Eczematous Dermatitis

Clinical Overview of Eczema/
Rich Callahan MSPA, PA-C
ICM I – Summer 2009
• Eczema and dermatitis are two different words
which essentially have the same meaning:
Inflammation of the epidermis and dermis.
• This group of diseases includes Atopic Dermatitis,
commonly known as “eczema” or “winter dry
• All diseases in this group share the primary
characteristics of pruritis, inflammation and
disruption of the skin barrier.
Eczematous Dermatitis is a family of diseases
• Non-allergic, or irritant Contact Dermatitis
• Allergic Contact Dermatitis (ACD)
• Atopic Dermatitis, or “Eczema”
• Lichen Simplex Chronicus (LSC)
• Seborrheic Dermatitis (Dandruff)
• All primarily characterized by pruritis,
inflammation and scratching.
Other Diseases in the Group
• Nummular Eczema: A variant of Atopic Dermatitis
• Dyshidrosis: A vesicular form of hand dermatitis which
often affects patients with a history of atopic dermatitis.
Can be precipitated by stress.
• Asteatotic Eczema and Stasis Dermatitis: Both are
pruritic, eczematous eruptions primarily affecting the
lower legs of elderly patients.
• Contact Urticaria: Hives brought on by contact with a
• We will focus on the more common diseases for this
Dermatitis presents in many different ways
• Moderate to Severe – Well-defined, erythematous and
edematous plaques with superimposed vesicles, weeping
erosions and crusts.
• Mild to moderate – Less defined, mildly erythematous to
pink plaques with dry adherent scale, superficial
desquamation (skin looks peeled off). Sometimes also has
pink to erythematous papules mixed in.
• Chronic – Pink to purple, thickened, lichenified papules
and plaques. Lesions can be quite hyperpigmented in
darker-skinned individuals. Constant scratching is the
main driving force with these lesions.
Urticaria (hives)
• Urticaria means an outbreak of wheals (hives)
which are caused by contact with an irritant (nonallergic) or an immunologic antigen (allergic.)
• Wheals are essentially areas of localized edema in
the deep dermis which show at the skin surface as
relatively featureless bumps. As you would
expect, there are no epidermal changes apparent.
• Urticaria can be caused by both external contact
with a substance, or internal ingestion.
(Non-allergic or Irritant Contact Dermatitis)
• Comes from exposure to any irritating substance, and can
happen to anyone. Mediated by the substance’s direct
toxicity to skin cells.
• Can occur immediately after a patient’s first exposure to
the substance, or can take months to develop over the
course of repeated exposures.
• Patients who do a lot of “wet work” either at home or on
the job are especially predisposed to contact hand
dermatitis as frequent wetting/drying of the hands leads to
breakdown of the skin barrier and better penetration of
irritating substances.
ICD: Clinical Presentation
• Large variance in clinical presentation:
• Mild/Early: Pink to mildly erythematous patches, or
slightly raised papules and plaques. Lesions may/may not
be scaly or vesicular. Can be distributed randomly or
present in a symmetrical pattern (I.e., if a patient develops
ICD from the dye in a new pair of sandals, you could see
ICD lesions develop in the pattern the straps make across
the top of the foot.)
• Severe/Late: Eroded, crusted, fissured patches and plaques
which frequently bleed and become secondarily infected.
Just about any substance can cause contact dermatitis
in the right individual, but here’s a short list of
frequent culprits:
• Croton oil, kerosene, gasoline,
detergents of all kinds,
cinnamic, sorbic and benzoic
acids, insect stings, moths,
nickel, polyethylene glycol,
animal keratin (hairs.) Also
includes many ingredients in
common household and
industrial products. Always
suspect sizing chemicals in
unwashed new clothing. This is
but any tiny sample of the
potential list.
• Clinical Pearl: Topical
antibiotics are common
contact irritants! Approx.
1/10 of my patients have
some sensitivity to
neosporin and 1/20 to
Bacitracin and Polysporin
almost never. Confusing
this with bacterial
infection can lead to
unnecessary antibiotic
prescriptions. Switch to
straight vaseline when this
These cases of ICD often require some detective
work to figure out – Clinical Case Example:
• Referred by PCP, 52 y/o male city municipal employee presents with
recurrent, chronic bilateral hand dermatitis characterized by patches of
dry, fissured, desquamated (peeling) skin which were prone to
bleeding and secondary infection.
