3: Body dermatitis

Abstract:

There are an almost uncountable number of rashes that affect the trunk and extremities. This chapter reviews the most common causes of body rashes and includes discussions of atopic dermatitis, allergic contact dermatitis, nummular dermatitis, psoriasis, urticaria, scabies, bullous pemphigoid, pemphigus vulgaris, and more.

Key terms:

atopic dermatitis

allergic contact dermatitis

nummular dermatitis

psoriasis

urticaria

scabies

bullous pemphigoid

pemphigus vulgaris

pityriasis rosea

confluent and reticulated papillomatosis

tinea corporis

Chapter outline

Atopic Dermatitis—Trunk and Extremities
Allergic Contact Dermatitis—Trunk
Nummular Dermatitis
Psoriasis
Urticaria
Id Reaction/Autoeczematization
Xerosis Cutis
Scabies
Bullous Pemphigoid
Seborrheic Dermatitis—Trunk
Notalgia Paresthetica
Tinea Corporis
Pemphigus
Pityriasis Rosea
Confluent and Reticulated Papillomatosis
Herpes Zoster
Necrobiosis Lipoidica
Leukocytoclastic Vasculitis

Atopic dermatitis—trunk and extremities

Clinical features

The American Academy of Dermatology (AAD) has developed atopic dermatitis (AD) criteria that are useful in evaluating patients for AD. The three essential criteria (pruritus, typical AD pattern, and chronic/relapsing course) should be used for screening patients with possible AD. If a patient does not display all three of these features, then they are very unlikely to have AD.

• The typical AD pattern is an eruption affecting predominantly flexural surfaces (e.g., flexural neck, antecubital fossa, flexural wrists, popliteal fossa), except during infancy, when it classically affects extensor surfaces and the face.
• Other clinical findings suggestive of AD include xerosis, keratosis pilaris (follicular-based, erythe-matous or hyperpigmented papules best appre-ciated on the arms and thighs), hand dermatitis (see Chapter 4), palmar hyperlinearity, ichthyosis (chronic, genetically mediated fish like scaling best appreciated on the lower extremities), and nipple dermatitis.
• Importantly, by definition, all AD is itchy. Patients with a nonpruritic, eczematous-appearing eruption are highly unlikely to have AD.
• For most patients, AD flares during the dry, winter months; however, a small subset of patients flare with sweating or light exposure during the summer.

Most adults with AD have had it since childhood, with many patients developing the condition during infancy.

Some children present with a variant of AD called “follicular AD,” which is characterized by the development of itchy, follicular-based papules predominantly on the trunk.

• This variant is most common in darker-skinned children and can develop in the absence of typical eczematous plaques.

Differential diagnosis

The differential diagnosis for AD is broad and is often confounded by the fact that AD frequently coexists with other conditions, predominantly allergic contact dermatitis (ACD) and irritant contact dermatitis (ICD). The differential diagnosis includes ACD, ICD, asteatotic or dry skin dermatitis, stasis dermatitis, cutaneous T cell lymphoma (CTCL) seborrheic dermatitis, and psoriasis.

• As previously noted, we recommend initially evaluating all patients with possible AD using the AAD’s three essential criteria (pruritus, typical AD pattern [Fig. 3.1], and chronic/relapsing course).
- • Using these criteria alone is highly sensitive for detecting AD.
  
  • Patients meeting these criteria in whom an alternate diagnosis is still being considered can then be further evaluated for important and associated criteria (see “AAD Criteria”, above) using a 3:2:1 approach, where a patient with AD would be expected to display all 3 essential criteria, 2 important criteria, and 1 associated criteria.
• Recognizing the typical AD pattern is essential for differentiating AD from mimickers. Unlike some mimickers, AD is almost always symmetric and AD plaques are ill defined (i.e., do not have distinct borders).
• Patients with AD frequently develop superimposed/concomitant ACD.

• Concomitant ACD can present either in a clinically obvious manner, such as a new eczematous rash in areas that are not typical for AD, or as AD that is refractory to or worsens with topical therapy, such as in cases where individuals are allergic to components of topical therapy.

