Differentiate, diagnose, and treat the various forms of dermatitis and stop the ‘itch that rashes’ with this in-depth, myth-busting episode of “The Dermsiders” with Dr. Kalman Watsky Clinical Professor of Dermatology at Yale Medical School. Topics include: how to differentiate between and diagnosis various forms of dermatitis, topical therapies, common pitfalls, patch testing, and more! Special thanks to Bryan Brown and Beth Garbitelli who wrote and produced this episode and the show notes!
Written by: Bryan Brown, MD and Beth Garbitelli
Edited by: Matthew Watto, MD
Infographics by: Bryan Brown, MD
Cover image by: Beth Garbitelli
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Case from Kashlak Memorial:
A 45-year-old man with a history of childhood eczema and asthma, but asymptomatic during young adulthood, now presents with two months of itchy scaly rash of the bilateral upper extremities, including the palms. He works as a cement mixer during the day, and washes dishes for a restaurant at night. On exam, there is flaking skin in his bilateral palms, and red pruritic patches scattered on his forearms.
Pre-test Questions (click link below)
Boost retention! Test yourself before and after listening.
How to Describe a Derm Lesion:
1) LOOK AT LESION THOROUGHLY AND DESCRIBE VIVIDLY.
Stop calling everything maculopapular! Important to describe lesions with accurate medical language. A vivid description allows both the internist and the dermatologist to develop a differential.
2) USE MEDICAL TERMS.
‘Flaking skin’ is not a medical term, doctors should be more specific. Is it desquamating? Is the skin flayed? Is this superficial desquamation? Is there adherent scale? Is there crust? The term ‘flaking’ fails to indicate any of these specifics.
3) USE DESCRIPTORS, NOT SYMPTOM
Determine if flat or elevated. Identify size
Flat lesions: macule (<1cm) or patch (>1cm)
Elevated lesions: papule (<1cm) or plaque (>1cm)
Identify the primary lesion
For example, if you have mostly macules, it can be called a macular eruption.
(Note: You may have both macules and papules, but uncommon)
Note any presence of blood in skin
Petechiae: Superficial bleeding.
Purpura: More confluent, deeper bleeding.
Ecchymosis: Blood pooled under skin.
Describe any blistering and fluid type/color
Vesicle: small, fluid-filled blister, generally <1cm
Bulla: slightly larger, fluid-filled blister, generally >1cm
Catalog Secondary Lesions
Identify signs of pruritus. E.g. excoriations (linear erosions), lichenification (thickened skin). Hyperkeratosis is a pathologic term
Atopic Dermatitis vs. Eczema: Eczema and Dermatitis mean essentially the same thing: inflamed skin. Modify them with additional terms e.g. Atopic dermatitis, contact dermatitis, etc.
Definition of Atopic Dermatitis: Process that begins in childhood, may be genetic and involves two main features. Tends to be associated with asthma and seasonal allergies.
1) Barrier Function Problem: Stratum corneum with increased permeability. Small fissures lead to excessive dryness and scratching. “The itch that rashes”.
2) Immune Dysregulation: Causes over reaction to antigens. Often associated with asthma and seasonal allergies.
How to Treat Atopic Dermatitis?
What are the Mimics of Atopic Dermatitis?
NOTE: Patients with atopic dermatitis are at higher risk for contact dermatitis. Contact and atopic dermatitis often coexist.
Seborrheic dermatitis: Dandruff on scalp, and red scaly patches on central part of face, nose, eyebrows, chest. Clinical diagnosis is based on distribution and loose, greasy scale. Consider diagnosis of HIV in severe or refractory cases. Also has association with Parkinson’s.
Pityriasis rosea: Lesions are discrete. Initial lesion is large/solitary, round/oval, scaly patch or plaque. Subsequent lesions are numerous, scattered and generally follow the relaxed skin tension lines. Self-limited disorder, likely caused by virus. Can be mistaken for tinea.
Tinea (Ringworm) and Fungal Infections: Can use a KOH test (potassium hydroxide preparation). Distribution is helpful: Rashes tend to be in groin, soles of feet, interdigital spaces, toenails.
