Contact Dermatitis


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Contact Dermatitis:

Contact Dermatitis Dermatology Module Family Nurse Practitioner Program K. M. Pendergrass PhD(c), PNP, FNP-BC

Contact Dermatitis:

Contact Dermatitis Contact dermatitis is any inflammatory reaction of the skin that results from direct contact with an offending agent. Most common are: Allergic contact dermatitis (ACD) Irritant contact dermatitis (ICD) Additional types of contact dermatitis Photodermatitis contact urticaria

PowerPoint Presentation:

Contact dermatitis from latex gloves in a health care worker. Note the sharp demarcations at the perimeter of the area of contact. Latex, in this case, is causing a type IV delayed allergic reaction.

Pathophysiology: Contact Dermatitis:

Pathophysiology : Contact Dermatitis Main pathologic feature of contact dermatitis is intercellular edema of the epidermis Acute: intraepidermal vesicle and bullae formation Chronic: papules, scaling, and lichenification Within the dermal layer, various cells congregate around the dilated capillaries to aid in inflammatory response

Pathophysiology: ICD:

Pathophysiology : ICD Results from direct injury to the skin. Affects individuals exposed to specific irritants and generally produces a stinging or burning sensation within seconds of exposure. Alternatively, extended exposure to a mild irritant can cause a chronic form of ICD. In this case, dryness precipitates an erythematous state, which ultimately leads to cracking and the formation of painful fissures.

Pathophysiology: ACD:

Pathophysiology : ACD Affects only individuals previously sensitized to the contactant Delayed (cell-mediated, type IV) hypersensitivity reaction Classically requires several hours to complete the cascade of cellular immunity before symptoms manifest

Incidence: Contact Dermatitis:

Incidence: Contact Dermatitis Greatest single risk for ICD is history of atopic dermatitis Most common allergens are nickel, potassium dichromate, and paraphenylenediamine Most cases easily treated if etiology recognized Rarely, contact with an allergen results in anaphylactic shock Can present concomitantly with chemical burns, which can be life-threatening, depending on the severity of exposure

Incidence (2):

Incidence (2) Low humidity and cold temperatures increase incidence of contact dermatitis. One notable contrast is ICD due to cement exposure, which is more common in the summer in hot and humid areas. F:M=2:1; Women more at risk after childbirth

Incidence (3):

Incidence (3) ACD most common during adulthood, but affects all ages. Frequent cause of ACD in elderly is topical medication. ICD affects very young and very old patients more severely. ICD is common in infants. Most common is diaper dermatitis.

Clinical Presentation: ACD:

Clinical Presentation: ACD Lesions appear w/ i 24-96 hours of exposure to allergen Main symptom, in addition to the lesion, is pruritus Location of the dermatitis is helpful in identifying the cause Most heavily contaminated areas break out first , followed by areas of lesser exposure. In more severe reactions, lesions can form in adjacent areas of the skin that never had direct contact with the offending agent.

Clinical Presentation: ICD: 2 types:

Clinical Presentation: ICD: 2 types Mild irritants require prolonged or repeated exposure before inflammation is noted. Strong irritants ( eg , strong acids, alkalis) can produce immediate reactions similar to thermal burns. Unlike ACD, ICD will only erupt in areas of the skin that have had direct contact with the irritant

Other Contact Dermatitis:

Other Contact Dermatitis Photodermatitis is diagnosed by the presence of lesions limited to sun-exposed body areas Burning is the primary complaint in phototoxic reactions Pruritus is the main complaint in photoallergic reactions Skin contact with photosensitizing agents found in some plants (notably limes) followed by UV irradiation can precipitate a type of photodermatitis called phytophotodermatitis Contact urticaria reactions occur within 1 hour of exposure to the inciting agent

Clinical Presentation (cont):

Clinical Presentation (cont) Most cases of contact dermatitis have a similar appearance regardless of the mechanism or cause of inflammation Inflammatory responses can be categorized into acute, subacute , and chronic phases. In all phases, a key feature is localization to the area of contact .

Inflammatory Response: Acute:

Inflammatory Response: Acute Bright red edematous skin Moderate-to-severe may have clear fluid-filled vesicles or bullae As lesions break, skin becomes exudative and weeps clear fluid In acute ICD, these lesions and surrounding erythema are sharply demarcated and located in the distribution of the area of contact

Inflammatory Response :

Inflammatory Response Contact dermatitis on the thigh of a recreational jogger after a long run. This individual noted running through shrubs, which likely caused the rash. The linear plaques and confluent vesicles and papules on the inferior aspect of the thigh are a common presentation of rhus dermatitis

Clinical Presentation Bullous:

Clinical Presentation Bullous Contact dermatitis with bullous formation caused in this case by a new pair of shoes

Inflammatory Response: Subacute:

Inflammatory Response: Subacute Characterized by the formation of papules instead of the vesicles (see the image-next slide). Additionally, less edema is seen in the subacute phase. Dry scales are sometimes seen in subacute contact dermatitis.


