September 23, 2008
Accurately Diagnosing Commonly Misdiagnosed Circular Rashes
By Popovich, Debbie McAlhany, Allison
Rashes are common in the pediatric population yet can be quite problematic for nurse practitioners to diagnose. A thorough history and physical examination, along with some simple procedures, will aid in identifying these skin conditions. Four cases are presented, which may initially prove challenging to diagnose, and symptoms are categorically examined to arrive at the accurate diagnoses. Treatment guidelines, options, and the role of parental education and involvement also are discussed. Skin lesions are common and encountered in all pediatric practice environments. It is therefore important to understand the fundamentals of diagnosing common skin conditions, appropriate therapy, and parental education. Rashes in children can affect their daily lives by exclusion from school or daycare. Parents who are required to miss work while awaiting proper diagnosis and treatment contribute to the financial burden of these commonly seen and easily treatable skin conditions. Infections such as tinea and impetigo may stigmatize children and their family due to their communicability and appearance. Several of the rashes presented can be spread among children and their playmates, classmates, and family members. Early access to treatment can avoid this transmission and further reduce the financial impact. In this era of rising methicillin-resistant Staphylococcus aureus (MRSA) rates, prompt treatment of infectious skin rashes may reduce the potential progression to bacterial infections and ultimately decrease cost and social handicap. Differentiating between rashes with similar presentation is essential for the astute pediatric nurse practitioner.Four Cases Involving Circular Rashes
Case 1 (Granuloma Annulare, see Figure 1). A 2- year-old boy presents with a circular lesion, which he has had for over 6 months, on the dorsal aspect of the left foot. The mother believes it may be spreading, having noticed the development of a second lesion just above the first. The child has given no indication that the lesions are irritating or pruritic, and no other family members have similar lesions.
Case 2 (Bullous Impetigo, see Figure 2). A 6-yearold boy presents with multiple lesions on both elbows and hands. They are pruritic and increasing in number. Each lesion forms a blister. The family denies noticing any fluid when the blisters rupture.
Case 3 (Tinea Corporis, see Figure 3). A 5-year-old girl presents with a 2-day history of circular rash on her anterior lateral thigh. She was recently seen by a pediatric nurse practitioner for her routine wellness examination and appeared symptom free at the time.
Case 4 (Tinea Capitis, see Figure 4). A 4-year-old female presents with a 1-week history of hair loss in the left temporal region.
Cases 1 and 2 demonstrate a lengthy list of possible diagnoses, so it is prudent to begin by evaluating for the most common presenting skin infections in childhood. Potassium hydroxide (KOH) scrapings are essential to rule out tinea as the cause of annular lesions based on the frequency of diagnosis. Cultures of fluid- filled lesions will determine the causative organism, be it viral (such as HSV) or bacterial (such as S. aureus). See Table 1 for differential diagnoses for annular lesions of the head and Table 2 for differential diagnoses of annular lesions of the body.
Although often confused with tinea corporis, the correct diagnosis in this case is granuloma annulare. A KOH scraping may help differentiate the two in the clinic setting. Granuloma annulare is a self-limiting inflammatory skin lesion occurring in both adults and children (Barron, Cootauco, & Cohen, 1997).
Diagnosis. These lesions are often seen on the hands, arms, and ankles. Granuloma annulare is characterized by rings of closely set, small, smooth, firm papules, usually skin colored, but they also may be slightly erythematous or have a purplish hue. Lesions vary in size from 1 cm to 5 cm. They are generally asymptomatic and nonpruritic (Fairlie, 2004). Reports of associations between granuloma annulare and diabetes mellitus, thyroid disease, malignancies, drug allergies, hypertension, arthritis, AIDS, and other conditions are being evaluated, but to date, no consistent association has been found (Rigopoulos et al., 2005). Thus, what causes these types of lesions remains unknown although evidence exists that they generally regress on their own within 2 years (National Institutes of Health, 2004).