• Individuals with AD are most commonly allergic to fragrances, preservatives, and topical antibiotics. These contactants are frequently present in both prescription and nonprescription topical treatments for AD and therefore are a frequent cause of treatment failure.

• AD patients with a new rash in areas that are atypical for AD or that are not responding to conventional therapy should undergo patch testing.
• ICD can be misdiagnosed as AD and can occur concomitantly with AD. Individuals with AD are predisposed to developing ICD because of their underlying skin barrier impairment.

• ICD on the trunk and extremities most frequently develops from use of personal care products or from cases of obvious occupational exposure (occupational exposure will not be further discussed because it is unlikely to be misdiagnosed as AD).

• ICD is most commonly a clinical mimicker of trunk and extremity AD when it presents as generalized xerosis and pruritus.

• This type of ICD can flare existing AD or can exist in the absence of AD, in which case it is characterized by generalized xerosis in the absence of any primary inflammatory skin lesions.
• Stasis dermatitis can be distinguished from AD because it typically presents in individuals older than 50 years of age on the bilateral lower extremities in the absence of rash elsewhere and is often associated with varicosities.
• Psoriasis presents with well-demarcated plaques on extensor surfaces, whereas AD presents with poorly demarcated plaques on flexural surfaces.
• CTCL is the most feared mimicker of AD because it is often very difficult to confirm a diagnosis of CTCL, even histologically, and it can clinically look very similar to AD (Fig. 3.2). CTCL should be considered in patients with atypical-appearing patches and/or plaques, with unusual distribution of disease (e.g., predominant involvement of sun-protected areas, such as the buttocks, inner thighs, and/or breasts), with disease refractory to topical therapy, or with onset of disease in adulthood. Differentiating CTCL from AD is notoriously difficult, and it is prudent to obtain an evaluation from a dermatologist who is experienced in managing CTCL if it is in the differential.

Fig. 3.1 **Atopic Dermatitis.** Notice the flexural distribution and characteristic ill-defined plaques. *Source:* (From the UConn Grand Rounds Collection.)

Work-up

All patients with presumed AD should be approached systematically using the AAD criteria as previously discussed.

A full-body skin examination should be performed in all patients to identify affected areas and to rule out signs of mimickers/concomitant skin conditions.

Histopathologic examination is almost never necessary to confirm a diagnosis of AD; however, it can be important in ruling out mimickers, such as CTCL.

Initial steps in management

Initial management of AD involves a four-pronged approach of dry skin care, topical antiinflammatory agents, trigger avoidance, and itch management.

Dry skin care

Dry skin care involves obtaining a list of all personal care products used and having an understanding of an individual’s bathing techniques (e.g., use of a luffa).

• Patients should be counseled that it is okay/encouraged to bathe daily as long as they use appropriate bathing techniques followed by lubrication.

• Patients should be counseled to use a mild, unscented bar soap, such as Dove White Unscented Bar Soap, CeraVe Hydrating Cleanser Bar, or Cetaphil Gentle Cleansing Bar.

• Soap should only be routinely applied to the axilla, groin, and overtly dirty areas. A luffa should not be used to apply soap because it may harbor bacteria and is abrasive.

• Hot water should be avoided and showers should not last longer than 10 minutes.

• Patients should pat dry with a towel rather than rub the towel against their skin.

• Immediately after bathing, individuals should moisturize.
• Barrier care should be performed by moisturizing at least twice daily (including immediately after showering). Thick moisturizing creams (e.g., Vanicream, CeraVe Moisturizing Cream, Eucerin Advanced Barrier Repair) or ointments (e.g., Vaseline, Aquaphor, Vaniply, Healing Ointment) should be applied to the entire body. Some patients prefer using oils or products containing natural ingredients. Patients should be provided with a list of acceptable moisturizers so that they can identify the products they are willing to use.

