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2. S upporting data from relevant diagnostic tests a. Di agnosis of AD is most often a clinical diagnosis, and immunologic testing is reserved for moderate to severe disease (T able 11-1). i. A lo w accuracy of food allergy tests has been reported in children with AD. ii. Di agnostic testing for skin allergies should be reserved for children who are nonresponsive to traditional therapies or who may have gastrointestinal symptoms of AD. b. A t 6 months of age, 83% of children with severe AD show positive Ig E sensitization to milk, eggs, and peanuts. III. Assessment A. Determine the diagnosis Differential diagnoses ( Figure 11-5 ) B. Assess the severity of the disease SCORAD is a clinical tool used by dermatologists to assess the extent and the severity of AD in children and to determine the effectiveness of the treatment regimen. The tool is available at http://dermnetnz. org/dermatitis /scorad. html C. Assess the significance of the problem to the child and family D. Assess the family functioning and ability to follow the treatment regimen IV. Goals of clinical management A. Improve quality of life for children with AD and their families 1. N o nighttime awakening because of itching 2. N o daytime discomfort or itching 3. N o missed school because of AD 4. N o missed workdays for the parents because of their child's symptoms B. Prescribe medications that allow the minimum effective dose to prevent adverse reactions C. Educate families so they understand and adhere to optimum skin care and medication regimenspruritus, and difficulty in identifying and avoiding triggers. ) 6. S ymptom history a. C ommon constitutional signs and symptoms of AD include pruritus, sleep disturbance, nasal congestion, age-specific patterns, or distribution of skin involvement, sparing of diaper area in infants, and sparing of groin and axillae in older children and adolescents; occasionally, irritabil-ity in infants with moderate-to-severe disease. b. S kin, hair, and nails i. Dr y skin (xerosis), erythema, occasional pap-ules, vesicles, weeping lesions, and crusting ii. C hronic skin changes include hyperpigmen-tation on lighter skin; hypopigmentation on darker skin; lichenification or leathery, thickened skin; and scarring from scratching c. L ymphadenopathy i. E nlarged lymph glands can be a common associated finding of children with AD, particularly in areas localized to exacerba-tions of AD or in children with associated bacterial, viral, or fungal infections. d. R espiratory i. P ulmonary findings of wheezing are com-mon in children with atopic disease and asthma is a common associated condition. B. Objective 1. P hysical examination findings a. A D presents differently at different ages. There are three distinct phases of clinical features: (1) infan-tile phase, (2) childhood phase, and (3) adult phase (see Figure 11-2). b. C onditions and features often associated with AD in children and adolescents (see Figure 11-3). c. O pportunistic infections are common in infants and children with AD (see Figure 11-4). d. Add itional physical examination findings of atopic disease:i. Ge neral appearance: pallor, allergic shiners, allergic salute, and xerosis ii. H ead, eye, ear, nose, and throat: periorbital puffiness; tympanic membranes with effu-sion unilaterally or bilaterally; boggy nasal mucosa or erythematous turbinates with enlarged adenoids; and tonsilar hypertro-phy, nonerythematous, nonexudative iii. N eck: enlarged lymph nodes (cervical, occipital, postauricular) iv. C hest: adventitious sounds such as wheezing72 CHAPTER 11 | Atopic Dermatitis in Children

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

V. p lan A. Develop an optimum skin care routine with the family New data have established that AD results from primary abnormalities of the skin barrier, suggesting the impor-tance of skin-directed management of the disease D. Control environmental factors that may adversely affect the child's skin (Note: Food avoidance is no longer first-line management or mainstay of treatment for AD. ) E. Provide ongoing emotional and medical support for children and their families FIGure 11-2 p hases of Atopic Dermatitis in c hildren ph Ases cl INI c A l F e Atures (may or may not include) Infantile phase Begins from birth to 6 months of age: May begin on cheeks and progress to scalp, arms, trunk, and legs; generalized dry skin (xerosis) including scalp Progresses to lateral extensor surfaces of arms and legs Pruritus and itch-scratch-itch cycle develops Acute phase with intense itching causing irritability in infant; vesicle formation, oozing, and crusting with excoriated areas on the skin Hallmark sign is diaper area and groin are usually spared of lesions May resolve by 2 years of age but can continue into childhood; symptoms may become milder as the child ages and disappear at adolescence or may continue throughout life Childhood phase Begins around 2 years of age: Involves wrists, hands, neck, ankles, popliteal and antecubital spaces, commonly on flexural surfaces Lesions tend to be dry, papular, circumscribed, scaly patches Pruritus is often severe Chronic manifestations include: Lichenification, thickening of skin causing leathery appearance Hyperpigmentation Scratch marks Often worse during winter dryness or summer heat. Adult phase Begins at puberty or ~12 years of age: Most commonly involves flexural skin folds; bends of elbows and knees; face; neck; upper arms; back; and dorsa of the hands, feet, fingers, and toes May be a new occurrence or reoccurrence of chronic condition Often postinflammatory hyperpigmentation and hypopigmentation disappear in adolescence or young adulthood. Data from Habif, T. P. (2010). Atopic dermatitis. In T. P. Habif (Ed. ), Clinical dermatology: A color guide to diagnosis and therapy (5th ed. ). Philadelphia, PA: Elsevier. Plan 73

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(T ollefson & Bruckner, 2014). Develop an optimum skin care routine with the family. Instruct the family to use the following “soak and seal” technique: 1. D aily bath with lukewarm water for about 10 to 15 minutes. Use a minimal amount of fragrance-free and dye-free gentle soap or cleanser that is formulated for sensitive skin, such as Cetaphil Cleanser, at the end of the bath. If the child is not too dirty, use soap or cleanser only on hands, feet, armpits, and genital area, not all over the body. a. I f the child complains of burning when sitting in a bathtub, the addition of one cup of table salt may make the bath more tolerable (Paller & Mancini, 2011). 2. Ge ntly pat away excess water, leaving skin slightly damp. 3. I f rash is present, apply skin medication to the rash on body and face. Prescription medications should be applied to areas of the skin that are red, rough, or itchy, or where there is a rash when the skin is slightly damp. Apply in a thin layer and rub in well. 4. A fter drying, apply a generous amount of moisturizing cream or ointment to the entire body and face. This seals in the water from bathing and makes the skin less dry and itchy. Eucerin cream, Aquaphor™ ointment, and Cetaphil™ cream are effective products. Lotions are not recommended for adequate moisturizing in children with AD. Vaseline or petroleum jelly can be used as an inexpensive moisturizer and sealer, and it is a good occlusive preparation, although not a moisturizer. This application should be done within 3 minutes of exiting the bath before water loss in the FIGure 11-3 c onditions and Features Associated with Atopic Dermatitis Assoc IAte D co NDI t I o N s cl INI c A l F e Atures (may or may not include) Dennie line or Dennie-Morgan fold Extra grooves or accentuated lines seen below lower eyelids bilaterally; may result from chronic edema of the eyelids and skin thickening Allergic shiners Dark discoloration below lower eyelids in lighter skin; slate-gray discoloration in individuals with darker skin; a result of vascular stasis Allergic salute Crease over the nasal bridge or exaggerated linear nasal crease caused by frequent rubbing of nose or nasal tip; most often associated with allergic rhinitis but common in atopic children Pityriasis alba Hypopigmented, slightly elevated plaques; occasionally with fine scaling, irregular borders; nonpruritic; occurring most often on the face of young children; also may appear on the upper arms and thighs; ~2-4 cm in diameter round-to-oval, often occur in summer or fall Keratosis pilaris Most predominant on the lateral aspects of the upper arms, buttocks, and thighs; appears in early childhood and persists into adulthood; papular with plugged hair follicles and surrounding inflammation; characterized by redness on lighter skin Nummular eczema Coin-shaped lesions or plaques ~1 cm or greater in diameter; erythematous and formed by confluent papules or occasionally vesicles Ichthyosis vulgaris T ransmitted as an autosomal-dominant trait; can be associated with AD but a separate disease; may occur as early as 3 months of age, but most common onset in later childhood; characterized by large scales on extensor surfaces of extremities, particularly on lateral aspect of the lower legs in plate-like scales; flexural surfaces are spared Data from Paller, A. S., & Mancini, A. J. (2011). Eczematous eruptions in childhood. In A. S. Paller & A. J. Mancini (Eds. ), Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence (4th ed. ). Philadelphia, PA: Elsevier ; Habif, T. P. (2010). Atopic dermatitis. In T. P. Habif (Ed. ), Clinical dermatology: A color guide to diagnosis and therapy (5th ed. ). Philadelphia, PA: Elsevier. 74 CHAPTER 11 | Atopic Dermatitis in Children

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

B. Avoid factors or allergic triggers that lead to flares 1. I rritants: things that may cause the skin to be red or itchy or to burn a. W ash all new clothes before wearing to remove chemicals. Double rinse the child's laundry so that the skin is not in contact with residual deter-gent in clothing. b. D o not use fabric softeners. c. A void clothes made of wool and artificial fibers. Dress the child in loose-fitting cotton clothes that allow air to pass freely to the skin. d. A void contact with harsh household cleaners. Use natural, environmentally safe products. skin occurs from evaporation. It can be repeated as needed to dry, itchy skin (Paller & Mancini, 2011). This bath routine should be continued even after the skin has improved and the prescription medication is no longer necessary. 5. W hen moisturizing products are not effective, some children may need a special preparation containing ammonium lactate or alpha-hydroxy acid lotion for maintenance care. These products have increased ability to hold water in the skin and the products may limit desquamation. However, they frequently cause burning of the affected skin and so should be used with caution with young children (Fitzpatrick & Wolff, 2005). Table 11-1 Common Laboratory Tests test Definition c linical Implications c omments Skin prick test Wheal response after skin prick with antigen Ig E-mediated food hypersensitivity Often does not correlate with clinical manifestations in children with AD Radioallergosorbent test Circulating specific Ig E Ig E-mediated food hypersensitivity False-positive findings are common, particularly in older children Data from Paller, A. S., & Mancini, A. J. (2011). Eczematous eruptions in childhood. In A. S. Paller & A. J. Mancini (Eds. ), Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence (4th ed. ). Philadelphia, PA: Elsevier. FIGure 11-4 s econdary o pportunistic s kin Infections opportu NIst Ic INFect Io Ns A ssoc IAte D FINDING s (may or may not include) Staphylococcus aureus Erythematous with pustular, exudative lesions and crusting; the most common opportunistic infection in AD and recovered in 93% of patients with AD lesions, 79% from nares of atopic children Streptococcus pyogenes A less common opportunistic infection in children with AD than S. aureus; skin findings as above Herpes simplex V esicles often become umbilicated; eczema herpeticum, rapid development of vesiculopustular lesions over the sites of dermatitis, can occur in individuals with AD Viral molluscum contagiosum Small, dome-shaped papules often with central umbilication; commonly af fect trunk, axillae, and antecubital and popliteal fossae in 25% of children with AD Data from Habif, T. P. (2015). Atopic dermatitis. In T. P. Habif (Ed. ), Clinical dermatology: A color guide to diagnosis and therapy (6th ed. ). Philadelphia, PA: Elsevier. Plan 75

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e. W ear long pants and long sleeves when playing around irritating substances, such as sand, dirt, and plants. f. El iminate the child's exposure to secondhand smoke because it can increase irritation and pru-ritus and may also increase the tendency for the development of asthma (Paller & Mancini, 2011). g. Ke ep the child's fingernails short, smooth, and clean to help prevent skin irritation, infection, and damage caused by scratching. Explain to the family that when the child scratches the rash becomes worse and the skin becomes thicker. 2. P roved or suspected allergens a. C onsider food allergy only in children who have reacted immediately to a certain food and in infants and young children with moderate or severe uncontrolled AD, particularly with gastro-intestinal symptoms or failure to thrive (National Institute for Health and Clinical Excellence [NICE], 2007). The National Institute of Allergy and Infection Disease (NIAID) guidelines state that allergy evaluation, specifically to milk, eggs, peanuts, wheat, and soy, should be considered in children less than 5 years with severe AD if the child has persistent AD despite optimal manage-ment. The guidelines state that food allergies can induce hives and itching, which may aggravate AD but do not cause AD. Egg allergy may be one exception. Up to half of infants with egg-specific Ig E may have improvement in their AD when fol-lowing an egg-free diet (T ollefson & Bruckner, 2014). i. I f cow's milk allergy is suspected, offer a 6- to 8-week trial of an extensively hydrolyzed protein formula as a substitute for cow's milk formula for bottle-fed infants younger than 6  months of age with moderate or severe AD. Refer to a dietary specialist if the baby needs to be on cow's milk-free diet for more than 8 weeks (Paller & Mancini, 2011). ii. I nform breastfeeding mothers that it is not known whether altering a mother's diet is effective in reducing symptoms. However, if a food allergy is strongly suspected consider a trial of elimination of the more allergenic foods, such as cow's milk, soy, wheat, tree nuts, peanuts, fish, and egg, under dietary supervision. b. C onsider inhalant allergy in children with sea-sonal flares, associated asthma, and allergic rhini-tis and in children older than 3 years of age with AD on the face. After 3 years of age, many children FIGure 11-5 c ommon Differential Diagnosis of Atopic Dermatitis co NDIt Io N A ssoc IAte D FINDING s (may or may not include) Contact dermatitis Irritant or allergic contact dermatitis is generally milder than AD; occurs on the cheeks and chin, extensor surfaces or diaper area of infants and young children; caused by harsh soaps, vigorous bathing, or saliva on cheek and chin area. Seborrheic dermatitis Greasy, yellow scales that involve the scalp, eyebrows, behind the ears, cheeks, and can spread to neck and chest area; generally nonpruritic. Often AD appears as seborrheic dermatitis subsides. Psoriasis Round, erythematous, well-marginated plaques; covered by grayish or silvery-white scales; ~1 cm or greater in diameter; commonly found on the scalp, elbows, knees, and lumbosacral area. Scabies Pruritic papules, nodules, vesiculopustules, and burrowing lesions; commonly occur on infants and young children; seen on trunk, between the fingers, wrists, ankles, axillae, waist, groin, palms of hands, and soles of feet; occasionally seen on the head of infants. Data from Paller A. S., & Mancini, A. J. (2011). Eczematous eruptions in childhood. In A. S. Paller & A. J. Mancini (Eds. ), Hurwitz clinical pediatric dermatology: A textbook of skin disorders of childhood and adolescence (4th ed. ). Philadelphia, PA: Elsevier. 76 CHAPTER 11 | Atopic Dermatitis in Children

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outgrow food allergies but become sensitive to airborne allergens, such as dust mites (Leong et al., 2004). Some children have shown improve-ment in symptoms when dust mites are controlled in their environment, especially in their bedroom:i. El iminate floor coverings and curtains ii. El iminate all upholstered furniture except the bed iii. C over box springs, mattress, and pillows in plastic zippered covers or obtain allergy-proof covers iv. El iminate clutter and limit the toys, espe-cially stuffed animals v. W ash all bedcovers and stuffed animals at least once a week in hot water vi. Ke ep pets with fur or feathers out of the room because they attract dust c. A void only substances that are documented to cause an increase in symptoms. It is important not to deny children things unnecessarily, such as foods or outdoor activities. d. M ost children with mild AD do not need diag-nostic testing for skin allergies (NICE, 2007). C. Treat symptoms when they occur 1. T opical corticosteroids are the therapeutic mainstay for AD. They not only suppress the inflammation and pruritus associated with AD, but they may also have an effect on bacterial colonization. Choosing which corticosteroid to prescribe depends on the severity and distribution of the lesions and the age of the child. Preparations are divided into seven groups based on relative potency, from very low preparations, such as hydrocortisone acetate, to very high preparations, such as clobetasol propionate. Ointment-based prepara-tions are more potent, more occlusive, and less drying than chemically equivalent cream-based agents. The most effective, but least potent, should  be used to prevent thinning of the skin. For children with mild-to-moderate disease, a group VII drug, such as hydro-cortisone ointment 1% or 2. 5%, is usually sufficient. When corticosteroids are prescribed, consider the following: a. P rescribe in adequate amounts to optimize con-trol. Prescriptions that require frequent refills may lead to undertreatment or nonadherence. b. P rescribe for application only once or twice a day. c. C orticosteroids should be applied to areas of active lesions, not to clear skin for prophylaxis. d. C onsider the possibility of secondary bacterial or viral infection if the regular application of cortico-steroids has not controlled the AD within 2 weeks. e. C onsider changing to a different topical cortico-steroid of the same potency as an alternative to stepping up treatment if tachyphylaxis is suspected (NICE, 2007). f. D o not use potent topical corticosteroids on the face or neck. g. W hen inflammation is widespread, avoid high-potency corticosteroids because of the risk of systemic adverse effects. h. R efer to a specialist if potent corticosteroids are needed for children younger than 12 months of age. i. E xplain to families that the benefits of topical cor-ticosteroids outweigh the risks if applied correctly. 2. T opical calcineurin inhibitors are an option for treatment if the child's AD has not shown a satisfactory clinical response to adequate use of topical corticosteroids at the maximum strength and potency that is appropriate for the child's age and the area being treated (NICE, 2007). Both pimecrolimus cream 1% (Elidel) and tacrolimus ointment 0. 03% and 0. 1% (Protopic) are approved for treating AD in children 2 years of age and older. a. P imecrolimus is efficacious in children with mild-to-moderate AD. b. T acrolimus is appropriate for children with mod-erate-to-severe disease, and its effectiveness has been compared to midpotency topical steroids. c. Both medications are safe for use in the perior-bital areas and on the head, neck, and intertrigi-nous area (Paller & Mancini, 2011). d. A bur ning sensation may occur during the first few days of application in children with either medication, especially in children with more severe dermatitis. e. U se sun protection when using either medication. 3. W et-wrap dressings reduce itching and inflammation by cooling the skin and improving penetration of topical corticosteroids for acute exacerbations. They also prevent excoriation from scratching. In the hospital, gauze is usually used for this procedure. At home, a method used for years at the National Jewish Medical and Research Center, Denver, Colorado, is a simpler approach. It uses wet clothing, such as long underwear and cotton socks, applied over an undiluted layer of topical corticosteroids with a dry layer of clothing on top. a. U se blankets to prevent chilling. b. S hould not be used for more than 7-14 consecu-tive nights (NICE, 2007). 4. A ntihistamines are thought to have little direct effect on pruritus. However, the tranquilizing and sedating effects of sedating antihistamines, such as hydroxyzine, diphenhydramine, and doxepin, may provide symptomatic relief if given at bedtime. Cetirizine may have limited value, but it is also somewhat sedating. Plan 77

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Nonsedating antihistamines are not effective in alleviating pruritus (Paller & Mancini, 2011). a. E nsure that the medication does not interfere with the child's functioning during the daytime. b. T opical antihistamines should be avoided because of possible local allergic reactions. 5. P hototherapy could be considered for severe AD or when other management options have failed. Refer to a pediatric specialty clinic where staff is experienced in dealing with children. 6. S ystemic corticosteroids should be avoided except in rare instances (Fitzpatrick & Wolff, 2005). Although effective for most patients with AD, the rapid rebound after discontinuation and high risk of potential side effects make their use impractical in children. 7. T reating flares of symptoms is an important area of patient education. Flares can occur at any time and the family should be prepared to step up treatment when needed. a. O ffer information on how to recognize flares. b. G ive written instructions, such as an Eczema Action Plan, on how to manage flares by step-ping up treatment and prescribe treatments accordingly. c. T reatment of flares should be started as soon as symptoms appear and should be continued for 48 hours after acute symptoms subside (NICE, 2007). D. Treat complications 1. B acterial superinfection with S. aureus is common in children with AD. First-generation cephalosporins, such as cephalexin, 25-50 mg/kg divided two or three times daily for 10 days, are commonly used, although in some communities it may be advisable to culture for methicillin-resistant S. aureus and then treat accordingly. The addition of one-quarter to one-eighth cup of chlorine bleach to a full tub of water, intermittent application of mupirocin ointment to the nares and hands of patients and caregivers daily for 3 weeks, and the use of a gentle antibacterial soap may decrease colonization (Paller & Mancini, 2011). Control of pruritus and prevention of excoriation with proper skin care and medications also helps prevent cutaneous infections. 2. H erpes simplex virus infection (eczema herpeticum) is a potentially life-threatening complication. a. C onsidered if the following is observed: i. A reas of rapidly worsening and painful dermatitis ii. S ystemic symptoms, such as fever, lethargy, or distressiii. C lustered blisters with the appearance of early-stage cold sores iv. P unched-out erosions that are uniform in appearance and that may coalesce (NICE, 2007) v. C hild's infected dermatitis fails to respond to antibiotic treatment and appropriate corticosteroids b. I f suspected, treat immediately with systemic acy-clovir and refer for same-day dermatologic advice. c. I f there is involvement of the skin around the eyes, refer for a same-day consultation with an ophthalmologist and dermatologist. VI. s elf-management A. Patient and family education and home management of bathing and medication regimens are the key factors in determining successful outcomes for children with AD. It is important to: 1. I nvolve the family in all treatment decisions. The family is likely to be more adherent with the treatment plans if they have been part of the decision-making process. Consider the family's cultural skincare and bathing practices when discussing options. 2. E xplain that AD often improves with time, but not all children grow out of the condition; at times it becomes worse as the child gets older. 3. E ducate families regarding the avoidance of environmental, behavioral, or emotional factors that may trigger symptoms. Referral to a public health nurse or community health worker for an environmental assessment in the home may be helpful. 4. C learly explain the quantity of moisturizer to use on the child's skin. Applying an insufficient amount of moisturizer is a common problem. B. Families need comprehensive written and verbal information in their native language regarding maintenance therapy, when and how to step treatment up and down, how to treat flares, and how to recognize complications. All procedures, even the application of ointments, should be demonstrated. C. Discuss complementary therapies with the family and explain that their effectiveness and safety for AD has not been adequately assessed (NICE, 2007). 78 CHAPTER 11 | Atopic Dermatitis in Children

