Body dermatitis

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.

  

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.

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.

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.

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

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.

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.

Differential diagnosis

The differential diagnosis for nummular dermatitis includes other pruritic skin conditions, such as AD, ACD, psoriasis, tinea corporis, CTCL, and lichen simplex chronicus (LSC). In all cases, geographic morphology (well-circumscribed, coin-shaped lesions) and a patient history of skin irritation/xerosis are helpful in supporting the diagnosis of nummular dermatitis.

• Although AD can present with pruritic and eczematous patches on the upper extremities, these plaques are typically less circumscribed and widespread. Typically, AD presents early in life and is associated with an atopic diathesis (e.g., allergic rhinitis, asthma). In clinical practice, these conditions may occur in an overlap state.

• Plaques from ACD are often less symmetric and monomorphous than those of nummular eczema. Patients with ACD may be able to identify a direct contactant that triggered their skin eruption. Additionally, it would be very unusual for ACD to present with multiple, discrete, coin-shaped lesions.

• Subacute and chronic skin lesions from nummular eczema may mimic psoriasis. In these cases, it is important to question patients regarding the initial appearance of their skin lesions (e.g., vesicular or eczematous). Additionally, pruritus is characteristic of nummular eczema and less typical in psoriatic lesions. Psoriatic lesions also have a strong predilection for extensor surfaces.

• During the early stages, tinea corporis is pruritic, erythematous, and well-circumscribed, sharing a similar geographic morphology to nummular dermatitis. Tinea lesions are typically localized and unilateral, whereas nummular dermatitis is usually bilateral and symmetric. A potassium hydroxide (KOH) preparation can be useful in ruling out tinea when available.

• LSC is characterized by the development of hyperpigmented, thickened, lichenified plaques incited by frequent skin rubbing and scratching. Although LSC most frequently presents with a solitary lesion, it can present similarly to chronic nummular dermatitis because nummular dermatitis may become lichenified over time because of how itchy it can be.

• CTCL can mimic many eczematous conditions. Generally, CTCL plaques are polymorphic and affect sun-protected areas (e.g., the buttocks). Biopsy can be helpful in distinguishing between the two entities.

Work-up

Nummular dermatitis is a clinical diagnosis based on patient history and examination. In general, a skin biopsy is not necessary to make the diagnosis.

• A total-body skin examination is recommended to demonstrate the presence of well-circumscribed, eczematous, coin-shaped plaques located in classic skin regions (upper and lower extremities).

  • Identification of diffuse xerosis may support the diagnosis of nummular eczema.

• A targeted patient history should be obtained to assess for the presence of a relapsing pattern of skin involvement; pruritus that is worse during the evening hours; and recent history of skin irritation, trauma, or bites.

• In patients with excessive exudation or crusting, a skin swab and culture may be used to identify the presence of secondary bacterial infection.

• Although rarely performed on initial presentation, patch testing (through a dermatologist) may be suitable for individuals with persistent skin lesions to better characterize whether ACD is contributing to the patient’s rash.

Initial steps in management

Warning signs/common pitfalls

The biggest pitfall when managing nummular dermatitis is prescribing systemic corticosteroids because the patient will flare after they are discontinued.

Other pitfalls include misdiagnosis and failure to use potent enough corticosteroids.

• Misdiagnosis as tinea corporis and subsequent treatment with a topical antifungal medication will delay the improvement of skin lesions. Therefore, when there is diagnostic uncertainty, we recommend testing for the presence of tinea through a KOH preparation.

• Failure to use high-potency corticosteroids (e.g., clobetasol, halobetasol) to affected areas is another potential pitfall.

• Failure to re-enforce the importance of skin barrier protection through the use of emollients may result in further relapses of nummular eczema. Although patients may be inclined to restrict emollient use to areas with active involvement, they should be counseled on using emollients in all areas of xerosis to prevent the development of skin fissures and entry points for allergens.

Counseling

You have a skin rash called “nummular eczema.” This is an especially itchy type of eczema that occurs more often in people who have dry skin. Although there is no cure for your rash, we can take steps to improve it.

Your doctor is prescribing you a topical corticosteroid ointment. You should apply this ointment to areas of your skin that are affected by the rash two times per day for 2 to 4 weeks. This is a very strong medication and therefore should not be applied to normal-appearing skin.