Treatment. Several treatment options exist with varying success. The current consensus is that no treatment is necessary because this skin eruption is generally asymptomatic and self-limiting (Felner, Steinberg, & Weinberg, 1997; Kowalzick, 2005). Treatment options for those concerned with the cosmetic aspect of the condition include topical steroids, ultraviolet light (Schnopp et al., 2005), and cryosurgery (Blume-Peytavi et al., 1994). Several newer treatment options have been studied with small sample sizes that demonstrated promising results, including pimecrolimus 1% (Rigopoulos et al., 2005), tacrolimus 0.1% (Jain & Stephens, 2004), vitamin E (Burg, 1992), and others. Although lesions may improve with intervention, recurrence is common with or without therapy. Additional studies are needed to further investigate the efficacy of these interventions.
Parental role. Parents should continue to assess the lesions and prevent irritation and potential infection with the use of clothing barriers such as socks, long sleeves, and pants.
Impetigo is a common and highly contagious pediatric skin infection. Intact skin is an effective barrier that decreases the risk of infection. When the child scratches a lesion, bacteria are introduced, causing inflammation and infection. This infection is most commonly seen in children aged 2 to 5 years but can occur at any age. Impetigo may be bullous or nonbullous and is usually caused by Staphylococcus aureus or Group A beta-hemolytic streptococci (GABHS) organisms.
Diagnosis. Although it was once thought that the organism causing impetigo could be predicted based on its bullous or nonbullous honey- colored crusted appearance, there is some evidence indicating that lesions may be affected by (or associated with) both S. aureus and GABHS (Stulberg, Penrod, & Blatny, 2002). The bullous form of impetigo presents as a large, thin-walled bulla (2 to 5 cm) containing serous yellow fluid. It often ruptures, leaving a complete or partially denuded area with a ring or arc of remaining bulla (Stulberg et al., 2002).
Treatment. Localized areas of impetigo are most commonly treated with antibacterial ointment such as 2% mupirocin (Bactroban(R)) cream or ointment. This preparation covers the organisms responsible for impetigo: GABHS, methicillin-sensitive S. aureus (MSSA), and MRSA. Oral antibiotics that cover gram-positive skin organisms, such as first generation cephalosporins, should be started if widespread impetigo is present or if localized lesions do not improve with topical medication. When an oral antibiotic is used, the additional use of mupirocin is not necessary to eradicate the bacteria (Bell, 2002). Topical bactericidals may decrease dissemination to other vulnerable individuals. It has also been suggested that oral antibiotics should be seriously considered when lesions occur near the patient's mouth, since a topically applied antibiotic may be frequently licked off, especially by younger patients (Bell, 2002).
Lesions that do not improve with oral medications should be suspect for community-acquired MRSA and cultured to identify the organism responsible and determine sensitivity. In the event of community-acquired MRSA, evaluating the sensitivity will allow the practitioner to make the best treatment choice for the patient. Trimethoprim-sulfamethoxazole (Septra(R)) should not be considered a firstline treatment (without MRSA positive cultures and demonstrated sensitivity) due to potential risk of Stevens-Johnson syndrome and increasing resistance to S. aureus from overuse of antibiotics. Practitioners should be aware of MRSA rates in their communities when considering the best course of action.
Potential but uncommon complications of impetigo include cellulitis, superinfection, and acute poststreptococcal glomerulonephritis (APSGN), but outbreaks of impetigo do not result in rheumatic fever (American Academy of Pediatrics [AAP], 2003; Kaplan, 2005). Prompt treatment of GABHS infections does not decrease the incidence of glomerulonephritis (Pichichero, 1998). APSGN can occur approximately 2 weeks after impetigo infections due to nephritogenic strains of GABHS. This post-streptococcal illness is the consequence of the host's immune response to a non-renal infection. Although this process is not fully understood, antigenic mimicry may be the triggering factor, leading to autoimmunity (Hahn, Knox, & Forman, 2005). Patients with any type of streptococcal infection should be monitored for decreased urine output, tea- colored or dark urine, headache, nausea, vomiting, and evidence of edema. Physical examination may reveal hypervolemia, edema, or hypertension. Although rare, parents should be alerted to this possible complication and the accompanying symptoms.
