Management Of Pediatric And Adolescent Populations
Management Of Pediatric And Adolescent Populations
Wk 7 – Clinical Case SOAP Note 1. Identify a patient from your pediatric clinicals who provided you with a learning experience. 2. Write a complete SOAP note for the patient encounter. 3. Include the following: • A brief case scenario, including pertinent aspects of the history and physical exam • Your assessment and plan • The patient’s vaccine status, BMI percentiles, nutrient status, and development status. 4. Include a minimum of 2 scholarly peer-reviewed journal articles that support your differential diagnosis and plan. 5. Cite and reference according to 7th edition APA guidelines. 6. References must be from within the last five years. 7. All treatment regimens, diagnosis, medications, diagnostic testing, etc… need to have proper reference citations for each item. 8. Textbook for NRP/543: Burns, C. E., Dunn, A. M., Brady, M. A., Barber Starr, N., Blosser, C. G., & Garzon, D. L. (2017). Pediatric primary care (6th ed.). Elsevier. Grading Criteria Weeks 7: Clinical Case SOAP Note Content: 20 points possible Points Possible Points Earned Provided patient history and physical exam 5 Provided assessment and plan 5 Included the following components in the SOAP note; • patient vaccine status • BMI percentile assessment Management Of Pediatric And Adolescent Populations • Nutrition intake and activity pattern • developmental assessment 10 Office Visit Scenario • A mother brings her 11-month-old daughter to the clinic because of a persistent facial rash that has been present for 3 to 4 weeks. The child is restless at night and scratches in her sleep. She is otherwise healthy. Physical examination reveals a well-nourished, healthy-appearing girl with dry, red, scaly areas on the cheeks, chin, chest, and around the mouth, as well as on the extensor surfaces of her extremities. The areas on the cheeks have a plaque-like, weepy appearance with papules. The diaper area is spared. The remainder of the child’s examination is normal. Questions • What is the most likely diagnosis? Atopic Dermatitis • What is the most appropriate next step in the evaluation? Elicit further history to determine rash duration and exacerbating factors, as well as any family history of atopic dermatitis, allergic rhinitis, and asthma.
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• What is the best management for this condition? Use emollients frequently, control pruritus, and use a topical corticosteroid intermittently. Summary: An 11-month-old girl presents with a 3- to 4-week history of a dry, red, scaly areas on extensor surfaces of extremities, cheeks, chin, trunk, and around the mouth that spares the diaper area. An otherwise normal examination. Objectives • Describe the incidence, etiology, and risk factors for atopic dermatitis. • Discuss diagnostic criteria and the differential diagnosis for atopic dermatitis. • Describe the treatment and follow-up of atopic dermatitis. • Describe other conditions associated with atopic dermatitis. Management Of Pediatric And Adolescent Populations Considerations This is an infant with a rash that has been persistent for 3 to 4 weeks. A new rash can reflect a viral exanthem, which is a skin manifestation of a viral infection. However, the lack of associated symptomatology such as fever makes infection unlikely. This child’s history and physical examination findings are consistent with atopic dermatitis. Further history may reveal additional risk factors for allergic disease. Treatment involves avoiding aggravating factors and ensuring intensive skin hydration. Definitions • ATOPIC DERMATITIS (AD): The most common chronic inflammatory dermatologic disorder in children, characterized by pruritic patches or plaques with age-dependent distribution, usually with a remitting and relapsing course. Atopic dermatitis and eczema are frequently used interchangeably, but atopy, as well as contact dermatitis and irritant dermatitis, are different subtypes of eczema. • CONTACT DERMATITIS: Delayed-type or type IV hypersensitivity reaction due to an offending agent with the skin. The reaction involves an allergen-specific T-cell response. Includes primary irritant dermatitis (eg, irritant diaper rash) and allergic contact dermatitis (eg, poison ivy, nickel allergy). • ECZEMA: General term for a skin condition consisting of acutely inflamed papules and plaques, frequently associated with serous discharge and pruritus; eczematous eruptions include atopic, seborrheic, and