In addition to the prescription cream, you should also hydrate your skin with a moisturizer. You should moisturize your entire body, including unaffected areas. It is important to use the moisturizer even after your rash improves. We recommend that you shower in warm (not hot) water, pat your skin dry, and apply the emollient liberally on your skin while it is still damp. Additional moisturizing during the day can be helpful.

If your rash fails to improve in the next few weeks, we may consider referring you to a dermatologist for further testing and treatment.

Clinical features

Psoriasis is a chronic, immune-mediated disease that presents with a waxing and waning course and is characterized by hyperplasia of the epidermal keratinocytes. It predominantly affects the skin, nails, and joints. It impacts approximately 2% of the U.S. population, and roughly one-third of impacted patients have moderate to severe disease characterized by involvement of more than 10% BSA. Onset typically occurs in two age ranges: 20 to 30 years old and 50 to 60 years old. Evaluation for family history is essential in patients with psoriasis because approximately 30% of individuals with psoriasis have a first-degree relative with the disease. The goal of treatment for psoriasis is to achieve complete or near-complete skin clearance and improve patient quality of life.

Most cases of psoriasis are readily identifiable based on the presence of well-demarcated (i.e., a circle can easily be drawn around the plaque), scaly plaques on extensor surfaces (e.g., elbows, knees, scalp, lower back).

There are several major subtypes of psoriasis that are classified based on skin morphology, with some patients demonstrating overlap between classification types.

• Plaque psoriasis presents with well-demarcated, scaly, and erythematous patches and plaques ( Fig. 3.5 ).

  • The plaques are typically symmetric, bilateral, and are most commonly found on the scalp, extensor elbows, knees, and gluteal cleft.

  • Clinical findings include pinpoint bleeding after removal of scale (Auspitz sign), as well as lesions appearing after trauma (Koebner phenomenon).

  

• Inverse/flexural psoriasis is characterized by erythematous patches primarily localized to the skin fold regions (axilla, groin) with minimal scaling.

• Guttate psoriasis presents with small, inflammatory plaques (raindrop-sized) with a fine scale that may follow streptococcal pharyngitis.

  • It is more common in children and young adults with no prior history of psoriasis. It may follow Group A Streptococcus infections.

• Pustular psoriasis involves a pustular cutaneous eruption, which may be generalized (von Zumbusch) or localized to the palms and soles (palmoplantar) and often follows infection or withdrawal from corticosteroids.

• Erythrodermic psoriasis is defined by cutaneous erythema and scale covering a large portion of the body area; it is often associated with systemic manifestations of illness (e.g., fever, chills, malaise).

Patients with psoriasis may also develop manifestations in special sites, including the nails, periocular area, skin folds (intertriginous, inverse psoriasis), and palms/soles (palmoplantar).

• Nail psoriasis can occur in adults or children and is seen in 10% to 55% of patients with psoriasis and 80% to 90% of patients with psoriatic arthritis. It is clinically distinguished by the presence of pitting, onycholysis (separation of the nail from the nail bed), subungual hyperkeratosis, and nail plate crumbling ( Chapter 16 ], “Nail Psoriasis”). In cases where psoriasis is suspected, fingernail examination is incredibly helpful for confirming the diagnosis.

• Patients with psoriasis are at an increased risk for ocular disorders, such as blepharitis, conjunctivitis, xerosis, corneal lesions, and uveitis. Patients may also develop psoriatic lesions on the eyelids with eyelid flaking.

• Patients with intertriginous psoriasis present with well-demarcated, shiny plaques with limited scale and must be distinguished from fungal infections, which also commonly present in similar regions.

• Palmoplantar psoriasis presents with erythematous, hyperkeratotic plaques, along with fissures > It is sometimes considered a form of pustular psoriasis.

Differential diagnosis

The differential diagnosis for psoriasis depends on the subtype. For chronic plaque psoriasis (80%–90% of patients), alternative considerations include LSC, seborrheic dermatitis, AD, and cutaneous fungal infections.

• Patients with LSC can also develop plaques with overlying scale, but they are typically less erythematous than those from psoriasis, are incited by chronic scratching, and are therefore more likely to be located in regions that patients can reach (e.g., the scalp, nape of the neck, extensor forearms, thighs).

  • In any event, a patient history of excessive scratch–itch cycles can help distinguish LSC from psoriasis.