• On physical exam lesions were discrete and affected both palms in an
asymmetric pattern which suggests chronic contact with a specific
• The patient mostly operates the same truck, which is a snowplow in
the winter. His truck “dumps a lot of salt.”
• I had him show me how he habitually holds the steering wheel, and the
areas of dermatitis directly corresponded to where his hands would
touch it.
Hand Dermatitis – The Plot Thickens!
• Through further questioning we found that this problem
started when the city switched to a new road salt, which he
called “magnesium chloride.”
• In the winter, his hands were in constant contact with this
substance while at work, and he had never cleaned the
steering wheel of the truck. Steering wheel described by
patient as “totally dirty with caked-on grime.”
• Treatment included cleaning the steering wheel, always
wearing gloves when in contact with road salt, a course of
topical steroids.
• The Problem resolved approx. 1 months later.
ACD – Clinical Presentation
• Poison Ivy is the classic example: Gradual, random
development of intensely pruritc papules, vesicular plaques
and outright groups of vesicles (blisters) which quickly
erode into weepy, crusted lesions.
• Tends to be randomly distributed in cases of contact with
plants, liquids/powders, etc.
• Tends to be arranged in a symmetric pattern when
secondary to chronic contact with offending substances in
clothing or footwear.
Allergic Contact Dermatitis
• Poison Ivy is the classic example – a type of delayed type
IV hypersensitivity in which a strong sensitizer (like the
urushiol resin in poison ivy) is recognized and taken up by
Langerhans cells in the epidermis, which then process the
urushiol and present it as an antigen to specialized T-cells.
The activated T-cells then multiply and spread throughout
the entire body, sensitizing all skin surfaces to the
offending contactant.
• This is why p. ivy can give the illusion of “spreading” over
a period of several weeks, leading patients to think they are
getting new exposures.
Poison Ivy dermatitis does not spread from one part
of the body to another.
• The main property of urushiol that makes it such an effective
contactant is that the molecule has qualities that allow it to penetrate
the skin easily to a depth of about 1mm, and then adhere to
surrounding cells.
• People often don’t recognize they were in poison ivy until way too
late, and the oily resin spreads around so well from one object (animate
or inanimate,) to another that diverse and scattered areas of the body
can become involved.
• The hypersensitivity reaction proceeds in a gradual progression around
the body, seeming to focus on one area, and then move on to
previously unaffected areas.
• This is why it can start on the face, move to the chest 3 days later and
then to the legs 7 days later.
Atopic Dermatitis aka “Eczema”
• An inherited disorder usually accompanied by
personal/family history of allergic rhinitis, asthma and hay
• Characterized by chronically dry, itchy skin which gets
scratched/rubbed, breaking down the skin barrier and
increasing susceptibility to contact allergens, bacteria and
• Usually first presents before the age of 12, but can rarely
start in adulthood also.
• Often chronic over periods of months to years.
Atopic Dermatitis – Clinical Presentation
• When it comes on acutely: Widespread erythematous
patches, papules and plaques which are often excoriated
and weeping/crusting. Lesions are often scaly.
• When it’s chronic: Affected areas become thickened and
lichenified (skin markings are accentuated.) Over a period
of time, hypopigmentation, fissuring and cracking can
• In any case, it’s always itchy. Pruritis is the hallmark of
this disease, and because they’re human, patients are
inevitably lead to scratch and exacerbate their condition.
Atopic Dermatitis – Clinical Presentation
• Usually involved areas are ears, face, eyelids, occipital
scalp/posterior neck, ventral upper extremity (especially in
antecubital regions,) lower legs, popliteal fossae and dorsal
• Can be a child with a new diagnosis, or an adult already
experienced with the disease.
• Usual flare precipitants include stress and onset of cold
weather (heat turns on, inside humidity drops, TEWL
(transepidermal water loss) increases, skin dries out and
becomes itchy, patient starts scratching.)
Clinical Pearl: Tinea Incognito –Fungus
masquerading as something else
• If it scales, scrape it: If you are questioning the diagnosis
in a new patient and the lesions have scale, it is always a
good idea to scrape it and prepare a KOH slide.
Occasionally you will find fungus either masquerading as
atopic dermatitis or exacerbating an already existing case.
• Also suspect bacterial colonization in all severe cases that
respond poorly to treatment or show symptoms and signs
suggestive of infection. Topical and oral antibiotics may
be necessary.
Clinical Presentation – Lichen
Simplex Chronicus
• Often secondary to chronic Atopic Dermatitis.