Subacute Subacute contact dermatitis, in this case due to bacitracin

Inflammatory Response: Chronic:

Inflammatory Response: Chronic Scaling, skin fissuring, and lichenification but only minimal edema. Excoriations can also be observed in chronic contact dermatitis.


Causes Causes of contact dermatitis are classified into 4 groups according to mechanism of response: ACD ICD Photodermatitis Contact urticaria Repeated exposures to an ACD-inducing allergen tend to cause incrementally more severe reactions

Causes: ACD:

Causes: ACD Cell-mediated type IV delayed hypersensitivity reaction results from specific antigens penetrating the epidermal skin layer Antigen combines with a protein mediator and travels to the dermis, where T lymphocytes become sensitized Allergic reaction on the subsequent exposure Contributing factors: Allergen concentration Duration of exposure Presence of other skin diseases.

ACD: Most common agents:

ACD: Most common agents Most common agents are plants of the Toxicodendron genus eg : poison ivy poison oak poison sumac

ACD: Other common agents:

ACD: Other common agents Nickel sulfate (various metal alloys) Sunscreens Potassium dichromate (cements, household cleaners), Formaldehyde Ethylenediamine (dyes, medications) Mercaptobenzothiazole (rubbers) Thiram (fungicides) Paraphenylenediamine (dyes, photographic chemicals)

ICD: Causes:

ICD: Causes Irritant produces direct local cytotoxic effect on the cells of the epidermis, with a subsequent inflammatory response in the dermis Most common site is the hand The risk of developing ICD is particularly high in individuals with eczema affecting the hands ICD is mostly caused by chemicals ( eg , acids, alkalis, solvents, oxidants, rubber, latex) Plants ( eg , hot peppers, garlic, tobacco) have also been implicated

ICD: Causes:

ICD: Causes Severity of the reaction is related to the amount and duration of exposure to the irritant. Most cases are acute in onset; symptoms develop within seconds of exposure. Prolonged exposure to a low-level irritant can lead to chronic ICD. Soaps and prolonged exposure to water, often due to occupational soaking of the hands, are typical causes of chronic ICD

Causes: Photodermatitis:

Causes: Photodermatitis Irradiation of certain substances by UV light results in the transformation of the substance into allergens ( photoallergic ) or irritants (phototoxic) Common example is phytophotodermatitis : phototoxic reaction occurs after skin that has been in contact with citrus fruit (or another plant contact) is exposed to sunlight. This exposure to sun chemically alters a previously benign agent in citrus (called furocoumarin or psoralen ) into a skin allergen. Medications (particularly sulfa drugs, thiazides , tetracycline) have also been implicated in photodermatitis .

Causes: Contact urticaria (immunologic, nonimmunologic):

Causes: Contact urticaria (immunologic, nonimmunologic ) Immunologic reaction is a type I IgE -mediated process caused by the immediate release of inflammatory mediators, resulting in a wheal-and-flare reaction. In rare cases, anaphylactic shock can result. Foodstuffs and latex have been implicated. Nonimmunologic contact urticaria results in local edema and erythema . It is more common than the immunologic mechanism. Substances containing benzoic, sorbic , cinnamic , or nicotinic acids often are the cause.

Differential Diagnoses:

Differential Diagnoses Bites, Insects Herpes Zoster Cellulitis Herpetic Whitlow Dermatitis, Atopic Impetigo Dermatitis, Exfoliative Psoriasis Erysipelas Scabies Erythema Multiforme Vulvovaginitis Herpes Simplex

Workup Laboratory Studies:

Workup Laboratory Studies Laboratory for ACD focuses on patch testing Dermatologist or an allergist applies multiple potential allergens into the skin of the patient The presence of erythema , papules, or vesicles can indicate a positive test


Treatment Definitive tx of ICD and ACD is ID and removal of causal agents Topical soaks with cool tap water, Burow solution (1:40 dilution), saline (1 tsp/pint), or silver nitrate solution (25.5%) Lukewarm water baths ( antipruritic ) Aveeno (oatmeal) baths Large vesicles may benefit from therapeutic drainage (but not removing vesicle tops). Lesions should then be covered with dressing soaked in Burow solution.