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re Fere Nces Boguniewicz, M. (2005). Atopic dermatitis: Beyond the itch that rashes. Immunology and Allergy Clinics of North America, 25, 333-351. Fitzpatrick, T., & Wolff, K. (2005). Fitzpatrick's color atlas and synopsis of clinical dermatology (5th ed. ). New Y ork, NY: Mc Graw-Hill. Goodhue, J. G., & Brady, M. A. (2009). Atopic and rheumatic disorders. In C. E. Burns et al. (Eds. ), Pediatric primary care (4th ed., pp. 553-583). St. Louis, MO: Saunders/Elsevier. Habif, T. P. (2010). Atopic dermatitis. In T. P. Habif (Ed. ), Clinical derma-tology: A color guide to diagnosis and therapy (5th ed. ). Philadelphia, PA: Elsevier. Leong, D. Y. M., Boguniewicz, M., Howell, M. D., & Hamid, Q. A. (2004). New insight into atopic dermatitis. Journal of Clinical Investigation, 113, 651-657. National Institute for Health and Clinical Excellence (NICE). (2007). Atopic eczema in children (NICE clinical guideline 57). London, UK: Author. National Institute of Arthritis and Musculoskeletal and Skin Diseases Information Clearing House, National Institutes of Health. (2009). Atopic dermatitis: Handout on health. Bethesda, MD: Author. Full text available online: www. niams. nih. gov Paller, A. S., & Mancini, A. J. (2011). Eczematous eruptions in childhood. In A. S. Paller & A. J. Mancini (Eds. ), Hurwitz clinical pediatric derma-tology: A textbook of skin disorders of childhood and adolescence (4th ed. ). Philadelphia, PA: Elsevier. Porth, C. M., & Matfin, G. (2009). Pathophysiology: Concepts of altered health states (8th ed. ). Philadelphia, PA: Wolters Kluwer/Lippincott, Williams & Wilkins. T ollefson, M. M., & Bruckner, A. L. (2014). Atopic dermatitis: Skin-directed management. Pediatrics, 135(6), 1735-1744. VII. p sychosocial and emotional support A. Considering the effect of AD on the quality of life of patients and their families, it is important to address possible psychosocial issues and to offer support: 1. P arents may feel guilty about the child's condition and they may be exhausted from sleep deprivation and from caring for the child's needs. 2. S chool-age children may be teased by their peers about the appearance of their skin and may also fall behind in their schoolwork because of absences. 3. Ado lescents may be particularly self-conscious about their appearance and may be leading isolated lives. B. Refer the family and child to a local support group or for counseling if needed. C. AD education resources: 1. N ational Eczema Association Support Network: www. nationaleczema. org/support 2. N ational Jewish Medical and Research Center: www . nationaljewish. org 3. N ational Institute for Health and Clinical Excellence “Understanding NICE Guidance—Information for Patients and Caregivers”: www. nice. org. uk/CG57 4. N ational Eczema Society (UK): www. eczema. org 5. C hanging Faces: www. changingfaces. org. uk References 79

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symptoms in the categories described next for older adoles-cents and young adults, and added examples of core behav-iors that are more applicable to adolescents and adults (APA, 2013). These changes were made in recognition of the developmental changes in behaviors across the lifespan and the difficulties adults might have in recalling child-hood symptoms when presenting for diagnosis. Because current practice guidelines still follow the DSM-IV TR diagnostic criteria (Pliszka and AACAP Work Group on Quality Issues, 2007; Subcommittee on Attention-Deficit/Hyperactivity Disorder et al., 2011), it is important for the APN to be familiar with both sets of criteria. Fortunately, the core behaviors of ADHD remain the same across DSM versions (Dalsgaard, 2013). T o be diagnosed with ADHD under DSM-V criteria, the child or adolescent (under 17) must display at least six inat-tentive behaviors and/or at least six impulsive or hyperac-tive behaviors (APA, 2013). Adolescents and adults 17 and older must display at least five behaviors in either or both categories. Examples of inattentive behaviors include diffi-culty in performing tasks that require sustained attention, distractibility, difficulty in organizing sequential tasks, poor time management, forgetfulness, and appearing not to lis-ten when spoken to directly. Examples of hyperactive or impulsive behaviors include fidgeting, leaving one's seat or running around in inappropriate settings or difficulty stay-ing still in restaurants or meetings, difficulty taking turns, blurting out answers, taking over what others are doing and acting as if “driven by a motor” (APA, 2013, p. 60). In adolescents and young adults, hyperactive behaviors may be more subtle, and impulsivity may manifest as impaired decision making or impulsive driving errors (Adler, Mattingly, Montano & Newcorn, 2011). Many of the symptoms and behaviors diagnostic of ADHD can be considered developmentally normal in younger children. Nevertheless, the current American Academy of Pediatrics (AAP) guidelines state that primary care clinicians can diagnose ADHD as young as 4  years of age, as long as the child is showing behavior that is out I. Intr oduction and general background Attention-deficit/hyperactivity disorder (ADHD) is one of the most common chronic conditions in childhood and the most common of the chronic neuropsychiatric conditions (Merikangas et al., 2010), with an estimated prevalence rate of 7. 2% (Thomas, Sanders, Doust, Beller, & Glasziou, 2015). The major pediatric and child psychiatric organizations recognize the benefits and role of primary care providers in diagnosing and treating this condition in childhood and adolescence (Pliszka & American Academy of Child and Adolescent Psychiatry [AACAP] Work Group on Quality Issues, 2007; Subcommittee on Attention-Deficit/Hyperactivity Disorder et al., 2011). The advanced practice nurse (APN), working in either primary or specialty care, is well suited to detect, follow, refer, and manage children with ADHD (Vierhile, Robb, & Ryan-Krause, 2009). II. Overview A. Definitions ADHD is defined by its features as a syndrome involv-ing inattentiveness, hyperactivity, impulsivity or a com-bination (Feldman & Reiff, 2014). Diagnostic criteria for ADHD have been set historically by the Diagnostic and Statistical Manual for Mental Disorders (DSM). The cur-rent edition, DSM-V (American Psychiatric Association [APA], 2013, p. 61), describes the “essential feature” of ADHD as “a persistent pattern of inattention and/or hyperactivity-impulsivity that interferes with functioning or development. ” Under the current diagnostic criteria, the individual must have displayed some of these behaviors before age 12 years, and they must be present in at least two areas of the child's life, such as home and school. Changes from the DSM-IV-T ext Revision (TR; APA, 2000) include a move of the upper limit for appearance of first symptoms from age 7 to age 12, a lowering of the number of required Naomi Schapiro Atte Nt ION-Def Ic It/ Hyper Act I v I ty D ISO r D er IN c HI l D re N AND A DO le S ce N t S© Eliks/Shutterstock; © donatas1205/Shutterstock 8012Chapt Er

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C. Theories of pathophysiology Studies of heritability have found that 60% to 76% of the variance in ADHD could be explained by genetic factors, with multiple potential genetic contributions (Cortese, 2012). Genome-wide association studies have shown that heritability is polygenic, with a mixture of common and rare DNA variants (Faraone, 2014). Dopamine and adren-ergic systems have been implicated in the core symptoms of ADHD, with alpha-2-adrenergic receptors responsible for inhibitory control of motor activity (Cortese, 2012). There may be involvement of serotonin and cholinergic systems, although animal studies are less consistent, and there is no animal model that completely replicates the core symptoms of ADHD. Current theories suggest struc-tural abnormalities and delays in maturation in the prefron-tal cortex, caudate, and cerebellum (Sharma & Couture, 2014). Functional brain studies reveal low activation in areas related to cognition, executive function, emotion and sensorimotor functions, and altered connectivity between regions (Cortese, 2012). Up to 45% of children with ADHD exhibit emotional dysregulation, with less sensi-tivity to positive stimuli than children without ADHD, problems regulating attention to emotional stimuli, and misperception of the emotions of others (Shaw, Stringaris, Nibb, & Leibenluft, 2014). III. Database: History A. Chief complaint: referrals from parents, teachers, and family members Parents may initiate care if they have noticed disruptive or attention problems at home or at school and are also frequently encouraged by school personnel to have their child evaluated for ADHD. The initiating symptoms, and motivation for seeking a diagnosis or treatment, are an important part of the history. Because specific behaviors are both part of the diagnostic criteria and help guide the treatment plan, it is important to have parents and children be as specific as possible about the core behavioral symp-toms and how they manifest in all the areas or domains of the child's life, particularly at home, at school, and with friends. Just as with a purely physical chief complaint, the APN can be guided in diagnosis by asking for the duration of the behaviors, specifically when they manifest (during which activities at home or which parts of the school day), any environmental characteristics or interventions that have made the behaviors better or worse, any associated problems, and any previous efforts by parents or teachers to manage the behaviors. For older adolescents and young adults, the functional impairment in school-and work-related settings may be the most salient part of the present-ing complaint, and it may take skillful questioning to elicit of range for developmentally appropriate peers and func-tional impairment in two domains (Subcommittee on Attention-Deficit/Hyperactivity Disorder et al., 2011). B. Incidence and prevalence According to the 2011 National Health Interview Survey (NHIS), 8. 4% of U. S. children were reported by their par-ents to have been diagnosed with ADHD (Perou et al., 2013). Using part of the National Health and Nutrition Examination Survey sample, over 8% of children who were given a structured mental health diagnostic interview fit diagnostic criteria for ADHD (Merikangas et al., 2010). Only half of the children in this study with diagnosable mental health conditions had sought treatment with a mental health professional. A meta-analysis of 179 global prevalence studies over 36 years show a pooled prevalence rate of 7. 2%, with somewhat increased rates using the DSM-IV and DSM-IV-TR criteria over earlier DSM ver-sions (Thomas et al., 2015). Prevalence studies of coexisting conditions in children with ADHD come from samples of children referred to psychiatric care, and so should not be interpreted as being representative of all children: 35% of children with ADHD in referral samples have oppositional defiant disorder, 26% have conduct disorder, 26% have anxiety, and 18% have depressive disorders (Stein & Perrin, 2003). A retrospective chart review of children from ages 5 to 10 diagnosed with ADHD found that African-American children, girls, and children of parents with lower educational levels were less likely to receive a comprehensive neurodevelopmental eval-uation for coexisting conditions (Gipson, Lance, Albury, Gentner, & Leppert, 2015). There was no difference in polypharmacy or special education evaluation between those who did and did not receive this evaluation; however, authors expressed concern about potential differences in long-term outcomes. The APN should be alert to the pos-sibility of coexisting conditions while taking a comprehen-sive history and performing a physical exam. An estimated 60% to 80% of the behavioral problems of children with ADHD persist into adulthood (Sharma & Couture, 2014). In one 6-year follow-up study of adoles-cents with ADHD, Cheung and colleagues (2015) found that 79% of adolescents with ADHD still met diagnostic criteria for ADHD into adulthood, with hyperactivity and parent ratings in childhood predicting adult persistence, and low income and lower cognitive function in child-hood predicting higher adult functional impairment. In an earlier 10-year longitudinal study, boys with ADHD who were treated with stimulants had lower rates of psychiatric disorders and academic failure than boys with ADHD who were not treated (Biederman, Monuteaux, Spencer, Wilens, & Faraone, 2009). These findings reinforce the importance of early diagnosis and effective treatment for children and adolescents with ADHD. Database 81

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Hyperactivity Disorder, 2011). The screening question-naire in the AAP ADHD T oolkit, the Vanderbilt ques-tionnaire (Wolraich, Bard, Neas, Doffing, & Beck, 2013; Wolraich et al., 2003), is available without cost on several websites in English and Spanish (see T able 12-1 ). Broader questionnaires, such as the Achenbach Child Behavior Checklist, have not been found to be specific or sensitive enough for the diagnosis of ADHD in primary care set-tings (Subcommittee on Attention-Deficit/Hyperactivity Disorder, 2011) but may be used by psychiatric and men-tal health professionals as part of their assessment. Most clinical questionnaires for identifying ADHD include parent forms and teacher forms, and it is crucial to collect information directly from the child's teacher. Asking the parent to deliver and retrieve screening forms from the teacher saves the APN time and ensures that parents con-sent to the collection of this information. C. Screening for coexisting psychiatric and behavioral issues Screening questionnaires, such as the Vanderbilt or Conners forms, include questions whose positive answers raise the clinician's suspicion of coexisting oppositional, anxiety, or mood disorders. Children who are suffering the the core behavioral symptoms that fit diagnostic criteria for ADHD and the age at which they began to manifest (Adler et al., 2011). Sleep problems, including sleep apnea, may result in daytime fatigue and inattention. Seizure disorders, espe-cially absence seizures, may masquerade as inattention (Subcommittee on Attention-Deficit/Hyperactivity Dis-order, 2011). Allergy symptoms, and the medications used to treat them, can also be related to inattention (Selekman, 2010). The APN's documentation of patient history should include questions about sleep, snoring, and nighttime awakening and specific descriptions of inattentive behavior. Children with hearing impairments or learning disabilities, such as reading disorders and receptive language delays, and other psychiatric conditions, such as anxiety or depres-sion, may also seem distractible and inattentive. History should include questions about any unusual movements or habits, such as tics or obsessive-compulsive behaviors, which may coexist with ADHD. B. Screening for ADHD The AAP states that primary care clinicians may use ADHD-specific screening scales to aid in the diagno-sis of ADHD (Subcommittee on Attention-Deficit/ Table 12-1 Screening T ools for ADHD (Partial List) Name contact Info c ost Individuals Screened l anguages Additional Information Vanderbilt Forms in Caring for Children with ADHD: A Resource Toolkit for Clinicians, 2nd ed. American Academy of Pediatrics http://www2. aap. org/pubserv/adhd2/1sted. html$94. 95 Parents Teachers English Spanish Screening forms Educational handouts Behavioral treatment guidelines Vanderbilt Forms National Institute for Children's Health Quality (NICHQ)http://www. nichq. org/childrens-health/adhd /resources/vanderbilt-assessment-scales No Cost Parents Teachers English Screening forms (1st ed. )Educational handouts Modified Vanderbilt Forms San Diego ADHD Projecthttps://research. tufts-nemc. org/help4kids /forms. asp No Cost Parents Teachers English Spanish Screening forms Educational handouts Links to behavioral treatment guidelines Conners Formshttp://www. mhs. com/product. aspx?gr=cli&id=overview&prod=conners3$269-$795, paper, online, software Parents Teachers Youth (8-18)English Spanish French Screening—long & short forms Barkley scales for children and adultshttp://www. guilford. com/search-products /ADHDvariable Parents Teachers Adults English CHADD list of screening resourceshttp://www. help4adhd. org/en/treatment /scales Links to rating scales listed here and others Partial list of screening forms. Additional forms described in Pliszka, S., & AACAP Work Group on Quality Issues. (2007). Practice parameter for the assessment and treatment of children and adolescents with attention-deficit/hyperactivity disorder. Journal of the American Academy of Child & Adolescent Psychiatry, 46, 894-921. 82 CHAPTER 12 | Attention-Deficit/Hyperactivity Disorder in Children and Adolescents

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sequelae of family disruption, child abuse, or other trau-mas may exhibit distractibility, inattention, and fatigue from sleep problems related to anxiety or mood changes (Gerson & Rappaport, 2013; Selekman, 2010). Careful history-taking, including the use of additional screening questionnaires for depression, anxiety, and substance use (Levy & Kokotailo, 2011; Zuckerbrot, Cheung, Jensen, Stein, & Laraque, 2007), will aid in assessment of children with more complex behavioral and emotional symptoms. Unless the APN and collaborating clinicians within the practice are very experienced at diagnosing and manag-ing mental health conditions in the primary care setting, children who may have coexisting conditions should be referred to mental health clinicians for diagnosis and co-management. D. Screening for learning disabilities If the child's functioning at school indicates the possibility of both learning disabilities and ADHD, both evaluations should proceed. Most health insurance plans, private or public, do not cover learning evaluations, which must be requested by the parent from an overburdened public school system. Although these evaluations are legally required for children who may need special education services, par-ents may need assistance from the APN in advocating for them (Selekman & Vessey, 2010). For children who do not improve in academic performance within 1 or 2 months of ADHD diagnosis and treatment, the AACAP recommends an evaluation at that point for learning disorders (Pliszka & AACAP Work Group on Quality Issues, 2007). Iv. p hysical examination A. Overview The physical examination in ADHD should help the APN eliminate potential physical causes of inattention, hyper-activity, and disruptive behavior and any contraindica-tions to medication that might be used to treat ADHD. There are no specific physical findings that confirm or rule out a diagnosis of ADHD. B. Important to eliminate other potential physical causes of attention issues and disruptive behavior The physical examination should include a thorough head, eye, ear, nose, and throat examination; a thorough cardio-vascular evaluation; a thorough neurologic examination including documentation of any tics; and hearing and vision screening. Many examiners look for signs of hyperthyroidism or hypothyroidism, anemia, or lead poisoning. These condi-tions typically present with more symptoms than just inat-tention or impulsivity (Pliszka & AACAP Work Group on Quality Issues, 2007). Most children with ADHD have a normal physical examination (Pliszka & AACAP Work Group on Quality Issues, 2007), although some children may have “soft neurologic signs” (Gustafsson et al., 2009), demonstrating more clumsiness on tasks requiring cer-ebellar integration, such as rapid-finger or alternating hand tests, than most children of their age. A frankly abnormal neurologic examination should prompt a search for other diagnoses, additional testing, and referral. Children with normal examinations do not need labora-tory or other imaging tests (Pliszka & AACAP Work Group on Quality Issues, 2007). In particular, brain imaging studies, electroencephalograms, and continuous perfor-mance tests have not been found to be useful diagnosti-cally, and the AAP recommends ordering laboratory tests for hematocrit, blood lead levels, and thyroid hormone only if concerns are raised from the history and physical exam (Subcommittee on Attention-Deficit/Hyperactivity Disorder, 2011). If the child also has symptoms of anxiety or mood disturbances, complete blood count, thyroid, lead, and metabolic panels may be indicated. C. Monitor for possible cautions or contraindications to treatments Concerns about possible cases of sudden death in chil-dren treated with stimulants for ADHD have prompted a call for screening all children with ADHD for cardiovas-cular disease before initiating treatment with medications (AAP & American Heart Association, 2008). This rec-ommendation reinforces the need to take a history and perform a thorough physical examination to exclude car-diovascular disease (Subcommittee on Attention-Deficit/Hyperactivity Disorder, 2011). The joint statement recom-mends the clinician use judgment as to whether an electro-cardiogram (ECG) should be done on any particular child before beginning medication to treat ADHD but does not recommend universal use of premedication ECGs. In a clarification, Vetter and colleagues (2008) recommended that all children with a family history of such conditions as hypertrophic cardiomyopathy, prolonged QT interval, and Wolff-Parkinson-White syndrome, which carry an increased risk for sudden cardiac death, be evaluated by a cardiologist before beginning stimulant medication. When a range of medications is being considered, con-sulting mental health professionals may ask for chemistry panels that could reassure prescribers about kidney func-tion (creatinine and blood urea nitrogen) and a lack of liver inflammation (aspartate aminotransferase and alanine aminotransferase). D. Neuropsychiatric conditions and ADHD: tic disorders Between 3% and 6% of all school-age children exhibit chronic vocal or motor tics, lasting over 1 year, and fewer than 1% have T ourette syndrome. However, up to 55% of Physical examination 83