Parental role. Parental education is paramount in the prevention and successful treatment of impetigo. Children's fingernails should be kept clean and short, and antibacterial soap used at the first sign of altered skin integrity. Nasal S. aureus has been implicated in recurrent impetigo (Raz et al., 1996), so parents should consistently encourage the use of tissues and handwashing. Children infected with impetigo should not bathe together, share towels, or have skin-to-skin contact. Topical treatment of Bactroban is applied three times a day for 7-14 days. Over-the-counter Neosporin may be effective for impetigo if MRSA is not involved. If the infection does not improve in 14 days or worsens despite therapy, children should be evaluated by their health care provider. Tinea Infections
Dermatophyte (tinea) infections are the most common recurrent and persistent fungal infections of the hair, skin, and nails in children of all ages. In the United States three types of dermatophytes account for the majority of fungal infections: Trichophyton, Epidermophyton, and Microsporum. Tinea corporis can be caused by any of these dermatophytes (Rinaldi, 2000; Tosanger & Crutchfield, 2004). The source of transmission is direct contact with humans, animals, or fomites infected with the organism. Greater than 90% of tinea capitis infections are caused by Trichophyton tonsurans (Schwartz, Bell, Bingham, Chung, & Cohen, 2003). Cats and dogs are a major source of Microsporum canis.
Diagnosis. On physical exam, tinea corporis presents as a circular or oval erythematous scaling lesion, hence the term "ringworm." The circular area has a pale center with mildly erythemic raised borders due to inflammation. The interior is dry, scaly, and may be pruritic. The affected area may closely resemble other dermatologic conditions that can manifest as round patches or plaques such as pityriasis rosea, nummular eczema, granuloma annulare, psoriasis, tinea versicolor, and annular contact dermatitis.
Children exposed to the dermatophytes may be at increased risk of infection if they are immunocompromised, have areas of skin trauma, or remain in moist and/or occlusive clothing. Once the organism has invaded the stratum corneum, the central clearing of the infected site will occur in a few weeks, resulting in the pathognomonic appearance.
History taking includes the onset, duration of infected areas, any changes in appearance over time, and any prior treatment and its effectiveness in relieving symptoms. Assessment of changes in children's scalps, hair, nails, and mucous membranes, plus queries about the health of the family's pet(s) and interactions between pet(s) and children, should be ongoing.
The diagnosis of tinea corporis usually is made by visual assessment, but the diagnosis can be augmented by microscopic examination. The erythematous border is the active area and the ideal spot for obtaining scrapings. The scaling border is scraped with a blade. The material is placed on a glass slide with one drop of 10% KOH, allowed to dry, and a cover slip is placed on the slide. Branching hyphae are characteristic.
Treatment. Solitary or non-inflammatory lesions are treated with twice-daily applications of the topical class of imidazoles such as 1% clotrimazole and 2% miconazole. Ketoconazole 2% is applied once daily. Treatment should last for 2 to 4 weeks or 2 weeks beyond when lesions have disappeared, not merely when the lesions have resolved or are no longer pruritic (Wichmann, 1994). Burning, itching, and stinging may occur as a result of local irritation. Steroids can act like fertilizer and actually increase tinea growth. Alston, Cohen, and Braun (2003) found the use of combination clotrimazole 1% cream/ betamethasone diproprionate 0.05% cream (Lotrisone(R)) to be associated with persistent/recurrent tinea corporis infection. "Tinea incognito" is the term applied to tinea corporis lesions that have undergone topical steroid treatment and are no longer red and scaly, making typical presentation unlikely and difficult to diagnose (Hines & Paniker, 2005). Parents should be instructed to apply the antifungal cream as often as prescribed (typically in the morning and evening for twice daily dosing) and after swimming, bathing, or play/exercise. Pets should be examined by a veterinarian. Normally, children can return to daycare or school without threat of transmitting the infection after topical treatment has begun (Wichmann, 1994).
Extensive, highly inflammatory lesions or those that do not respond to topical treatment usually require systemic therapy. Griseofulvin is an antifungal antibiotic produced by a species of Penicillium, administered orally, and is effective against dermatophytes only. It remains the drug of choice for tinea corporis (AAP, 2003). Its effectiveness on superficial fungal infections lies in its ability to penetrate keratin precursor cells. This creates an unfavorable environment for hyphae to reproduce, thus facilitating the exchange of infected skin cells for those not infected with the dermatophyte. For children over 2 years of age, the AAP recommends a dose of 10 to 20 mg/kg/day (maximum: 1 g) of microsize griseofulvin given in one to two divided doses. Dosages up to 20 to 25 mg/kg/day have been used (AAP, 2003). The suggested therapy length is 2 to 4 weeks.