Topical antiinflammatory agents

First-line treatment for AD should include a medium-potency topical corticosteroid, such as triamcinolone 0.1% cream, applied twice daily for several weeks (with avoidance of application to facial skin or intertriginous areas to avoid skin thinning).

• Patients who have difficulty complying with twice-daily corticosteroid applications can be offered a slightly more potent topical corticosteroid for once-daily application (e.g., mometasone 0.1% cream)
• Patients should be prescribed 1 gram of cream per day for each percentage of body surface area (BSA) affected.
• Patients who frequently flare in the same locations (e.g., antecubital fossa) despite excellent dry skin care can be counseled to apply a medium-potency topical corticosteroid, such as triamcinolone 0.1%, to flare-prone areas three times weekly, even in the absence of rash.

Topical calcineurin inhibitors, such as tacrolimus or pimecrolimus 0.1%, can be used for maintenance therapy or for patients experiencing cutaneous adverse events from topical corticosteroid use.

• Topical calcineurin inhibitors can be applied to flare-prone areas three times weekly to decrease flares.
• Topical calcineurin inhibitors should not be applied to actively inflamed skin because they can cause severe stinging and burning.
• This treatment is not recommended by the U.S. Food and Drug Administration (FDA) for infants and children between 2 and 15 years of age; instead, tacrolimus 0.03% should be used.

• Given their relatively higher cost and lack of conferred benefit over medium-potency topical corticosteroids, topical calcineurin inhibitors should not be used in lieu of topical corticosteroids as a first-line antiinflammatory.

• Another steroid-sparing alternative, crisaborole (commercially available as Eucrisa), is a phosphodiesterase-4 inhibitor that is an ointment approved for the use of AD in patients older than 2 years of age.

• Using steroid-sparing agents intermittently is advised in those patients with chronic persistent AD to avoid the side effects of topical steroids.

Trigger avoidance

Identifying triggers in patients with AD can be very difficult but is necessary to avoid flares. There are now smartphone-based applications (colloquially known as “apps”) that can help patients track disease activity and input exposures to help identify possible triggers and predict possible flares.

• Patients should be questioned about their bathing and personal care regimens at every visit to identify behaviors that may be contributing to the worsening of AD.
• All patients who are not responding to appropriate therapy should undergo patch testing to assess for concomitant ACD.

Itch management

The most bothersome symptom of AD is intractable pruritus. Control of cutaneous disease correlates with itch control; however, itch-directed therapies are currently frequently ineffective.

• Oral H1 antihistamines (both sedating and nonsedating) are commonly used to treat AD-related itch; however, recent evidence suggests that histamine is not a primary mediator of itch in AD and that H1 blockers are ineffective. Sedating antihistamines are still considered to have a role as adjuncts for sleep.

• Other agents, including naltrexone and neural modulators (e.g., gabapentin, amitriptyline, mirtazapine), are also occasionally used for itch control.

• Topical antihistamines (such as Benadryl cream) and other soothing topical antipruritic agents (e.g., doxepin cream, creams with menthol, creams with colloidal oatmeal) might help.

Other therapies

• Bleach baths can be used.

• Twice-weekly dilute bleach baths (one-half cup of household bleach mixed into a 40-gallon bath of water) have long been recommended to prevent pathologic bacterial growth on patients with AD; however, recent evidence suggests that routine use of bleach baths is unnecessary.

• Bleach baths are indicated for patients with recurrent skin and soft tissue bacterial infections or who are known to be colonized with Staphylococcus aureus.
• Wet wraps are used to improve both skin hydration and the efficacy of topical corticosteroids.

• Wet wraps are very effective for treating severe AD; however, compliance is often poor. Wet wraps should be considered for any patient who has an acute flare that cannot be managed with traditional topical therapies alone.

• Written instructions on how to properly perform a wet wrap are available from the National Eczema Association at: https://nationaleczema.org/eczema/treatment/wet-wrap-therapy/.
• Phototherapy, pills, and injectables for AD can be prescribed by a specialist.

• Patients with disease that is refractory to topical management and those who present with disease affecting more than 10% BSA should be referred to a dermatologist who specializes in the use of phototherapy, systemic medications, or biologics for the treatment of AD.

