |
Differential Diagnosis
An early IH (macular phase) may be difficult to distinguish from a port wine stain
Pityriasis Alba
Pityriasis alba is a common skin condition affecting children and adolescents aged 3 to 16 years. The name refers to its appearance; pityriasis refers to its characteristic fine scale, and alba to its pale color (hypopigmentation).
The hypopigmented spots are mostly seen on the face in children who have atopic dermatitis. In fact, pityriasis alba is considered to be a low-grade type of atopic dermatitis.
A history of preceding inflammation is generally absent. The patches of pityriasis alba are more apparent in summer, especially in patients who have darker skin because lesional skin does not tan as well as surrounding uninvolved skin.
Distinguishing Features
Asymptomatic or slightly itchy
Present as one or more round, oval, or irregular whitish patches or thin plaques, with or without fine surface scale
Often appears following sun exposure because tanning of surrounding skin unmasks affected areas
Diagnosis
Clinical, atopic dermatitis may be noted elsewhere on the body
 Figure 7-6 Pityriasis alba. Ill-defined hypopigmented slightly scaly patches on the cheeks are characteristic of pityriasis alba. |
Management
No treatment is necessary, but a moisturizing cream may improve the dry appearance
If the patches are red or itchy, a low-potency topical steroid cream such as hydrocortisone 1% can be applied
Keratosis Pilaris
Keratosis pilaris (KP), also known as “allergic bumps” because it most often arises in individuals who are atopic, is also often referred to as “chicken-skin” because of its rough texture. KP appears most often during childhood or the teen years and is frequently mistaken for acne, particularly when it involves the malar area of the face.
KP is also commonly seen on the deltoid and posterolateral upper arms (see Fig. 13-1), the shoulders, upper back, buttocks, and thighs. KP often improves, especially during the summer months and with time. It runs in families, especially families that tend to have KP, hay fever, asthma, sinusitis, some allergies, or atopic dermatitis.
Distinguishing Features
KP presents as an eruption of grouped, follicular, tiny keratotic papules resulting in a sandpaper-like texture when palpated
Distributed in a grid-like pattern
In children, the lateral sides of the cheeks are frequently involved (Fig. 7-7)
Usually worsens during the winter months
Figure 7-7 Keratosis pilaris.
Small, follicular, rough-textured, hyperkeratotic, papules are present on this 2-year-old’s cheeks. Note similarity to infantile acne in Fig. 7-10.
Figure 7-8 Keratosis pilaris rubra faciei, inflamed.
Multiple hyperkeratotic follicular papules overlying facial erythema. (Image courtesy of Robert I. Rudolph, MD.)
When erythematous and inflamed, KP is referred to as keratosis pilaris rubra faciei (Fig. 7-8)
The condition is mostly of cosmetic significance
Diagnosis
Clinical
Management
There is no cure or very effective treatment for KP; however, the roughness can be lessened temporarily by applying certain moisturizers, exfoliating or barrier creams or lotions such as:
Ammonium lactate (Lac-Hydrin), or other alpha- or beta-hydroxy acids, available in a cream or lotion, reduces roughness and softens the keratin plugs. It does not, however, lessen the redness caused by the condition
Urea-containing products, such as Carmol and Keralac, moisturize and soften dry, rough skin. They also help loosen and remove the dead skin cells
Gentle exfoliation twice per week with a loofah or a body scrub can help remove skin that has been softened by the urea or the alpha and beta hydroxy acid creams.
Topical retinoids may be an effective temporary treatment, but they can also cause bothersome skin irritations and exfoliation. Tretinoin (Retin-A Micro), tazarotene (Tazorac), adapalene (Differin), and trifarotene (Aklief) are examples of topical retinoids
Neonatal Acne (Neonatal Cephalic Pustulosis)
Acne, also known as acne vulgaris, is most commonly seen in adolescence, but it also may occur during the neonatal period and infancy. Neonatal acne is a benign eruption that self-resolves without sequelae, whereas infantile acne often requires treatment.
Neonatal acne is currently referred to as neonatal cephalic pustulosis (NCP) to distinguish it from infantile and adolescent acne. NCP is a benign self-limiting condition that is estimated to occur in 25% of neonates. Recent data suggest the papules and pustules in this condition may be the result of an inflammatory response to Malassezia spp. Increased rates of sebum secretion during the neonatal period are also thought to play a role.