• Both plaque psoriasis and seborrheic dermatitis may involve the scalp and intertriginous areas. Seborrheic dermatitis, however, is often localized to specific facial regions (eyebrows, nasolabial folds, postauricular areas), occasionally involves the trunk and upper chest, and rarely involves the extremities.

  • Additionally, lesions from seborrheic dermatitis are poorly-circumscribed and are characterized by patchy scaling or crusting that has a greasy texture, unlike the well-circumscribed plaques with abundant scale seen in psoriasis.

• AD classically presents with pruritic papules and patches with erythema and scale, but the raised, well-defined borders of plaque psoriasis are not typically seen. Involvement of the flexural surfaces is also common in AD, whereas chronic plaque psoriasis involves the extensor surfaces.

  • Furthermore, patients with AD frequently have a history of involvement from a young age and may have associated atopic conditions, such as asthma and allergic rhinitis.

• Cutaneous fungal infections, such as tinea, can present with erythematous plaques and with nail changes (onychomycosis) similar to those in nail psoriasis. Like psoriasis, tinea can involve the scalp (tinea capitis) or body (tinea corporis), but there are typically a limited number of lesions. Plaques may be further distinguished by their fine scale with a well-defined, reddish margin. Importantly, onycholysis (separation of the nail from the nail bed) is frequently seen in nail psoriasis but less commonly noted in fungal infections of the nail.

  • A KOH preparation can be useful in distinguishing these two etiologies.

Work-up

The diagnosis of psoriasis can typically be made through physical examination and supported by patient history, with skin biopsy reserved for challenging cases.

• A total-body skin examination is warranted and should include an assessment of the scalp and nails.

  • Visualization of well-demarcated, inflamed plaques in characteristic skin regions (elbows, areas, scalp, knees) with significant scaling supports the diagnosis of plaque psoriasis.

• Routine biopsy and histologic confirmation is not indicated, except in atypical-appearing cases or in cases that fail to respond to treatment as expected.

  • Importantly, a biopsy should not be obtained from plaques that are actively receiving treatment with topical corticosteroid.

• A patient history indicative of specific risk factors, including family history and obesity, can support a diagnosis of plaque psoriasis.

• Worsening of longstanding psoriasis should prompt a review of medications to identify exacerbating factors.

  • Frequently implicated medications include lithium, beta blockers, antimalarials (e.g., chloroquine, hydroxychloroquine), nonsteroidal antiinflammatory drugs (NSAIDs), and tetracycline.

• A KOH preparation can be employed to rule out a superficial fungal infection if this is suspected, especially in the case of intertriginous lesions, but this examination only has utility if performed by an experienced user.

• It is critical to evaluate for the presence of psoriatic arthritis at the time of initial diagnosis to avoid irreparable joint disease. Even a 6-month delay in treatment of psoriatic arthritis can result in irreversible joint damage.

  • Patients should be questioned regarding the presence of joint pain, joint stiffness, and back pain.

    • Screening tools for psoriatic arthritis exist; however, their sensitivity is limited. Patients who have any joint symptoms whatsoever should be referred to a rheumatologist or dermatologist for evaluation.

• It is not necessary to evaluate for the presence of systemic triggers, such as HIV or streptococcal pharyngitis, in the absence of clinical suspicion (e.g., presence of guttate psoriasis).

Initial steps in management

Warning signs/common pitfalls

• It is highly recommended to screen patients with psoriasis for psoriatic arthritis at regular intervals. If this is deemed a diagnostic possibility, urgent referral to a rheumatologist is necessary. There are validated screening tools (e.g., the Psoriasis Epidemiology Screening Tool [PEST]) that can easily be implemented in the clinical setting.

• It is important to ask patients about prior experiences with treatment efforts to guide current efforts. Additionally, it is recommended to discuss with patients how they plan to incorporate treatment into their daily routine to gauge medication compliance.

• After initiating treatment, having the patient return for a follow-up visit in 1 to 2 weeks can be useful in increasing rates of compliance.

• Oral corticosteroids should never be used in psoriasis because flare-ups are inevitable after medication tapering. Some patients develop erythroderma or pustular psoriasis from this, which can require hospitalization.