Warning signs/common pitfalls

The biggest pitfall when managing AD in any location is failure to promote patient adherence to a dry skin care management regimen. Such a regimen is essential for achieving disease control and maintaining disease control in patients with AD; failure to implement a daily dry skin care regimen ensures treatment failure.

• Patients must specifically be counseled that twice-daily use of their prescription topical antiinflammatory is not a substitute for frequent moisturization.
• Avoidance of harsh soaps and irritating cosmetics/perfumes is essential. Patients need specific product recommendations because the cosmetic aisle in drugstores is confusing and the internet is full of misinformation on this subject.

Failure to identify coexisting dermatoses, such as ICD to soaps and ACD (including to topical corticosteroids), can interfere with successful AD management.

Many patients with AD develop superinfections of their AD lesions because their skin barrier is impaired. The most common are impetigo and eczema herpeticum.

• Impetigo, a bacterial superinfection most commonly caused by S. aureus, is characterized by the development of yellow crusts superimposed on AD lesions. Impetigo can trigger a full-body AD flare.

• Impetigo should be treated with oral or topical antibiotics (depending on the severity) that provide S. aureus coverage.

• Patients with recurrent impetigo should consider undergoing Staph decolonization with topical mupirocin 2% or initiating bleach baths.

• Oral antibiotics should not be prescribed to AD patients in the absence of clinical evidence of superinfection.
• Eczema herpeticum, or superinfection of AD lesions by herpes simplex virus (HSV), is a dermatologic emergency characterized by the development of punched-out, herpetic lesions within AD plaques and with or without the presence of fever. Eczema herpeticum should be suspected in any patient who develops acute onset of skin pain superimposed on AD lesions.

• Eczema herpeticum with fever requires hospitalization for intravenous (IV) antivirals.

• All patients with possible eczema herpeticum should be started on valacyclovir at the first sign of an outbreak.

Many patients or their parents request referral for food allergy testing because they want an explanation for why they or their child have developed AD. Blind elimination diets or use of immunoglobulin E (IgE) testing without confirmation with a double-blind food challenge is not recommended because it is rarely helpful.

A diagnosis of CTCL should always be considered in patients with disease refractory to topicals, with new onset of disease in adulthood, with atypical-appearing patches/plaques, and/or with atypical distribution of patches/plaques. These patients require biopsies of untreated lesional skin. Specimens must be evaluated by a dermatopathologist given the difficulty of rendering a histologic diagnosis of CTCL.

Counseling

You have atopic dermatitis, also known as “eczema.” Atopic dermatitis is usually an inherited chronic skin condition (meaning there is no cure) that occurs in people who have skin that does not retain enough water and that does not adequately protect itself from outside allergens. Your skin is sensitive, prone to dryness, and susceptible to becoming itchy and developing rashes.

Individuals with atopic dermatitis develop skin inflammation in response to the environment around them. This inflammation makes the skin red and itchy. Importantly, there is no one allergen that causes your skin disease. Additionally, dietary changes have not been reported in the medical literature to cure your disease.

Treating your skin disease requires that you keep your skin healthy by moisturizing it and by avoiding exposing it to things that may irritate it. To keep your skin healthy, it is important that you have a special bathing regimen that promotes your skin health. When you shower, it is important that you use tepid water and that you limit your shower to less than 10 minutes. In the shower, you should use a gentle, unscented bar soap and should only apply soap to the armpits, groin, and areas that are visibly dirty. Do not use a luffa or a washcloth to apply soap because this may further irritate your skin. Pat, rather than rub, yourself dry with a towel. Immediately after drying off, you should apply a moisturizer to lock in the hydration that your skin received while you were showering. It is important that you not only hydrate your skin with a moisturizer after showering, but also that you moisturize at least twice a day. While your skin is still red and irritated, it is important that you do not apply any cosmetics or fragrances because these can inflame or irritate your skin.