contact dermatitides. • EMOLLIENT: Cream or lotion that restores water and lipids to the epidermis; those containing urea or lactic acid are more lubricating and may be more effective; creams lubricate better than lotions. • FLEXURAL AREAS: Areas of repeated flexion and extension, which often perspire on exertion (eg, antecubital fossae, neck, wrists, ankles). • LICHENIFICATION: Epidermal thickening with normal skin lines resembling a washboard. • SEBORRHEIC DERMATITIS: Self-limited scaly, erythematous, and/or crusty eruption limited to areas of the skin with a high concentration of sebaceous glands (eg, cradle cap). Clinical Approach to Atopic Dermatitis Epidemiology Atopic dermatitis (AD) is a chronic skin disorder characterized by pruritic plaques or papules with an age-dependent distribution. AD affects approximately 12.5% of children in the United States, with 60% of children presenting in the first year after birth and 90% presenting by age 5. Sixty-seven percent of patients present with mild disease, whereas the remaining patients present with moderate to severe disease. AD is considered the first manifestation of the “atopic march,” followed by development of food allergies, allergic rhinitis, and asthma. Pathophysiology The pathogenesis of AD is thought to be multifactorial, involving genetic abnormalities of the epidermal barrier, immune dysregulation, and environmental exposures. Experts debate whether the condition is primarily driven by immune abnormalities (inside-out theory) or epidermal barrier dysfunction (outside-in theory). Management Of Pediatric And Adolescent Populations Recent studies have noted variations of the filaggrin (FLG) gene in AD patients, which has a role in epidermal differentiation, aids in barrier function, and promotes skin hydration. Abnormal epidermal barrier function results in increased transepidermal fluid losses, leading to the ubiquitous finding of dry skin in AD patients. The abnormal epidermis also allows easier entrance of allergens and bacteria, stimulating an immune reaction. Although the exact genetic role is unclear, more than two-thirds of children with AD have an immediate family member with atopic disease. Differential Diagnosis • The differential diagnosis includes seborrheic dermatitis (cradle cap), which usually begins on the scalp in the first few months of life and may involve the ears, nose, eyebrows, and eyelids. The greasy brown scales of seborrheic dermatitis are in contrast to the erythematous, weeping, crusted lesions of infantile AD. • Other considerations include scabies, irritant dermatitis (perioral dermatitis), allergic contact dermatitis (poison ivy), and eczematoid dermatitis (infectious lesion near a draining ear). Rare conditions might include ichthyosis, severe combined immune deficiency, Wiskott-Aldrich syndrome (eczema, thrombocytopenia, and immunodeficiency in boys), zinc deficiency, and drug reactions. Comorbidities The most common comorbidity of AD is sleep disruption, present in up to 60% of children with AD. Children with AD are also more likely to have attention deficit hyperactivity disorder (ADHD), potentially caused by frequent sleep disturbance and chronic pruritus. Clinical Presentation Phases of AD • AD occurs in three often-overlapping phases. Management Of Pediatric And Adolescent Populations • Infants (birth to 3 years) present with central distribution of lesions on their scalp, forehead, cheeks, trunk, and extensor surfaces of the extremities with sparing of the diaper region. The lesions are erythematous, pruritic papules or plaques that ooze and crust. • The childhood phase (4-10 years) is notable for lesions on the wrists, ankles, perioral region, neck, and flexural surfaces such as the antecubital and popliteal fossa; the lesions typically are dry, pruritic papules or circumscribed scaly patches. • The adult phase (older than 12 years) is marked by lesions on the face (periorbital, perioral), flexural areas, and the dorsum of the hands and feet; marked lichenification can be found. History and Physical Examination Evaluation of the child with AD involves eliminating other potential causes of the child’s rash through a complete personal history, family history, and physical examination to obtain a proper diagnosis and initiate treatment (Table 32–1). Skin is evaluated for locations and nature of affected areas (patches, weepiness, lichenification), extent of skin dryness, and warmth or tenderness (possible secondary infection). Eyes, nose, throat, and chest are examined for