What is Eczema?


Eczema (AKA Atopic Dermatitis) is an itchy skin condition characterized by scaly red patches with bumps, oozing, and crusting. People suffering from eczema have intense itching relieved by scratching which produces secondary thickening of the skin. The hallmark of eczema is recurrence of itchy red skin in typical locations.
Eczema usually starts in childhood with more than 50% affected before one year of age, and 85% affected by five years of age. Although eczema often improves or resolves in many children over time, the disease may persist into adulthood. Those with more severe disease during childhood and those whose eczema started later in life have a higher likelihood of persistence.

About Eczema

Eczema treatment

Educational videos created by the Society for Pediatric Dermatology


Frequently Asked Questions (FAQ)

What does eczema look like?

How often should someone with eczema bathe? Can I swim if I have eczema?

What cleanser and moisturizer should I use?

What triggers eczema? What about food allergy?

What are topical steroids? Are they safe to use?

Examples of Topical Steroids that we routinely prescribe

Do I have to use topical steroids? Are there other options?

Are there complications of eczema?

My eczema is really bad. Is there systemic treatment for eczema?

What does Atopic Dermatitis look like?

The appearance and distribution of atopic dermatitis differs depending upon the age of the patient. These have been arbitrarily divided into infantile, childhood, and adult forms of the disorder.

Infantile atopic dermatitis (seen between birth and one year of age) is characterized by sudden onset of redness, scaling, crusting, oozing, rubbing and scratching.  Lesions typically start on the cheeks and chin and scalp, and then spread to the trunk and extensor aspects of the arms and legs. There typically is sparing of the nose and diaper region. Many infants with atopic dermatitis have difficulty sleeping due to itching.

Photos courtesy of Dermnet NZ

The childhood form of atopic dermatitis (seen between two years of age and puberty) and is characterized by chronic areas of scaly red patches and papules typically on the antecubital fossa (i.e. front of the elbows), popliteal fossa (i.e. behind the knees), ankles and wrists, hands and feet. Facial involvement typically involves areas around the mouth (lip licking dermatitis), around the eyes, and corners of the ear lobes. In patients with darker skin types, atopic dermatitis may manifest as papular or follicular based lesions often with white discoloration (hypopigmentation). As in all forms of eczema, itching is a hallmark of the disease.

Photos courtesy of Dermnet NZ

The adult form of atopic dermatitis (which develops at puberty and extends into adulthood) will usually shows area of chronic scaly red patches on the wrists, hands, neck and ankles, and sometimes involvement on the face, back, and upper arms. Secondary areas of thickening and lichenification may be seen from scratching.

Photos courtesy of Dermnet NZ


Atopic dermatitis in patients with skin of color

Some of the classical signs of atopic dermatitis are less visible in patients with skin of color. Sometimes redness of the skin is hard to appreciate. However, lichenification and follicular accentuation may be more prominent. In addition hypopigmentation (i.e. lightening of the skin color) in active or previous areas of eczema are common and sometimes quite distressing to the patient and his/her family. Fortunately, this discoloration is temporary and will resolve once the eczema is completely controlled.


What is the cause of Atopic Dermatitis?

Atopic dermatitis (AD) is strongly linked to genetics, family history and environmental factors. Approximately 70% of patients with AD have a family history of atopic disease (eczema, allergies, hay fever, or asthma). Many patients with atopic dermatitis have mutations in a gene called Filaggrin, which is essential in forming a normal skin barrier. Recent studies have shown that overactivity of the immune system (TH2 cells via cytokines IL-4 and IL-13) can reduce expression of Filaggrin in patients with no known mutation.

Ultimately patients with AD have an abnormal skin barrier, with an inability to retain water in the skin, and are more susceptible to the penetration of allergens (e.g dust mites) and infections (e.g. staph aureus, molluscum, and warts). Extremes in temperature (e.g. cold weather), low humidity, harsh soaps and detergents, prolonged water exposure, and cigarette exposure can worsen AD.


Treatment of Atopic Dermatitis


There are no official guidelines which dictate the frequency with which patients with atopic dermatitis should bathe. Dr. Singer’s opinion is that patients with eczema (atopic dermatitis) should bathe once or twice daily under the following conditions:

1. The cleanser must be a gentle fragrance free soap-less cleanser. Some suggestions include liquid Dove®, Cerave®, Vanicream® cleansing bar, and Cetaphil® cleanser. (Soaps such as Dial®, Ivory®, Irish spring®, etc. dry out the skin and should be avoided.)