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treatment, or both (Subcommittee on Attention-Deficit/ Hyperactivity Disorder, 2011), with medication considered if behavioral treatments are insufficient. A. Behavioral approaches (Subcommittee on Attention-Deficit/Hyperactivity Disorder, 2011) 1. P sychoeducation a. L ong-term developmental implications of ADHD b. Effe cts on self-esteem and strategies for positive parenting c. Go als of treatment d. B ringing in school personnel as part of the team 2. P arent behavioral training to help parents work more effectively with their children, specifically using: a. P ositive reinforcement (including point systems, token economy) b. M ethods of negative reinforcement (e. g., cost response) c. G iving commands, shaping behavior effectively B. Medication 1. S timulant medications Although the exact mechanism of action is unclear, stimulant medications affect core symptoms of ADHD in up to 75% of children if tried systematically (Pliszka & AACAP Work Group on Quality Issues, 2007) and are still considered first-line treatment by most clinicians (see T able 12-2). All have potential side effects of appetite suppression, sleep disturbance (although this is also a core ADHD symptom), head-aches, constipation, and irritability during the day as medication wears off. Stimulants can worsen anxiety or mania in children with anxiety or bipolar disorder or a family history of bipolar disorder. Although dex-troamphetamine and mixed amphetamine salts are approved for children as young as 3, stimulants are not generally recommended for preschool-age chil-dren, because they seem to have increased adverse effects and may not be as effective as behavioral treat-ment in this age group. Extended-release medications can last anywhere from 6 to 12 hours, depending on the medication and absorption formulation. These medications obviate the need for midday dosing, may decrease irritability because the medication wears off more slowly, and may have less potential for abuse. They also offer coverage for after-school or after-work tasks, such as homework or driving (Adler et al., 2011; Pliszka & AACAP Work Group on Quality Issues, 2007; T aketomo, Hodding, & Kraus, 2014). a. S hort-acting: rapid onset, duration of action 3-4 hoursi. Adv antages: dose clears system rapidly, effect rapidthis group has ADHD as a coexisting condition, and chil-dren with tics or T ourette syndrome should be evaluated for ADHD (Cohen, Leckman, & Bloch, 2013). Although most children with tics can suppress them for a time in public settings, they may show up on examination. v. Assessment A. History and examination that support a diagnosis of ADHD No coexisting mental or behavioral health conditions are present. The child may be treated in a primary care setting or comanaged with mental health and learning professionals. B. History and examination that support a diagnosis of ADHD and coexisting conditions If additional coexisting conditions are suspected, consulta-tion or referral to mental health and learning professionals for more definitive diagnosis is recommended, and the APN may comanage the conditions. Coexistence of anxiety, mood disorders, or tic disorders may complicate treatment, and children with a family history of bipolar disorder may react poorly to stimulant medications, even if they them-selves do not have coexisting conditions. C. History and examination that do not support a diagnosis of ADHD Refer to psychiatric or mental health professionals or a neurologist, as indicated by the findings. v I. p lan Current practice guidelines recommend treating ADHD as a chronic condition, centered in the healthcare home, and recommend medication, psychosocial treatment, or both, depending on the age of the child (Pliszka & AACAP Work Group on Quality Issues, 2007; Subcommittee on Attention-Deficit/Hyperactivity Disorder, 2011). The AAP (2001) in particular recommends the choosing of three to six target behaviors that the parent and child would specifically like to improve. For school-age children and adolescents, the AAP and the AACAP have found that medication is the most effec-tive treatment for core ADHD behaviors, with behavioral and educational interventions helpful in combination or instead, depending on severity of symptoms and family preference. For children from 4 to 6 years of age, the AAP recommends coordinated family and school behavioral interventions as first-line treatment. Current practice guidelines recommend treating ADHD as a chronic condition, centered in the health-care home, and recommend medication or psychosocial 84 CHAPTER 12 | Attention-Deficit/Hyperactivity Disorder in Children and Adolescents

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Table 12-2 ADHD Medications: Food and Drug Administration (FDA) Approved class Medication Dur ation e xamples Advantages Disadvantages Dosing Stimulants Short-acting (3-6 hr)Methylphenidate (chewable, liquid available)Dextroamphetamine Dexmethylphenidate Quick onset Ease of making dosage adjustments without changing prescription Must be dosed midday to last through school or work day. Higher abuse potential Individualized, not mg/kg dosing, but starting dose adjusted to weight Medium-acting (4-8 hr)Mixed amphetamine salts (sometimes listed as short acting, however effects may last through school day)May last during school day, lower abuse potential. Steady release during day, less effective for some children than bursts of medication Individualized, not mg/kg dosing, but starting dose adjusted to weight Long-acting, variable forms of absorption/release (8-12 hr)OROS methylphenidate Methylphenidate ER, SRMethylphenidate-LA*Methylphenidate CD*Methylphenidate patch Methylphenidate XR solution Dextroamphetamine XRDexmethylphenidate XR*Mixed amphetamine salts XR*Lisdexamfetamine#Last during entire school day, better coverage for driving, lower abuse potential Cannot be crushed or altered, may effect sleep more Dosing less flexible, conversion charts available from short-acting medications Norepinephrine reuptake inhibitor Long-acting, 24-hr effect, half-life 5-21 hr Atomoxetine 24-hr coverage, low abuse potential, may be effective for depression Extensive drug interactions, black box warnings re suicidality Weight-based dosing for children < 70 kg Alpha-2-agonist Short-or long-acting (only extended-release FDA approved 2009), half-life 17 hr Guanfacine Guanfacine ERMore effective for impulsivity, hyperactivity than for inattention Rebound hypertension if withdrawn too quickly, some children c/o headache, somnolence; drug interactions Start with 1 mg oral daily, may increase in increments of 1 mg/wk, weight-based suggested upper limits * = capsule may be opened and sprinkled on applesauce # = capsule may be opened and dissolved in water Data from Feldman, H. M., & Reiff, M. I. (2014). Clinical practice. Attention deficit-hyperactivity disorder in children and adolescents. New England Journal of Medicine, 370, 838-846; Pliszka, S., & AACAP Work Group on Quality Issues (2007). Practice parameter for the assessment and treatment of children and adolescents with attention-deficit/hyperactivity disorder. Journal of the American Academy of Child and Adolescent Psychiatry, 46, 894-921; Taketomo, C. K., Hodding, J. H., & Kraus, D. M. (2014). Pediatric dosage handbook: 2014-2015 (21st ed. ). Hudson, OH: Lexi-Comp. Plan 85

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v. M ay increase effects of albuterol, sympatho-mimetic drugs in general vi. B lack box warnings of suicidality b. α2-Adrenergic agonists i. M ore effective for impulsivity than for inattention ii. G uanfacine approved for children 6 years and older in extended-release form only; clonidine used off label iii. C lonidine patch available (off label) when steady dose reached; medication must be tapered off slowly iv. S ometimes used for children with impul-sive ADHD and tics (off label for tics and aggression) v. S ide effects: depression, headache, dizzi-ness, fatigue, constipation, decreased appe-tite; rebound hypertension if discontinued suddenly; drug interactions c. T ricyclic antidepressants (off label for ADHD): imipramine, nortriptyline, and desipraminei. N ot considered first line ii. M ay be effective for ADHD combined with other conditions, such as anxiety, tics, or enuresis iii. M any drug interactions (neuroleptics, selec-tive serotonin reuptake inhibitors, H2 block-ers, combined hormonal contraceptives) iv. R ate of metabolism may decrease after puberty v. S ide effects: anticholinergic; weight gain; cardiac arrhythmias (need premed ECG and repeat with increasing doses), dangerous in overdose d. B upropion i. O ff-label use for ADHD, Food and Drug Administration approved for depression, smoking cessation ii. N ot approved for children younger than 18 years iii. S ide effects: insomnia, fatigue, agitation, dry mouth, headaches, rash, and lower seizure threshold iv. C ontraindicated if history of seizures, trau-matic head injury, or eating disorders C. General considerations about medication 1. C ontraindications for stimulants a. S ymptomatic cardiovascular disease (adults and children) b. Gl aucoma c. F ood and Drug Administration lists tics as a contraindication to stimulant medication; how-ever, several studies of children with T ourette ii. Di sadvantages: given two or three times a day, including midday; issues of convenience (parent, school personnel), training, safety, and child's embarrassment; and more reports of irritability as medication wears off b. I ntermediate-and long-acting medication i. L onger acting: 6-12 hours, no need for midday dose ii. M ay start long acting directly, no need to start with short acting first, except in very young children iii. M ay have slower onset, depending on formulation iv. M ay have decreased abuse potential relative to short-acting medication v. I f slower, steady release, child may not “feel” that the medication is working as much as the short acting or medication released in several bursts, but literature shows equiva-lent effect c. A bsorption mechanisms available in long-acting medications (current available medications in parentheses accurate at time of publication)i. O smotically released oral therapy: shorter release and nonabsorbable plastic shell con-tains some medication for later release; later onset; longer effect than spheroidal oral drug absorption system (methylphenidate) ii. S pheroidal oral drug absorption system: combination of immediate-release and lon-ger release beads; capsules may be opened up and sprinkled on food (methylphenidate, dexmethylphenidate) iii. T ransdermal patch: releases medication over 9 hours; onset within 2 hours; dura-tion 12 hours; applied on hip; site and patch changed daily (methylphenidate) iv. P rodrug, converted slowly to active drug, in intestines and liver; slower onset and 10 hours of active effect; lower abuse poten-tial (lisdexamfetamine to dexamphetamine) 2. N onstimulant medication a. A tomoxetine: affects norepinephrine receptors i. S low onset, effects may not be felt for several weeks ii. 24-hour coverage, longest coverage iii. More acceptable to child and adolescent if first medication, rather than switching from stimulant (patient may not “feel” that medication is taking effect) iv. R are reports of liver toxicity, cleared through CYP2D6 pathway, half-life up to 21 hours in individuals with less active CYP2D686 CHAPTER 12 | Attention-Deficit/Hyperactivity Disorder in Children and Adolescents

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syndrome randomized to various treatment arms for ADHD showed no increase in tics with stim-ulant medicine 2. T racking medication short-term effects a. E ncourage systematic follow-up of ADHD core symptoms: designation of core symptoms and follow-up with parent, child, and school about effects of medication b. I nitial dose should be increased weekly until core symptoms show improvement or side effects increasei. C linician and family should expect some loss of appetite during the dosing period for stimulants, with normal appetite before dose and after wearing off; lack of this effect may indicate subtherapeutic dose ii. C arefully monitor side effects if child is on nonstimulant medication or if taking additional medications iii. C heck in weekly with parent and child by telephone or in office when starting medi-cation and increasing dose. Stimulants are Schedule II medications: no refills by tele-phone and new prescriptions must be writ-ten and picked up when continuing these medications. iv. F ollow-up blood pressure, heart rate, and weight for stimulants; other medications as indicated (e. g., possible liver inflammation for atomoxetine) c. T rack adherence and diversion: especially an issue for adolescent and young adult patients taking shorter acting stimulant medication d. S timulant medication holidays i. S ometimes used or recommended on weekends and summer if core symptoms manageable outside of school; medication holidays are controversial ii. M ay increase side effects on restarting iii. M ay not be beneficial for adolescents, especially if they drive 3. T racking medication long-term effects a. Effe cts on academic and job performance and home and peer relationshipsi. M ost documented benefits early in treat-ment (first 3 years) may be partly caused by more intensive management ii. M ay be more effective if started earlier in the course of ADHD iii. I nteraction of ADHD and substance abuse is complex: in general, adolescents and adults with ADHD have higher rates of substance abuse compared to non-ADHD peers; effective treatment with stimulants seems to lower this risk while treatment is maintained b. E mergence or persistence of any mood-related symptoms c. Gr owth (height, weight) and blood pressure d. Div ersion or substance use issues: in-depth psychosocial screen for adolescents D. Follow-up and indications for referral 1. L ack of expected improvement a. M ost children respond to stimulants, but may require a switch in specific type, adjustments in dose, or addition or switch to a nonstimulant medication b. R esponse to behavioral approaches 2. C oexisting learning, mood, or behavioral problems not improving or worsening E. Parental/Patient Education Encourage parental connection with other parents, peer support for children and youth, and community resources (see Box 12-1) F. Long-term issues and transition to adulthood 1. C ondition trajectory (Adler et al., 2011; Obioha & Adesman, 2014). a. I nitial presenting behavioral symptoms may diminish, functional impairments may improve or worsen b. I ncreasing appearance of coexisting conditions (anxiety, mood, conduct, substance abuse); may be mitigated by appropriate medication and behav-ioral treatment in childhood and adolescence c. S ignificantly increased risks of driving accidents, tickets, and impulsive errors, especially if not properly medicated 2. L ong-term planning should begin with early adoles-cent and parent a. S kill building to increase confidence, offer alterna-tives to risky behavior, and aid in career planning i. R eframing ADHD to highlight positive aspects of behavioral characteristics for appropriate careers ii. J obs, chores to give youth a sense of accom-plishment, instill work ethic iii. F ocusing on strengths and interests b. Adv ocating for educational accommodations as needed, involving the adolescent as a self-advocate (Selekman, 2010) c. S hift to long-acting medication with decreased abuse potential and greater coverage for evening behaviors, especially driving Plan 87

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3. T ransition to adult systems of care a. Adult pr oviders are often unfamiliar with ADHD, relative to pediatric providers b. L oss of insurance coverage and difficulty con-tinuing stimulant medications through publicly funded or indigent mental health carei. M ay be greatly mitigated through 2010 healthcare reforms ii. D ecreased access to care affects educational and job trajectories iii. S everities of coexisting conditions may increase and risk of substance abuse increas-es without access to effective care refere Nce S Adler, L. A., Mattingly, G. W., Montano, C. B., & Newcorn, J. H. (2011). Optimizing clinical outcomes across domains of life in adolescents and adults with ADHD. Journal of Clinical Psychiatry, 72, 1008-1014. doi: 10. 4088/JCP. 10063ah1 American Academy of Pediatrics. (2001). Clinical practice guideline: T reatment of the school-aged child with attention-deficit/hyperactivity disorder. Pediatrics, 108, 1033-1044. American Academy of Pediatrics, & American Heart Association. (2008). American Academy of Pediatrics/American Heart Association clarifica-tion of statement on cardiovascular evaluation and monitoring of children and adolescents with heart disease receiving medications for ADHD: May 16, 2008. Journal of Developmental Behavioral Pediatrics, 29, 335. American Psychiatric Association. (2000). Diagnostic and statistical manual of mental disorders (4th, T ext Revision Ed. ). Washington, DC: Author. American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed. ). Washington, DC: Author. Biederman, J., Monuteaux, M. C., Spencer, T., Wilens, T. E., & Faraone, S. V. (2009). Do stimulants protect against psychiatric disorders in youth with ADHD? A 10-year follow-up study. Pediatrics, 124, 71-78. Cheung, C. H., Rijdijk, F., Mc Loughlin, G., Faraone, S. V., Asherson, P., & Kuntsi, J. (2015). Childhood predictors of adolescent and young adult outcome in ADHD. Journal of Psychiatric Research, 62, 92-100. doi: 10. 1016/j. jpsychires. 2015. 01. 011 Cohen, S. C., Leckman, J. F., & Bloch, M. H. (2013). Clinical assessment of T ourette syndrome and tic disorders. Neuroscience Biobehavioral Review, 37, 997-1007. doi: 10. 1016/j. neubiorev. 2012. 11. 013 Cortese, S. (2012). The neurobiology and genetics of attention-deficit/ hyperactivity disorder (ADHD): What every clinician should know. European Journal of Paediatric Neurology, 16, 422-433. doi: 10. 1016 /j. ejpn. 2012. 01. 009 Dalsgaard, S. (2013). Attention-deficit/hyperactivity disorder (ADHD). European Child Adolescent Psychiatry, 22(Suppl. 1), S43-S48. doi: 10. 1007/s00787-012-0360-z Faraone, S. V. (2014). Advances in the genetics of attention-deficit /hyperactivity disorder. Biological Psychiatry, 76(8), 599-600. doi: 10. 1016/j. biopsych. 2014. 07. 016 Feldman, H. M., & Reiff, M. I. (2014). Clinical practice. Attention deficit-hyperactivity disorder in children and adolescents. New England Journal of Medicine, 370, 838-846. doi: 10. 1056/NEJMcp1307215 Gerson, R., & Rappaport, N. (2013). T raumatic stress and posttraumatic stress disorder in youth: Recent research findings on clinical impact, BOx 12-1 r esources National Institute for Children's Health Quality (NICHQ)Caring for Children with ADHD: A Resource Toolkit for Clinicians (first edition open access) http://www. nichq. org/adhd_tools. html American Academy of Pediatrics Children's Health Topics—ADHD—with links to resource for parents (ADHD Toolkit second edition available for purchase) http://www. healthychildren. org/English/health-issues/conditions/adhd/Pages/Attention-Deficit-Hyperactivity-Disorder. aspx Implementing the Key Action Statements: An algorithm and explanation of care for the evaluation, diagnosis, treatment, and monitoring of ADHD in children and adolescents http://pediatrics. aappublications. org/content/suppl /2011/10/11/peds. 2011-2654. DC1/zpe611117822p . pdf Developmental Behavioral Pediatrics Online Materials related to screening and early identification of behavioral/mental health problems http://www. dbpeds. org/ American Academy of Child and Adolescent Psychiatry http://www. aacap. org/ Help4Kids with ADHD Tufts University site with resources in Spanish and English, including San Diego ADHD Project Screening Packets in Spanish and English, parent and teacher educational forms Last updated 2008https://research. tufts-nemc. org/help4kids/default. asp CHADD Children and Adults with Attention Deficit Hyperactivity Disorder http://www. chadd. org/ Adolescent Health Working Group Behavioral Health: An Adolescent Provider Toolkit Screening and treatment guidelines for providers, handouts for youth and parents, symptom and medication side effect tracking forms http://www. ahwg. net/uploads/3/2/5/9/3259766 /behavioral_health. pdf88 CHAPTER 12 | Attention-Deficit/Hyperactivity Disorder in Children and Adolescents