• It is critical to screen patients for the psychosocial aspects of their disease because some patients can develop depression or low self-esteem as a result of the appearance of their skin. Reassurance can be an important tool at follow-up visits, and referral to a psychiatrist or counselor may be useful in some cases.

• In the case of intertriginous psoriasis, we recommend the use of low-potency topical steroids to avoid skin atrophy of the flexural surfaces.

Counseling

Psoriasis is a skin condition that occurs because your immune system is inappropriately attacking your own skin. Although psoriasis is not curable, meaning it will be present for years, it can be managed with certain medications that can relieve the symptoms and improve the rash. Almost all patients can achieve satisfactory disease control with appropriate therapy. Although psoriasis is not life-threatening, it can increase your risk of several other diseases that are harmful to you.

I have prescribed you a topical corticosteroid. You should apply the corticosteroid twice daily to skin areas that have the rash on them. You should continue using this cream until the rash is no longer red and raised. The inflammation caused by psoriasis may discolor your skin. This discoloration should not be treated with the cream. Once you take a break from using the cream, your psoriasis will come back. You can then continue to use the cream up to twice daily as needed to keep it under control. The major side effect of the corticosteroid is that it can cause the skin to become a bit thinner and therefore cause some of the blood vessels to show more than usual. Taking breaks when the rash has gone away can help to prevent this side effect from happening. It is important to use the medication consistently each day because it is most effective that way. Patients say that they start to see an improvement within a week of using the medication.

Clinical features

Urticaria (or hives) is characterized by the sudden development of swollen-appearing, variably pink-red papules or plaques on the skin, which are referred to as wheals and/or angioedema ( Fig. 3.6 ).

• Urticarial wheals have three key features:

  • They have a central swelling with or without surrounding erythema.

  • They usually itch, but they can also tingle or burn.

  • They are evanescent, lasting from 30 minutes to 24 hours.

• Urticarial angioedema has three key features as well:

  • It presents with sudden dermal, subcutaneous, and/or mucous membrane swelling.

  • It is typically more painful than itchy.

  • It resolves in less than 72 hours.

• Urticaria is divided into two major subtypes based on the duration of symptoms.

  • Acute urticaria lasts less than 6 weeks.

    • It frequently has an inciting trigger (e.g., illness, medication, food).

  • Chronic urticaria lasts longer than 6 weeks.

    • It can be further subdivided into chronic spontaneous urticaria and chronic inducible urticaria (CIU).

      • Chronic spontaneous urticaria has no known or identifiable specific eliciting trigger.

      • CIU consistently and reproducibly occurs in response to a specific eliciting trigger.

        • Subtypes of CIU include dermographism, delayed pressure urticaria ( Fig. 3.7 ), vibratory angioedema, contact urticaria, aquagenic urticaria, solar urticaria, cholinergic urticaria, cold urticaria, and heat urticaria.

          

Differential diagnosis

The differential for urticaria is broad and includes dermal hypersensitivity reaction, urticarial bullous pemphigoid (BP), urticarial vasculitis, and autoinflammatory disorders (e.g., familial Mediterranean fever [FMF]).

• Dermal hypersensitivity reactions can clinically and histologically overlap with CSU; however, dermal hypersensitivity skin lesions last longer than 24 hours and present with erythema throughout the area of dermal swelling rather than at the periphery of the swelling, as is typically seen in urticaria. Furthermore, dermal hypersensitivity reactions are much less responsive to antihistamines than urticaria is.

• Urticarial BP has an urticaria-like appearance, as its name suggests. It can be distinguished from urticaria because its lesions last longer than 24 hours; there can be a history of bullae development; BP is not antihistamine responsive; and a direct immunofluorescence examination of the perilesional skin will reveal a linear deposition of immunoglobulin G (IgG) with or without C3 at the basement membrane zone.

• Urticarial vasculitis is a form of leukocytoclastic vasculitis that presents with urticaria-like lesions. It can be distinguished from urticaria because it burns more than it itches; its lesions persist longer than 24 hours; its lesions are typically dusky/purpuric appearing; and a histopathologic examination shows small-vessel vasculitis.

• Patients presenting with angioedema without concomitant wheals should be evaluated for non-mast cell–related angioedema, of which there are many etiologies (e.g., hereditary angioedema, angiotensin-converting enzyme [ACE] inhibitor–induced angioedema). The presence of both wheals and angioedema differentiates urticaria from other causes of angioedema.