Your doctor has prescribed a topical steroid cream that you should use twice daily only for 7 to 10 days, at which time the redness and irritation should be gone. Do not apply this cream to your face, groin, underarms, or under your breasts unless told specifically to use the cream in these locations. Alternative steroid-sparing creams may also be prescribed for more chronic or intermittent use.

These prescription creams are not a substitute for your moisturizer and should be used with your moisturizer, not instead of your moisturizer. Once the redness and irritation has resolved, you can stop the prescription cream, although you may want to restart it when the redness and irritation return. The topical steroid prescribed cream can cause side effects if you use it too frequently or if you use it for too long. These side effects include potential thinning of the skin, dilatation of blood vessels that can become more visible in the area of application, discoloration of the skin, and even an acne like rash. Continue your routine of twice-daily lubrication and shortened tepid bathing as part of your skin regimen.

Atopic dermatitis is cyclical, meaning you will have times when your rash is much better and times when it is much worse. Different people flare for different reasons. You should try your best to identify things that are unique triggers for your atopic dermatitis. You will have to work with your doctor over time to find a skin care regimen that is right for you and that keeps your skin disease under control.

Allergic contact dermatitis—trunk

Christian Gronbeck and Diane Whitaker-Worth

Clinical features

ACD is a delayed-type hypersensitivity reaction to immunogenic agents that come into contact with the skin. Many patients who develop ACD have an impaired skin barrier, allowing small compounds to penetrate the skin and initiate an antigenic response. After initial allergen exposure, affected individuals progress through a sensitization phase, which involves the proliferation of antigen-specific T cells. After reexposure, activation of these T cells leads to an inflammatory response, which prompts more immediate cutaneous symptoms.

Although the skin can be allergic to an innumerable number of compounds, the most common causes of ACD are nickel, fragrance mixtures, preservatives (e.g., formaldehyde), detergents, dyes (often in hair products), sunscreens (especially those containing benzophenones), topical medications (e.g., minoxidil, neomycin, bacitracin), acrylates, and urushiol (a chemical in poison ivy, poison sumac, and poison oak). Although ACD occurs equally among all races, it is more commonly seen in female patients, likely because of the higher prevalence of piercings and the increased number of personal care products used by women.

Course of development

Initial exposure

• After exposure to a new allergen, individuals become sensitized to the particular antigen over the course of 10 to 14 days.

• After 2 weeks, some patients may develop a mild inflammatory dermatitis, consisting of erythematous plaques and papules in the exposed skin region.

• In some cases, continuous low-grade exposure to an allergen can incite sensitization over an extended period of time.

Subsequent exposures

• Because of the persistence of memory T cells in the dermis, subsequent antigen exposure leads to a more profound and immediate dermatitis, generally within 12 to 48 hours of exposure.

• Affected individuals will classically develop intense pruritus in exposed areas, along with the development of erythematous, edematous plaques that may develop scale and vesiculation in the following days.

Chronic allergic contact dermatitis

• Repeated exposures to the allergen can lead to chronic disease, in which the skin becomes thickened, lichenified, hyperpigmented, and hyperkeratotic.

• Reexposure once every 28 days is frequent enough to maintain ACD.

• Chronic disease is more likely to occur in individuals who do not receive proper treatment for acute episodes.

Common clinical presentations

• ACD can present with different patterns based on the most likely cause of exposure and the specific body region.

• ACD on the face may be the result of cleansing products, hair products, cosmetics, or airborne allergens.

• A rinse-off pattern that affects the sides of the face and upper chest may be the result of shampoos, conditioners, and other cleansing products.

• A hairline pattern that impacts the superior forehead and nape of the neck may be caused by dyes and perming solutions.

• Patchy, bilateral plaques on the bilateral cheeks are typically caused by application of a cosmetic product.

• Involvement of the upper eyelids, nasolabial fold, and submental region generally signifies exposure to airborne allergens (e.g., small particles like powder or gas).

• ACD on the hands may stem from objects in everyday use or occupational exposures.

• Plaques on the palms may be incited by use of computer mice, cell phones, or stair rails.

