Pediatric Primary Care Case Studies (120 page)

Clark, L. R. (2003). Tips for clinicians: approaching the adolescent patient from a psychodevelopmental framework.
Journal of Pediatric and Adolescent Gynecology, 1
, 327–330.

Gerlt, T. J., Blosser, C. G., & Dunn, A. M. (2009). Sexuality. In C. E. Burns, A. M. Dunn, M. A. Brady, N. B. Starr, & C. Blosser (Eds.),
Pediatric primary care
(4th ed., pp. 395–410). Philadelphia: Elsevier.

Gerlt, T. J., Kollar, L. M., & Starr, N. B. (2009). Gynecologic conditions. In C. E. Burns, A. M. Dunn, M. A. Brady, N. B. Starr, & C. Blosser (Eds.),
Pediatric primary care
(4th ed., pp. 906–941). Philadelphia: Elsevier.

Murphy, N. A., & Elias, E. R. (2006). Sexuality of children and adolescents with developmental disabilities.
Pediatrics, 118
, 398–403. Retrieved September 20, 2008, from
http://aappolicy.aappublications.org/cgi/content/full/pediatrics;118/1/398

Rakel, R. E. (2002).
Textbook of family practice
(6th ed.). Philadelphia: WB Saunders.

Reddy, D. M., Fleming, R., & Swain, C. (2002). Effect of mandatory parental notification on adolescent girls’ use of sexual health care services.
Journal of the American Medical Association, 288
, 710–714.

Saslow, D., Runowicz, C. D., Solomon, D., Moscicki, A. B., Smith, R. A., Eyre, H. J., et al. (2002). American Cancer Society guideline for the early detection of cervical neoplasia and cancer.
CA: A Cancer Journal for Clinicians, 52
, 342–362.

Shrier, L. A. (2005). Bacterial sexually transmitted infections: gonorrhea, chlamydia, pelvic inflammatory disease, and syphilis. In S. J. Emans, M. R. Laufer, & D. P. Goldstein (Eds),
Pediatric and adolescent gynecology
(5th ed., pp. 565–614). Philadelphia: Lippincott Williams & Wilkins.

Spigarelli, M. G., & Biro, F. M. (2004). Sexually transmitted disease testing: evaluation of diagnostic tests and methods.
Adolescent Medicine Clinics, 15
, 287–299.

Stamm, C. A., & McGregor, J. A. (2001). Diagnosing and treating STDs in young women.
Contemporary Pediatrics, 18
, 53–67.

Chapter 30

The Child with an Itchy Rash

Donald W. Kennerley

The child who presents in a clinic with an itchy rash is usually miserable and the parents are anxious for a quick fix to the problem. The dilemma for the healthcare provider is to quickly identify the problem and find a treatment plan that provides immediate relief as well as a long-term cure, or amelioration in the chronic case that won’t be cured. The source of the problem may be an infection, infestation, environmental toxin/irritant, or allergy/immunologic problem. This scenario will help the clinician sort through those issues.

Educational Objectives

1.   Develop a multimodal approach for the treatment of atopic dermatitis.

2.   Understand the complex role that the environment and aeroallergens have in the development of atopic dermatitis.

3.   Review and understand new therapies for compromised barrier function.

4.   Understand the effects that atopic dermatitis has on the social, financial, and psychological well-being of a family with a child affected with this disorder.

   Case Presentation and Discussion

Anna Logan is a 3-year-old white female who comes into the office accompanied by her mother. She has come today because of a persisting rash that the mother indicates comes and goes and was first noted when her daughter was 1 year old. Though the rash does at times get better, it has never left her daughter. In fact, as her daughter gets older the intensity of the rash worsens and is spreading to other areas of her body. Originally the rash started on Anna’s face but is now on her neck, arms, and legs. Mrs. Logan indicates that her daughter is scratching more now than in the past and is often awake at night due to the scratching. Further questioning of the mother reveals that, apart from the rash, her daughter also has trouble with chronic sneezing and a constant running nose. The child does not have a history of asthma. The mother is concerned about the spreading rash and is worried about the possibility of her daughter causing further damage to her skin as a result of her constant scratching. The mother comes with her daughter to find out what the rash is and how to get rid of it.