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assessment, and treatment. Journal of Adolescent Health, 52, 137-143. doi: 10. 1016/j. jadohealth. 2012. 06. 018 Gipson, T. T., Lance, E. I., Albury, R. A., Gentner, M. B., & Leppert, M. L. (2015). Disparities in identification of comorbid diagnoses in children with ADHD. Clinical Pediatrics (Phila), 54, 376-381. doi: 10. 1177/0009922814553434 Gustafsson, P., Svedin, C. G., Ericsson, I., Linden, C., Karlsson, M. K., & Thernlund, G. (2009). Reliability and validity of the assessment of neurological soft-signs in children with and without attention-deficit-hyperactivity disorder. Development Medicine and Child Neurology, 52, 364-370. Levy, S. J., & Kokotailo, P. K. (2011). Substance use screening, brief inter-vention, and referral to treatment for pediatricians. Pediatrics, 128, e1330-e1340. doi: 10. 1542/peds. 2011-1754 Merikangas, K. R., He, J. P., Brody, D., Fisher, P. W., Bourdon, K., & Koretz, D. S. (2010). Prevalence and treatment of mental disorders among US children in the 2001-2004 NHANES. Pediatrics, 125, 75-81. Obioha, O., & Adesman, A. (2014). Pearls, perils, and pitfalls in the assess-ment and treatment of attention-deficit/hyperactivity disorder in adolescents. Current Opinion in Pediatrics, 26, 119-129. doi: 10. 1097 /mop. 0000000000000053 Perou, R., Bitsko, R. H., Blumberg, S. J., Pastor, P., Ghandour, R. M., Gfroerer, J. C., et al. (2013). Mental health surveillance among chil-dren—United States, 2005-2011. MMWR Surveillance Summaries, 62(2), 1-35. Pliszka, S., & AACAP Work Group on Quality Issues. (2007). Practice parameter for the assessment and treatment of children and adolescents with attention-deficit/hyperactivity disorder. Journal of the American Academy of Child and Adolescent Psychiatry, 46, 894-921. Selekman, J. (2010). Attention-deficit/hyperactivity disorder. In P. J. Allen, J. A. Vessey, & N. A. Schapiro (Eds. ), Primary care of the child with a chronic condition (5th ed., pp. 197-217). St. Louis, MO: Mosby Elsevier. Selekman, J., & Vessey, J. A. (2010). School and the child with a chronic con-dition. In P. J. Allen, J. A. Vessey, & N. A. Schapiro (Eds. ), Primary care of the child with a chronic condition (5th ed., pp. 42-59). St. Louis, MO: Mosby Elsevier. Sharma, A., & Couture, J. (2014). A review of the pathophysiology, etiology, and treatment of attention-deficit hyperactivity disor-der (ADHD). Annals of Pharmacotherapy, 48(2), 209-225. doi: 10. 1177/1060028013510699Shaw, P., Stringaris, A., Nigg, J., & Leibenluft, E. (2014). Emotion dysregu-lation in attention deficit hyperactivity disorder. American Journal of Psychiatry, 171, 276-293. doi: 10. 1176/appi. ajp. 2013. 13070966 Stein, M. T., & Perrin, J. M. (2003). Diagnosis and treatment of ADHD in school-age children in primary care settings: A synopsis of the AAP practice guidelines. Pediatrics in Review, 24, 92-98. Subcommittee on Attention-Deficit/Hyperactivity Disorder, Steering Committee on Quality Improvement and Management. (2011). ADHD: clinical practice guideline for the diagnosis, evaluation, and treatment of attention-deficit/hyperactivity disorder in children and adolescents. Pediatrics, 128(5), 1007-1022. doi: 10. 1542 /peds. 2011-2654 T aketomo, C. K., Hodding, J. H., & Kraus, D. M. (2014). Pediatric dosage handbook: 2014-2015 (21st ed. ). Hudson, OH: Lexi-Comp. Thomas, R., Sanders, S., Doust, J., Beller, E., & Glasziou, P. (2015). Prevalence of attention-deficit/hyperactivity disorder: A systematic review and meta-analysis. Pediatrics. doi: 10. 1542/peds. 2014-3482 Vetter, V. L., Elia, J., Erickson, C., Berger, S., Blum, N., Uzark, K., et. al. (2008). Cardiovascular monitoring of children and adolescents with heart disease receiving medications for attention deficit/hyperactivity disorder [corrected]: A scientific statement from the American Heart Association Council on Cardiovascular Disease in the Y oung Congenital Cardiac Defects Committee and the Council on Cardiovascular Nursing. Circulation, 117, 2407-2423. Vierhile, A., Robb, A., & Ryan-Krause, P. (2009). Attention-deficit/hyper-activity disorder in children and adolescents: Closing diagnostic, communication, and treatment gaps. Journal of Pediatric Health Care, 23(Suppl. 1), S5-S23. Wolraich, M. L., Bard, D. E., Neas, B., Doffing, M., & Beck, L. (2013). The psychometric properties of the Vanderbilt attention-deficit hyperactivity disorder diagnostic teacher rating scale in a community population. Journal of Developmental Behavioral Pediatrics, 34, 83-93. doi: 10. 1097/DBP. 0b013e31827d55c3 Wolraich, M. L., Lambert, W., Doffing, M. A., Bickman, L., Simmons, T., & Worley, K. (2003). Psychometric properties of the Vanderbilt ADHD diagnostic parent rating scale in a referred population. Journal of Pediatric Psychology, 28, 559-567. Zuckerbrot, R. A., Cheung, A. H., Jensen, P. S., Stein, R. E., & Laraque, D. (2007). Guidelines for Adolescent Depression in Primary Care (GLAD-PC): I. Identification, assessment, and initial management. Pediatrics, 120, e1299-e1312. References 89

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illness (American Psychiatric Association [APA], 2013). In any of these cases, or in any case in which the clinician suspects or elicits the presence of depressive symptoms or other behavioral or mental health concerns, safety must be assessed as a priority. Suicidal ideation as well as bully-ing, sexual or physical abuse, and neglect should be chief among the safety concerns explored when a behavioral or mood change is the focus of the presenting complaint in the child or adolescent. Mental health treatment and medication are not synony-mous. It should be remembered that primary screening for and assessment of mood and behavioral disorders in the pediatric population is an essential component of the psychi-atric assessment and treatment process and does not always necessitate prescription of psychotropic medication. All psychiatric treatment—pharmacologic and otherwise—including family and patient education, behavioral training, and play-or talk-based psychotherapies as well as specialty evaluation typically proceed from primary care screening and referral. The primary care provider is encouraged to appreciate the importance of their gatekeeping and educa-tional function, regardless of comfort level in prescribing psychotropic medication in children. Additionally, it should be kept in mind that although reassurance and normalizing are necessary and useful practices, the primary care provid-er should not preference these activities above mood and behavioral assessment—especially in reference to safety, onset, duration, precipitants, severity, and extent of symp-tomatology. Screening instruments in the public domain—such as the PHQ-A (Patient Health Questionnaire for Adolescents)—can be invaluable in this regard, providing a quantifiable reference point for assessing symptomatology and treatment response over time. Research suggests clinical depression is a relatively common occurrence in the pediatric population, with some estimates showing adolescents mirroring adult life-time prevalence rates of 15-25% (March et al., 2004; Rao & Chen, 2009). Depression in younger children is not as prevalent but does occur. According to Cheung, Kozloff, I. Intr oduction A. General background Clinical depression is a disease state with physical, emo-tional, and cognitive effects burdening children, adoles-cents, and adults. It is characterized by persistently low mood or loss of interest/pleasure (anhedonia) such that the patient's subjective quality of life is lessened. Functional impairment in school, work, home, and peer relationships is also often objectively observed, but this is not required for diagnosis. Subjective report of depressive symptoms by the patient suffices. This is an important distinction in evaluat-ing the adolescent or child who, because of developmental misunderstanding or caregiver bias, may not be perceived as depressed or impaired. Alternatively, lack of emotional and intellectual insight by the child/adolescent may lead to a discrepancy between the caregiver's observation of depressive symptoms and the child/adolescent's ability to acknowledge or name these symptoms. The clinician should keep in mind that the presenting symptomatology of the depressed child or adolescent may differ from that of the adult patient and that problematic behavior cannot be assumed to be developmentally nor-mative or caused by depression. Popular wisdom sug-gests that adolescents go through expectable “phases” of depression or irritability (Arnett, 1999). Although this may be true to a minor degree (Hines & Paulson, 2006), the typically developing child or adolescent should not go through an extended period of depression, irritabil-ity, or rebelliousness as a part of normative development: any report by the parent, caretaker, or child of a prolonged period of irritability or oppositional behavior should trig-ger suspicion of depressive or other psychiatric illness and further inquiry. Additionally, a presenting recurrent or acute somatic complaint (stomachache, headache, etc. —especially in very young children), feeling “blah,” appetite loss, appetite increase, weight fluctuation, or anxi-ety complaints may indicate the presence of depressive Damon Michael Williams Ch Il Dhoo D Depress Ion© Eliks/Shutterstock; © donatas1205/Shutterstock 9013Chapt Er

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nervosa, a diagnosable disorder) or hyperphagia (increased appetite); insomnia or hypersomnia; or fatigue (APA, 2013). However, the primary care clinician evaluating the child or adolescent for depressive illness should keep in mind that mood may show more as “irritability” (excessive anger or feeling mad) rather than sad and that the child may not report subjective change in appetite but instead show observable “failure to make expected weight gains” (APA, 2013, p. 163). C. Major depressive disorder MDD is the prototypical disease usually referred to when depression is spoken of generically. It is diagnosed based on the occurrence of one or more major depressive episodes (APA, 2013). A major depressive episode con-sists of 2 (or more) weeks of depressed mood/irritability or anhedonia and a minimum of four additional depressive symptoms (APA, 2013). The neurobiology underlying depression is not well understood, and continues to evolve. Current theories suggest more complicated and nuanced processes than the simplified vision of deficient serotonin or norepinephrine many were taught, though this remains the most credible explanation vis-à-vis the effects of anti-depressants such as SSRIs (selective serotonin reuptake inhibitors) and SNRIs (serotonin norepinephrine reup-take inhibitors). Researchers have theorized depression from a strictly behavioral perspective as caused by a loss of environmental reward (positive reinforcement) leading to avoidance, withdrawal, and isolation via negative reinforce-ment (Dimidjian et al., 2011; Dobson et al., 2008). In addition to depressed/irritable mood or anhedonia, depressive symptoms can include fatigue, psychomotor agitation or slowing, feelings of worthlessness or guilt, decreased ability to think or concentrate, indecisiveness, unintentional weight changes, and suicidal ideation (APA, 2013). The reader is referred to DSM-V directly for com-plete diagnostic criteria. Note that in the case of MDD and most other depressive syndromes, DSM-V qualifies most of these symptom criteria as “most of the day, nearly every day” or “nearly every day” (APA, 2013). According to DSM-V, in diagnosing any of the depressive syndromes, symptoms caused by a general medical condition or substance use or abuse must first be ruled out. D. Persistent depressive disorder (dysthymia) Persistent depressive disorder is similar in symptom profile to MDD but lacks its severity and demonstrates a course that is constant over a longer period of time without distinct episodes (APA, 2013). DSM-V criteria for persis-tent depressive disorder are not significantly different from the DSM-IV criteria for dysthymia. The major difference is that chronic major depressive disorder, which had been a distinct and separate diagnosis, was integrated into the single diagnosis of persistent depressive disorder along with dysthymia (APA, 2013). & Sacks (2013), it has been “reliably diagnosed in children as young as 3 years of age. ” Onset of depression in chil-dren (especially the very youngest children) rarely arises de novo because of purely internal biologic or psycho-logic factors as the young child's psyche is developmen-tally predicated upon the family environment, especially the relationship with the primary caregiver(s). Therefore, onset of depression in the very young child warrants assess-ment of abuse, neglect, trauma, child-caregiver fit, paren-tal mental health, parenting styles, discipline approaches, parental/family conflict, and interactions with siblings. Genetic, biologic, and environmental etiologic factors (Rao & Chen, 2009) are suggested as contributing to depression. Despite clear evidence of familial transmission of depression in the case of children and adolescents, it is unclear to what degree childhood depression is influenced by genetics, environment, or some combination thereof (Rao & Chen, 2009). In any case, it is believed that the single greatest risk factor for developing major depressive disorder (MDD) in childhood or adolescence is paternal or maternal loading for the disorder (Birmaher & Brent, 2007). Thus, the subjective and family history should include any history of depression in the family, especially the child's parents or siblings, any parental or family history of bipolar disorder, or alcohol or substance abuse. B. Definition of clinical depression In the clinical setting, diagnosis and assessment of the clinical syndromes of depression are defined and guided by the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM) published by the APA (2013). DSM-V includes the following depressive syndromes, which have depressive features: Major Depressive Disorder (MDD) Persistent Depressive Disorder (includes DSM-IV diagnoses of Dysthymia & Chronic Major Depressive Disorder) (APA, 2013) Unspecified Depressive Disorder Bipolar Affective Disorder I and II (variously abbrevi-ated as BAD or BPD) Cyclothymia Seasonal Affective Disorder Disruptive Mood Dysregulation Disorder Adjustment Disorder with Depressed Mood or Mixed Depression and Anxiety Note: A review of the latter five diagnoses is beyond the scope of this chapter and the reader is referred to the 2013 DSM-V. Presentation of depressive illness in the pediatric popu-lation shows remarkable similarity to the adult popula-tion. These symptoms can include sad, low, or disinterested mood; anhedonia; felt or observed decreased effectiveness at school; feelings of guilt; feelings of hopelessness; anorexia (literally “without appetite” as a symptom, versus anorexia Introduction 91

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the clinician may mistakenly diagnose unipolar depres-sion rather than bipolar depression if inquiry is not made about mood and behavior over the lifetime of the patient rather than the limited course of the current episode alone. In cases of undiagnosed bipolar disorder, psychotropic medications (especially antidepressants) may precipitate hypomanic or manic mood or behavior when admin-istered—this is known as “activation” or an “activated mania. ” Thus, in the interest of “doing no harm,” the clini-cian evaluating clinical depression in the child, adolescent, or adult must always entertain the possibility of a bipolar illness presenting in its depressed phase, especially if anti-depressant medication is being considered. This evalua-tion can be assisted by asking about family history of mood lability or bipolar disorder and substance abuse, though the absence of these in the family history does not rule out bipolar disorder. Finally, in many cases of MDD, bipo-lar spectrum illness remains a “rule out” diagnosis; one should advise the patient and family about the possibility of activation when reviewing the risks and benefits of anti-depressant medication. II. Database (may include, but not limited to) A. Subjective data The primary care provider evaluating the child or adoles-cent is in an excellent position to assess for depression. The primary care provider usually has an established relation-ship with the child and family and some familiarity with the family dynamics and the child's developmental and other medical history, all essential components of a com-petent evaluation for pediatric depression. If this is not the case, the treating clinician should gather information from the child and parents about the family situation and the child's emotional, physical, and cognitive development and history since birth, including intrauterine conditions. Gathering these data may take several visits, especially with adolescents, as the clinician may choose to meet first with the family together and then on separate occasions with the child/adolescent alone and then the parents alone (or vice versa). Regardless of the number of visits, always prioritize the safety screening first. The safety screening will then provide the initial data to determine a referral course, if indicated. As the clinician lays out an initial plan for screening and assessment with the child and family, it is useful to clarify the parameters of confidentiality and what information will and will not be shared and how this will occur. Clarity around confidentiality is essential for main-taining rapport with the child and the caregivers through-out this process and may assist in data gathering. The presence of MDD and comorbid dysthymia identi-fied in a single individual is commonly known as “double depression. ” The clinician should keep in mind that 5-10% of children and adolescents have depressive symptoms that are not severe enough to warrant diagnosis of a depressive syndrome, such as MDD or dysthymia, but that are debili-tating to some degree nonetheless (Birmaher & Brent, 2007); in some cases these depressive symptoms are attributable to an adjustment disorder caused by an acute stressor. Additionally, of those children and adolescents with diagnosable depressive syndromes, 40-90% have other psychiatric disorders (Birmaher & Brent, 2007). Thus, the clinician should observe for any potential signs of other comorbid psychiatric illness, such as attention-deficit/hyperactivity disorder, anxiety disorders, and autism spectrum disorder. In terms of the diagnostic nomenclature used by DSM-V, a child with depressive symptoms that does not have enough signs and symptoms to meet criteria for MDD or dysthymia could be identified as having unspecified depressive disorder—formerly depressive disorder not otherwise specified (NOS) in DSM-IV-TR. E. Bipolar spectrum Clinical depression is also a significant component of the bipolar “spectrum” of illnesses, which include bipolar affective disorder I, bipolar affective disorder II, and cyclo-thymia. As would be suggested by the idea of a “spectrum,” these three illnesses are differentiated from one another by severity and duration but all show similar cyclical episodic variations in mood reflecting elevated, expan-sive, energized mood symptoms (mania or hypomania) alternating or sometimes even intermixed with depres-sive symptoms. Patients experiencing a bipolar spectrum illness, like those with MDD, may also spend a period of time in a euthymic (“normal') mood state. Mania is differ-entiated from (less severe) hypomania by a greater dura-tion (at least 1 week) and greater intensity of symptoms (more symptoms, need for hospitalization or presence of psychotic symptoms, among others) (APA, 2013). One might characterize the bipolar spectrum from most severe to least severe as follows: bipolar affective disorder I, bipolar affective disorder II, and cyclothymia. The DSM-V, in an effort to address the controversy over the upswing in diagnosis of pediatric patients with bipolar disorder, also now includes a diagnosis called disruptive mood dysregulation disorder (APA, 2013). The differen-tial between the two is best left to a specialist in mental health; suffice to say this diagnosis categorizes “children who present with chronic, persistent irritability relative to children who present with classic (i. e., episodic) bipolar disorder” (APA, 2013, p. 157). Children and adults with bipolar illness often present in a depressed, rather than elevated state. In these cases, 92 CHAPTER 13 | Childhood Depression

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Depending on age-appropriateness of the patient, the database review should include the following elements: 1. C ardiovascular, seizure, endocrine, and metabolic problems, and chronic conditions, such as diabetes, physical impairments, sleep-related disorders (including insomnia), pain, or other relevant medical conditions 2. M edications (prescribed and over-the-counter, includ-ing herbs and supplements) 3. D evelopmental data a. T emperamental or developmental difficulties b. Be havioral problems 4. E ducation a. Aca demic difficulties (“How is school going for you?” “What kind of grades are you getting?”) b. L earning disabilities 5. P sychiatric history a. S elf-injurious behavior, such as “cutting” b. P revious outpatient mental health treatment or inpatient psychiatric hospitalization c. P revious suicidal ideation (in the school-aged child this may be described as the desire to “disappear” or “not be here anymore”) d. P revious suicide attempt (including type and lethality) e. A nxiety (“What worries you?” “Do you ever get so worried that you start to feel sweaty or like you can't breathe or are having an anxiety attack?”) f. H allucinations (“Besides my voice, do you hear anything or anyone else right now?” “Do you ever hear or see anything that other people cannot?” If the answer is affirmative: “Describe that for me” or “T ell me more about that. ”) g. D o you ever have trouble paying attention or getting assignments completed? h. D o your parents or teachers complain about you being “fidgety” or get on your case to hurry up? Do you do things without thinking that get you into trouble? 6. S ubstance use and abuse a. C igarette, alcohol, marijuana, or other illicit or licit drug abuse. Often teens are more forthcoming when the clinician educates them regarding con-fidentiality and the fact that in most cases there is not an obligation to report such use to parents or law enforcement (reference your local laws, poli-cies and other professional guidelines). Interview using the term “recreational drugs” and framing in terms of experimentation can also be useful. 7. S ocial and family history a. P eer relationships, including identifiable (namable) friends and peer support, and any peer bullyingb. R omantic relationships or break-ups (“ Are you dating anybody?” rather than “Do you have a girlfriend/boyfriend?”) c. S exual debut (e. g., “Have you ever had sex with anyone else?”) d. T raumatic events (“Has anything really bad ever happened to you?” and “Has anything happened that you think about a lot or can't stop thinking about?”) e. S exual or physical abuse f. F amily conflict (e. g., “How does your family get along?” “What's your relationship like with your parents?” “Is there any yelling or arguing in the household?”) B. Objective data The mental status examination (MSE) is the psychiat-ric equivalent to the physical examination and it must be included in any evaluation of depressive conditions or other psychiatric illness. However, the MSE does not substitute for the physical examination, if indicated to rule out organic factors in a depressive presentation or identify other comor-bid medical illness. Generally speaking, the MSE begins with gross physical observations and progresses to description of the internal cognitive and emotional processes as observed by the clinician in the course of the interview, visit, or interaction, however brief. The MSE typically includes the following observations, adapted from Saddock and Saddock (2007): 1. Ge neral demeanor, response to clinician, and appearance (including remarkable identifiers) and grooming 2. M otor status: slowing, agitation, tremor, and hyperac-tivity 3. S peech: tone, volume, rate, rhythm, and production 4. E ye contact 5. A ffect 6. M ood: the patient's direct report of how they feel in quotation marks (e. g., “sad,” “tired,” “bored,” “none of your business,” etc. ) 7. Thou ght process: how organized, linear, cogent vs. disorganized, circumstantial/tangential, loose 8. Thou ght content: includes suicidal and homicidal ide-ation, perceptual changes, paranoia, intrusive thoughts/memories/worries or hallucinatory experience 9. J udgment 10. I nsight 11. S ome sources include impulsivity (important for safety assessment)Database 93