Medication Treatment of contact dermatitis depends on the type (irritant or allergic), extent, and area of skin lesions on initial presentation Preventive advice is as important as the prescription of medications Once an allergen or irritant is identified as the cause of contact dermatitis, eliminate further exposure

Medication: Wet compresses with an astringent:

Medication: Wet compresses with an astringent soothing, have a mild antipruritic effect, and keep affected areas clean. Aluminum acetate solution Dissolve aluminum acetate tabs in water for a 1:40 solution. Apply as compress for 20-30 min 4-6 times/d

Meds: Topical Steroids:

Meds: Topical Steroids Mainstay of treatment Topical agents of medium-to-high strength (class I-IV) should be adequate to treat most cases. In general, ointments are preferred over creams. Triamcinolone topical ( Aristocort ) Treats inflammatory dermatosis responsive to steroids. Decreases inflammation A moderate potency is available in both ointment (0.1%) and cream (0.5%). Apply tid initially; reduce as lesions remit

Meds: t. steroids (2):

Meds: t. steroids (2) Hydrocortisone valerate 0.2% ( LactiCare HC, DermaGel , Cortaid, Dermacort ) Lower-potency cream useful on the face. Suitable for skin or external mucous membranes. Has mineralocorticoid and glucocorticoid effects resulting in anti-inflammatory activity. Apply tid initially; reduce as lesions remit

Systemic steroids:

Systemic steroids Use in severe cases that involve more than 10-20% of total body surface area (TBSA) or bullae . May also be considered when sleep or ADLs are impaired Glucocorticoids cause profound and varied metabolic effects. Also these agents modify the body's immune response to diverse stimuli.

Meds: s. steroids:

Meds: s. steroids Prednisone ( Deltasone , Orasone , Sterapred ) Used for treatment of a variety of diseases, including adrenocortical insufficiency. Prednisone is inactive and must be metabolized to the active metabolite prednisolone . Conversion may be impaired in patients with liver disease. Use for 2-3 weeks with taper. Too short a course results in recurrence of lesions. Adult 50 mg PO qd for 1 wk; taper by a 10-mg reduction in dose q3d Pediatric 1 mg/kg PO for 1 wk; taper by a 20% reduction in dose q3d; available in 5 mg/5 mL elixir ( prednisolone sodium phosphate); prolonged use in children can suppress growth

Meds: Antihistamines:

Meds: Antihistamines May be used as adjuncts to relieve pruritus associated with contact dermatitis. Diphenhydramine (Benadryl) Used for the symptomatic relief of allergic symptoms caused by histamine released in response to allergens. Adult: 25-50 mg cap PO q6h prn Pediatric: 5 mg/kg/d (12.5 mg/5 mL elixir) PO divided qid

Hydroxyzine HCl (Atarax, Vistaril):

Hydroxyzine HCl ( Atarax , Vistaril ) Antagonizes H1 receptors in the periphery and may be used as alternative to diphenhydramine . May also suppress histamine activity in subcortical region of the CNS. Available in 10 mg/5 mL elixir. Adult: 25-50 mg PO tid / qid prn Pediatric: <6 years: 30-50 mg/d PO divided tid >6 years: 50-100 mg/d PO divided tid


Emollients may be used as adjuncts to moisturize dry skin in subacute and chronic contact dermatitis. Urea ( Ureacin , Ureaphil ) Both promote hydration and removal of excess keratin in conditions of hyperkeratosis. Dosing: Apply to affected area prn Mineral oil (Fleet, Zymenol ): same as urea

Barrier creams:

Barrier creams Primary agents for diaper dermatitis. Zinc oxide paste ( Desitin ) Provides relief of minor skin irritations. Pediatric: Apply to affected area after gentle cleansing and drying, between each diaper change Camphor and menthol (0.5% each) in emollient base ( Sarna Anti-Itch) Topical drug combination that consists of mild local anesthetics, counterirritants, and antipruritic formulations. Generally safe and effective for symptomatic relief Adult: Apply to affected area prn Pediatric: <12 years: Not established >12 years: Apply as in adults

Medications Summary:

Medications Summary Acute contact dermatitis (mild, moderate) Astringents with wet compress Topical steroids (ointments are recommended over creams) Systemic antipruritics Acute ACD with marked edema and bullae (severe) Above treatment with addition of systemic steroids Acute ICD secondary to strong acids and alkalis (severe) Prolonged irrigation with water; further treatment same as for burns Chronic dermatitis Topical steroids, emollients, and barrier agents


Consultations Dermatology consult for recurrent episodes of contact dermatitis or rash of unclear etiology


Deterrence/Prevention Prevention is better than cure. Most important part of treatment: Identify Eliminate further exposure to the causative agent. Use appropriate protective clothing. Rubber-based products protect against water-based products but not solvents.


Complications/Prognosis Treat secondary bacterial infections with systemic antibiotics. Following adequate removal of the offending agent, the prognosis excellent for ICD and ACD Most contact dermatitis resolves without intervention in 4-6 weeks IF further exposure is prevented. Long-term success in treatment is poor if HCP does not identify the etiology

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