Physical Examination

Upon general physical examination you notice that Anna appears healthy with a slight paleness in her color and darkness beneath her eyes. She scratches during the entire examination. She has a red, dry, inflamed rash on her face, neck, wrists, and antecubital and popliteal fossae. Some of the areas show scratch marks and are lichenified. There are no areas of weeping. She has signs of chronic rhinitis with redness of the nasal turbinates. The rest of her physical examination is unremarkable.

What questions do you feel would help you to make a diagnosis?

Before proceeding with those questions, let us now look at atopic dermatitis in more detail.

Atopic Dermatitis

Epidemiology

Atopic dermatitis (AD) is a common skin condition in children, often beginning in early childhood. Its presentation can be quite severe. Approximately 15–20% of school-age children are affected, with 1–2% having severe involvement. About 1–3% of adults are affected by this condition (Barclay, 2008; Krakowski, Eichenfield, & Dohil, 2008). Approximately 60–65% of patients with atopic dermatitis develop their disease before age 1 year, and by age 5 years, 85–90% of patients have developed signs of their disease (Krakowski et al., 2008; Lewin Group, 2005). The prevalence of atopic dermatitis, asthma, and allergic rhinitis has been rising in industrialized countries (Spergel & Paller, 2003).

Atopic dermatitis is a chronic and relapsing disease and persists from an average of 4.4 years in children to 18.2 years in adults (Lewin Group, 2005). Most forms of this childhood disease improve with the onset of puberty, but up to 40% of cases do not and can recur even into adulthood. AD is often associated with other atopic predispositions; many patients suffering with atopic dermatitis will go on to develop asthma or allergic rhinitis in what is known as the “atopic march” (Spergel & Paller, 2003). Up to 30–60% of patients with atopic dermatitis will go on to develop asthma and 35–66% will go on to develop allergic rhinitis (Lewin Group).

This condition has a significant impact on the quality of life of the individual and his or her family. Cost estimates for the United States range from $364 million to $3.8 billion annually, depending upon the study parameters (Carroll et al., 2005; Mancini, Kaulback, & Chamlin, 2008). The condition accounts for an estimated 7.4 million office visits in the United States alone (Krakowski et al., 2008). Studies have shown that AD can affect sleep, negatively affect school performance, cause low self-esteem, decrease participation in sports and other social activities, and induce stress and anxiety (Krakowski et al.).

Pathophysiology

Although the pathogenesis of atopic dermatitis is not completely understood, in the simplest terms it is believed to be due to a combination of T-cell downregulation and skin barrier dysfunction (Gilliam & Frieden, 2006). The underlying immunologic abnormality for acute disease appears to be related to the overex-pression of T-helper-cell type 2 hypersensitivity, whereas chronic disease is related to augmented T-helper-cell type 1 activity (Novark, Bieber, & Leung, 2003). Genetic studies have found that AD has a complex genetic pattern. Some studies have shown that a primary defect in the skin barrier may be one central factor in the condition. Other factors are still being studied (Spergel, 2008).

The permeability barrier, which relies on the functional integrity of the stratum corneum, is altered in patients with atopic dermatitis, leading to accelerated transepidermal water loss and skin dryness. Improving that functional permeability barrier is a cornerstone of AD treatment.