• Isolated involvement of the thumb and ring ringer can signify ACD from occupational exposures, such as from using acrylates (dentists) or handling plants (florists).

• ACD on the trunk and extremities may be the result of a nickel allergen or textile products.

• Involvement of the earlobes, neck, wrists, and skin beneath the umbilicus are likely caused by a nickel allergen.

• Textile products typically incite reactions along the inferior neck, axillae, and internal surface of the arms and thighs because of more frequent friction from clothing in these regions.
• Regardless of location, the identification of several patterns should clue the clinician in that ACD is the likely culprit:

• A geometric pattern (e.g., an adhesive reaction that is clearly square shaped).

• Linear and other so-called “outside job” morphologies (i.e., where the morphology of the rash-like lines can only be explained by exogenous contact with something).

• This pattern is particularly common in ACD caused by poison ivy, sumac, and oak (Fig. 3.3).

• Disease isolated to one anatomic unit (e.g., just hands) may be ACD.
• The rash typically develops at the site of primary contact with the allergen (e.g., application of eye shadow leading to periocular dermatitis); however, in some cases, dermatitis occurs at a site distant from where the allergen is applied to the skin (e.g., nail polish causing eyelid dermatitis from touching thin eyelid skin).
• ACD often becomes superimposed atop other background skin diseases (e.g., atopic dermatitis, venous stasis ulcers).

• In these settings, ACD usually develops to an ingredient in a topical formulation used for treating the background disease (e.g., neomycin, lanolin, topical corticosteroid).

Differential diagnosis

The differential for ACD includes AD, ICD, psoriasis, and seborrheic dermatitis.

• The primary morphology of both AD and ACD is an eczematous dermatitis that can vary in appearance depending on chronicity. ACD can be distinguished from AD by distribution (AD typically affects all flexural areas, whereas ACD is typically more localized), age at onset (AD typically presents in early childhood), and presence/absence of other atopic features (e.g., nasal salute, thinning of lateral third of eyebrow). Many individuals with AD develop ACD to the topical creams used to treat their AD, which is suggested by the development of treatment-refractory disease.
• ICD can also present with the development of erythematous, scaly plaques; however, it can be distinguished from ACD because it is frequently painful and not pruritic and has an irritated rather than inflamed appearance characterized by fissuring. In reality, distinguishing between these two entities is frequently very difficult and patch testing may be required.
• Psoriasis is another mimicker of ACD; however, it should be distinguishable from ACD clinically because psoriasis is well circumscribed, has thick overlying silvery scale, and has a characteristic distribution overlying the extensor surface. Psoriasis is most frequently confused with ACD when it affects the eyelids.
• ACD can be distinguished from seborrheic dermatitis by distribution and morphology.

• Seborrheic dermatitis affects predominantly seborrheic areas (e.g., scalp, eyebrows, nasolabial folds, beard, chest).

• Seborrheic dermatitis presents with thin pink plaques with overlying greasy scale.

Work-up

A total-body skin examination and patient history is necessary to support the diagnosis of ACD. Patch testing is the gold standard in confirming the diagnosis of ACD and identifying likely allergens:

• A total-body skin examination may reveal classic ACD lesions, including well-circumscribed, pruritic, eczematous plaques and papules in areas that were recently exposed to allergens.

• Acute reactions may further exhibit vesiculation or weeping, whereas chronic lesions are typically lichenified.

• A patient history of a chronic, multi-year course that follows contact with specific allergens will further support a diagnosis of ACD.

• Nevertheless, it is important to recognize that patients’ susceptibility to certain allergens may vary over time and that they may develop new-onset sensitization to products they previously tolerated.
• If a single offending agent is strongly suspected, removal can be both therapeutic and diagnostic (if the patient demonstrates resolution of symptoms).

• If a particular allergen is suspected, it is recommended to provide patients with a list of products containing this allergen so that they can perform targeted removal of the offending agent.