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for the child and adolescent. It is available for free from the AACAP website; a link is provided in the “Resources” section. IV. p lan A. Diagnostics Diagnostic laboratory tests are not used to establish or rule out a diagnosis of depression. However, a number of disease states can present with low energy, fatigue, loss of motivation, and other symptoms of depression. The follow-ing tests may be used to differentially assess an identifiable organic pathology (e. g., hypothyroidism or anemia) from a nonmedical depressive syndrome: 1. Th yroid-stimulating hormone (TSH), free T4 2. C omplete blood count 3. C omprehensive metabolic panel 4. 25-OH-Vitamin D Keep in mind that a patient may have a diagnosable depres-sive syndrome along with other pathology such as anemia, hypothyroidism, diabetes mellitus, or low vitamin D, which may exacerbate depressive symptoms and require concurrent treatment. B. Treatment 1. M edications and the black box warning The Food and Drug Administration (FDA) issued a ruling in 2007 directing antidepressant manufacturers to include “black box” labeling identifying the pos-sibility of increased suicidal ideation in children and adolescents up through age 24. The announcement of this black box warning was widely reported in the media. Since that time, there has been a marked drop in the prescription of first-line antidepressant treatment by primary care providers (Gibbons et al., 2007) and subsequent increase in completed suicides. The pru-dent clinician should continue circumspect prescribing and vigilant monitoring for increased suicidal ideation or behavior in the child or adolescent (through age 24) continuing on or initiated on antidepressant medica-tion. However, considerable data continue to accumu-late regarding the benefit of antidepressant treatment in children and adolescents and the importance of early intervention and potential negative sequelae associ-ated with failure to prescribe (Gibbons et al., 2007; Hammad, Laughren, & Racoosin, 2006a, 2006b; March et al., 2004). With this in mind, the primary care provider who has identified a child or adolescent with uncomplicated unipolar depression is encouraged to consider the benefits and risks with the family of cau-tiously initiating first-line antidepressant treatment. III. Assessment DSM-V provides clear diagnostic criteria for each syndrome involving depressed mood and guidance on differential diag-nosis. The primary care clinician is encouraged to refer to DSM-V for complete diagnostic criteria and procedures. No assessment of depressive illness in the child or adoles-cent is complete without assessment of suicide risk and any self-injurious behaviors. Since 2000, suicide has remained the third leading cause of death among 10-to 14-year-olds and 15-to 19-year-olds in the United States (Gould, Greenberg, Velting, & Shaffer, 2003). Risk of suicide and lethality must be assessed on an individual basis. Keeping this in mind, the clinician must be aware that the following factors (not listed in order of importance) confer higher risk for suicide attempt and completed suicide and may warrant emergent referral to a psychiatric provider or hospital emergency room (Gould et al., 2003; Pelkonen & Marttunen, 2003): Male gender White race Substance abuse or dependence Posttraumatic stress disorder Panic attacks Prior suicide attempt or suicidal behavior Poor interpersonal problem-solving ability Aggressive-impulsive behavior Same-sex sexual orientation Family history of suicidal behavior Parental psychopathology, particularly depression and substance abuse Impaired parent-child relationship Family violence and arguments Precipitating incident or life stressors (e. g., interpersonal loss, legal problem, school change, being kicked out of school, disciplinary problems, or physical changes) Physical abuse Sexual abuse Difficulties in school Media coverage of suicide Nonintact family of origin Psychiatric disorder Presence of plan Intent to act on the plan Access to means to execute the plan A comprehensive review of assessment, evaluation, and treat-ment of suicidal ideation in the child or adolescent is beyond the scope of this chapter. However, the reader is referred to the American Academy of Child and Adolescent Psychiatry (AACAP)'s Practice Parameter on the topic. Included in this parameter is a more thorough treatment of risk factors, safety planning, national resources on suicide for the family and clini-cian, and a comparative review of suicide screening instruments 94 CHAPTER 13 | Childhood Depression

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child's psychotherapist(s) and teachers to assist in monitoring. At a minimum, medication monitoring visits should include the following parameters:a. P atient's subjective response to the medication b. Obj ective evaluation of demeanor, energy, and affect c. R eport of any adverse effects, including any changes in weight, sleep, behavior (activation), and sexual problems (adolescents). The clinician is referred to the manufacturer's literature for a comprehensive listing of drug side effects with frequency of occurrence. d. D osing record and any difficulties with or obsta-cles to adherence, such as gastrointestinal com-plaints or sleep changes e. S uicidal ideation and self-harming behaviors f. P rogress with psychiatric referral or response to psychotherapy or other nonpharmacologic treatments. 3. P sychotherapy and combined treatment Psychotherapy either alone or combined with phar-macotherapy is effective in treating pediatric depres-sion. Specifically, cognitive behavioral therapy (CBT) shows the strongest evidence for improved outcome (March et al., 2004; Weisz, Mc Carty, & Valeri, 2006). Developed by Aaron Beck (and since elaborated by many other clinician-researchers), CBT uses behavioral interventions, structured exercises, and talk therapy to change negative thinking. In the depressed child, CBT is thought to exert a therapeutic effect because it leads to restructuring of the negatively distorted cognitions that engender and accompany depressive symptoms. The best data concerning CBT and depression in the pediatric population come from the T reatment for Adolescents with Depression Study (TADS). The TADS is a highly powered 13-site, national study funded by the National Institute of Mental Health that tested three conditions in randomized controlled trial design from spring through summer 2003 (March et al., 2004): fluoxetine alone, CBT alone, and fluoxetine plus CBT. The study was conducted with the adoles-cent population, so conclusions should be applied only to that population. Among the conclusions reached by the TADS team: “despite calls to restrict access to medications, medical management of MDD with fluoxetine, including careful monitoring for adverse events, should be made widely available, not discour-aged” (March et al., 2004, p. 819). “given incremental improvement in outcome when CBT is combined with medication and, In addition to the very small but real potential risk of increased suicidal ideation and behavior, selective serotonin reuptake inhibitors (SSRIs), including esci-talopram and fluoxetine, often have significant gas-trointestinal, nervous system, and sexual side effects predominantly because of the effect on nontargeted serotonin receptors. Risk of various potential side effects (additional to suicidal ideation) must be reviewed with the child and their parents or guardians as part of the process for obtaining informed consent (T able 13-1). The medication guide in T able 13-1 may be helpful in assisting families through this pro-cess. For the most current version and other prescrib-er-directed medication advisories, see www. fda. gov. The process of initiating first-line antidepressant treat-ment for the child or adolescent with uncomplicated unipolar depression may be done in tandem with referral to a pediatric psychiatric specialist. 2. FD A-approved antidepressant agents Only two agents have FDA approval for use as anti-depressants in children and adolescents: the SSRIs fluoxetine (Prozac TM) and escitalopram (Lexapro TM). T able 13-2 summarizes data on these agents. Note that sertraline (Zoloft TM) and fluvoxamine (Luvox TM)—also SSRIs—do not have FDA approval for use in the pediatric age group for depressive disor-ders. They do, however, have FDA approval for treat-ment of obsessive-compulsive disorder in children and adolescents, the former for ages 6-17 years and the latter for ages 8-17 and have been used off-label for treatment of depressive disorders. After gaining appropriate consent, the clinician choosing to initiate antidepressant treatment in an uncomplicated case of major depressive disorder should begin with the lowest dose possible (often one-quarter to one-half the recommended adult dose depending on other factors) and titrate in very slow intervals, generally not sooner than every 3-4 weeks. However, face-to-face monitoring at more frequent intervals than those required to make a dosage change is recommended for children and adolescents receiv-ing antidepressant medication. Vigilance is especially warranted when initiating, increasing, reducing, or otherwise changing dosage. The FDA recommends “at least weekly face-to-face contact with the prescriber during the first 4 weeks of treatment, then visits every other week for the next 4 weeks, then at 12 weeks, and as clinically indicated beyond 12 weeks” (Hughes et al., 2007, pp. 667-686), and this is now generally accepted as the standard of care. The provider should enlist parents in monitoring for adverse effects and, with proper consent, could consider educating the Plan 95

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Table 13-1 Revisions to Medication Guide Read the Medication Guide that comes with your or your family member's antidepressant medicine. This Medication Guide is only about the risk of suicidal thoughts and actions with antidepressant medicines. Talk to your, or your family member's, healthcare provider about: All risks and benefits of treatment with antidepressant medicines All treatment choices for depression or other serious mental illness What is the most important information I should know about antidepressant medicines, depression and other serious mental illness, and suicidal thoughts or actions? 1. Antidepr essant medicines may increase suicidal thoughts or actions in some children, teenagers, and young adults when the medicine is first started. 2. Depr ession and other serious mental illnesses are the most important causes of suicidal thoughts and actions.  Some people may have a particularly high risk of having suicidal thoughts or actions. These include people who have (or have a family history of) bipolar illness (also called manic-depressive illness) or suicidal thoughts or actions. 3. How can I watch for and try to pr event suicidal thoughts and actions in a family member or myself? Pay close attention to any changes, especially sudden changes, in mood, behaviors, thoughts, or feelings. This is very important when an antidepressant medicine is first started or when the dose is changed. Call the healthcare provider right away to report new or sudden changes in mood, behavior, thoughts, or feelings. Keep all follow-up visits with the healthcare provider as scheduled. Call the healthcare provider between visits as needed, especially if you have concerns about symptoms. Call a healthcare provider right away if you or your family member has any of the following symptoms, especially if they are new, worse, or worry you: Thoughts about suicide or dying Attempts to commit suicide New or worse depression New or worse anxiety Feeling very agitated or restless Panic attacks Trouble sleeping (insomnia) New or worse irritability Acting aggressive, being angry, or violent Acting on dangerous impulses An extreme increase in activity and talking (mania) Other unusual changes in behavior or mood What else do I need to know about antidepressant medicines? Never stop an antidepressant medicine without first talking to a healthcare provider. Stopping an antidepressant medicine suddenly can cause other symptoms. Antidepressants are medicines used to treat depression and other illnesses. It is important to discuss all the risks of treating depression and also the risks of not treating it. Patients and their families or other caregivers should discuss all treatment choices with the healthcare provider, not just the use of antidepressants. Antidepressant medicines have other side effects. Talk to the healthcare provider about the side effects of the medicine prescribed for you or your family member. Antidepressant medicines can interact with other medicines. Know all of the medicines that you or your family member takes. Keep a list of all medicine to show the healthcare provider. Do not start new medicines without first checking with your healthcare provider. Not all antidepressant medicines prescribed for children are FDA approved for use in children. Talk to your child's healthcare provider for more information. The U. S. Food and Drug Administration has approved this Medication Guide for all antidepressants. Reproduced from U. S. Food and Drug Administration. Medication guide: Antidepressant medicines, depression and other serious mental illnesses, and suicidal thoughts or actions. Retrieved from http://www. fda. gov/downloads/drugs/drugsafety/informationbydrugclass/ucm100211. pdf. 96 CHAPTER 13 | Childhood Depression

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as importantly, increased protection from suicidality, CBT also should be readily available as part of comprehensive treatment for depressed adolescents” (March et al., 2004, p. 819). In addition to CBT, family therapy and interpersonal therapy are often used in the treatment of pediatric depression (Weisz et al., 2006). The clinician should keep in mind that all therapeutic interventions must be chosen on the basis of the child's particular con-text, family situation, and unique presentation. It should be noted that most of the research into psychotherapy treatment of pediatric depression has focused particularly on adolescents and only rarely on young school-age children. Although some CBT models have been adapted for use in younger children, generally speaking, for a chronologically preadolescent child (or developmentally young older child), play psychotherapies are going to be both more accessible and developmentally appro-priate, though they may seem like a waste of time or simply esoteric to the parent or caregiver. CBT requires a certain level of cognitive, verbal, and social development on the part of the child. Very young or developmentally impaired persons do not and cannot process thoughts and feelings like some adolescents and adults. For these young chil-dren, expressing themselves with and through play is the developmental equivalent for the adult or older adolescent of talking through something using spoken words and conversation. Typically, a play psychotherapist will use the play itself to help the child explore feelings and thoughts by acting them out in the therapy room using toys, puppets, paint, drawing, and the like. The primary provider can facilitate a successful referral for evaluation or psy-chotherapy of the young child by helping to frame the caretaker's expectations of psychotherapy in a developmentally appropriate way. C. Referral Children and adolescents with depression and other psychiatric illness are optimally treated in the context of their families, school, and community within a develop-mental framework. Often the collateral contacts required for optimal assessment and treatment are not easily conducted within the confines of the 15-minute medical office visit. Thus, the primary care clinician should always feel free to consult with or refer to a pediatric psychiatric specialist. Referral or consultation should definitely be sought depending on severity, lethality, complexity, and comorbidity of the case. Cases in which emergent or urgent referral to a psychiatric colleague or hospital emergency room should be made include the following: 1. S uspected bipolar illness 2. P resence of suspected or identified suicidal ideation or suicide-related behavior or nonsuicidal self-harming behavior 3. A ggressive behavior 4. C omorbid or suspected psychiatric or medical illnesses 5. C omorbid or suspected substance abuse 6. I mpaired parent-child functioning or other dysfunction in the family or support system 7. S ignificant family pathology or history of suicide in the family 8. C omorbid or suspected learning disability 9. A ny case in which the treating clinician desires consultation or believes that the presenting problem exceeds his or her scope or knowledge base to provide competent care Table 13-2 Antidepressant Medications with FDA Approval for Use in the Pediatric Population proprietary name Generic n ame Generic Available FDA-Approved pediatric Indication Dosage Prozac TMFluoxetine hydrochloride Yes MDD, 8-18 years (also OCD, 7-17 years)Initial: 10-20 mg/day, depending on weight (initial dose in OCD is 10 mg) Lexapro TMEscitalopram Yes MDD, 12-17 years Initial: 10 mg once daily Recommended: 10 mg once daily Maximum: 20 mg once daily MDD = major depressive disorder; OCD = obsessive-compulsive disorder. Data from U. S. Food and Drug Administration. Plan 97

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V. s elf-management resources A. For providers 1. I nformation on antidepressant use in children, adolescents, and adults with advisories from the FDA available at http://www. fda. gov/Drugs/Drug Safety /Informationby Drug Class/ucm096273. htm. 2. A t oolkit for child and adolescent depression treatment in primary care, developed from consensus guidelines, available at www. glad-pc. org. 3. The g eneral AACAP website also offers param-eters for competent prescribing and evaluation in the child and adolescent population for licensed professionals available at http://www. aacap. org /AACAP/Resources_for_Primary_Care/Practice _Parameters_and_Resource_Centers/Practice _Parameters. aspx. B. For patients and families 1. The g eneral AACAP website also offers excellent educational material for families on a number of topics including medications available at http://www. aacap. org/AACAP/Families_and_Y outh/Facts _for_Families/Facts_for_Families_Keyword. aspx. 2. A lso from AACAP resources on the depression resource center available at http://www. aacap. org /AACAP/Families_and_Y outh/Resource_Centers /Depression_Resource_Center/Home. aspx. 3. A merican Academy of Pediatrics resources on child health topics including depression and suicide available at https://healthychildren. org/English/health-issues /conditions/emotional-problems/Pages/default. aspx. 4. I nformation on depression in children and adoles-cents, available at http://www. nami. org/Content /Navigation Menu/Mental_Illnesses/Depression /Depression_in_Children_and_Adolescents. htm. 5. C hild and adolescent mental health resources available at http://www. nimh. nih. gov/health/topics /child-and-adolescent-mental-health/index. shtml. 6. The N ational Center for Infants, T oddlers, and Families has excellent educationsal materials for parents and providers available at http://www. zerotothree. org /child-development/temperament-behavior/. re Feren Ces American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed. ). Washington, DC: Author. Arnett, J. J. (1999). Adolescent storm and stress, reconsidered. American Psychologist, 54(5), 317-326. Birmaher, B., & Brent, D. (2007). Practice parameter for the assessment and treatment of children and adolescents with depressive disorders. Journal of the American Academy of Child & Adolescent Psychiatry, 46(11), 1503-1526. Cheung, A. H., Kozloff, N., & Sacks, D. (2013). Pediatric depression: An evidence-based update on treatment interventions. Current Psychiatry Reports, 15(8), 1-8. Dimidjian, S., Barrera, M., Martell, C., Muñoz, R. F., & Lewinsohn, P. M. (2011). The origins and current status of behavioral activation treat-ments for depression. Annual Review of Clinical Psychology, 7, 1-38 Dobson, K. S., Hollon, S. D., Dimidjian, S., Schmaling, K. B., Kohlenberg, R. J., Gallop, R., et al. (2008). Randomized trial of behavioral activa-tion, cognitive therapy, and antidepressant medication in the prevention of relapse and recurrence in major depression. Journal of Consulting and Clinical Psychology, 76(3), 468-477. Food and Drug Administration. (2007). FDA proposes new warnings about suicidal thinking, behavior in young adults who take antidepres-sant medications. Retrieved from http://www. fda. gov/News Events /Newsroom/Press Announcements/2007/ucm108905. htm. Gibbons, R. D., Brown, C. H., Hur, K., Marcus, S. M., Bhaumik, D. K., Erkens, J. A., et al. (2007). Early evidence on the effects of regulators' suicidality warnings on SSRI prescriptions and suicide in children and adolescents. American Journal of Psychiatry, 164, 1356-1363. Gould, M. S., Greenberg, T., Velting, D. M., & Shaffer, D. (2003). Y outh suicide risk and preventive interventions: A review of the past 10 years. Journal of the American Academy of Child & Adolescent Psychiatry, 42(4), 386-405. Hammad, T. A., Laughren, T. P., & Racoosin, J. A. (2006a). Suicidality in pediatric patients treated with antidepressant drugs. Archives of General Psychiatry, 63, 332-339. Hammad, T. A., Laughren, T. P., & Racoosin, J. A. (2006b). Suicide rates in short-term randomized controlled trials of newer antidepressants. Journal of Clinical Psychopharmacology, 26(2), 203-207. Hines, A. R., & Paulson, S. E. (2006). Parents' and teachers' perceptions of adolescent storm and stress: Relations with parenting and teaching styles. Adolescence, 41(164), 597-614. Hughes, C. W., Emslie, G. J., Crismon, M. L., Posner, K., Birhamer, B., Ryan, N., et al. (2007). T exas children's medication algorithm project: Update from the T exas consensus panel on medication treatment of childhood major depressive disorder. Journal of the American Academy of Child & Adolescent Psychiatry, 46(6), 667-686. March, J., Silva, S., Petrycki, S., Curry, J., Wells, K., Fairbank, J., et al. (2004). Fluoxetine, cognitive-behavioral therapy, and their combination for adolescents with depression. JAMA, 292, 807-820. March, J. S., Silva, S., Petrycki, S., Curry, J., Wells, K., Fairbank, J., et al. (2007). T reatment for Adolescents with Depression Study (TADS): Long-term effectiveness and safety outcomes. Archives of General Psychiatry, 64(10), 1132-1144. Pelkonen, M., & Marttunen, M. (2003). Child and adolescent suicide: Epidemiology, risk factors, and approaches to prevention. Pediatric Drugs, 5(4), 243-265. Rao, U., & Chen, L. (2009). Characteristics, correlates, and outcomes of childhood and adolescent depressive disorders. Dialogues in Clinical Neuroscience, 11, 45-62. Saddock, B. J., & Saddock, V. A. (2007). Kaplan & Saddock's synopsis of psychiatry (10th ed. ). New Y ork, NY: Lippincott, Williams & Wilkins. Weisz, J. R., Mc Carty, C. A., & Valeri, S. M. (2006). Effects of psycho-therapy for depression in children and adolescents: A meta-analysis. Psychological Bulletin, 132(1), 132-149. 98 CHAPTER 13 | Childhood Depression

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nonorganic pediatric feeding disorders (Romano, Hartman, Privitera, Cardile, & Shamir, 2015). 2. P revalence and incidence a. FTT is usually identified during the first 2 years of life; 80% are identified by 18 months of age (Cole & Lanham, 2011). b. I t affects up to 5-10% of infants and children in primary care settings, although less than 10% can be attributed to a recognized disorder, such as cardiac disease or inborn errors of metabo-lism (Atalay & Mc Cord, 2012; Block et al., 2005; Stephens et al., 2008). c. H owever, because there is a lack of consensus regarding criteria to establish the diagnosis, this likely affects the reported incidence. B. FTT caused by inadequate caloric intake 1. O verview FTT may be the result of poorly sustained nutrient availability, infant inability to consume adequate foods, or ineffective feeding interactions leading to decreased intake (the most common cause of FTT). a. I mproper formula preparation, limited formula or food availability, insufficient breastmilk pro-duction, or overuse of fruit juices at the expense of more nutrient-dense foods b. M otor feeding issues interfering with consuming adequate intake, such as inability to suck, chew, or swallow effectively c. P oor appetite d. Or al aversion e. Di sturbed caregiver-infant interactions affecting feeding interest or success, including behavioral problems during the meal, caregiver inattention, or outright neglect (Gahagan, 2006; Stephens et al., 2008) f. One e ndocrinology clinic reported an associa-tion with family stress (34% of patients), ineffec-tive feeding such as poor attention to cues or I. Intr oduction and general background Growth failure in childhood, defined as inadequate sustained growth and/or weight gain compared to age-appropriate norms, must be appropriately identified and managed to optimize out-comes (Al Nofal & Schwenk, 2013). Weight is primarily affect-ed when nutritional intake cannot support growth demands, although height and head circumference are affected by increas-ing malnutrition. Failure to thrive (FTT) is a sign of growth fail-ure with multiple interacting causes, yet is itself poorly defined in the literature. Formerly labeled “organic” and “inorganic,” FTT is now thought of in more useful terms based on its presumed etiology: (1) inadequate caloric intake, (2) inadequate caloric absorption or use, or (3) excess caloric consumption. Regardless of the etiology, growth failure and FTT may have long-term effects on cognitive and behavioral development and long-term growth (Al Nofal & Schwenk, 2013; Cole & Lanham, 2011; Jaffe, 2011; Stephens, Gentry, Michener, & Kendall, 2008). A. FTT from all causes 1. O verview The most common cause of FTT worldwide is pov-erty and poor access to adequate nutrition (Block, Krebs, Committee on Child Abuse and Neglect, & Committee on Nutrition, 2005). It occurs across all populations, although the risk is increased in impov-erished urban and rural populations (Gahagan, 2006; Rabinowitz, 2015). a. I n developed countries, it is also commonly asso-ciated with poor caretaking skills, reflecting a disparity between infant interactive and growth needs and caretaker attentiveness. b. FTT m ay be the sole clinical finding suggesting neglect or abuse. c. FTT a ccounts for up to 5% of pediatric hospi-talizations (Stephens et al., 2008; Rabinow-itz, 2015) and is associated with 40-50% of Annette Carley FAIlure to t hr I ve Dur I ng In FA n C y© Eliks/Shutterstock; © donatas1205/Shutterstock 9914Chapt Er