• Lesions present as lichenified, thickened, well-defined
plaques, occasionally scaly, and violaceous to pink color.
• Lesions often brown or black in darker-skinned patients.
• Driving force formation of LSC is repeated scratching –
lesions of crusted and excoriated from recent picking.
• Lichenified lesions become hypersensitive over time –
lesions itch at the slightest provocation and patients will
admit taking great pleasure in itching them.
• Male = Female. Any age.
Clinical Presentation – Asteatotic
• Usually presents in elderly patients, especially those in
nursing homes, on arms, legs, hands and occasionally on
• Used to be called “eczema craquele” or “marred with
cracks” because skin acquires a cracked-china appearance.
• Primary precipitating factors are low indoor relative
humidity and over bathing/over washing of the skin.
• Lesions are erythematous-to-pink, dry, scaly patches and
plaques with “crazy pavement” skin markings. Lesions
usually excoriated. Extreme pruritis.
Clinical Presentation - Dyshidrosis
• Dyshidrosis is a vesicular form of hand (and occasionally
foot) dermatitis. Patients often have prior history of AD.
• Tends to occur in acute episodes lasting 2-3 weeks each.
Often chronic over months to years.
• Presents as crops of tiny translucent papules and vesicles
on all hand surfaces, which develop over several weeks,
rise to the surface and rupture. Secondary cracking,
peeling and fissuring are the rule.
• Lesions tend to have a classic “tapioca pearl” appearance.
Patients often describe burning, itching and tingling.
• Usually seen in adults. Men = Women.
Clinical Presentation of Seborrheic
• Pruritic, scaling dermatitis occurring in areas of skin rich
in sebaceous glands: Face, scalp, ears and sternum.
• Usually chronic and recurrent over long periods of time.
• Men = Women. First episodes in childhood/teenage yrs.
• Lesions present as erythematous papules and plaques with
loosely adherent yellowish, greasy scale. Scale can be
gently peeled back to reveal raw, erythematous skin.
• Etiology not entirely understood, but thought to be related
to over activity of the yeast Malassezia furfur accompanied
by excessive inflammatory response to its presence.
Diagnosis of Eczema/Dermatitis
• Almost always a clinical diagnosis based on patient history
and PE.
• Rarely biopsy is needed to diagnose cases with atypical
• Patients with Atopic Dermatitis are usually easy to sort out
because they often already have a chronic history of the
disease and other features that go along with it like hay
fever, allergic rhinitis and history of asthma.
• If it scales, scrape it.
Diagnosis of Eczema/Dermatitis
• In cases of chronic ICD and ACD where poison ivy is not
the obvious culprit, allergy patch testing may be necessary
to find out what’s causing it.
• In these cases it is critical to take a good, thorough history
focusing on all skin contactants: Soaps, detergents, fabric
softeners, moisturizers, new household/workshop
chemicals, shaving cream/aftershave, perfumes, bug
sprays, chemicals at work, etc. Also watch for history of
recently trying on/wearing new clothes that have never
been washed (sizing chemicals,) and heavily colored/dyed
clothing warn next to skin on hot day.
• The basic principles of treatment apply to all forms of
eczema/dermatitis, as outlined below. Specific variations
will be pointed out.
• Treatment is geared towards reducing inflammation first
and foremost, with secondary goals of
• Improving skin hydration/skin barrier through treatment
and personal habits.
• Preventing/treating secondary infection.
• Decreasing pruritis
• Decreasing picking/scratching which can perpetuate
lesions in some cases.
• Topical Steroids are first line (Classes 1-7.)
• Moisturizing emollients. (New line of Rx non-steroidal
anti-inflammatory emollients including Mimyx and
• AD patients need thorough education on appropriate
bathing, moisturization, humidification and avoidance of
trigger factors.
• Interventions include short, tepid showers with moisturizer
application immediately after bathing. Limit soap use to
• Non-steroidal topical anti-inflammatories: tacrolimus
(Protopic) and pimecrolimus (Elidel.) Inhibit cutaneous
activity of T-Cells. Often used in place of topical steroids
when development of skin atrophy is an issue.
• Oral/IM steroids. (Don’t under treat poison ivy!)
• Immunosuppressants: Cyclosporine and mycophenolate
mofetil. Potent drugs with risk/SE profiles – only for cases
of severe, refractory AD.
Specific Treatments
• Seborrheic Dermatitis – topical steroids will clear, but
quickly recurs when steroids are withdrawn, leading to
dependence and skin atrophy issues. Only exception is
scalp, where pulsed treatment with Class 1 topical steroids
can provide long-term improvement.