2. The bath or shower should last no more than 10 minutes.

3. Upon exiting the bath or shower, pat dry lightly, trying to keep some water droplets on the skin.

4. Then immediately moisturize with either a cream or ointment (never a lotion) within three minutes of exiting of bathing/showering. – a regimen referred to as “soak and seal.”

Examples of moisturizers include Vaseline petroleum jelly, Aquafor Healing ointment, Cetaphil moisturizing cream, Cerave cream, Vanicream moisturizer, Aveeno eczema moisturizer, etc.

The addition of bleach to the bath water also known as a “bleach bath” has been recently shown to reduce colonization of Staphylococcus aureus on the skin with subsequent reduction of flares of eczema. Dr. Singer may discuss this treatment option with the patient at the time of the visit.

Avoidance of triggers

Eczema may be triggered by a number of environmental factors including extremes in temperature and humidity. During the wintertime, patients with eczema are more prone to dryness due to the lower humidity and cold temperatures. It is especially important to moisturize twice daily during colder months. On the flip side, during the summer it is important to maintain an indoor temperature of 72°F as heat and sweating may exacerbate itch and eczema.

As mentioned above, harsh soaps can trigger eczema. In addition, bubble baths and fragrances should be avoided. To that end, it is advisable to use hypoallergenic detergents that are “free and clear ” and avoid fragranced fabric softener and dryer sheets. Perfumed and fragranced products from Bath and Body Works, Lush, etc. should also be avoided.

It is okay for patients with eczema to swim as long as the exposure to water is not prolonged, and he/she must rinse off immediately after exiting the pool and apply a thick emollient.

In infantile eczema, applying Vaseline to the face before eating may be beneficial.

Cotton clothing is preferable to wool and other harsh textiles.

The role of food allergy in patients with atopic dermatitis is controversial. Although up to 35% of patients with severe eczema have food allergy, only a small percentage of these patients have food allergies relevant to their eczema. Recent studies support early introduction of peanut to reduce the incidence of peanut allergy. Those infants with moderate to severe eczema, however, should probably consult an allergist prior to introduction of peanut.


Complications of Eczema

In addition to disruption of normal daily activities and sleep, disruption of normal family dynamics, and disruption of psychological well being, patients with eczema are prone to secondary infections. Overgrowth of Staphylococcus bacteria has been shown to produce flares of atopic dermatitis. Sometimes oral systemic antibiotics such as cephalexin are necessary to treat obvious secondary bacterial infection. In addition, bleach baths and intranasal mupirocin are sometimes necessary to control bacterial counts on the skin. In addition, patients with atopic dermatitis are also prone to secondary viral infections with molluscum contagiosum and herpes simplex virus. Molluscum contagiosum has been known to flare eczema and spreads with scratching. Herpes simplex virus infection of eczema requires oral or intravenous systemic antiviral therapy. And in addition, some patients with atopic dermatitis may develop a secondary allergic contact dermatitis. to topical creams, cosmetics, nickel, and even to topical steroids.

Steroid Potency Chart

Class I topical steroid (super high potency)
-Augmented betamethasone cream, ointment 0.05%
-Clobetasol dipropionate cream, ointment, foam 0.05%
-Desoximetasone 0.25% spray

Class II (high potency)
-Fluocinonide 0.05% cream, ointment
-Desoximetasone 0.25% cream, ointment

Class III/IV medium potency
-Triamcinilone 0.1% cream, ointment
-Fluticasone 0.005% ointment, cream

Class V (low medium potency)
-Hydrocortisone butyrate 0.1% cream, ointment
-Triamcinilone 0.025% cream, ointment

Class VI topical (low potency)
-Desonide 0.05% ointment, cream, foam
-Aclomethasone 0.05% cream, ointment
-Fluocinolone acetonide 0.01% cream, oil