Lichen Planus: Purple, polygonal, papular, pruritic. Lesions are typically on wrists and ankles, but can be in other areas.
Psoriasis: Lesions are more brightly red, scale very characteristic: ivory white scale called micaceous scale. Scale is tightly adherent and bleeding points can be seen if plucked (Auspitz sign)
Stasis dermatitis: Typically on lower extremities. Patients will present with red, scaly areas overlying edema. Often hyperpigmented.
What is dyshidrotic eczema?
It’s a clinical phenotype, not a true entity, with tiny vesicles on the lateral aspects of the digits. May be seasonal, intermittent and made worse by environmental exposures. It can exist independent of other types of dermatitis, but usually present in patient with history of atopic dermatitis.
Behavior modification for Atopic Dermatitis
Be mindful of handwashing frequency and type of soap used. Pat dry after bathing (don’t rub) and moisturize while skin is damp. Moisturize at night and wear loose fitting plastic gloves to bed.
Can the wild wet pajama trick work for full body eczema?! Dr. Watto describes a technique used which involved a patient with scaly rash slathering up in emollient and then dressing in wet pajamas before bed. Yes, it can work! Especially for children, or in a hospital setting.
Open Wet Dressing: Take a single thickness cotton sheet, soak in water, ring out so damp and add over affected body part. Allow to evaporate. Will take the heat out of a dermatitis before adding moisturizer. Good for localized dermatitis e.g. face.
Occlusive Therapy: Add clothing on top of where you apply the topical.
NOTE: Cotton is more absorptive than skin. So advise patients to use rubber or latex gloves for overnight hand therapy.
What about bleach baths? No more effective than plain water in relieving symptoms of dermatitis, but good for decolonizing Staph infections. Superinfection common since skin barrier impaired.
Contact dermatitis can be endogenous, or exogenous (primarily caused by external factors).
Allergic contact dermatitis requires a genetic predisposition (endogenous), but irritant contact dermatitis does not (exogenous).
Irritant Contact Dermatitis: Anyone can get this. Although, people with a barrier issue (i.e. atopic dermatitis) are more susceptible.
Allergic Contact Dermatitis: Only occurs once patient has been sensitized to an allergen. Requires a genetic predisposition. We cannot predict who will become allergic with exposure. Poison ivy, nickel, and chromate (found in cement in US) are strong sensitizers compared to other allergens.
Phototoxic dermatitis: Photo activated chemical produces an exaggerated sunburn e.g. certain types of weeds
Photoallergic dermatitis: Allergy to a given chemical is activated by sun exposure e.g. sun block.
Psoralens = photosensitizing agents.
Patch Testing Basics
What’s patch testing and when should it be used? To identify allergens that are responsible for type 4 hypersensitivity reactions (allergic contact dermatitis). Does not identify immediate hypersensitivity reactions. Technique requires lots of experience for proficiency. There are kits available for dermatologists that can test up to 36 allergens, there are some that have have 65, 80, even 100+ allergens.
Who merits patch testing? 1) Patient with new, severe, or recurrent dermatitis. 2) Change in status of character of chronic atopic dermatitis. (E.g. Patient has atopic dermatitis and every winter, they develop some hand dermatitis. But they suddenly develop new severe dermatitis on face or other part of body) 3) Patient who suspects they have a product allergy. 4) Dermatitis impairing livelihood (E.g. Dental worker suspicious they have a contact allergy to something at work)
Note on Case Study: Likely an irritant component to diagnosis. Cement mixing is known to cause sensitization to chromate.
What are the topical treatments for dermatitis?
Topical steroids come in a range of potencies: high, medium, low
We grade potency from class 1 (most potent) to class 7 (least potent)
Be comfortable with a high potency steroid but know when/where to use it. High potency steroids can cause skin atrophy and other serious side effects, including suppression of the HPA access (especially if used over large area). Always have a course of time for use for these types of steroids.
High Potency Steroid Examples
CLASS 1 EXAMPLE: Clobetasol. Useful, widely available as cream, ointment, solution or lotion. Good for thick skin of hands and feet. NEVER use Class 1 agent on skin folds, face or genitals.