• Better treatment strategy is decreasing population of M.
furfur yeast and exfoliating the oily scale that it lives in.
• Selenium sulfide 1-2.5% shampoos.
• Sodium sulfacetamide/Sulfur creams
• Ketoconazole shampoos.
Specific Treatments
• Lichen Simplex Chronicus (LSC) - #1 goal is get the
patient to stop scratching. If they stop scratching, will
clear in 4-6 weeks. This is easier said than done.
• Flurandrenolide (Cordran) tape – steroid-impregnated tape
worn over lesions for 12-24 periods of time, 7 days/week,
2 weeks on/1 week off. Has dual function of protecting
lesions from direct contact and delivering steroid.
• Need to break the itch/scratch cycle for any kind of
improvement to occur.
• Nocturnal scratching patients may need to wear cotton
gloves to bed.
Specific Treatments
• Dyshidrosis – First line is Class 1 topical steroid ointment
under plastic wrap occlusion at qhs; 2 weeks on/1 week
off. Acutely vesicular cases may need Burrow’s dressings
to desiccate lesion.
• In severe cases, occasionally use oral/IM steroids.
• Rarely strong immunosuppressants needed to return patient
back to ADL’s. (Cyclosporine.)
• Always be on the alert for secondary infection by
opportunistic organisms (bacteria/fungus.) Topical
steroids/oral steroids/immunosuppressants treat the
inflammation of dermatitis, but also dampen the body’s
immune response to foreign invaders. Topical steroids =
miracle grow for fungus.
• Watch for signs including excessive erythema/edema,
tenderness to palpation, pus-like exudate and/or history of
rapid worsening in one area in short period of time.
• Don’t be afraid to perform bacterial cultures/KOH for
fungus if indicated clinically!
Clinical Pearl: Be wary of treating
anything you haven’t seen!
• Here’s a clinical case example that will illustrate secondary
infection of eczema, and drive home an important lesson:
Be wary of treating anything you haven’t seen.
• CF was a 22 year old male with long history of Atopic
Dermatitis since childhood. He was a typical case with
concurrent history of hay fever, allergic rhinitis, multiple
environmental allergies and active asthma needing daily
use of an inhaler.
• I had been treating him for 6 months for a chronic,
stubborn patch of AD on his left dorsal foot.
Clinical Pearl: Be wary of treating
anything you haven’t seen!
• The lesion was scraped for KOH at his first visit and no
fungal elements were seen.
• He was treated chronically with clobetasol 0.05% ointment
at qhs, 2 weeks on/1 week off.
• We had also recently treated with a short course of oral
prednisone with excellent improvement.
• After not having seen the patient for several months, we
get an urgent phone call from his wife, stating “the rash on
the top of his left foot is really bad again, can you call in
some more prednisone.”
Clinical Pearl: Be wary of treating
anything you haven’t seen!
• I called CF’s wife back for more information. On
further questioning, she recounted a history of
sudden, severe worsening of the rash. She said that
“his toes are purple and his foot hurts to walk on.”
• What I was hearing on the phone was more
consistent with infection than severe flare of AD.
• I told her I needed to see him within 24 hours, and
had the receptionist make a slot for him at the end
of the next day.
Clinical Pearl: Be wary of treating
anything you haven’t seen!
• The patient came the following day, removed his Italian
leather boots (not a lot of air exchange in there) and
showed me his inflamed, purple left foot.
• There was a large, scaly erythematous patch with a hint of
raised border and central clearing (a characteristic of Tinea
Corporis, or “ringworm.”) It was in the same place where
his chronic AD patch had been.
• Entire left foot was tender to palpation; arterial pulses
palpably stronger compared with other foot. Toes had a
dusky, violaceous color although cap refill in all digits was
Clinical Pearl: Be wary of treating
anything you haven’t seen!
• Dry scale was scraped around the periphery of the lesion with a #15
blade, placed on a glass slide w/1 drop KOH.
• Prep was heated and viewed under the microscope.
• It was immediately obvious that the specimen was loaded to the gills
with fungal hyphae – a sign of severe infection.
• Patient treated with oral terbinafine (Lamasil) for 14 days which
cleared the rash and all symptoms.
• Now think what would have happened if I had just called in
another prescription for prednisone instead of having the patient
come back in. (Active infection + potent oral immunosuppressant =
potential catastrophic worsening of infection.)