• Many autoinflammatory conditions (e.g., FMF, Muckle-Wells syndrome) present with urticarial lesions. These are unlikely to be misdiagnosed as urticaria because these patients present with fever and other systemic findings and often have a family history of their condition.

Work-up

Acute urticaria does not usually require any work-up because frequently, the history elicits the precipitating allergen. Nevertheless, in some cases, referral for allergy testing may be helpful for identifying the culprit and thereby preventing recurrences.

The work-up of patients with suspected chronic urticaria is divided into confirmation of the diagnosis and identification of the triggers/underlying causes.

• A thorough history ascertaining lesional history; concomitant systemic symptoms; inciting/exacerbating factors; personal history of allergies, infections, and autoimmune disease; family history of urticaria; current medications; and prior treatments should be obtained from all patients.

• Extensive laboratory work-up is not recommended in patients with acute urticaria who lack an obvious trigger and who are without systemic symptoms because lab work is unlikely to reveal an underlying cause; those with chronic urticaria should have an age-appropriate cancer work-up, a thorough review of systems, and a physical examination.

  • Patients with chronic fever and/or systemic symptoms in addition to their urticarial lesions should be referred to an allergist for evaluation for an autoinflammatory syndrome.

Patients with angioedema who do not have concomitant wheals should be worked up for non-mast cell–induced angioedema. This work-up is broad and includes but is not limited to a search for external agents such as a drug or food; history of previous treatment with an ACE inhibitor; an underlying autoimmune disease or infection; and C1 inhibitor deficiency. Referral of these patients to a specialist is recommended if the identifying cause is not easily identified.

Initial steps in management

The first-line treatment for chronic urticaria is second-generation antihistamines (e.g., loratadine, cetirizine, fexofenadine, levocetirizine, desloratadine).

• Antihistamines should be initially dosed daily at their usual dose (e.g. cetirizine 10 mg BID).

  • Dosage should be increased up to 4 times the recommended daily dose (20 mg BID) if symptoms are not adequately controlled within 2 weeks of initiating the antihistamine.

    • The same treatment algorithm is used for children; however, lower doses are recommended (e.g., cetirizine 5 mg instead of 10 mg).

    • High-dose antihistamines are effective in around 70% of cases.

  • Mixing different antihistamines is not recommended (e.g., loratadine and cetirizine).

  • Use of a nightly sedating first-generation antihistamine (e.g., hydroxyzine) is not recommended.

  • Previously, H2 blockers (e.g. ranitidine, cimetidine) were added when H1 blockers were inadequate; however, this is no longer recommended.

• Patients who are not successfully controlled with a trial of high-dose H1 blockers should be referred to a dermatologist or an allergist for a trial of high-dose varied and disparate antihistamines and, if that fails, initiation of omalizumab.

Warning signs/common pitfalls

Most patients with chronic urticaria are antihistamine responsive and respond quickly. Initiation of systemic corticosteroids is almost never indicated because most patients have chronic urticaria for around a year and discontinuation of corticosteroids often results in significant disease flare.

• Similarly, first-generation antihistamines (e.g., diphenhydramine, hydroxyzine) are not generally recommended as first-line therapy because of their side effects.

Many patients with urticaria want an explanation as to why they have urticaria. Extensive laboratory evaluations and allergy testing are expensive and typically add to patient anxiety and therefore should not be performed unless the patient history suggests a specific trigger.

CIU represents only approximately 15% to 25% of all cases of chronic urticaria. Nevertheless, many patients (around two-thirds) with chronic urticaria have a component of CIU. Identification of this component is essential for successfully managing these patients.

Fever and/or systemic symptoms in the setting of chronic urticaria can represent a serious underlying illness. These patients should be referred urgently for additional evaluation.

Counseling

You have chronic urticaria, which is also known as “hives.” Hives are a type of skin reaction that occur from either an allergy, an autoimmune condition, an underlying disease, an infection, a medication, or something in your environment. Although we do not know why you are developing these hives, they often go away on their own within about a year.

You should attempt to identify what brings out your hives or worsens them. For example, some people’s hives worsen with they take nonsteroidal antiinflammatory medications, such as ibuprofen; other people have their hives brought out by emotions and sweating.