Nurse practitioners must carefully consider the child's medical history for contraindications to the use of griseofulvin, such as hepatic disease, pregnancy, and systemic lupus erythematosus. Practitioners also should use caution when prescribing griseofulvin in a patient with a history of penicillin hypersensitivity. The hepatic metabolism of estrogencontaining oral contraceptives can be accelerated by griseofulvin, rendering them less effective. Female adolescents must be instructed to use a back-up method of birth control while taking the antifungal and for 1 month after it is discontinued (Archer & Archer, 2002). Due to potential harmful effects on human sperm, it is recommended that males wait at least 6 months after completing griseofulvin treatment before attempting to father a child (Grifulvin V, 1982). In addition, the excretion of griseofulvin in breast milk has not been well documented; possible effects on breast-feeding infants are unknown, thus breast-feeding is not recommended during use (Griseofulvin, 2006). Food also can affect the medication's bioavailability (Schmidt & Dalhoff, 2002). The absorption of microsized griseofulvin may be enhanced by the intake of food high in fat such as whole milk, ice cream, cheese, and peanut butter. It also may induce photosensitivity, requiring extra sunscreen or protective clothing in intense sunlight. Tanning beds are absolutely contraindicated.
Parental role. In addition to topical and systemic medication, there are practical interventions to be discussed with the parents or guardians. These include keeping the infected area clean and dry. Wet, damp, or tight-fitting clothing should be avoided. Clothing or linen having contact with the infection should be washed. Fingernails need to be kept clean and trimmed short to prevent secondary bacterial infections.
T. tonsurans (the most common cause of tinea capitis) and M. canis account for the majority of tinea capitis infections in the United States and Europe (Chan & Friedlander, 2004). T. tonsurans is associated with human-to-human contact and with fomites such as combs, hats, seatbacks, and telephones. An endothrix, T. tonsurans' growth and spore formation is largely confined to the hair shaft, where the spores increase hair follicle fragility.
Diagnosis. In non-inflammatory tinea capitis, the hair breaks off just above the level of the scalp. The black tips of the hair follicles remain, causing the typical black-dot appearance. Another common presentation resembles seborrheic dermatitis; the scalp appears scaly rather than blackdot. This inflammatory type of tinea capitis is characterized by pustules, papules, and crustiness of the scalp. Cats and dogs are natural reservoirs of M. canis fungal infections of the commonly inflammatory type. Infected cats contaminate the environment with microsporum through airborne arthrospores. Dogs are more likely than cats to contaminate surfaces and are less likely to cause infections in humans (Mancianti, Nardoni, Corazza, D'Achille, & Ponticelli, 2003). The organism is transmitted through direct contact of an exposed area such as the face, scalp, or arms, with an infected animal or its dander (Fitzpatrick, Eisen, Wolff, Freedburg, & Austin, 1993). The spores of M. canis, an ectothrix, grow on the outside of the hair shaft and produce a substance that fluoresces green under a Wood's lamp. This aids in the species diagnosis (as T. tonsurans does not fluoresce).