• Importantly, if a particular allergen or product is not strongly suspected, it is not recommended to blindly remove potential allergens because many products share similar allergens and this does not frequently lead to identification of the allergen.
• Patch testing is typically indicated: (1) when distributions are highly indicative of ACD; (2) when clinical history, as described previously, is consistent with ACD; (3) when the patient is involved in high-risk occupations for ACD, including health care professionals, florists, and cosmetologists; (4) when the cause for the dermatitis cannot be otherwise established; (5) if there is acute worsening of an underlying dermatitis; and/or (6) if the patient proves refractory to initial treatment efforts.

• Patch testing is typically performed through a dermatologist and involves securing several potential allergens to the skin surface for 2 days with subsequent monitoring for signs of an eczematous reaction.

• Note that patch testing is unique from prick testing, which is an alternative allergy test performed by an allergist.

• Patch testing is the necessary test to identify allergens for ACD (delayed hypersensitivity reaction) as opposed to those causing an immediate (Type 1) hypersensitivity reaction.

Initial steps in management

General management comments

• Definitive management involves avoidance of allergen-containing products, if successfully identified through patch testing (see indications for testing in “Work-Up”).
• For existing lesions, antiinflammatory medications are used to prompt symptomatic improvement and resolution of lesions.
• Patients with chronic or persistent ACD or extensive skin involvement may benefit from the use of oral immunosuppressive agents or referral to a dermatologist for further management.

Allergen avoidance and protection

Patients should be counseled to avoid identified or highly suspected allergens.

• Patients should be educated that many products share similar allergens, and they should reference manufacturer websites to identify common household products that may contain their allergen.
• If possible, an informational leaflet can be provided to patients to educate them on common uses of their identified allergen.
• If patients are at risk for workplace exposures, they should be advised to use personal protective equipment (PPE; e.g., laminate gloves).
• Emollients (e.g., Vaseline, Aquaphor) can offer additional skin protection by acting as barriers against external allergens.

Minimization of existing skin inflammation

• To target skin inflammation of the hands, feet, or nonflexural surfaces, we recommend high-potency topical corticosteroids (clobetasol propionate 0.05% cream) twice daily for 2 to 4 weeks.
• To target the skin inflammation of the flexural surfaces or face, we recommend treating patients with mild- to moderate-potency topical corticosteroids (fluocinolone acetonide 0.01% cream) twice daily for 2 to 4 weeks.
• Patients with ACD of the hairbearing scalp may benefit from high-potency corticosteroids (clobetasol propionate 0.05% solution or fluocinonide 0.05% solution) nightly.
• As an alternative to steroids, topical calcineurin inhibitors (tacrolimus 0.1% cream) can be used twice daily for 2 to 4 weeks

Management of chronic allergic contact dermatitis

Patients with chronic ACD may require more extensive management that includes oral immunomodulatory drugs (e.g., methotrexate, mycophenolate) or ultraviolet (UV) light treatment. Nevertheless, these patients are typically best referred to a dermatologist for close management and to ensure their allergens have been adequately identified through patch testing.

Partial but inadequate response

If there is a partial but inadequate response after a 4-week trial of topical corticosteroid monotherapy:

• Confirm patient compliance with the recommended treatment regimen and address any compliance barriers.
• Reconsider the diagnosis of ACD and ensure that the patient has received patch testing.
• For extensive or severe skin involvement that is secondary to an acute exposure (e.g., poison ivy), a 20-day course of oral corticosteroids (e.g., prednisone) is suggested alongside referral to a dermatologist.

• Dosing should be weight-adjusted at a rate of 1 mg/kg.

• A typical 20-day taper of oral prednisone for an average-weight patient would include 40 mg daily for 5 days, 30 mg daily for 5 days, 20 mg daily for 5 days, and 10 mg daily for 5 days, with all doses taken in the morning.

• Shorter, 5- to 7-day doses typically result in rebound flaring after cessation.

• Systemic comorbidities, such as heart failure, glaucoma, poorly controlled hypertension, and diabetes mellitus should be taken into account when prescribing oral corticosteroids.