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A. Subjective 1. H istory and review of systems A thorough history, the most critical element in estab-lishing the diagnosis, uncovering causes, and posing a therapeutic plan (Block et al., 2005; Cole & Lanham, 2011; Gahagan, 2006; Jaffe, 2011; Rabinowitz, 2015), includes:a. P ast health history i. P renatal history, including gravida and par-ity of mother, maternal weight gain during pregnancy, pregnancy complications, prena-tal care access ii. I ntrauterine growth history ( Jaffe, 2011) iii. B irth history, including gestational age, weight, type of delivery, infant Apgar scores, and delivery complications iv. N eonatal history; including weight at dis-charge; complications; congenital disorders; and oral instrumentation, such as intubation v. Ea rly childhood history, including acute and chronic illness, hospitalizations, inju-ries, and developmental status vi. C urrent history, including presenting com-plaint onset and duration and associated symptoms vii. El imination history, including voiding and frequency and character of stools b. F amily history i. A ge and health of parents, grandparents, and primary caretakers ii. B irth weight and height of parents and siblings iii. C ongenital disorders; chronic illness; and mental health disorders, such as anxiety or depression c. S ocial and environmental history i. M arital status, education, and literacy of parents ii. O ccupation and source of financial support and access to public assistance programs, such as the Special Supplemental Nutrition Program for Women, Infants, and Children (WIC) or food stamps iii. T ype of housing and number of persons in household iv. S ocial or environmental concerns, such as unemployment, marital problems, abuse, and substance exposure v. F amily and peer relationships, including physical and emotional closeness, communi-cation, support, history of abuse or neglect, adaptive behaviors, positive social affect, and ability to ask for and receive supportinadequate mealtime structure (28% of patients), and overreliance on a liquid diet such as excess juice (38% of patients) in their referred patients (Atalay & Mc Cord, 2012). C. FTT caused by inadequate caloric absorption or use 1. O verview A number of genetic, structural, or functional condi-tions may create ineffective nutrient absorption or use and must be recognized. Included among these con-ditions are:a. C eliac disease b. C ystic fibrosis c. C ow milk protein allergy d. V itamin or mineral deficiencies e. B iliary atresia or hepatic dysfunction f. S hort gut syndrome g. Ge netic abnormalities, such as trisomy 13, 18, and 21 h. S hort-stature syndromes including Russell-Silver syndrome, Turner syndrome, Down syndrome, hypothyroidism, hypophosphatemic rickets, growth hormone deficiency, and fetal alcohol syndrome i. M etabolic disorders, such as glycogen storage disease and aminoacidopathies j. C hronic vomiting k. G astroesophageal reflux l. C hronic renal disease (Gahagan, 2006; Jaffe, 2011; Stephens et al., 2008) D. FTT caused by excess caloric consumption needs 1. O verview Increased metabolic demands may interfere with growth, which may occur with such conditions as:a. C hronic lung disease b. C ongenital heart disease c. C hronic infection d. H yperthyroidism e. A nemia f. D iabetes g. R enal tubular acidosis h. Fe ver i. I mmunodeficiency j. M alignancy k. I ntrauterine growth restriction (Cole & Lanham, 2011; Jaffe, 2011; Stephens et al., 2008) II. Database (appropriate for the evaluation of FTT in developed countries) may include but is not limited to:100 CHAPTER 14 | Failure to Thrive During Infancy

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beyond age 2 years, the CDC growth charts are recommended (Al Nofal & Schwenk, 2013). i. W eight-for-age ratio is not sufficient as the sole indicator of FTT because it does not accurately address infants who are geneti-cally or constitutionally small or those born premature or small for gestational age ( Joosten & Hulst, 2011). ii. P ersistent weight below the third to fifth percentile on standardized curve, down-ward growth trend crossing two percentile lines, or change in weight-to-height ratio currently recommended in the determina-tion of FTT ( Joosten & Hulst, 2011). iii. J oosten and Hulst summarized multiple cri-teria to determine FTT and direct immedi-ate nutritional management, based on age, weight, and/or height including:a. in adequate weight gain or growth for more than 1 month in a child less than age 2 b. w eight loss or failure of weight gain for more than 3 months in a child over age 2 c. mor e than-1 standard deviation (SD) change in weight: age over 3 months in a child less than 1 year of age d. mor e than-1 SD change in weight: height over 3 months in a child over 1 year of age e. de crease in height gain of 0. 5-1 SD per year in a child less than 4 years of age, or 0. 25 SD per year in a child over age 4 years f. de crease in height gain of more than 2  cm compared with preceding year during early and middle puberty ( Joosten & Hulst, 2011) b. V ital signs, including blood pressure 2. Obs ervation and documentation of caregiver-child interactions a. P resence of eye contact, holding close to body, calling infant by name b. Obs ervation during feeding 3. S upportive data from relevant diagnostic tests are rarely needed, although may be dictated by positive findings in the history (Stephens et al., 2008). III. Assessment A. Determine the diagnosis Identify other causes of diminished growth, including those constitutionally small or genetically small. vi. P arenting skills, including previous experi-ence caring for children, attendance at par-enting classes, ability to interpret infant cues, daily routines, play activity with child, care-taking routines related to behavior, crying, and elimination vii. Di sorganized or disruptive household envi-ronment, erratic family meals, and multiple caretakers viii. C aretaker concerns about growth and development d. N utrition history i. M aternal nutrition before, during, and after pregnancy, including number of meals per day, type, and amount of food and fluid intake ii. I nfant feeding history, including type of milk, volume and frequency of feedings, proper preparation of formula, strength of suck, burping, use of supplemental foods, and tolerance of food texture iii. Obt ain minimum 24-hour dietary recall (Rabinowitz, 2015) e. F or breastfed infants: frequency of feeding, duration of feeding, perceived satiety, strength of suck, single or two breasts at feeding, and maternal breast fullness before feeding and emp-tying after feeding f. F or bottle-fed infants: frequency of feeding, duration of feeding, perceived satiety, strength of suck, and proper formula preparation g. F or infant transitioning to solid foods: time of introduction of solids and foods self-fed by infant h. R eview of systems and clinical findings may reveal i. D ysmorphic features suggesting a syn-drome, such as low-set ears, hypertelorism, or long philtrum ii. P allor iii. H air loss iv. Thin or w asted appearance, loose folds of skin v. I rritability vi. S leepiness or easy fatigue vii. P oor eye contact or social smile viii. D elayed vocalization ix. D elayed motor development, including late rolling, sitting, crawling, or walking (Lucile Packard Children's Hospital, 2009) B. Objective 1. P hysical examination findings a. Es tablish a growth trend, including measuring and plotting head circumference, weight, and length (height). For children less than 2 years of age, the WHO growth charts are recommended; Assessment 101

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B. Severity Assess severity of the condition: severe malnutrition, dehydration, and suspected abuse are indications for hos-pitalization. Rarely hospitalization may be indicated for accurate observation of feeding interactions or to optimize investigation (Block et al., 2005; Cole & Lanham, 2011; Gahagan, 2006; Stephens et al., 2008). C. Significance Assess significance of the problem to caregiver and family. D. Motivation and ability Determine caregiver and family willingness and ability to follow through with the treatment plan. Iv. g oals of clinical management A. Screening or diagnosing FTT Choose a practical, cost-effective approach to screening and diagnosis. B. Treatment Select a treatment plan that achieves appropriate growth and growth velocity, provides necessary micronutrients and macronutrients, and is individualized for the caregiver and child as part of a therapeutic alliance C. Patient adherence Select an approach that maximizes caretaker compliance. v. Plan A. Screening Elicit a thorough history and perform a thorough physical examination; assess growth and development at all well-child visits. B. Diagnostic tests Laboratory or radiographic tests are rarely necessary, because the diagnosis is generally apparent after review of history and physical examination findings (Cole & Lanham, 2011). In addition to routine childhood screening at 6-18 months for iron deficiency and lead poisoning, sup-portive testing suggested by positive findings may include: 1. U rinalysis and urine culture, urine p H 2. C omplete blood count with smear 3. S tool p H, reducing substances, and ova and parasites or occult blood 4. S weat chloride 5. T uberculosis testing: skin (Mantoux tuberculin skin test) or blood (interferon-gamma release assays)6. R adiographic studies, including skeletal survey and bone age (Al Nofal & Schwenk, 2013, 2010; Gahagan, 2006; Stephens et al., 2008). C. Management 1. FTT is a chronic process, and management continues long term (Block et al., 2005). 2. Ade quate growth is essential for survival, and interventions begin before completion of the diagnostic evaluation (Gahagan, 2006). 3. M ost FTT cases can be managed on an outpatient basis, unless malnutrition is severe; hospitalization is indicated for evidence of severe dehydration, weight less than 70% of predicted weight-to-height, or suspected neglect or abuse (Block et al., 2005; Gahagan, 2006; Jaffe, 2011; Stephens et al., 2008). 4. A m ultidisciplinary approach is strongly encouraged, involving input from medicine, nursing, lactation specialists, pediatric nutritionist, physical therapy, behavioral psychology, and social services as part of a therapeutic alliance with the family (Cole & Lanham, 2011; Jaffe, 2011) 5. F or breastfed infants, efforts should support breastfeeding where possible, including: a. B reast pumping using dual-pump b. C onsidering galactalogues to increase milk production c. E ncouraging maternal nutrition, fluids, and rest d. D eveloping strategies to modify maternal and environmental stress and its negative impact on milk production e. I dentifying sources of home and social support for breastfeeding f. I f formula supplementation is deemed neces-sary to ensure sufficient nutrient intake, support the mother in efforts to resume or continue breastfeeding 6. F or formula-fed infants, efforts to optimize intake include: a. I ncreasing the number of feeds per day, with a goal of 100-120 kcal/kg/d b. D emonstrating techniques to awaken a sleepy feeder c. R eviewing formula preparation with the caretaker 7. F or infants consuming solid foods, encourage self-feeding while ensuring adequate intake of nutritious foods and nutritionally competent choices of finger foods. Discourage excess juice as this may interfere with more appropriate nutritional intake. Consider instructing parents to complement foods with calorie-dense supplements such as gravy, cream sauces, olive oil, or butter (Cole & Lanham, 2011; Gahagan, 2006). 102 CHAPTER 14 | Failure to Thrive During Infancy

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1. C hildren's National Medical Center, Washington, DC http://childrensnational. org/choose-childrens /conditions-and-treatments/stomach-digestion-gi /poor-growth-failure-to-thrive 2. J ohns Hopkins Children's Center, Baltimore, MD http://www. hopkinschildrens. org/Failure-to-Thrive . aspx 3. L ucile Packard Children's Hospital, Palo Alto, CA http://www. stanfordchildrens. org/en/topic/default ?id=failure-to-thrive-90-P02297 4. U niversity of California, San Francisco School of Medicine/Department of Pediatrics http://pediatrics. ucsf. edu/blog/failure-thrive -rethinking-our-approach#. Vaw Hp Sp Viko 5. M edscape e Medicine http://emedicine. medscape. com/article/985007 -overview re Feren Ces Al Nofal, A., & Schwenk, W. F. (2013). Growth failure in children: A symp-tom or a disease? Nutrition in Clinical Practice, 28(6), 651-658. Atalay, A., & Mc Cord, M. (2012). Characteristics of failure to thrive in a referral population: Implications for treatment. Clinical Pediatrics, 51(3), 219-225. doi: 10. 1177/000992281142100 Block, R. W., Krebs, N. F., & Committee on Child Abuse and Neglect, & Committee on Nutrition. (2005). Failure to thrive as a manifestation of child neglect. Pediatrics, 116(5), 1234-1237. Cole, S. Z., & Lanham, J. S. (2011). Failure to thrive: An update. American Family Physician, 83(7), 829-834. Gahagan, S. (2006). Failure to thrive: A consequence of undernutrition. Pediatrics in Review, 27(1), e1-e11. Jaffe, A. C. (2011). Failure to thrive: Current clinical concepts. Pediatrics in Review, 32(3), 100-108. doi: 10. 1542/pir. e2-3-100 Joosten, K. F. M., & Hulst, J. M. (2011). Malnutrition in pediatric hos-pital patients: Current issues. Nutrition, 27, 133-137. doi: 10. 1016 /j. nut. 2010. 06. 001 Lucile Packard Children's Hospital. (2009). Failure to thrive. Retrieved from http://www. stanfordchildrens. org/en/topic/default?id=failure-to -thrive-90-P02297 Nutzenadel, W. (2011). Failure to thrive in childhood. Deutsches Arzteblatt International, 108(38), 642-649. Rabinowitz, S. S. (2015). Nutritional considerations in failure to thrive. Retrieved from http://emedicine. medscape. com/article/985007 -overview Romano, C., Hartman, C., Privitera, C., Cardile, S., & Shamir, R. (2015). Current topics in the diagnosis and management of the pediatric non organic feeding disorders (NOFEDs). Clinical Nutrition, 34, 195-200. doi: 10. 1016/j. clnu. 2014. 08. 013 Stephens, M. B., Gentry, B. C., Michener, M. D., & Kendall, S. K. (2008). Clinical inquiries. What is the clinical workup for failure to thrive? Journal of Family Practice, 57(4), 264-266. 8. A ttention to optimizing interest by including appealing food textures, colors, or temperatures and rewarding desirable eating behaviors ( Jaffe, 2011). 9. C atch-up growth should be promoted until previous growth percentiles have been attained. The refeeding plan is determined by the degree of malnutrition, with attention to potential risks from exceeding the child's absorptive capacity or creating refeeding syndrome. This condition is not well understood but may create electrolyte and fluid balance abnormalities that contrib-ute to edema and impaired cardiac performance. The therapeutic nutrition plan must attend to careful moni-toring of serum electrolytes, glucose, and acid-base bal-ance as well as growth measures (Nutzenadel, 2011). D. Client education Offer ongoing caretaker support and education and rein-force consistent effective nutritional practices at all office visits by: 1. P roviding a supportive environment for parents to discuss concerns or conflicts related to the infant or home setting 2. R ole modeling infant feeding, holding, and stimulation 3. Di scussing normal development and infant behavior 4. R einforcing proper nutritional practices, such as discussing caloric needs to optimize growth, dem-onstrating proper formula preparation, proposing a regular feeding schedule with written instructions, and directly assessing a feeding interaction 5. M aintaining ongoing contact with the caregiver and family and modifying the nutritional plan accordingly 6. R eferral to public health or home care nursing, as available in the community, for ongoing evaluation and support E. Outcome Most children with poor growth can demonstrate adequate improvement with intensive intervention. However, both cognitive and school outcomes of children with FTT are worse than their non-FTT counterparts, likely representing the cumulative effects of undernutrition and other envi-ronmental risks, such as inattention or lack of appropriate stimulation. These infants need ongoing developmental, behavioral, and growth monitoring to detect and manage long-term consequences of FTT (Gahagan, 2006). v I. r esources A. Patient-client education The following resources provide online health library information for clients and professionals. References 103

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neglect in the pediatric population. Cumulative estimates from the National Child Abuse and Neglect Data System (NCANDS) are that 12. 5% of all children will be reported and confirmed as maltreated during their childhood (Wildeman et al., 2014). A recent household survey of caregivers and older children found that 12% of children in the sample experienced some form of maltreatment just in the past year (Finkelhor, Vanderminden, Turner, Hamby, & Shattuck, 2014). Assessing and responding to child maltreatment can be chal-lenging for the APN, because the abuse or neglect may not be readily apparent and may not be the specific reason that the child is presenting for care. Epidemiologic risk factors for child maltreatment may be helpful in planning population-level inter-ventions but are not as helpful in the clinical setting, where the APN should always keep maltreatment in mind as part of the differential diagnosis (Schapiro, 2008). Child abuse and neglect involve injuries to children or failure to protect them from harm; maltreatment assessments and reports are made to protect chil-dren, not to punish “bad” parents (Keeshin & Dubowitz, 2013). Keeping the child in mind helps the APN to sort through what is often a confusing and emotion-laden situation. Child maltreatment has been associated in the litera-ture with a variety of risk factors including poverty; income inequality; single parenthood; intimate partner violence; parental physical and mental illness; substance abuse; and child factors, such as disability, special healthcare needs, or temperamental mismatch with a parent (Eckenrode, Smith, Mc Carthy, & Dineen, 2014; IOM & NRC, 2014; T esta & Smith, 2009). Protective factors may include extended fam-ily cohesiveness; personal, financial, and community resourc-es; religiosity; optimism on the part of the caregiver; and an engaging child (IOM & NRC, 2014). Just as it is important for the APN to explore the resources and coping strategies of all families who seem to have risk factors for maltreatment, it is also important to remember that child maltreatment can occur in families who do not have known risk factors. Research has shown that healthcare providers may underreport maltreat-ment in families they know well and assume to be socially and economically stable ( Jones et al., 2008). I. Intr oduction and general background Child maltreatment encompasses physical, sexual, and emo-tional abuse and child neglect. Healthcare providers have legal, professional, and ethical responsibilities to assess children for maltreatment and to report suspected cases. Each of the 50 states, the District of Columbia, and territories such as Puerto Rico has its own definitions of child abuse and neglect, but all must conform to minimum federal standards set in the Child Abuse Prevention and T reatment Act: Any recent act or failure to act on the part of a parent or caretaker, which results in death, serious physical or emotional harm, sexual abuse, or exploitation, or an act or failure to act that presents an imminent risk of serious harm (Child Abuse Prevention and T reatment Act, 1998; Child Welfare Information Gateway, 2014). Advanced practice nurses (APNs) can consult the website https://www. childwelfare. gov /topics/systemwide/laws-policies/state/ for the specific defini-tions and reporting responsibilities in their own states. The professional and ethical responsibilities to assess for, detect, and report child maltreatment are reinforced by a steadily accumulating body of literature on the myriad and long-lasting effects of these adverse events, including greater rates of depression and substance abuse, early onset of sexual activity, greater likelihood of becoming a teenage parent, and higher rates of type 2 diabetes mellitus and other adult chronic conditions (Herrenkohl, Hong, Klika, Herrenkohl, & Russo, 2013; Mersky, T opitzes, & Reynolds, 2013; Shonkoff & Garner, 2012). In 2013, 3. 5 million reports were made to child protection agencies in the United States. From these reports, 678,932 children were deemed to be victims of child maltreat-ment, with a victimization rate of 9. 1 per 1,000 children. An estimated 1,520 children died as a result of abuse or neglect, with a rate of 2. 04 deaths for 100,000 children. Children who were less than 1 year old were most vulnerable to fatal maltreat-ment, at a rate of 18. 09 per 100,000 infants (U. S. Department of Health and Human Services, 2015). However, these annual reporting rates understate the prevalence of child abuse and Naomi Schapiro Ch Ild Maltreat Me Nt© Eliks/Shutterstock; © donatas1205/Shutterstock 104 15Chapt Er