Correct and early diagnosis of tinea capitis is necessary to prevent significant hair loss, scarring, and pain. The evidence of hair loss or scaling on the scalp of any child is suspect for this fungal infection. Other common skin infections frequently mistaken for tinea capitis (resulting in delay of correct treatment) are seborrheic dermatitis, atopic dermatitis, trichotillomania, alopecia areata, psoriasis, folliculitis, and impetigo. In a study of 100 children presenting with at least one fungal symptom indicative of tinea capitis, Hubbard (1999) found that abnormal enlargement of the lymph nodes (lymphadenopathy) had the highest positive predictive value. Definitive diagnosis is made by KOH preparation or fungal culture. If the provider is unskilled in KOH interpretation, a fungal culture may be obtained in one of three ways, although the first two methods, hopefully archaic by now because of unnecessary discomfort for children and families, involve plucking hairs or scraping the scalp with a blade. Friedlander, Pickering, Cunningham, Gibbs, and Eichenfield (1999) found a third method of obtaining a specimen that was easy, reliable, inexpensive, and painless. A cotton swab moistened with tap water is rubbed against the infected area and plated on fungal culture medium. The swab specimen may also be inserted into a culturette system and transported to a laboratory. According to Friedlander's (1999) study, both in-office and laboratory cultures showed the same results. Treatment. Griseofulvin is the drug of choice for tinea capitis, either as a dose of microsized liquid (20-25 mg/kg/ day in a single dose) or divided into two daily doses for children over 2 years of age (Chan & Friedlander, 2004; Elewski & Krowchuk, 2001). Heightened photosensitivity associated with griseofulvin can be reduced by once daily dosing with the evening meal (Silverman, 2001). Treatment is for 4 to 8 weeks (or longer as needed) until the symptoms are resolved and the organism eradicated. Higher dosing and duration of treatment may result in increased noncompliance as children experience the side effects of headache, nausea, and diarrhea. Therapeutic alternatives to griseofulvin include terbinafine or fluconazole. Friedlander and colleagues (2002) found that when efficacy, cost, and compliance were taken into consideration, 2 weeks of terbinafine at a dose of 3 to 6 mg/kg/day (compared at 1 and 4 weeks with typical griseofulvin treatment), appeared to be an optimal duration for patients with T. tonsurans tinea capitis. Gaughan and Aronoff (2004) determined that a 2 to 4 week course of terbinafine was as effective as a 6 to 8 week course of griseofulvin for treating trichophyton infections of the scalp. Although the cost of griseofulvin is approximately one-half that of terbinafine, a typically shorter course of terbinafine implies its cost effectiveness. Fluconazole dosed at 6 mg/kg/day, once daily for 2 to 6 weeks, is available as a suspension. Approved to treat systemic fungal infections in all age groups, it is a reasonable therapeutic alternative. Practitioners must keep in mind, however, that griseofulvin is the only antifungal medication the Food and Drug Administration approved for tinea capitis. Ketoconazole 2% and selenium sulfide 1% shampoos, used concurrently with oral antifungal therapy, also have been recommended as therapeutic adjuncts to reduce the spread of infection and allow children to return to school once therapy has been initiated (Chan & Friedlander, 2004). These shampoos should be used at least 3 times a week and remain on the scalp for 5 to 10 minutes. Chan and Friedlander (2004) also recommend that asymptomatic family members use the shampoo for several weeks to prevent infection.
Parental role. Parents play the most critical role here. First, they need education to understand why they must insist on preventive measures (having all family members use antifungal shampoos) or if necessary, insist on getting the entire family tested (and treated with antifungals if cultured positive for tinea capitis). Parents need to understand that sharing brushes, combs, hats, hair ties, headbands, or any other items in contact with the head (e.g., pillows or sheets) is to be strictly policed and avoided. In addition, they need to be taught the specific protocols for administering medication, particularly griseofulvin. Occasionally children may develop a fine pink pruritic, papular, or vesicular exanthem on the head, neck, and shoulders once griseofulvin is initiated. Parents need to know this is a hypersensitivity reaction to a fungal agent and not a drug reaction (Elewski & Krowchuk, 2001). True allergic urticaria and angioedema are rare (Elewski & Krowchuk, 2001). Finally, one other preventive measure may prove helpful. A multicenter study involving three national urban referral centers used a convenience sample of 66 children with clinical symptoms of tinea capitis. Although Sharma and colleagues (2001) failed to find an association of tinea capitis with hair care styling practices, a protective effect was found for the use of hair conditioners. They recommend larger studies be conducted to further analyze the use of conditioners as a method of preventing the spread of tinea capitis.
