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Pediatric Considerations

Increased incidence of positive patch testing due to better delayed hypersensitivity reactions (3)

ETIOLOGYAND PATHOPHYSIOLOGY

Hypersensitivity reaction to a substance generating cellular immunity response (4)

Plants

–Urushiol (allergen): poison ivy, poison oak, poison sumac

–Primary contact: plant (roots/stems/leaves)

–Secondary contact: clothes/fingernails (not blister fluid)

Chemicals

–Nickel: jewelry, zippers, hooks, and watches (5)

–Potassium dichromate: tanning agent in leather

–Paraphenylenediamine: hair dyes, fur dyes, and industrial chemicals

–Turpentine: cleaning agents, polishes, and waxes

–Soaps and detergents

Topical medicines

–Neomycin: topical antibiotics

–Thimerosal (Merthiolate): preservative in topical medications

–Anesthetics: benzocaine

–Parabens: preservative in topical medications

–Formalin: cosmetics, shampoos, and nail enamel

Genetics

Increased frequency of ACD in families with allergies

RISK FACTORS

Occupation

Hobbies

Travel

Cosmetics

Jewelry

GENERALPREVENTION

Avoid causative agents.

Use of protective gloves (with cotton lining) may be helpful.

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DIAGNOSIS

HISTORY

Itchy rash

Assess for prior exposure to irritating substance.

PHYSICALEXAM

Acute

–Papules, vesicles, bullae with surrounding erythema

–Crusting and oozing

–Pruritus

Chronic

–Erythematous base

–Thickening with lichenification

–Scaling

–Fissuring

Distribution

–Where epidermis is thinner (eyelids, genitalia)

–Areas of contact with offending agent (e.g., nail polish)

–Palms and soles relatively more resistant, although hand dermatitis is common

–Deeper skin folds spared

–Linear arrays of lesions

–Lesions with sharp borders and sharp angles are pathognomonic.

–Well-demarcated area with a papulovesicular rash

DIFFERENTIALDIAGNOSIS

Based on clinical impression: appearance, periodicity, and localization

Diffuse bullous or vesicular lesions

– Bullous pemphigoid Groups of vesicles

– Herpes simplex Photodistribution

– Phototoxic/allergic reaction to systemic allergen Eyelids

– Seborrheic dermatitis Scaly eczematous lesions

– Atopic dermatitis

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–Nummular eczema

–Lichen simplex chronicus

–Stasis dermatitis

–Xerosis

DIAGNOSTIC TESTS & INTERPRETATION

Diagnostic Procedures/Other

Consider patch tests for suspected allergic trigger (systemic corticosteroids or recent, aggressive use of topical steroids may alter results).

Test Interpretation

Intercellular edema Bullae

TREATMENT

GENERALMEASURES

Remove offending agent:

–Avoidance

–Work modification

–Protective clothing

–Barrier creams, especially high-lipid content moisturizing creams (e.g., Keri

lotion, petrolatum, coconut oil)

Topical soaks with cool tap water, Burow solution (1:40 dilution), saline (1 tsp/pt water), or silver nitrate solution

Lukewarm water baths

Aveeno oatmeal baths

Emollients (white petrolatum, Eucerin)

MEDICATION

First Line

Topical medications (5)[A]

–Lotion of zinc oxide, talc, menthol 0.15% (Gold Bond), phenol 0.5%

–Corticosteroids for ACD as well as ID

High-potency steroids: fluocinonide (Lidex) 0.05% gel, cream, or ointment TID–QID

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Use high-potency steroids only for a short time and then switch to lowor medium-potency steroid cream or ointment.

Caution regarding face/skin folds: Use lower potency steroids, and avoid prolonged usage. Switch to lower potency topical steroid once the acute phase is resolved.

Calamine lotion for symptomatic relief

Topical antibiotics for secondary infection (bacitracin, erythromycin) Systemic

–Antihistamine

Hydroxyzine: 25 to 50 mg PO QID, especially useful for itching

Diphenhydramine: 25 to 50 mg PO QID

Cetirizine 10 mg PO BID–TID

Corticosteroids

–Prednisone: Taper starting at 60 to 80 mg/day PO, over 10 to 14 days.