CLASS 2 EXAMPLE: Betamethasone. Note: Betamethasone+clotrimazole is a combination steroid/antifungal. While clotrimazole is safe for use in skin folds, betamethasone is a potent steroid and can cause ulceration/skin thinning. Avoid this combo!
How quickly can skin thinning from potent steroid occur?
Skin thinning can happen within a week on delicate skin. Generally takes several weeks. Emphasize risks to patients in clear terms. NEVER use super potent steroid to treat folds.
Medium Potency Steroid Example
Triamcinolone- range of concentrations (0.1, 0.5, 0.025%) and available in a 1 lb jar, good to manage large rash. Inexpensive. Available in multiple formulations: cream, ointment, and lotion. Should be workhorse for most.
Low Potency Steroid Example
Hydrocortisone- 2.5 %, slightly stronger than OTC (1%), go-to for low potency
Does Carrier Molecule of steroid matter?
Yes. Carrier molecule can matter as one can have allergic contact dermatitis to the actual moiety/active ingredients. There are certain steroids that have a lower risk for allergic dermatitis. Worth noting that Triamcinolone is not considered a lower risk for allergic reaction. If a patient has a steroid responsive condition and they do not improve with topical steroid, you may need to consider they had allergic reaction to the steroid (and/or that they do not have a steroid-responsive condition…) Hydrocortisone also can have allergic contact dermatitis but it is still a rare condition.
Re: calcineurin inhibitor black box warning:
Some patients tested in clinical trials with calcineurin inhibitors developed T-cell lymphoma. In actuality, the patients enrolled in these trials did not have atopic dermatitis, they had cutaneous T-cell lymphoma, which is a mimic for atopic dermatitis. They did not get better and the medication became implicated because it DOES suppress T-cells.
Takeaways for calcineurin inhibitors: Tacrolimus and pimecrolimus are incredibly useful, but first use a topical steroid to calm dermatitis and then transition patient to calcineurin inhibitor. Patients are much more likely to tolerate the calcineurin inhibitors after passing the acute phase. Cost, black box warning, and burning sensation are barriers.
When would you move to calcineurin inhibitor versus a stronger topical steroid?
Depends on location. Calcineurin inhibitors are not necessarily stronger than a topical steroid. Calcineurin inhibitors work best on thin skin e.g. face, skin folds, genitals. Ineffective for hand dermatitis. Note: Calcineurin inhibitors burn for first few applications until substance P is depleted. Must warn patients about this barrier to use.
Are ointments better than creams?
Not necessarily. Medication that patient will use is best. Be flexible in delivery. Potency not hugely different.
Chronic Dermatoses: How long does it take for it to clear up?
Continuous use of topical steroids is not recommended. Ask patients how long it takes for dermatitis to clear up and how long it takes to come back once off therapy. Intermittent use works and is generally safe (twice weekly or once a week) Example: Dermatitis flares up after 10 days, then may work to have patient use topical use once a week.
What if a single lesion doesn’t resolve?
Suspect cancer if solitary skin lesion fails to resolve despite 1 month of topical therapy. Inform patient that if a discrete lesion is not completely gone in a month, they will need to be tested further.
What about oral steroids?
Use 10-15 days of oral steroids if an allergic contact dermatitis (i.e. poison ivy) affects larger than 15 percent of body surface area OR severe regional disease (face, hands, feet, groin, eyes, ears). Note: Quick taper (e.g. 5 days) will result in rebound and patient will return with worsening symptoms. Start at 60 mg (or 1mg/kg), then taper e.g. 60 mg → 40mg→ 20mg, 5 days per dosage.
Thoughts on PUVA for atopic dermatitis?
Phototherapy is very helpful. Narrowband UVB = current industry standard and has mostly supplanted PUVA. UVB = safe and effective for atopic dermatitis. Consider phototherapy if dermatitis is widespread and not responsive to topicals or steroid taper. Ensure patch testing to rule out allergic contact dermatitis.
Is CeraVe better than Vaseline?
Patient preference is important. Barrier repair creams do seem to have advantage over pure emollients. Products that contain ceramides and/or dimethicone may be superior to petroleum products.
Take Home Points
Disclosures: Dr Watsky is a contributor to Up-To-Date. The Curbsiders report no relevant financial disclosures.
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