Class VII (lowest potency)
Hydrocortisone acetate 1%, 2.5% cream, ointment

Treatment of Atopic Dermatitis

Products We Recommend to Treat Eczema






Laundry Detergent



Topical Steroids

Topical corticosteroids (AKA topical steroids) are the first-line therapy for treatment of atopic dermatitis. Many patients and their parents are fearful of using topical steroids due to potential side effects. Local side effects of topical steroids can include thinning of the skin, stretch marks, visible blood vessels, pimples, etc. However, if applied properly, topical steroids rarely produce local side effects. Topical steroids are graded as strong, mid-potency and weak based upon vasoconstrictive assays. Class I topical steroids are consider superpotent and are only indicated for adults and children over 12 years of age. Areas of skin that have been scratched at frequently may require more potent topical steroids. Class VII steroids are considered the weakest and are found in over-the-counter preparations such as 1% hydrocortisone® Cortaid®. Typically class III and IV topical steroids are used on thicker skin regions of the body such as the arms, legs, and trunk. Low potency, class VI and VII topical steroids, are reserved for sensitive skin areas such as the face, armpits, groin and inner thighs. Younger children typically receive lower strength topical steroids. In general, steroids ointments are more effective than creams and lotions because they are more occlusive. In addition, sometimes saran wrap or wet wraps are used to further occlude topical steroids to increase their potency.

What is the proper application of topical steroids?

The topical steroid of the appropriate potency is applied twice daily to active patches of eczema until the site is “itch free and flat.” What does “itch free and flat” mean? – It means that the active areas of eczema are no longer itchy to the patient and they feel smooth to the touch just like normal skin. Even if the skin looks discolored (i.e. lighter or darker in color) it is considered to be “itch free and flat”  as long as it is smooth to the touch and not itching. – At this point, the topical steroid is no longer applied every day. Instead, the patient may be instructed to apply topical steroid to the previous area of eczema twice a week (e.g. Mondays and Thursdays) in order to prevent flaring of the eczema. Twice-weekly application of  appropriate strength topical steroid rarely produces local side effects. The reason is that the skin has a chance to recover during the other five days a week that the topical steroid is not applied.

So the first goal is to calm down active areas of eczema until there is no more itching and the skin is smooth. The next phase of treatment is to maintain clear skin without producing side effects of the topical medications. This may be accomplished sometimes with moisturizers and avoidance of triggers, but other times may require twice weekly topical steroid, or non-steroidal anti-inflammatory medications such as Elidel and Protopic, or newer non-steroid agents such as Eucrisa.

Finally it is important to remember that topical steroids should always be applied before application of moisturizers to ensure that the topical steroid penetrates the areas of eczema properly.

How much topical steroid is appropriate to use on a given site?

In general, a very thin layer of topical steroid is typically applied to the skin, just enough to produce a nice shine to the skin. If one were to squirt a thin strip of cortisone cream from the last crease of the index finger to the tip of the finger (i.e a finger tip unit), this would provide enough cream to cover the size of one hand. It takes about 30 g of cream to cover an entire adult body.


Non-Steroidal Eczema Therapy Elidel and Protopic

A variety of steroid free topical anti-inflammatory agents have been introduced to allow patients to decrease their application of topical steroids and reduce the local side effects of topical steroids. Around 2002, topical calcineurin inhibitors (TCI’s) tacrolimus and pimecrolimus (Protopic and Elidel) became FDA approved for the treatment of atopic dermatitis in children older than two years of age and adults. These agents have a long history of safety and efficacy in patients with atopic dermatitis. Unlike topical corticosteroids, these agents can be used on any body surface area, even thin skin areas such as the groin, axilla and eyelids.

Elidel and Protopic work by inhibiting cytokines responsible for T cell activation. The result is reduction in inflammation and redness of the skin. Elidel and Protopic 0.03% are FDA approved for both active treatment and as maintenance therapy for atopic dermatitis in adults and in children older than two years of age. Protopic 0.1% is FDA approved for patients older than 16 years of age. Elidel and Protopic 0.03% are equivalent in strength to a low potency topical steroids, whereas Protopic 0.1% is equivalent to a mid-potency topical steroid.

Since Elidel and Protopic are not steroids, they do not produce local side effects that topical steroids do such as thinning of the skin, stretch marks, bruising etc. However, these agents have been associated with a stinging and burning sensation upon application which typically improves after using the medication for a week. Sometimes, topical steroids are used for several days first before the application of Elidel or Protopic in order to reduce burning and stinging sensations.

Elidel and Protopic are FDA approved for intermittent use (i.e three times a week long-term) and are best used in conjunction with topical steroids.

In 2006, the FDA issued a black box warning regarding TCI’s and a theoretical increased risk of lymphoma and skin cancer. These risks were mainly based upon patients receiving these medications by mouth for transplantation and in animal studies where 30 times the human dose was used. Many human scientific studies since then have confirmed the safety of these topical therapies. Data over the past 10 years has not shown any increased risk of lymphoma or skin cancer with topical use of Elidel and Protopic. Finally, the American Academy of Dermatology has found no evidence to support the issuance of this black box warning.