Encouraging Collaboration of Parents/Adult Caretakers and School Personnel
Parents. Although nurse practitioners' knowledge of appearance, etiology, and choice of treatment are critical factors, parent education and compliance greatly contribute to decreasing the spread of infection among siblings, families, and contacts. Many factors are involved in parental and child health care education, but attendance and adherence to treatment are arguably the most basic necessities for effective treatment delivery (Nock & Ferriter, 2005). Obviously, compliance in small children is highly dependent on their parents (Niggemann, 2005). When parents believe that the disease itself puts their child at risk, the medication is safe, and the health care provider is trustworthy, they are more compliant with treatment. For example, Mann, Eliasson, Patel, and ZuWallack (1992) found that parental influence on child compliance in the acute phase of asthma was greater than that in maintenance therapy. Similarly, several of the skin disorders presented here have an acute phase followed by a lengthy maintenance period requiring compliance. Lack of compliance may result in treatment failure, antibiotic resistance, recurrent morbidity, missed school time, and consequently, loss of parental work and wages.
In addition, the infected child's self-esteem may be negatively affected if a persistent unsightly appearance and infectious status around peers and others is not resolved as quickly as possible (Harrison & Sinclair, 2003). "Children with visible skin disease affecting their appearance are negatively impacted the most. They have the challenge of having to prove that they demand the same level of respect and social regard" (Hilton, 2004). This sometimes not-so-subtle form of intolerance may extend beyond the classroom to the child's own home environment as well.
Because the skin is the most visible portion of the body, defects in its surface that alter its appearance are sometimes a source of distress to the child and a source of revulsion and rejection by others. Parents of other children may fear that their children will "catch" the disorder. Occasionally the affected child's own family members will reduce their interaction with him or her, especially close physical contact, or otherwise demonstrate a distaste for the condition, which the child may interpret as rejection (Hockenberry, 2003).
With this in mind, health care providers should first carefully assess the extent of parents' knowledge about the skin disorder. What gaps in understanding need to be filled in? What concerns, especially ones resulting in actions the child may perceive as rejection, need to be addressed? Next, treatment rationale and ramifications of noncompliance need to be firmly and factually presented. Finally, instructions for treatment need to be clarified, simplified, adjusted, written out, and/or interpreted (if English is not the native language) to ensure understanding. Andal (2006) suggests a diary be kept of any concerns that arise, a verbal commitment be made to comply with the treatment outlined, and there be a discussion of positive and negative consequences associated with compliance and noncompliance.
School personnel. Although parental understanding and compliance are critical, alone, they are often not enough to ensure treatment success. According to Mears, Charlebois, and Holl (2006), school- based clinics are becoming an integral part of the health care system for low-income children. Obstacles to medication adherence are lack of health insurance, poverty, transportation dilemmas, health literacy, confidentiality, language barriers, and working parents who are unable to keep medical appointments. Their study of 81 students over the age of 10, found that only 55.6% of the students filled their prescription, 75.6% self- administered their medication at the correct time, and 22% sometimes forgot to take their medication. Therefore, ideally, a team approach involving parents/caregivers, health care providers, school nurses/teachers, and pharmacists is needed to encourage and influence adherence to treatment. Each team member offers important contributions to the treatment regimen and outcome.
Thus, the first step toward a successful outcome is the health care provider's initial accurate diagnosis of these common pediatric skin disorders. Then coordination of care involving a team approach will help ensure adherence to treatment and prevent risking further spread of the disease as well as further angst and embarrassment to the child.
Alston, S.J., Cohen B.A., & Braun, M. (2003). Persistent and recurrent tinea corporis in children treated with combination antifungal/ corticosteroid agents. Pediatrics, 111(1), 201-203.
Andal, E.M. (2006). Compliance: Helping patients help themselves. Clinician Reviews, 116(3), 23-25.
American Academy of Pediatrics (AAP). (2003). Report of the Committee on Infectious Disease: Group A Streptococcal Infections. Elk Grove Village, IL: Author.
Archer, J.M., & Archer, D.F. (2002). Oral contraceptive efficacy and antibiotic interaction: A myth debunked. Journal of the American Academy of Dermatology, 46, 917-923.
Barron, D.F., Cootauco, M.H., & Cohen, B.A. (1997). Granuloma annulare: A clinical review. Lippincott's Primary Care Practice, 1, 33- 39.