Warning signs/common pitfalls

• Patients with extensive skin involvement or severe plaque formation warrant referral to a dermatologist.
• It is important to monitor patients with ACD for secondary bacterial infection, which may be indicated by warmth, swelling, extensive erythema, or discharge from involved areas.

• In these cases, oral or topical antibiotics targeting the secondary bacterial infection are warranted.
• Although patch testing can be useful in identifying potential allergens, any identified allergens should fit in the patient history. For example, patients may test positive for certain preservative compounds that they do not readily encounter in their daily life, so these findings are therefore less relevant for future management.
• Prick testing is not equivalent to patch testing and is not suitable to identify the allergens that are causing the ACD.

Counseling

Allergic contact dermatitis is a skin rash caused by a skin allergy to certain products, chemicals, or medications in your day-to-day environment. Common allergens include shampoos, soaps, nickel (on your watch or pants button), fragrances, cosmetic agents, creams, and some plants, such as poison ivy. Importantly, this type of allergy is not life-threatening.

We generally manage this rash in a few ways. First, we want to identify what you are allergic to. To determine this, we will refer you to a dermatologist for patch testing. Patch testing is a painless procedure in which small pieces of potential allergens will be taped to your back and left in place for 2 days. If we identify what you are allergic to, we recommend that you avoid that allergen to see if your symptoms resolve.

We also have treatments available that can help to resolve your skin rash while we are waiting to determine what you are allergic to. We have prescribed you a topical corticosteroid cream, which you should apply to the rash twice daily. The most common side effect people notice from this cream is that it can cause the skin to thin slightly and the blood vessels to become more noticeable in the surrounding area. Most patients see their rash begin to resolve within a few weeks of consistently using the cream. In addition to using these treatments, you may also find it helpful to hydrate your skin with moisturizers.

Nummular dermatitis

Christian Gronbeck and Diane Whitaker-Worth

Clinical features

Nummular dermatitis (eczema) is an inflammatory skin condition that derives its name from its characteristic coin-shaped lesions (Fig. 3.4). Nummular dermatitis is likely a clinical variant of atopic eczema and ACD because it shares features of both conditions.

Fig. 3.4 **Nummular dermatitis.** *Source:* (From the UConn Grand Rounds Collection.)

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Tags: Dermatology for the Primary Care Provider

Jul 22, 2021 | Posted by admin in Dermatology | Comments Off

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Body dermatitis

3: Body dermatitis

Abstract:

Atopic dermatitis—trunk and extremities

Clinical features

Differential diagnosis

Work-up

Initial steps in management

Dry skin care

Topical antiinflammatory agents

Trigger avoidance

Itch management

Other therapies

Warning signs/common pitfalls

Counseling

Allergic contact dermatitis—trunk

Clinical features

Course of development

Initial exposure

Subsequent exposures

Chronic allergic contact dermatitis

Common clinical presentations

Differential diagnosis

Work-up

Initial steps in management

General management comments

Allergen avoidance and protection

Minimization of existing skin inflammation

Management of chronic allergic contact dermatitis

Partial but inadequate response

Warning signs/common pitfalls

Counseling

Nummular dermatitis

Clinical features

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Plastic Surgery Key

Fastest Plastic Surgery & Dermatology Insight Engine

Body dermatitis

Abstract:

Atopic dermatitis—trunk and extremities

Clinical features

Differential diagnosis

Work-up

Initial steps in management

Dry skin care

Topical antiinflammatory agents

Trigger avoidance

Itch management

Other therapies

Warning signs/common pitfalls

Counseling

Allergic contact dermatitis—trunk

Clinical features

Course of development

Initial exposure

Subsequent exposures

Chronic allergic contact dermatitis

Common clinical presentations

Differential diagnosis

Work-up

Initial steps in management

General management comments

Allergen avoidance and protection

Minimization of existing skin inflammation

Management of chronic allergic contact dermatitis

Partial but inadequate response

Warning signs/common pitfalls

Counseling

Nummular dermatitis

Clinical features

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