–Used for moderate to severe cases

–May use burst dose of steroids for up to 5 days

Antibiotics for secondary skin infections

–Dicloxacillin: 250 to 500 mg PO QID for 7 to 10 days

–Amoxicillin-clavulanate (Augmentin): 500 mg PO BID for 7 to 10 days

–Erythromycin: 250 mg PO QID in penicillin-allergic patients

–Trimethoprim-sulfamethoxazole (Bactrim DS): 160 mg/800 mg (1 tablet)

PO BID for 7 to 10 days, in suspected resistant Staphylococcus aureus Precautions

–Antihistamines may cause drowsiness.

–Prolonged use of potent topical steroids may cause local skin effects (atrophy, stria, telangiectasia).

–Use tapering dose of oral steroids if using >5 days.

Second Line

Other topical or systemic antibiotics, depending on organisms and sensitivity

Pregnancy Considerations

Usual caution with medications

ISSUES FOR REFERRAL

May need referral to a dermatologist or allergist if refractory to conventional treatment

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COMPLEMENTARY& ALTERNATIVE

MEDICINE

The use of complementary and alternative treatment is a supplement and not an alternative to conventional treatment.

ADMISSION, INPATIENT, AND NURSING CONSIDERATIONS

Rarely needs hospital admission

ONGOING CARE

FOLLOW-UPRECOMMENDATIONS

Stay active, but avoid overheating.

Patient Monitoring

As necessary for recurrence

Patch testing for etiology after resolved

DIET

No special diet

PATIENT EDUCATION

Avoidance of irritating substance

Cleaning of secondary sources (nails, clothes)

Fallacy of blister fluid spreading disease

PROGNOSIS

Self-limited

Benign

COMPLICATIONS

Generalized eruption secondary to autosensitization

Secondary bacterial infection

REFERENCES

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1.Sultan TA, Hatem AMA. Management of contact dermatitis. J Dermatol

Dermatol Surg. 2015;19(2):86–91.

2.Tan CH, Rasool S, Johnston GA. Contact dermatitis: allergic and irritant. Clin Dermatol. 2014;32(1):116–124.

3.Admani S, Jacob SE. Allergic contact dermatitis in children: review of the past decade. Curr Allergy Asthma Rep. 2014;14(4):421.

4.Martin SF. Contact dermatitis: from pathomechanisms to immunotoxicology. Exp Dermatol. 2012;21(5):382–389.

5.Usatine RP, Riojas M. Diagnosis and management of contact dermatitis. Am Fam Physician. 2010;82(3):249–255.

6.Pelletier JL, Perez C, Jacob SE. Contact dermatitis in pediatrics. Pediatr Ann. 2016;45(8):e287–e292.

SEE ALSO

Algorithm: Rash

CODES

ICD10

L25.9 Unspecified contact dermatitis, unspecified cause

L23.9 Allergic contact dermatitis, unspecified cause

L25.5 Unspecified contact dermatitis due to plants, except food

CLINICALPEARLS

May affect anyone exposed to irritants or allergic substances, especially in occupations that have high exposure to chemicals

The most common allergens causing contact dermatitis are plants of the Toxicodendron genus (poison ivy, poison oak, poison sumac).

Poison-ivy dermatitis typically requires 10 to 14 days of topical or oral steroid therapy to prevent recurrent eruption.

Worldwide, nickel is the number one patch-tested allergen causing ACD (6).

The usual treatment for contact dermatitis is avoidance of the allergen or irritating substance and temporary use of topical steroids.

Acontact dermatitis eruption presents in a nondermatomal geographic fashion due to the skin being in contact with an external source.

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DERMATITIS, DIAPER

Dennis E. Hughes, DO, FAAFP, FACEP

BASICS

DESCRIPTION

Diaper dermatitis is a rash occurring under the covered area of a diaper. It is usually initially a contact dermatitis.

System(s) affected: skin/exocrine

Synonym(s): diaper rash; nappy rash; napkin dermatitis

Geriatric Considerations

Incontinence is a significant cofactor.

EPIDEMIOLOGY

Incidence

The most common dermatitis found in infancy

Peak incidence: 7 to 12 months of age, then decreases

Lower incidence reported in breastfed babies due to lower pH, urease, protease, and lipase activity.

Prevalence

Prevalence has been variably reported from 4–35% in the first 2 years of life. Upward of 75% of infants will have episodes of varying duration and severity in United States.