Distinguishing Features
Erythematous papulopustules (Fig. 7-9)
Unlike infantile and adolescent acne, there are no comedones and the course is self-limiting
Eruption is asymptomatic
Resolves spontaneously in weeks to months
Diagnosis
Diagnosis is made clinically
A Giemsa stain may show yeast forms, neutrophils, and other inflammatory cells
When in doubt a Gram stain can rule out bacterial folliculitis, and a KOH fungal stain can rule out candidiasis
 Figure 7-9 Neonatal acne (neonatal cephalic pustulosis). Erythematous papulopustules on the cheeks resolved completely at 4 months of age in this infant. |
Management
No treatment is required, as the condition self-resolves by 3 to 6 months of age
In severe cases, the application of a topical antiyeast imidazole such as ketoconazole 2% cream or econazole 1% cream twice daily can lead to improvement
Topical hydrocortisone 1% cream can be helpful if lesions are very red
Infantile Acne
Infantile acne is an uncommon condition that is the result of increased androgens and sebum excretion. It is seen more often in boys.
Distinguishing Features
Appears similar to typical acne vulgaris that is seen in adolescence with an admixture of acneiform papules, pustules, open and closed comedones, and cysts (Fig. 7-10)
Lesions are typically located on the cheeks, but can also be seen on the forehead, chin, and back
Cysts, draining sinuses, and deep nodules with potential for scarring occasionally occur
Onset is between 3 and 6 months and subsides at around 1 to 2 years of age commiserate with the normalization of androgen levels
Diagnosis
Diagnosis is made clinically
Management
Most cases resolve by 1 to 2 years of age, even without treatment. In rare cases, the condition can persist until 4 to 5 years old and even through adolescence.
First-line treatments are similar to those used for adolescent acne and include topical tretinoin 0.025% cream or benzoyl peroxide with, or without, a combined topical antibiotic such as Benzaclin (benzoyl peroxide 5% and clindamycin 1%)
In severe cases, oral antibiotics may be required
Antibiotic choices for acne at this age include erythromycin and trimethoprim/sulfamethoxazole
Alert: Patients with infantile acne should have a complete physical examination with particular attention to other signs of androgen excess such as clitoromegaly, hirsutism, or pubic hair. If signs of androgen excess are present, referral to a pediatric endocrinologist is warranted. Figure 7-10 Infantile acne. In this 8-month-old boy there are acneiform papules, pustules, as well as open and closed comedones. |
Acne Vulgaris (Teenage Acne)
Acne vulgaris (AV), teenage acne, the most common skin disorder, is an embarrassing problem for many teenagers, but it is not limited to that age group. It may develop before puberty in either sex, or it may first present in adulthood, particularly in women (see below). In general, AV becomes less active as adolescence ends, but may continue into adulthood.
AV has a strong tendency to be hereditary and is less likely to be seen in Asians and dark-skinned individuals. Lesions begin during puberty when androgenic hormones cause increased sebum production and abnormal follicular keratinization that blocks the follicular orifice, forming a microcomedo, the primary acne lesion. The microcomedo enlarges to become the visible comedone, the “blackhead” or “whitehead.”
Enlargement and/or rupture of the comedone triggers inflammation and results in an acne papule, pustule, or cyst. Acne “cysts” are not really cysts (true cysts are neoplasms that have an epithelial lining). Instead, acne cysts are composed of poorly organized conglomerations of inflammatory material.
The anaerobe Cutibacterium acnes also plays a significant role in the pathogenesis of acne. This gram-positive rod is found in the sebaceous gland and hair follicle and releases enzymes that contribute to comedonal rupture and inflammation.
Distinguishing Features
Inflammatory lesions consist of papules, pustules (Fig. 7-11), and acne “cysts” (nodules)
Noninflammatory (comedonal acne) lesions appear as open comedones (“blackheads”) and closed comedones (“whiteheads”) (Fig. 7-12)
Mild acne consists of open and closed comedones and/or occasional papules and pustules
Management
Often managed successfully by topical treatments, including numerous over-the-counter benzoyl peroxide (BPO) preparations.
Treatment is often initiated with a topical retinoid alone (see Table 7.1) such as tretinoin, or in combination with a BPO agent or a topical antibiotic (see Table 7.2)
In addition, topical antibiotics alone or in combination with BPO such as Benzamycin, BenzaClin, and Duac gel may be prescribed (see Tables 7.3 and 7.4)
Azelex (azelaic acid cream 20% or gel 15%) can be useful to treat acne in pregnant women
Dapsone 5% or 7.5% gel (Aczone) is effective for inflammatory acne, particularly in adult females with acne
Topical minocycline 4% foam (Amzeeq) can be used to treat moderate to severe inflammatory acne in patients 9 years of age and older
Table 7.1 Topical Retinoids for Acne | |||||||||||||||||||||
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Table 7.2 Topical Combinations Containing Retinoids | ||||||||
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Table 7.3 Topical Antibioticsa | ||||||||||
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Table 7.4 Combination Topical Antibiotic and Benzoyl Peroxide Agentsa | ||||||||||
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