Bell, E.A. (2002). Topical products used for the treatment of common skin infections. Infectious Diseases in Children, 4(15), 20.
Blume-Peytavi, U., Zouboulis, C.C., Jacobi, H., Scholz, A., Bisson, S. & Orfanos, S.E. (1994). Successful outcome of cryosurgery in patients with granuloma annulare. British Journal of Dermatology, 130(4), 494-497.
Burg, G. (1992). Disseminated granuloma anulare: Therapy with vitamin E topically. Dermatology, 184(4), 308-309.
Chan, Y., & Friedlander, S.F. (2004). New treatments for tinea capitis. Current Opinion in Infectious Diseases, 17(2), 97-103.
Elewski, B.E., & Krowchuk, D.P. (2001, April). Reaching consensus. Contemporary Pediatrics, 18(Suppl.), 1-15. Fairlie, C. (2004). Granuloma annulare. Dermatology Nursing, 16, 526.
Felner, E.I., Steinberg, J.B., & Weinberg, A.G., (1997). Subcutaneous granuloma annulare: A review of 47 cases. Pediatrics, 100(6), 965- 967.
Fitzpatrick, T.B., Eisen, A.Z., Wolff, K., Freedburg, I.M., & Austin, K.F. (1993). Dermatology in general medicine. (4th ed.). New York: McGraw-Hill.
Friedlander, S.F., Aly, R., Krafchik, B., Blumer, J., Honig, P., Stewart, D., et al. (2002). Terbinafine in the treatment of Trichophyton tinea capitis: A randomized, double-blind, parallel- group, duration- finding study. Pediatrics, 109(4), 602-607.
Friedlander, S.F., Pickering, B., Cunningham, B.B., Gibbs, N.F., & Eichenfield, L.F. (1999). Use of the cotton swab method in diagnosing tinea capitis. Pediatrics, 104(2), 276-279.
Gaughan, F.D., & Aronoff, S.C. (2004). Griseofulvin versus terbinafine in the treatment of tinea capitis: A meta-analysis of randomized, clinical trials. Pediatrics, 114(5), 1312-1315.
Grifulvin V: (griseofulvin tablets) microsize and (griseofulvin oral suspension) microsize tablets/suspension. (1982, rev. insert, 1997). Drugs.com: Drug information online. Retrieved March 3, 2006, from http://www.drugs.com/PDR/Grifulvin_V_Tablets_Microsize_ and_Oral_Suspension_Microsize.html
Griseofulvin: Fulvicin(R) P/G | Fulvicin(R) U/F | Grifulvin(R) V | Gris-Peg(R) | Grisactin(R) (n.d., rev., 2006). Clinical pharmacology. Retrieved March 7, 2005, from http://cpip.gsm.com
Hahn, R.G., Knox, L.M., & Forman, T.A. (2005). Evaluation of poststreptococcal illness. American Family Physician, 71(10), 1949- 1954.
Harrison, S., & Sinclair, R. (2003). Optimal management of hair loss (alopecia) in children. American Journal of Clinical Dermatology, 4(11), 757-770.
Hilton, L. (2004). Psycho-social dysfunction: Psychosocial effects of skin disease impact on lives of the youngest patients. Dermatology Times, 25(3), 19-23.
Hines, W. A., & Paniker, P. (2005). Ring around the collar area. The American Journal of Medicine, 118(3), 217-218.
Hockenberry, M.J. (2003). Wong's nursing care of infants and children (7th ed.). St. Louis: Mosby.
Hubbard, T.M. (1999). The predictive value of symptoms in diagnosing childhood tinea capitis. Archives of Pediatrics & Adolescent Medicine, 153(11), 1150-1153.
Jain, S., & Stephens, C. (2004). Successful treatment of disseminated granuloma annulare with topical tacrolimus. British Journal of Dermatology, 150, 1042.
Kaplan, E.L. (2005) Rheumatic fever. In Kasper, D.L., et al. (Eds.), Harrison's principles of internal medicine (16th ed., pp. 1977-1979). New York: McGraw-Hill.