evidence of allergic rhinitis (clear rhinorrhea, itching of nose, allergic shiners, nasal crease) or asthma (wheezing, shortness of breath on exertion)Management Of Pediatric And Adolescent Populations. Dermatologic Findings Patients with active lesions are at increased risk of infection due to the loss of skin integrity and immunologic deficiencies, particularly in beta-defensin (antiviral) and cathelicidin (antibacterial) components. Cutaneous viral infections, such as herpes simplex, warts, and molluscum contagiosum, are common. With recurrent flare-ups and trauma due to scratching, skin often becomes lichenified, with thickening of the skin and development of a leathery appearance. White dermographism may be seen, demonstrated by stroking the skin of a patient with AD; after the initial red line develops, a white line replaces it without wheals. Other associated findings include keratosis pilaris, accentuated palmar creases, small fissures at the base of the earlobe, and Dennie-Morgan creases under the lower eyelid. Laboratory Values Laboratory studies are not particularly helpful in diagnosing AD. The diagnosis requires pruritus, chronic relapsing eczematous dermatitis, and age-specific distribution. A serum immunoglobulin E (IgE) level is often elevated, and eosinophilia may be seen on a complete blood count (CBC). Culture of the skin is performed if bacterial superinfection is suspected. Treatment Topical Treatment Options Treatment goals include restoring and preserving the skin integrity, trigger avoidance, antiseptic measures, and use of antipruritic agents. Skin care measures include use of nonsoap cleansers or mild soaps, hydration and lubrication of the skin, and reduction of irritants and bacteria in the skin. Applying moisturizers immediately after bathing reduces transepidermal water loss. First-line therapy for acute flares is topical corticosteroids (TCSs). The lowest effective potency steroid preparation should be used. Typically, lower-potency TCSs are preferred over medium-potency TCSs for longer periods of treatment and for larger areas of affected skin. Lower-potency steroids are not associated with adverse endocrinologic side effects. Fluorinated corticosteroids (classes I, II, and III) are generally avoided on the face, genitalia, and intertriginous area because they may depigment and thin the skin; they are typically used for short periods of time and on lichenified areas. Lubrication is continued after corticosteroids are discontinued. • First-line therapy for acute flares is topical corticosteroids (TCSs) used twice daily for up to 3 days after flare-up resolution • Mild disease: a low-potency class VII TCS (ie, hydrocortisone, methylprednisolone, dexamethasone) • Moderate to severe disease; medium-potency TCS (classes III and IV; eg, fluticasone, triamcinolone, or mometasone) • Patients older than 2 years who are unresponsive to therapy or who require maintenance therapy can use topical calcineurin inhibitors (TCIs; pimecrolimus or tacrolimus) for a short period of time until symptom resolution; these agents do not cause skin atrophy or other additional adverse effects seen with corticosteroids. In stubborn cases, “proactive” maintenance therapy with TCSs or TCIs once or twice weekly decreases flare frequency. • Topical phosphodiesterase-4 inhibitors (crisaborole 2% [Eucrisa]) are approved for children over the age of 2 years, are nonsteroidal, are not associated with skin atrophy, and are available as monotherapy or incorporated into the previously described regimens. Refractory AD may require immunosuppressive agents (eg, cyclosporine, methotrexate, mycophenolate mofetil), narrow-band ultraviolet B (UVB) phototherapy, and rarely, oral corticosteroids. Oral Treatment Options Oral antihistamines are used to reduce itching. Symptoms of AD are often worse at night; sedating oral antihistamines (eg, hydroxyzine, diphenhydramine) may offer an advantage over nonsedating agents. Nonsedating agents, such as loratadine (Claritin) and cetirizine (Zyrtec), may be useful for patients with concurrent atopic conditions (ie, allergic rhinitis). Topical antihistamines are avoided because of the potential for skin irritation or toxicity due to absorption. Fingernails should be cut short to prevent further skin damage from scratching. Antibiotics Patients with secondary bacterial infections (eg, Staphylococcus or Streptococcus sp) often require outpatient antibiotic therapy. For localized infection, topical antibiotics (eg, mupirocin) are sufficient, whereas more