On March 25, 2020, the FDA approved Pfizer’s supplemental new drug application for Eucrisa ointment, 2%, for children as young as age 3 months with mild-to-moderate atopic dermatitis. In the study, Eucrisa was well tolerated and demonstrated effectiveness in patients with eczema with no new safety signals identified.

In December 2016, the FDA approved a new boron based phosphodiesterase (PDE-4) inhibitor, Eucrisa, for the treatment of mild to moderate atopic dermatitis in adults and children older than two years of age.

Eucrisa works by inhibiting phosphodiesterase, an enzyme responsible for indirectly activating T cells in atopic dermatitis. The potency of Eucrisa is probably similar to that of Elidel and Protopic (TCI’s). Eucrisa produces no local steroid side effects such as thinning of the skin, stretch marks or bruising. The main side effects are burning and stinging, particularly noticed when used on the eyelids. Similar to the TCI’s, Eucrisa is probably best used in combination with topical corticosteroids.

In December 2016, the FDA approved a new boron based phosphodiesterase (PDE-4) inhibitor, Eucrisa, for the treatment of mild to moderate atopic dermatitis in adults and children older than two years of age. Eucrisa works by inhibiting phosphodiesterase, an enzyme responsible for indirectly activating T cells in atopic dermatitis. The potency of Eucrisa is probably similar to that of Elidel and Protopic (TCI’s). Eucrisa produces no local steroid side effects such as thinning of the skin, stretch marks or bruising. The main side effects are burning and stinging, particularly noticed when used on the eyelids. Similar to the TCI’s, Eucrisa is probably best used in combination with topical corticosteroids.

Systemic Therapy

For those patients with moderate to severe disease, those who are unresponsive to topical and preventative therapies, or those with extensive body surface area involvement (>10% BSA), systemic therapies are often necessary to control atopic dermatitis.

Narrowband UVB, which is frequently used for treatment of psoriasis, has been shown in some studies to be an effective treatment option in atopic dermatitis as well. Light therapy is required 2 to 3 times a week and the patient must protect the eyes and genital area from exposure to light. In addition, long-term maintenance therapy is required. Those with fair skin and blue eyes are at higher risk for long-term effects of light treatment.

Traditional systemic agents such as cyclosporine, methotrexate, and mycophenolate mofetil have been used off label for decades to treat severe atopic dermatitis in children and adults. These treatments may produce substantial improvement of atopic dermatitis; However, these agents also may lead to immune suppression, bone marrow suppression, liver and kidney damage, hypertension, and potentially increase the risk for secondary infection and malignancy.


More recently, improved understanding of the pathogenesis of atopic dermatitis has spurred the development of a new, safe and effective systemic treatment that appears to specifically target the underlying cause of atopic dermatitis. Dupixent, an inhibitor of the IL-4 receptor alpha subunit, inhibits signaling of TH2 cytokines IL-4 and IL-13.

Dupixent is the first systemic FDA approved therapy for moderate to severe atopic dermatitis. It was approved in 2017 for use in adults 18 years of age and older, and studies are currently being conducted to evaluate the safety in pediatric patients as young as 6 years of age. In the “SOLO 1” and “SOLO 2” studies, approximately 37% of patients with moderate to severe atopic dermatitis were clear or almost clear after 16 weeks of therapy and about half the patients noticed 75% improvement from baseline.

Unlike traditional systemic therapies, patients enrolled on Dupixent in the SOLO 1 and SOLO 2 studies showed no significant increased risk of systemic infection, lymphoma or other serious adverse events.

The most commonly reported adverse events in the treatment groups were injection site reaction (temporary redness and swelling) and conjunctivitis (eyelid swelling). No patients dropped out of the study because of an injection site reactions; one patient discontinued because of conjunctivitis.

Patients who start Dupixent should plan on remaining on this medication indefinitely as there is currently no cure for atopic dermatitis.


1. Paller, Amy S and Mancini T.; Hurwitz Clinical Pediatric Dermatology 4th edition
2. Eichenfeld LF, Stein Gold LF. CME supplement to Dermatology News; Meeting the Challenge of Atopic dermatitis from Infancy to Adulthood released April 2017
3. Eichenfeld et al. Guidelines of care for the management of atopic dermatitis, Section 2. Management and treatment of atopic dermatitis with topical therapies. JAAD 2014;71 116-132
4. Simpson EL et al. SOLO 1 and SOLO2 investigators. New England Journal of Medicine 2016; 375; 2335 – 2348


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