Kowalzick, L. (2005). Granuloma anulare. Der Hautarzt, 56(11), 1071-1083. Retrieved on March 7, 2005, from http://www. springerlink.com/(rmhonv45cocw0l45r1ghhr45)/app/home/ issue.asp?referrer=searchresults&id=L1H262104157&backto= searcharticlesresults,5,8
Mancianti, F., Nardoni, S., Corazza, M., D'Achille, P., & Ponticelli, C. (2003). Environmental detection of Microsporum canis arthrospores in the households of infected cats and dogs. Journal of Feline Medicine and Surgery, 5, 323-328.
Mann, M., Eliasson, O., Patel, K., & ZuWallack, R.L. (1992). A comparison of the effects of bid and qid dosing on compliance with inhaled flunisolid. Chest, 101, 496-499.
Mears, C.J., Charlebois, N.M., & Holl, J.L. (2006). Medication adherence among adolescents in a school-based health center. Journal of School Health, 76(2), 52-56.
National Institutes of Health. (2004, February 7). Medical encyclopedia: Granuloma annulare. Retrieved February 9, 2006, from http:// www.nlm.nih.gov/medlineplus/ency/article/000833.htm
Niggemann, B. (2005). How can we improve compliance in pediatric pneumology and allergology? Allergy, 60, 735-738.
Nock, M.K., & Ferriter, C. (2005). Parent management of attendance and adherence in child and adolescent therapy: A conceptual and empirical review. Clinical Child and Family Psychology Review, 8(2), 149-166.
Pichichero, M.E. (1998). Group A beta-hemolytic streptococcal infections. Pediatric Review, 19, 291-302.
Raz, R., Miron, D., Colodner, R., Staler, Z., Samara Z., & Keness, Y. (1996). A 1-year trial of nasal mupirocin in the prevention of recurrent staphylococcal nasal colonization and skin infection. Archives of Internal Medicine, 156, 1109-1112.
Rigopoulos, D., Prantsidis, A., Christofidou, E., Ioannides, D., Gregoriou, S., & Katsambas, A. (2005). Pimecrolimus 1% cream in the treatment of disseminated granuloma annulare. British Journal of Dermatology, 152, 1364-1365.
Rinaldi, M.G. (2000). Dermatophytosis: Epidemiological and microbiological update. Journal of the American Academy of Dermatology, 43(Suppl. 5), S120-124.
Schmidt, L.E., & Dalhoff, K. (2002). Food-drug interactions. Drugs, 62, 1481-1502.
Schnopp, C., Tzaneva, S., Mempel, M., Schulmeister, K., Abeck, D., & Tanew, A. (2005). UVA1 phototherapy for disseminated granuloma annulare. Photodermatology, Photoimmunology & Photomedicine, 21, 68- 71.
Schwartz, W.M., Bell, L., Bingham, P., Chung, E., & Cohen, D. (Eds.) (2003). The 5-minute pediatric consult (3rd ed.). Philadelphia: Lippincott Williams & Wilkins.
Sharma, V., Silverberg, N.B., Howard, R., Tran, C.T., Laude, T.A., & Frieden, I.J. (2001). Do hair care practices affect the acquisition of tinea capitis? Archives of Pediatric & Adolescent Medicine, 155(7), 818- 821.
Silverman, R. (2001). Using oral antifungals safely. Contemporary Pediatrics, 18(Suppl.), 9-11.
Stulberg D.L., Penrod, M.A., & Blatny, R.A. (2002). Common bacterial skin infections. American Family Physician, 66(1), 119- 124.
Tosanger, M., & Crutchfield, C.E. (2004). Tinea corporis. Dermatology Nursing, 16(5), 453.
Wichmann, K.M. (1994). Pediatric management problems. Pediatric Nursing, 20(5), 478-479.
Debbie Popovich, MSN, ARNP, is Clinical Assistant Professor, University of Florida College of Nursing, Gainesville, FL.
Allison McAlhany, MSN, ARNP, is Clinical Assistant Professor, University of Florida College of Nursing, Gainesville, FL.
Note: This article is reprinted with permission from Pediatric Nursing, 33(4), 315-320.
Copyright Anthony J. Jannetti, Inc. Aug 2008
(c) 2008 Dermatology Nursing. Provided by ProQuest LLC. All rights Reserved.