generalized involvement requires systemic antibiotics (eg, first-generation cephalosporin). A poor clinical response may require broader antibiotic coverage for methicillin-resistant Staphylococcus aureus (MRSA). Widespread infection or evidence of toxicity may require hospital admission for intravenous antibiotics. Eczema herpeticum, caused by herpes simplex virus, can present with a severe infection requiring hospital admission and intravenous acyclovir. Pediatric Dermatology Consultation Consultation with a pediatric dermatologist may be warranted for patients with an unclear diagnosis, patients who fail to respond to treatment, or patients who have extensive skin involvement. Consultation also may be appropriate for patients with ocular or serious infectious complications, for patients requiring steroid therapy, and for patients with atypical herpes simplex virus superinfection. Other Treatment Options Avoidance of irritants, such as fragrances, tobacco, temperature extremes, and certain chemicals, can lessen disease severity. Aeroallergens, such as animal dander, dust mites, and pollen, can also exacerbate AD. Bathing patients prone to bacterial superinfection in bleach baths twice weekly reduces AD severity by decreasing inflammation and cutaneous bacterial colonization. Clinical Approach to Contact Dermatitis Epidemiology AD can be confused with contact dermatitis, a reaction of skin to an outside agent. Management Of Pediatric And Adolescent Populations Contact dermatitis is defined as inflammation of the dermis and epidermis due to direct contact of a substance to the surface of the skin. The two varieties are primary irritant contact dermatitis and allergic contact dermatitis. It is estimated that 10% to 20% of pediatric patients will develop contact dermatitis some time in their childhood. Females are more often affected than males. Common exposures include nickel, fragrant mixes, and neomycin/bacitracin ointments. Genetic predisposition is a factor. Pathophysiology Primary Irritant Dermatitis Primary irritant dermatitis can be caused by harsh detergents and soaps, bubble baths, saliva, urine, and feces. Examples of primary irritant contact dermatitis include diaper dermatitis, lip-licker’s dermatitis, and shin guard dermatitis seen in soccer and hockey players. Allergic Contact Dermatitis Allergic contact dermatitis is a delayed T-cell hypersensitivity reaction (type IV) that occurs 7 to 14 days after initial exposure and 1 to 4 days after subsequent exposures. The most common cause is exposure to plants such as poison oak, ivy, and sumac. Also common in the pediatric population is nickel allergy, causing irritation below the umbilicus (where nickel-containing buckles or snaps make contact) and on pinnae (from nickel ear piercings). Allergic contact dermatitis can also trigger an “id” reaction of widespread pruritic papules in nonexposed areas. Clinical Presentation A history of exposure to a suspected irritant or contact with an erythematous, blistering, and pruritic rash is highly suggestive of contact dermatitis. The examination often shows a well-demarcated area of the skin indicating the shape of the exposure. Patch testing can confirm the diagnosis. Treatment The main treatment is avoidance of the irritant or exposure. Covering nickel metal tabs of clothing, wearing gloves to reduce exposure to detergents, or avoiding latex may be helpful. Antihistamines or topical corticosteroids may help somewhat in the acute phase, with systemic short-term steroids reserved for extensive or severe contact dermatitis. Clinical Pearls • Atopoic dermatitis (AD) is a chronic, itchy disease that often begins in childhood. • In infancy, the itchy eruption has a more central distribution, involving the face and cheeks; by childhood, the rash is noted in flexural areas, predominantly in the extremities. • The diagnosis of AD is clinical and is based on pruritus, chronic relapsing eczematous dermatitis, and age-specific distribution. • Seborrheic dermatitis (cradle cap) presents as an oily and scaly rash beginning on the scalp in the first few months of life and may involve the ears, nose, eyebrows, and eyelids. • Baseline therapy for AD is avoidance of drying soaps and replenishment of skin hydration with emollients; topical steroids may be required. • Contact dermatitis is a delayed or type IV hypersensitivity reaction. • The main treatment of contact dermatitis is avoidance, and corticosteroids in the short-term if severe Management Of Pediatric And Adolescent Populations.