There are an almost infinite number of causes of hives. We do not perform blood work or allergy testing to try to figure out why you have hives because it is almost never helpful.

Fortunately, most hives dramatically improve with antihistamines. You should take over-the-counter (OTC) cetirizine 10 mg by mouth twice daily. If your symptoms are not satisfactorily improved in 2 weeks, then you should increase the dose of the cetirizine to 20 mg twice daily.

If you do not improve despite taking antihistamines, we will refer you to a hive specialist for additional treatment options.

Clinical features

Autoeczematization, or id reaction, is a secondary skin eruption that results from a primary, inflammatory disorder in another part of the body. It is generally thought to be the result of hyperirritability of the skin elicited by immunogenic stimuli.

• In terms of geographic morphology, it presents with symmetric, erythematous, and pruritic papules and plaques with associated scale.

• It may be located at various sites on the body, either close to or distant from the inciting inflammatory disorder.

The type of primary skin infection varies and classically includes ACD, dermatophyte infections, and stasis dermatitis.

• Inciting dermatophyte reactions most classically include tinea pedis but may also be the result of tinea manuum, cruris, corporis, or capitis.

  • Patients with tinea pedis (athlete’s foot) commonly present with secondary vesicular eruptions on the hands, head, and neck.

  • Patients with dermatophyte infections may develop id reactions shortly after the initiation of antifungals, which should not be misdiagnosed as a medication allergy. Patients should continue on their antifungal and be treated symptomatically for the id reaction.

• ACD frequently occurs in children and commonly results in development of an id reaction distal to the initial site of irritation.

  • Development of an id reaction is particularly common with nickel dermatitis.

• Stasis dermatitis can give rise to an id reaction 1 to 2 weeks after the initial inflammation and is most frequently located on the forearms, thighs, trunk, and face.

Differential diagnosis

The differential diagnosis of an id reaction is broad and includes AD, ACD, drug eruptions, and scabies. In all cases, the diagnosis of an id reaction is made more likely by the identification of a primary rash in a separate body location.

• AD is distinguished from id reactions in that it frequently develops during early childhood, co-develops with other atopic conditions (e.g., allergic rhinitis, asthma), and develops in characteristic geographic regions (antecubital fossae, popliteal fossae, other flexural surfaces).

• ACD is distinguished from an id reaction in that it typically is asymmetrical and eczematous appearing.

• Drug eruptions have variable presentations; however, they are often in the differential for an id reaction because patients are started on new medications for their primary dermatoses, and there is suspicion that these new medications are responsible for a subsequent rash. Drug eruptions are typically generalized, usually develop within 1 month of initiating a new medication, and usually resolve with de-challenge.

• Patients with scabies primarily present with secondary lesions (i.e., excoriations) that develop from the intense pruritus that they experience. These lesions most frequently affect the interdigital web spaces of the hands, the wrists, and the genitals. The face is characteristically spared. Patients with scabies may also demonstrate linear burrow markings in the skin (see following section, “Scabies”).

Work-up

The diagnosis of an id reaction is a clinical diagnosis based on history and examination.

• In cases where an id reaction is suspected, patients should be questioned about whether they have a different rash elsewhere; however, history is typically not fruitful.

• A total-body skin examination should be performed to identify the primary dermatosis; if a primary rash is identified, management involves treatment of the primary dermatosis.

  • Patients with a primary fungal infection may exhibit erythematous, scaling plaques with central clearing (tinea corporis), erythematous patches affecting the medial thigh and intertriginous areas (tinea cruris), or erythematous erosions and scales between the toes (tinea pedis). If identified, a KOH preparation can be used to diagnose the presence of a primary fungal infection (see following section, “Tinea Corporis”).

  • Patients with primary stasis dermatitis will typically demonstrate erythematous, scaling, and hyperpigmented lesions on the lower legs, along with a history of venous insufficiency, varicosities, or pitting edema (see Chapter 4 ).

  • A patient with an id reaction secondary to primary ACD will exhibit erythematous, scaling plaques with intense pruritus in regions exposed to allergen exposures (see section, “ACD Overview”).

    • Patch testing can be performed if there is suspicion for a contact allergy; however, this is typically deferred until after the acute phase of the id reaction.

• If a work-up is not indicative of a primary etiology, we recommend referral to a dermatologist to pursue further testing, including a skin biopsy.

Initial steps in management