ETIOLOGYAND PATHOPHYSIOLOGY

Immature infant skin with histologic, biochemical, functional differences compared to mature skin (1)

Wet skin is central in the development of diaper dermatitis, as prolonged contact with urine or feces results in susceptibility to chemical, enzymatic, and physical injury; wet skin is also penetrated more easily.

Fecal proteases and lipases are irritants.

Superhydrase urease enzyme found in the stratum corneum liberates ammonia from cutaneous bacteria.

Fecal lipase and protease activity is increased by acceleration of GI transit;

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thus, a higher incidence of irritant diaper dermatitis is observed in babies who have had diarrhea in the previous 48 hours.

Once the skin is compromised, secondary infection by Candida albicans is common. 40–75% of diaper rashes that last >3 days are colonized with C. albicans.

Bacteria may play a role in diaper dermatitis through reduction of fecal pH and resulting activation of enzymes.

Allergy is exceedingly rare as a cause in infants.

RISK FACTORS

Infrequent diaper changes

Improper laundering (cloth diapers)

Family history of dermatitis

Hot, humid weather

Recent treatment with oral antibiotics

Diarrhea (>3 stools per day increases risk)

Dye allergy

Eczema may increase risk.

GENERALPREVENTION

Attention to hygiene during bouts of diarrhea

COMMONLYASSOCIATED CONDITIONS

Contact (allergic or irritant) dermatitis

Seborrheic dermatitis

Psoriasis

Candidiasis Atopic dermatitis

DIAGNOSIS

HISTORY

Onset, duration, and change in the nature of the rash

Presence of rashes outside the diaper area

Associated scratching or crying

Contact with infants with a similar rash

Recent illness, diarrhea, or antibiotic use

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Fever

Pustular drainage

Lymphangitis

PHYSICALEXAM

Mild forms consist of shiny erythema ± scale.

Margins are not always evident.

Moderate cases have areas of papules, vesicles, and small superficial erosions.

It can progress to well-demarcated ulcerated nodules that measure ≥1 cm in diameter.

It is found on the prominent parts of the buttocks, medial thighs, mons pubis, and scrotum.

Skin folds are spared or involved last.

Tidemark dermatitis refers to the bandlike form of erythema of irritated diaper margins.

Diaper dermatitis can cause an id reaction (autoeczematous) outside the diaper area.

DIFFERENTIALDIAGNOSIS

Contact dermatitis

Seborrheic dermatitis

Candidiasis

Atopic dermatitis

Scabies

Acrodermatitis enteropathica

Letterer-Siwe disease

Congenital syphilis

Child abuse

Streptococcal infection

Kawasaki disease

Biotin deficiency

Psoriasis

HIV infection

DIAGNOSTIC TESTS & INTERPRETATION

Initial Tests (lab, imaging)

Rarely needed

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Follow-Up Tests & Special Considerations

Consider a culture of lesions or a potassium hydroxide (KOH) preparation.

The finding of anemia in association with hepatosplenomegaly and the appropriate rash may suggest a diagnosis of Langerhans cell histiocytosis or congenital syphilis.

Finding mites, ova, or feces on a mineral oil preparation of a burrow scraping can confirm the diagnosis of scabies.

Test Interpretation

Biopsy is rare.

Histology may reveal acute, subacute, or chronic spongiotic dermatitis.

TREATMENT

Prevention is the key to treatment of this condition.

GENERALMEASURES

Expose the buttocks to air as much as possible.

Use mild, slightly acidic cleanser with water; no rubbing and pat dry.

Avoid impermeable waterproof pants during treatment (day or night); they keep the skin wet and subject to rash or infection.

Change diapers frequently, even at night, if the rash is extensive.

Superabsorbable diapers are beneficial, as they wick urine away from skin and still allow air to permeate (2)[C].

Discontinue using baby lotion, powder, ointment, or baby oil (except zinc oxide).

Use of appropriately formulated baby wipes (fragrance-free) is safe and as effective as water (3)[B].

Apply zinc oxide ointment or other barrier cream to the rash at the earliest sign and BID or TID (e.g., Desitin or Balmex). Thereafter, apply to clean, thoroughly dried skin (4)[C].

Cornstarch can reduce friction. Talc powders that do not enhance the growth of yeast can provide protection against frictional injury in diaper dermatitis, but do not form a continuous lipid barrier layer over the skin and obstruct the skin pores. These treatments are not recommended.

MEDICATION

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