The immune system response in atopic dermatitis involves both intrinsic (nonallergic) and extrinsic (allergic) components. Approximately 70–85% of cases of atopic dermatitis involve the extrinsic system whereas 15–30% of cases are intrinsic. Extrinsic atopic dermatitis is associated with high serum IgE levels and exhibits allergen-specific IgE to aeroallergens and foods, positive skin prick reactions, and a cytokine profile of high interleukin-4 (IL-4) and IL-13 levels (Bardana, 2004). Intrinsic atopic dermatitis is associated with normal IgE levels, negative skin prick reactions, and low IL-4 and IL-13 levels, and the individual does not have allergen-specific IgE to aeroallergens and foods (Bardana). Patients with intrinsic disease are characterized by an absence of other atopic diseases, asthma, and allergic rhinitis (Schmid-Grendelmeier, Simon, Simon, Akdis, & Wirthrich, 2001).

Presentation

There are three distinct phases, related to stages of growth, in which atopic dermatitis can present. They include an infantile phase, a childhood phase, and an adult phase. In the infantile phase, which occurs from birth up to age 2, the disease presents with pruritic, erythematous papules, patches, and vesicles on cheeks and extensor surfaces of the extremities (Peterson & Chen, 2006). Other areas of involvement may include the scalp, forehead, chin, and trunk, but not in the diaper area in the majority of cases (Spergel & Paller, 2003). In the childhood phase, from age 2 to puberty, lichenification and scarring appear as a result of chronic rubbing and scratching. Distribution of the lesions changes to the flexor surfaces, particularly the antecubital and popliteal fossae as well as the neck, periorbital, perioral, hands, feet, wrists, and ankles (Spergel & Paller). The adult phase begins at puberty and may follow a continuous course. Areas of involvement include the flexor folds, face, hands, upper arms, back, wrists, and the dorsa of the hands, fingers, feet, and toes (Spergel & Paller). Large lichenified plaques; scaly, erythematous papules and plaques; and pruritic papules are featured in the adult phase (Leung & Bieber, 2003).

A diagnostic formula was established in 1996 to aid in the diagnosis of atopic dermatitis. A patient has to have a history of itchy skin and three or more of the following presentations: a history of rash in skin folds, a personal history of asthma or hay fever, a history of dry skin, onset before age 2 years, and visible flexural dermatitis (Williams et al., 1996).

Triggers

Allergies play a major role in triggering atopic dermatitis. Approximately 20–40% of young children and infants with atopic dermatitis have clinically relevant food allergies that worsen their disease (Leung & Bieber, 2003). The most common food allergies include cow’s milk, eggs, fish, peanuts, soy, tree nuts, and wheat (Rudikoff & Lebwohl, 1998). Aeroallergens include animal dander, cockroaches, dust mites, human dander, molds, and pollens (Schmid-Grendelmeier et al., 2001). Tests for allergies are not necessary in most children with mild eczema. Radioallergosorbent/skin prick (RAST/SPT) testing has only a 20% positive predictive accuracy (Rowlands, Tofte, & Hanifin, 2006). A double blind placebo-controlled food challenge is considered the gold standard for diagnosing food allergies; however, if there is a history of anaphylaxis, a food challenge should be used with caution and only if the patient is closely monitored (Peterson & Chen, 2006).

Other triggers such as climate, irritants, and micro-organisms are also factors that have a pronounced effect on the severity of atopic dermatitis. Decreased humidity in winter allows the skin to dry out easier through increased transdermal water loss. Irritants such as hot water, soaps, cigarette smoke exposure, laundry detergents, household disinfectants, solvents, synthetic clothing fibers, and juice from fresh fruits are commonly implicated in atopic dermatitis (Abramovits, Goldstein, & Stevenson, 2003).

Bacteria, viruses, fungi, and yeast aggravate atopic dermatitis. Approximately 90% of atopic dermatitis lesions are colonized by
Staphylococcus aureus
, as opposed to only a 5% rate of colonization in skin of healthy controls (Abramovits, 2005; Chung, Jeon, Sung, Kim, & Hong, 2008). Community-acquired methicillin-resistant
S. aureus
(MRSA) accounted for 18.3% of those isolates in the Chung et al. study (2008).

Other information that should be ascertained includes the following:

•   Does this child have food or other types of allergies?

•   What type of clothing does the child wear?