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(Child Welfare Information Gateway, 2013a, p. 4). Emotional abuse is difficult to substantiate unless the child exhibits severe psychologic sequelae. Such abuse is also a component of other forms of child maltreatment, which impedes reporting and tracking of emotional abuse in itself. In some states, witness-ing domestic violence may be considered a form of child abuse, whereas in others committing intimate partner violence in the presence of a child may result in an enhanced sentence or a requirement to pay for counseling for the child (Child Welfare Information Gateway, 2013b). 2. I ncidence and prevalence In 2013, 8. 7% of child maltreatment victims were psychologically abused (U. S. Department of Health and Human Services, 2015). Prevalence studies over childhood in developed countries range from 4-9% of children (Gilbert, Widom et al., 2009). D. Neglect 1. D efinition and overview As the most commonly reported form of child mal-treatment, neglect has been understudied, yet its long-term consequences may be just as devastating as other forms of abuse (Keeshin & Dubowitz, 2013). Broadly, neglect involves the failure of a parent or caregiver to provide for a child's basic physical and emotional needs (Child Welfare Information Gateway, 2014), including food, clothing, shelter, educational needs, medical care, supervision, and emotional care. Although neglect may involve one instance of a dangerous failure to supervise or pro-vide care, it also may result from the accumulation of smaller lapses over time, making assessment a chal-lenge. The standard for reporting neglect involves the APN's suspicion of actual or imminent harm to a child (Schapiro, 2008). States vary widely in their specific definitions of neglect, with some including or excluding drug use, homelessness, or parental refusal of health care for their child for personal or religious reasons. In some states, failure to educate is covered under truancy rather than child abuse law (Child Welfare Information Gateway, 2014). Child neglect has been associated with substance abuse, depression, and other caretaker stressors (IOM & NRC, 2014). Neglect has also been strongly associated with poverty, with increasing reports of neglect directly related to increasing unemployment, decreasing income, stricter limits on welfare pay-ments, and decreased access to childcare and child health insurance, independent of parenting char-acteristics (IOM & NRC, 2014; Klevens, Barnett, Florence, & Moore, 2015. )A. Physical abuse 1. D efinition and overview Broadly, physical abuse is an inflicted (nonaccidental) injury to a child that results in physical impairment. Mechanisms of injury may include biting, burning, kicking, striking, shaking, grabbing, stabbing, dragging, throwing, strangling, or poisoning. Legal definitions of reportable physical abuse vary widely from state to state (Child Welfare Information Gateway, 2014). 2. I ncidence and prevalence During 2013, 18% of victims of child maltreatment were physically abused. Physical abuse accounted for 46. 8% of child fatalities, either alone or in com-bination with another type of maltreatment (U. S. Department of Health and Human Services, 2015). Lifetime prevalence estimates of severe physical abuse (not including hitting, slapping, or grabbing) from parental or self-reported surveys range from 5-35% (Gilbert, Widom et al., 2009). Widely differ-ing definitions and overlap with nonabusive physical punishment make estimation of prevalence difficult. B. Sexual abuse 1. D efinition and overview Sexual abuse includes sexual contact between adults and children, including fondling, penetration, expo-sure to sexual activity or involvement in pornogra-phy, and unwanted sexual contact between minors. This contact may be carried out through violence, coercion, emotional manipulation, or the child's developmental inability to understand or consent to the activity (Child Welfare Information Gateway, 2013a). Sexual abuse includes commercial sexual exploitation of children (Greenbaum, 2014). In many states, consensual sexual activity of a minor with either an older minor or an adult may be report-able under sexual abuse laws (Assistant Secretary for Planning and Evaluation, n. d. ). 2. I ncidence and prevalence During 2013, 9% of child maltreatment victims were sexually abused (U. S. Department of Health and Human Services, 2015). Lifetime prevalence estimates range from 15-30% of girls and 5-15% of boys (Gilbert, Widom et al., 2009). C. Psychologic or emotional abuse 1. D efinition and overview Under federal standards, emotional abuse involves “a pattern of behavior that impairs a child's emo-tional development or sense of self-worth. This may include constant criticism, threats, or rejection, as well as withholding love, support, or guidance” 105 Introduction and general background

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jokes, is developmentally normal and not in itself a sign of sexual abuse (Kellogg, 2010). In a media-saturated society in which sexual images are widely available, discerning age-appropriate from inappropriate sexual knowledge may be difficult. However, some activities should raise a suspicion of sexual abuse:i. S exual play involving penetration or use of objects. ii. S exual play that closely mimics adult sexual activity. iii. S exual play between children with an age difference of 3 or more years or suspicion of emotional coercion. d. P ersonal and social history and activities of daily livingi. H ow does the parent describe the child? Red flags include obvious lack of enjoyment of the child, labeling the child as bad, or inappropriate expectations for child's devel-opmental stage. ii. F amily routines and activities. iii. M ethods of discipline used and their per-ceived effectiveness. e. R eview of systems Recurrent headache, abdominal pain, or genito-urinary discomfort may be related to somaticiz-ing or actual recurrent injury. A thorough review of systems from both parent and child may be helpful in cases in which the history is confusing or inconsistent. 2. S ituations that may heighten the risk of child maltreatment Children and families in these situations may need extra support, and should be asked how they are coping if they are experiencing any of the following situations (Dubowitz & Leventhal, 2014; Christian & Committee on Child Abuse, 2015; Saul et al., 2014):a. S udden changes in family status Job loss, loss of health insurance, death, divorce, domestic violence, and parental illness, including mental health diagnoses and substance abuse, can all strain or overwhelm a parent's resources and ability to care for a child. b. C hallenging stages in child development i. The inc onsolable infant, the willful toddler, the school-age child with behavioral and learning difficulties, and normative develop-mental changes of adolescence can challenge all parents. ii. I n some cases these typical challenges of parenting can exacerbate a stressed family system. 2. I ncidence and prevalence During 2013, 79. 5% of child maltreatment victims in the  United States were neglected, and 2. 3% suffered from  medical neglect (U. S. Department of Health and Human Services, 2015). Prevalence estimates range from 6-11. 8% of children (Gilbert, Widom et al., 2009). II. d atabase (may include but is not limited to) A. Subjective As with other sensitive subjects, history-taking about child maltreatment may be enhanced when written ques-tionnaires on paper or computer are used in combination with direct questions by the practitioner (Gilbert, Kemp et al., 2009; Slep, Heyman, & Foran, 2015). Routinely asking questions about physical punishment or fighting, about forced or coerced sexual activity and inappropriate touching, and about general safety can send a message to the child and parent that these subjects are open topics of discussion during the visit, even if they do not answer them at first. 1. C hief complaint a. I njuries i. D etailed history of any new or old injuries: Is the injury consistent with the history? ii. H istory of similar injuries and general injury history. iii. C urrent or past history of delayed care for injuries. iv. H istory of seeking care for injuries at multiple facilities. b. S udden changes in behavior Because children vary widely in temperament, and cultural influences may also affect their behavior in clinical settings, a sudden change in behavior is an important indicator of some kind of emotional trauma (including but not limited to child maltreatment): for example, the outgo-ing child who suddenly seems withdrawn, or the quiet child who suddenly seems driven by a motor. c. S exual acting out Genital self-stimulation for pleasure, or mastur-bation, is a normal part of child development from toddlerhood through adolescence; chil-dren younger than school age may not have a well-developed sense of privacy and may mastur-bate in social settings considered inappropriate by adults. Sexual play between age mates, con-sisting of exploration of body parts and sexual 106 CHAPTER 15 | Child Maltreatment

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c. C hildren who are difficult to care for This category encompasses a wide variety of conditions, from children with difficult tem-peraments to children with neuromuscular dis-abilities. Children who require a great deal of additional care or who are less able to give the parent positive reinforcement for that care may be at greater risk for maltreatment. 3. S pecial considerations for taking histories from children about suspected maltreatment The APN should approach history-taking of injuries and physical complaints in a careful and systematic fashion. If children disclose abuse, the APN should avoid taking a comprehensive history of the disclo-sure, instead limiting questions to a brief review of who, what and when, gathering just enough information to report to Child Protective Services (CPS) or the police. The following are age-related considerations:a. T oddlers and preschool-aged children i. C hildren under the age of 6 have limited vocabularies and a relatively undeveloped sense of time and sequence and are best interviewed by a trained expert in child maltreatment. ii. W ell-meaning parents and healthcare profes-sionals can inadvertently feed the child infor-mation and unwittingly distort the story. b. S chool-age children i. S chool-age children have a developed sense of time and sequence. The challenge for the healthcare provider is to speak briefly with the school-age child without the parent present. ii. I f history-taking is not possible, the APN with a reasonable suspicion of maltreatment should still file a CPS report. c. Ado lescents i. Ado lescents may come in alone for care, and many clinics have established policies for taking written questionnaires and verbal histories from children over 12 without a parent in the room (see Chapter 7). ii. Ea ch state has its own parameters for con-fidential services (Guttmacher Institute, 2015), and it is important to let the adoles-cent know which parts of the history are truly confidential and what the APN must report related to both sexual assault and consensual sexual activity between dissim-ilar-aged minors and between minors and adults (Assistant Secretary for Planning and Evaluation, n. d. ; Child Welfare Information Gateway, 2014). B. Objective It is important to document any abnormal findings as thoroughly and accurately as possible, including measure-ment of injuries and drawings if appropriate. Photographic documentation may be useful if it conforms to local law enforcement standards for quality and chain of custody. 1. Ge neral overview of child's appearance and behavior The demeanor and behavior of the child or adoles-cent in the clinic can provide the APN with valuable information. However, it is important to remember that the APN is seeing just a snapshot of the child in an artificial and sometimes stressful setting. Behavioral changes commonly seen in maltreated children may also occur after other adverse events of childhood, including death, incarceration, or divorce of a parent, or sudden death of a close friend (Fairbank & Fairbank, 2009; Naughton et al., 2013). Children may be overly compliant for their developmental age, may be with-drawn or attach readily to adults they do not know well, may exhibit hypervigilance, or may fail to seek com-fort in the clinical setting from parents or caretakers (Child Welfare Information Gateway, 2013a). 2. P hysical examination findings consistent with physical abuse In some cases, an inflicted injury is obvious to the examiner. In other cases, it may be difficult to dis-tinguish between inflicted and accidental injury or between injury and infection or a chronic medical condition. Y et timely identification of physical abuse can protect vulnerable children and may be able to prevent serious injury or fatalities, especially in infants and young children. Reviews of missed cases of physi-cal abuse show that clinicians tend to miss “sentinel injuries” (Christian & Committee on Child Abuse, 2015, p. e1340) such as bruising, intraoral injuries including lingual and labial frena tears and fractures. Common errors include incomplete exams, failure to understand the significant of bruises in preambulatory children, failure to report discrepancies between the history and the physical findings, and failure to obtain imaging when recommended by protocols ( Jackson et al., 2015). T able 15-1 is a partial list of physical indi-cators of maltreatment and normal variants or medical conditions that may appear similar on exam. a. B ruises are the most common injuries in physi-cally abused children. Dating of bruises by appearance has been found to be unreliable (Grossman, Johnston, Vanezis, & Perrett, 2011). Bruising to the center of the face, ears, neck, back, buttocks, upper arms, and backs of the legs and any bruising in an infant that does not have a clear and plausible history raise suspicions of inflicted injury. Bruising over bony prominences is more consistent with accidental injury (Hornor, 2012). 107 Database

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b. B urns may be inflicted or accidental. Accidental burns from hot objects, such as heaters or irons, may be difficult to distinguish from inflicted burns, because both have patterning. Splash burns, occurring for example when a toddler pulls a hot pot or cup off a surface, have typical and irregular formation, with the burn degree lessen-ing as the liquid drips down the body. Immersion burns with a stocking or glove demarcation are more likely to be inflicted (T oon et al., 2011). c. F ractures are common in children, and distin-guishing inflicted from accidental fractures can be difficult. Spiral fractures and metaphyseal fractures can be the result of inflicted or acciden-tal trauma, and some preambulatory infants in walkers have sustained accidental fractures. The following findings on physical or radiologic exam-ination should raise suspicions of physical abuse:i. F ractures in a preambulatory infant. ii. F ractures in different stages of healing. Table 15-1 Physical Findings or Conditions That May Mimic Findings in Child Maltreatment Findings Inflicted Injury/ a buse Normal Variant or Medical Condition Circular crusted plaques with red margins Burns from cigarettes or other hot circular-tipped objects Impetigo Iatrogenic: wart removal Bullae Inflicted burns Accidental burns Bullous impetigo Marked erythema with or without vesicles or bullae Immersion burns Staphylococcal scalded skin syndrome Toxic epidermal necrolysis Red or hyperpigmented handprint Slapping In sun-exposed areas: phytophotodermatitis Ecchymoses Inflicted injury from punching or slapping Accidental injury Clotting or bleeding disorders, chronic or acute (e. g., hemophilia vs. idiopathic thrombocytopenic purpura) Infants: birthmarks (congenital dermal melanocytosis)Neonates: bruising from precipitous delivery Accidental impact to forehead with movement of ecchymoses during healing Allergic “shiners” Swollen red eyelid or orbital area Fresh inflicted injury Periorbital cellulitis Scratches on wrists, popliteal spaces, back Scratching, restraining child Self-inflicted secondary to atopic dermatitis or neuropsychiatric conditions Fractures inconsistent with history or child's developmental level; multiple fractures at different stages of healing Grabbing, twisting, throwing Pathologic fractures related to osteogenesis imperfecta or other bone abnormalities Mucopurulent vaginal discharge in prepubertal girl Neisseria gonorrhoeae or Chlamydia trachomatis infection [Absence of discharge does not indicate lack of infection]Streptococcus pyogenes or Salmonella shigella infection Intravaginal foreign body (e. g., toilet paper) Clear, gray, or whitish vaginal discharge in early puberty Nonspecific, or may indicate bacterial vaginosis, trichomoniasis Physiologic leukorrhea common in Tanner stages 2 and 3 Anal fissure Penetration (penis or foreign object) Functional constipation Weight loss or failure to thrive Neglect Metabolic, neuromuscular, or cardiac abnormalities, including malabsorption syndromes Depression Eating disorders108 CHAPTER 15 | Child Maltreatment

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iii. R ib fractures, especially posterior, in the absence of documented accidental trauma. iv. B ucket-handle or corner fractures (from shaking or squeezing). d. H ead trauma may be caused by shaking (coup contrecoup injuries), striking, or throwing an infant and is implicated in most cases of fatal phys-ical abuse. Presentations may be acute or subtle, with children often misdiagnosed in emergency settings as suffering from a viral illness because of lethargy, vomiting, and poor feeding (Herman, Makoroff, & Corneli, 2011; Leventhal, Asnes, Pavlovic, & Moles, 2014). The following findings can be associated with abusive head trauma:i. A ltered mental status. ii. R etinal hemorrhages (requires dilated exam-ination by a pediatric ophthalmologist, and finding can be nonspecific). iii. S kull fractures and possibly additional long bone or rib fractures. iv. I ntracranial hemorrhages (also may be pres-ent in coagulopathies and other medical conditions). e. Thor acoabdominal trauma: squeezing or punch-ing may result in rib fractures, trauma to under-lying structures, or abdominal trauma. Children may not have surface bruising, and the exami-nation can be confounded by other injuries or concurrent head injury. Imaging studies, including computed tomography, may be indi-cated (Hornor, 2012). Examination findings may include:i. D ecreased or absent bowel sounds. ii. G uarding or abdominal muscle rigidity. 3. P hysical examination findings consistent with sexual abuse a. I n examinations of sexually abused children, physical findings are rare ( Jenny & Crawford-Jakubiak, 2013); over 90% of examinations of children who are evaluated for sexual abuse show no evidence of trauma or infection (Heger, Ticson, Velasquez, & Bernier, 2002; Jenny & Crawford-Jakubiak, 2013). Sexual abuse of pre-pubertal children most often consists of oral or digital contact. The elastic nature of genital and rectal tissues, added to delays in disclosure or examinations, contribute to the lack of find-ings (Adams, 2011). Some trauma to the genital area can occur accidentally, as with the asym-metric vulvar trauma consistent with straddle injuries. The APN who regularly examines the genital area of prepubertal girls during well-child examinations is more confident in distinguishing normal from abnormal findings (Monasterio & Schapiro, 2014). However, apparently abnor-mal findings are often subtle, are difficult to determine without special magnification equip-ment (e. g., a colposcope), and can be caused by normal physiologic variations. Therefore, they should be confirmed by an expert in sexual abuse examinations. b. The fo llowing are findings that are consistent with sexual abuse:i. V aginal trauma: trauma may occur any-where in the vulvar area, the periurethral or perihymenal tissue, or in the perineum, from either forceful digital penetration, use of objects, or penile penetration. The following are consistent with sexual abuse (Adams, 2011):a. Ac ute trauma or notches or transactions of inferior hymenal tissue (caution: normally occurring redundant hymenal folds may appear to be notched). b. Thin or absent hymenal tissue. ii. A norectal trauma: penetration may cause fissures, and repeated penetration may lead to laxity of the sphincter. The most common cause of anal fissures is large hard stools, so fissures in themselves are nonspecific. Laxity of the anal sphincter should raise sus-picions of abuse, but may also be related to neurologic conditions. iii. P enile trauma: penile trauma is an uncom-mon finding in sexual abuse but may be associated with severe physical abuse. iv. S exually transmitted infections: most cases of vulvovaginitis in prepubertal children, including mucopurulent vaginal discharge, are caused by nonsexually transmitted infections, such as Streptococcus pyogenes and Salmonella shigella. Most cases of bala-nitis (inflammation of the foreskin) are also unrelated to sexual abuse. Gonorrhea and chlamydia are rare in sexually abused prepubertal children (0. 7-3. 7%) and are more common in sexually abused teenagers whose rates of infection (14%) are higher than teenagers who report only consensual activity with peers (Bechtel, 2010). Vertical transmission of gonorrhea, chlamydia, human papillomavirus, and herpes simplex virus is possible (Adams, 2011). Ulcers or verrucous papules in the genital area should be tested for herpes simplex virus and human papillomavirus typing. 109 Database

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this form of maltreatment should be in the differential when children have repeated visits or hospitalizations for serious symptoms with negative diagnostic tests. III. a ssessment Child maltreatment does not fit easily into a medical model or diagnostic algorithm in which one can “rule out” or “rule in” abuse or neglect. Many physical signs and behaviors associated with abuse are also associated with infections, serious chronic conditions, or variations of normal. Children and their care-takers, for a variety of reasons, may withhold elements of the history that could, alone or considered together with physical findings, aid in the determination or elimination of child mal-treatment as a likely explanation for a given clinical picture. However, the APN's legal responsibility usually hinges on a reasonable suspicion or concern, rather than a firm or even likely diagnosis (Child Welfare Information Gateway, 2014) (see T able 15-2). The following elements should be carefully assessed when the APN suspects child maltreatment: A. Safety 1. I s further testing or examination warranted by experts in child physical or sexual abuse? a. Ac ute disclosure of sexual abuse or assault, espe-cially involving penetration or exchange of body 4. P hysical examination findings consistent with neglect a. P hysical signs of neglect may include evidence of generally poor hygiene, inadequate clothing, and failure to grow and gain weight as expected during childhood. Most cases of failure to thrive have a variety of causes, including congenital heart disease, malabsorption syndromes, neu-romuscular disorders, and a variety of interac-tional failures between parent or caregiver and child (Cole & Lanham, 2011; Harper, 2014). These interactional failures may be related to neglect or to a parent's appropriate anxieties about a medically fragile child who does not respond easily to the parent's customary care-taking strategies. b. A r are and puzzling form of child maltreatment, pediatric symptom falsification or medical child abuse, involves elements of physical abuse, psy-chologic abuse, and child endangerment (a type of neglect) (Flaherty & Macmillan, 2013; Mash, Frazier, Nowacki, Worley, & Goldfarb, 2011). Formerly known as Munchhausen syndrome by proxy, parents in this form of maltreatment induce or falsify symptoms of illness in their children, presenting them as victims of rare and serious medical conditions. The parent is typi-cally a well-educated mother, often with training in a healthcare profession. Although uncommon, Table 15-2 Child Maltreatment: Associated Factors That May T rigger an Independent Report adverse Conditions Specific r eportable Behaviors Variations from State to State Domestic violence Domestic violence committed in front of a child Physical injury to a child reportable under child abuse laws Reportable in some states, but not others Adds to charges or sentencing of offender in some states Offender may have to pay for child's counseling Substance abuse Exposure of a child to substance abuse Manufacturing or using methamphetamine in front of a child Substance abuse affecting parenting ability Prenatal use of substances affecting a fetus Newborn testing positive for drugs of abuse Specifically reportable in some states, but not others Providing substances to a child or failure to prevent access reportable in all states Some states have mandated follow-up for prenatally exposed newborns with evaluation by CPS before discharge Poverty Homelessness Failure to provide adequate food, clothing, shelter, health care Homelessness reportable in some states, specifically excluded in others Inability to provide stable, adequate housing may be related to reporting in some states Some states have exemptions for personal or religious beliefs Truancy Failure to send child to school or provide home schooling, ensure child goes to school Check individual state laws: in some states a violation of truancy laws; not under child protection laws Data from U. S. Department of Health and Human Services, Child Welfare Information Gateway. (n. d. ). State statutes search. Retrieved from https:// www. childwelfare. gov/topics/systemwide/laws-policies/state/110 CHAPTER 15 | Child Maltreatment

