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Wk2Assgn1YepifanovaYiHumanRash.docx.docPrimary Diagnosis and ICD- 10 code: Allergic Contact Dermatitis L 23.9 Allergic contact dermatitis is a classic example of a cell mediated hypersensitivity reaction in the skin. This occurs as a result of xenobiotic chemicals penetrating into the skin, chemically reacting with self proteins, eventually resulting in a hapten-specific immune response. It is precisely because of this localized immune response that allergic signs and symptoms occur (redness, edema, warmth and pruritus).
Cellulitis: Cellulitis is a common bacterial skin infection, with over 14 million cases occurring in the United States annually. It accounts for approximately 3.7 billion dollars in ambulatory care costs and 650000 hospitalizations annually (Raff, Kroshinsky 2017). Cellulitis typically presents as a poorly demarcated, warm, erythematous area with associated edema and tenderness to palpation. It is an acute bacterial infection causing inflammation of the deep dermis and surrounding subcutaneous tissue. The infection is without an abscess or purulent discharge.
Impetigo: Impetigo is a contagious skin infection marked by a vesicle or bulla that later becomes pustular, ruptures and forms a yellow crust.
Impetigo is typically caused by staphylococcal or streptococcal bacteria. Predisposing factors include: poor hygiene, malnutrition, and anemia.
Sign and symptoms of impetigo. Lesions may begin as macules, vasacules, and pustules. Primary lesions rupture, leaving a honey colored liquid. This liquid hardens a thick yellow crust forms over the infected site. The most common locations are the mouth, nose, neck, or extremities.
Varicella-Zoster: Shingles also known as herpes zoster is a rash that occurs on one side of the face or body and consists of blisters that scab after week of infection. It results from the reactivation of the varicella-zoster virus (VZV) from its latent state. The primary and acute infection phase of the virus is chicken pox and shingles come as a result of the reactivation of the virus from the latent phase. Before the rash appears, the people experience pain, itching and tingling in the area of development. The rash is reddish with tiny blisters which eventually break, dry out and crust over (Waldman, 2019).
Diagnostic Test and Laboratory Values: ACD is diagnosed by a medical provider, no necessary test or laboratory values are necessary for the diagnosis, unless the condition persists.
Consult Dermatology: If condition (rash) worsens.
Therapeutic Modalities:
First line therapy for mild contact dermatitis reactions is topical steroids. Avoid prolonged topical steroids on sensitive areas such as the face, hands, or genitals. Hydrocortisone 0.1-0.2% or higher potency topical steroids, such as triamcinolone 0.1% (Kenalog, Aristocort) or clobetasol 0.05%. The rationale for the steroids is that steroids reduces inflammation (Huether & McCance, p. 1061, 2017).
None pharmacological treatment includes over-the-counter calamine lotions, cool compresses, lukewarm baths with oatmeal. For itching consider Benadryl 25 mg q6 hr or Hydroxyzine 25 mg q8h. Cortisteroids reserved for more significant contact dermatitis reactions. Prednisone 20-60 mg daily. Consider prolonged taper for severe dermatitis such as severe poison ivy to prevent rebound phenomenon.
Health Promotion: Avoid known allergens, wear full body coverage clothing while hiking.
Patient Education: Advised Pt on supportive measures, including taking cool showers, using Ivy Block or Aveeno or Calamine lotion, trimming nails and limiting excoriation, identifying and avoiding allergen source, washing suspected clothes and materials that may be allergen carriers in hot water and detergent, bathe pets, and cover any oozing blisters as they may form.
Disposition: Follow up in one week, return to clinic or urgent care with new or worsening symptoms.
References:
Raff AB, Kroshinsky D. Cellulitis: A Review. JAMA. 2016 Jul 19;316(3):325-37
Waldman, S. D. (2019). Atlas of common pain syndromes. Philadelphia
Nickoloff BJ, Nestle FO (eds): Dermatologic Immunity. Curr Dir Autoimmun. Basel, Karger, 2008, vol 10, pp 1-26
https://doi.org/10.1159/000131410
Nixon RL, Mowad CM, Marks JG. Allergic contact dermatitis. In: Bolognia JL, Schaffer JV, Cerroni L, eds. Dermatology. 4th ed. Philadelphia, PA: Elsevier; 2018:chap 14.