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fluids (within 72 hours, or in some states up to 108 hours): the child or adolescent should be transported to a specialized center for forensic examination, usually a designated emergency room or child advocacy center within or near the county where the abuse took place. b. E quivocal examination, for example an apparently abnormal genital examination, which warrants a specialized examination with magnification. c. E valuation to determine if serious physical injuries are accidental or inflicted. 2. I s it safe for the child or adolescent to go home? Although CPS ultimately makes this decision, the APN's concerns will affect the urgency of reporting and referral. a. D o the suspected injuries or overall physical con-dition warrant hospitalization? b. I s there a disclosure or suspicion of sexual abuse in the home or physical abuse with imminent danger to the child? c. C an the caretaker with the child keep or trans-port the child safely?i. W illingness or ability to protect the child. ii. S afe transport (e. g., intoxicated caregiver who drove to the clinic with the child). d. W ill the disclosure or reporting of maltreat-ment put the child or caretaker at risk in the home?i. F amily reactions to disclosure. ii. F or adolescents, potential harsh punish-ment for disclosing behaviors associated with extrafamilial abuse (e. g., going to a for-bidden party). 3. A re there potential safety issues for the APN in reporting? a. S uspected offending parent or caretaker in the clinic. b. R eactions of nonoffending parent of child or adolescent. B. Need to report 1. D oes the situation warrant mandatory reporting in the state in which the APN is practicing?a. C onsultation with other clinic providers. b. C onsultation with local child abuse reporting hotline. 2. H ow urgent is the report (related to safety issues described previously)?a. I mmediate. i. I mmediate safety issues. ii. L egal issues: evidence collection or docu-mentation. b. E nd of the day (disclosures of past abuse, child and caretaker currently safe, sexual abuse outside of home beyond 72-hour period). C. Are the child's and family's immediate needs being met? 1. W hen suspected maltreatment is part of the family's chief complaint a. D etermine their expectations for outcome regarding housing safety (e. g., shelter versus arrest of suspected offender, which is not always immediate). b. F urther testing desired by child and family that may or may not be indicated. 2. I f suspected maltreatment is not the chief complaint of the child or caregiver a. I t is important for APN not to lose sight of child and family priorities, which may be equally or more urgent than the investigation of maltreatment. b. I f a report is necessary, a collaborative approach with the family and a respect for their priorities can help preserve provider-family relationships IV. Plan A. Diagnostic testing 1. I maging: order in consultation with radiologist or child abuse specialist to determine occult, old, healing fractures. If inflicted fractures are suspected in children younger than 2 years, a full skeletal series should be ordered (Flaherty, Perez-Rossello, Levine, & Hennrikus, 2014; Hornor, 2012). Rib fractures, especially posterior, in children younger than 2, should prompt a head CT scan and ophthalmology consult to look for abusive head trauma (Hornor, 2012). 2. L aboratory testing a. I f there is fresh disclosure of sexual assault or abuse within time period for forensic evidence, examination and laboratory testing should be ordered by a specialized sexual abuse forensic testing center. b. B acterial or viral cultures as indicated for skin lesions or discharge in anogenital area and the oropharynx. Current guidelines recommend a NAAT (nucleic acid amplification test) from appropriate sites for gonorrhea, chlamydia, and Trichomonas vaginalis infections (Workowski & Bolan, 2015). c. S erologic testing as indicated (HIV, rapid plasma reagin, hepatitis panels). 111 Plan

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Child Welfare and Information Gateway at https://www . childwelfare. gov/ is an excellent site for parent and provider education, with some materials available in Spanish. re Fere NCe S Adams, J. A. (2011). Medical evaluation of suspected child sexual abuse: 2011 update. Journal of Child Sexual Abuse, 20, 588-605. doi: 10. 1080/10538712. 2011. 606107 Assistant Secretary for Planning and Evaluation. (n. d. ). Statutory rape: A guide to state laws and reporting requirements. Retrieved from http://aspe. hhs. gov/hsp/08/sr/statelaws/summary. shtml#_ftn9. Bechtel, K. (2010). Sexual abuse and sexually transmitted infections in children and adolescents. Current Opinions in Pediatrics, 22, 94-99. Child Abuse Prevention and T reatment Act (CAPTA). 42 U. S. C. A. § 5106g(2) (West Supp. 1998) Child Welfare Information Gateway. (2014). Definitions of child abuse and neglect: State statutes series. Washington, DC: U. S. Department of Health and Human Services. Retrieved from https://www. childwelfare . gov/topics/systemwide/laws-policies/state/. Child Welfare Information Gateway. (2013a). What is child abuse and neglect? Recognizing the signs and symptoms. Washington, DC: U. S. Department of Health and Human Services, Children's Bureau. Retrieved from https://www. childwelfare. gov/pubs/factsheets/whatiscan/. Child Welfare Information Gateway. (2013b). Child witnesses to domestic violence: Summary of state laws. Retrieved from https://www. childwelfare . gov/topics/systemwide/laws-policies/statutes/witnessdv/. Christian, C. W., & Committee on Child Abuse and Neglect. (2015). The evaluation of suspected child physical abuse. Pediatrics, 135, e1337-1354. doi: 10. 1542/peds. 2015-0356 Cole, S. Z., & Lanham, J. S. (2011). Failure to thrive: An update. American Family Physician, 83, 829-834. Dubowitz, H., & Leventhal, J. M. (2014). The pediatrician and child mal-treatment: Principles and pointers for practice. Pediatric Clinics of North America, 61, 865-871. doi: 10. 1016/j. pcl. 2014. 06. 001 Eckenrode, J., Smith, E. G., Mc Carthy, M. E., & Dineen, M. (2014). Income inequality and child maltreatment in the United States. Pediatrics, 133, 454-461. doi: 10. 1542/peds. 2013-1707 Fairbank, J. A., & Fairbank, D. W. (2009). Epidemiology of child traumatic stress. Current Psychiatry Reports, 11, 289-295. Finkelhor, D., Vanderminden, J., Turner, H., Hamby, S., & Shattuck, A. (2014). Child maltreatment rates assessed in a national household survey of caregivers and youth. Child Abuse & Neglect, 38, 1421-1435. doi: 10. 1016/j. chiabu. 2014. 05. 005 Flaherty, E. G., & Macmillan, H. L. (2013). Caregiver-fabricated illness in a child: A manifestation of child maltreatment. Pediatrics, 132, 590-597. doi: 10. 1542/peds. 2013-2045 Flaherty, E. G., Perez-Rossello, J. M., Levine, M. A., & Hennrikus, W. L. (2014). Evaluating children with fractures for child physical abuse. Pediatrics, 133, e477-e489. doi: 10. 1542/peds. 2013-379 Gilbert, R., Kemp, A., Thoburn, J., Sidebotham, P., Radford, L., Glaser, D., et al. (2009). Recognizing and responding to child maltreatment. Lancet, 373, 167-180. Gilbert, R., Widom, C. S., Browne, K., Fergusson, D., Webb, E., & Janson, S. (2009). Burden and consequences of child maltreatment in high-income countries. Lancet, 373, 68-81. Greenbaum, V. J. (2014). Commercial sexual exploitation and sex traffick-ing of children in the United States. Current Problems in Pediatric and Adolescent Health Care, 44, 245-269. doi: 10. 1016/j. cppeds. 2014. 07. 001B. Management 1. T reat injuries or infections as indicated. a. P rophylactic treatment of adolescents to prevent sexually transmitted infections in cases of sexual assault, including HIV prophylaxis if indicated (Workowski & Bolan, 2015). b. C urrent guidelines recommend prophylaxis for HIV only in prepubertal children, given low rates of infection and complications and importance of confirmed diagnosis; however, some parents and children may insist on treatment, which may be considered after all diagnostic testing has been done. 2. A s indicated previously, refer any child or adolescent with sexual abuse or assault of less than 72 hours (or longer in some localities) to police and specialized child sexual abuse forensic team. 3. M ake a child abuse report if maltreatment is suspected, following state and local procedures for verbal (telephone) and written reporting; usually both are required. a. C onsider informing the parent about a report if it is safe for the provider, in order to maintain trans-parency and trust in the therapeutic relationship. b. I nvolve the adolescent in making a report. i. I n most states, reporting is required by law, regardless of the adolescent's wishes; in some states, the provider has discretion and the adolescent can decline to report sexual abuse or assault if the suspected offender is not a parent or caretaker (Child Welfare Information Gateway, 2014). ii. Di scuss APN legal responsibilities and ado-lescent decision making about disclosing versus withholding information. 4. A rrange follow-up care a. C ounseling, if not arranged by law enforcement or CPS. b. F or suspected neglect, follow-up supports for family. i. P ractical and material (food banks, shelter assistance, transportation vouchers). ii. H ealth supervision and support: public health nursing and health education. c. C lose clinic follow-up as indicated. V. r esources A. Patient education Many states have excellent websites with parent and child educational material in multiple languages. The 112 CHAPTER 15 | Child Maltreatment

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Grossman, S. E., Johnston, A., Vanezis, P., & Perrett, D. (2011). Can we assess the age of bruises? An attempt to develop an objective technique. Medicine Science & Law, 51, 170-176. Guttmacher Institute. (2015). An overview of minors' consent law (State Policies in Brief). Retrieved from http://www. guttmacher. org/statecenter/spibs /spib_OMCL. pdf. Harper, N. S. (2014). Neglect: Failure to thrive and obesity. Pediatric Clinics of North America, 61, 937-957. doi: 10. 1016/j. pcl. 2014. 06. 006 Heger, A., Ticson, L., Velasquez, O., & Bernier, R. (2002). Children referred for possible sexual abuse: Medical findings in 2384 children. Child Abuse & Neglect, 26, 645-659. Herman, B. E., Makoroff, K. L., & Corneli, H. M. (2011). Abusive head trauma. Pediatric Emergency Care, 27, 65-69. doi: 10. 1097 /PEC. 0b013e31820349db Herrenkohl, T. I., Hong, S., Klika, J. B., Herrenkohl, R. C., & Russo, M. J. (2013). Developmental impacts of child abuse and neglect related to adult mental health, substance use, and physical health. Journal of Family Violence, 28. doi: 10. 1007/s10896-012-9474-9 Hornor, G. (2012). Medical evaluation for child physical abuse: What the PNP needs to know. Journal of Pediatric Health Care, 26, 163-170. doi: 10. 1016/j. pedhc. 2011. 10. 00 IOM (Institute of Medicine) & NRC (National Research Council) (2014). New directions in child abuse and neglect research. Retrieved from http://www. nap. edu/catalog/18331/new-directions-in-child-abuse -and-neglect-research. Jackson, A. M., Deye, K. P., Halley, T., Hinds, T., Rosenthal, E., Shalaby-Rana, E., & Goldman, E. F. (2015). Curiosity and critical thinking: Identifying child abuse before it is too late. Clinical Pediatrics (Phila), 54, 54-61. doi: 10. 1177/0009922814549314 Jenny, C., & Crawford-Jakubiak, J. E. (2013). The evaluation of children in the primary care setting when sexual abuse is suspected. Pediatrics, 132, e558-e567. doi: 10. 1542/peds. 2013-1741 Jones, R., Flaherty, E. G., Binns, H. J., Price, L. L., Slora, E., Abney, D., et al. (2008). Clinicians' description of factors influencing their reporting of suspected child abuse: Report of the child abuse reporting experience study research group. Pediatrics, 122, 259-266. Keeshin, B. R., & Dubowitz, H. (2013). Childhood neglect: The role of the paediatrician. Paediatric Child Health, 18, e39-e43. Kellogg, N. D. (2010). Sexual behaviors in children: Evaluation and management. American Family Physician, 82, 1233-1238. Klevens, J., Barnett, S. B., Florence, C., & Moore, D. (2015). Exploring policies for the reduction of child physical abuse and neglect. Child Abuse & Neglect, 40, 1-11. doi: 10. 1016/j. chiabu. 2014. 07. 013 Leventhal, J. M., Asnes, A. G., Pavlovic, L., & Moles, R. L. (2014). Diagnosing abusive head trauma: The challenges faced by clinicians. Pediatric Radiology, 44(Suppl. 4), 537-542. doi: 10. 1007/s00247-014-3074-1 Mash, C., Frazier, T., Nowacki, A., Worley, S., & Goldfarb, J. (2011). Development of a risk-stratification tool for medical child abuse in failure to thrive. Pediatrics, 128, e1467-e1473. doi: 10. 1542 /peds. 2011-1080 Mersky, J. P., T opitzes, J., & Reynolds, A. J. (2013). Impacts of adverse childhood experiences on health, mental health, and substance use in early adulthood: A cohort study of an urban, minority sample in the U. S. Child Abuse & Neglect. doi: 10. 1016/j. chiabu. 2013. 07. 011 Monasterio, E. B., & Schapiro, N. A. (2014). Female genitalia. In K. G. Duderstadt (Ed. ), Pediatric physical examination: An illustrated handbook (2d ed., pp. 242-258). St. Louis, MO: Mosby Elsevier. Naughton, A. M., Maguire, S. A., Mann, M. K., Lumb, R. C., T empest, V., Gracias, S., et al. (2013). Emotional, behavioral, and developmental features indicative of neglect or emotional abuse in preschool children: A systematic review. JAMA Pediatrics, 167, 769-775. doi: 10. 1001 /jamapediatrics. 2013. 192 Saul, J., Valle, L. A., Mercy, J. A., Turner, S., Kaufmann, R., & Popovic, T. (2014). CDC grand rounds: Creating a healthier future through pre-vention of child maltreatment. Morbidity and Mortality Weekly Report (MMRR), 63(12), 260-263. Schapiro, N. A. (2008). Medical neglect of children: Reporting issues for nurse practitioners. Journal for Nurse Practitioners, 4, 531-534. Shonkoff, J. P., & Garner, A. S. (2012). The lifelong effects of early childhood adversity and toxic stress. Pediatrics, 129, e232-e246. doi: peds. 2011 -2663 10. 1542/peds. 2011-2663 Slep, A. M., Heyman, R. E., & Foran, H. M. (2015). Child maltreatment in DSM-5 and ICD-11. Family Process, 54, 64-81. doi: 10. 1111/famp. 12131 T esta, M. F., & Smith, B. (2009). Prevention and drug treatment. Future of the Child, 19, 147-168. T oon, M. H., Maybauer, D. M., Arceneaux, L. L., Fraser, J. F., Meyer, W., Runge, A., et al. (2011). Children with burn injuries—assessment of trauma, neglect, violence and abuse. Journal of Injury & Violence Research, 3, 98-110. doi: 10. 5249/jivr. v3i2. 91 U. S. Department of Health and Human Services. (2015). Child maltreat-ment 2013. Washington DC: Administration for Children and Families, Administration on Children, Y outh and Families, Children's Bureau, U. S. Department of Health and Human Services. Retrieved from http://www. acf. hhs. gov/programs/cb/research-data-technology /statistics-research/child-maltreatment. U. S. Department of Health and Human Services, Child Welfare Information Gateway. (n. d. ). State statutes search. Retrieved from https://www. childwelfare. gov/topics/systemwide/laws-policies/state/. Wildeman, C., Emanuel, N., Leventhal, J. M., Putnam-Hornstein, E., Waldfogel, J., & Lee, H. (2014). The prevalence of confirmed maltreat-ment among US children, 2004 to 2011. JAMA Pediatrics, 168, 706-713. doi: 10. 1001/jamapediatrics. 2014. 410 Workowski, K. A., & Bolan, G. A. (2015). Sexually transmitted diseases treatment guidelines, 2015. MMWR Recommendation Report, 64(RR-03), 1-137. 113 References

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B. Obesity in early childhood Overweight and obesity in children between 2 and 5 years old are particularly concerning, and much attention is being paid to prevention in this age group. During this time, BMI generally reaches its minimum point before beginning to increase again (known as the “adiposity rebound”) in early school age. This is a critical point for prevention of obesity, as there is evidence that an early adiposity rebound can be predictive of obesity later in life (Brisbois et al., 2012; Hughes, Sherriff, Ness, & Reilly, 2014). Increased intake of sugar-sweetened beverages (SSBs), nonnutritious snack foods, large portion sizes, lack of physical activity, and decreased sleep duration are all contributors to early childhood overweight (IOM, 2011). C. Obesity in school-age children Between 6 and 12 years of age, self-regulation becomes increasingly important, especially with regard to nutritional intake, as children with compromised abilities to self-regulate tend to have a higher BMI (Francis & Susman, 2009). In addition to the risk factors in early childhood described previously, children in this group are also begin-ning to consume more food outside of the home, which can include high rates of fast food or other “junk” foods. As children spend more time in school and after school programs, time spent in sedentary behaviors also increases (T anaka, Reilly, & Huang, 2014), and opportunities for physical activity may be more difficult to find. Body aware-ness and teasing or bullying by peers may also surface dur-ing this period, which can negatively affect self-esteem and emotional health (Maggio et al., 2014; van Geel, Vedder, & T anilon, 2014). D. Obesity in adolescence Some consider adolescence to be one of the most chal-lenging periods with regard to overweight and obesity. Puberty brings physical and metabolic changes in the body that may exacerbate risk for negative sequelae such as insulin resistance ( Jasik & Lustig, 2008; Pilia et al., 2009). Developmentally, teens are increasingly more independent from their parents, which often includes I. Intr oduction and general background Over 30% of children and adolescents between 2 and 19 years old in the United States are overweight or obese (body mass index [BMI] ≥ 85%), as defined by the Centers for Disease Control and Prevention (CDC) sex-specific BMI-for-age growth charts (Ogden, Carroll, Kit, & Flegal, 2014). Although the prevalence of childhood overweight has remained relatively stable in the United States over the last decade (Ogden, Carroll, Kit, & Flegal, 2012), there is still much work to be done to address this epidemic. Overweight and obesity in childhood have been linked to numerous serious health conse-quences, including increased risk for obesity in adulthood, as well as metabolic and cardiovascular disease (Daniels, 2009; de Onis et al., 2013; Friedemann et al., 2012; Harrington, Staiano, Broyles, Gupta, & Katzmarzyk, 2013). Numerous changes in growth and development occur between infancy and adolescence. As such, it is important to consider the etiology and impact of overweight and obe-sity within a developmental context (National Association of Pediatric Nurse Associates & Practitioners, 2006). A. Obesity in infancy According to current statistics, approximately 8% of U. S. infants younger than 2 years of age have a high weight for recumbent length (≥ 95% on the CDC growth chart) (Ogden et al., 2014). Although the diagnosis of overweight or obesity is not generally used in this age group, there is increasing research to show that infants with high weight for length or rapid weight gain (Brisbois, Farmer, & Mc Cargar, 2012; Koontz, Gunzler, Presley, & Catalano, 2014) may be at greater risk for remaining overweight in the future. Contributing factors to overweight in infancy include maternal overweight (via fetal metabolic programming) and overfeeding (Brisbois et al., 2012; Institute of Medicine [IOM], 2011). Preventive factors against overweight in infancy may include breastfeeding and delay of the intro-duction of solid foods to 4-6 months of age (Hunsberger et al., 2013; Moss & Y eaton, 2014; Oddy, 2012). Victoria F. Keeton Ch Ildhood o Verwe Ight and  o bes I ty© Eliks/Shutterstock; © donatas1205/Shutterstock 114 16Chapt Er

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coping for some patients. Conversely, the presence of overweight in a child may also contribute to the emergence or worsening of mental health condi-tions, especially if negative self-esteem or bullying is present (Geoffroy, Li, & Power, 2014; Rottenberg et al., 2014). General mental health assessment of the parents or guardian should be considered as well, as caregivers with impaired mental health may have a compromised ability to promote healthy behaviors in their children (National Association of Pediatric Nurse Associates & Practitioners, 2006). II. d atabase Figure 16-1 shows an algorithm for obesity risk assessment and recommended steps for prevention and treatment in all children (Barlow & Expert Committee, 2007). The following provides a comprehensive overview of pertinent assessment of the overweight child. A. Subjective 1. P ast medical/developmental history a. I nvestigate history of any physical illnesses that may contribute to weight gain and/or limitations in physical activity, as well as any related comorbid conditions and their management plans. b. R eview current medications and note whether significant changes in weight occurred with their initiation or discontinuation. c. I f the child is 5 years old or younger or has a significant developmental delay, review the developmental history and note any impact of current or previous delays on nutrition or mobility status. 2. F amily history a. T ake an accurate history of obesity, cardiovas-cular disease (including hypertension and/or hyperlipidemia), and diabetes in the imme-diate family, especially siblings, parents, and grandparents. b. Obt ain a comprehensive family mental health history, including disordered eating and addiction. 3. Die t Request a detailed history of intake that includes type of food as well as serving size and overall quantity consumed per day or week. Consider hav-ing examples of cup sizes to help families accurately describe quantity of intake. a. B everages b. B reakfast consumption c. N onnutritious snack foods (sweets, chips, etc. )unsupervised decision making related to food and bev-erage choices. Excessive sedentary behavior and screen time are also a significant problem, when activities such as TV, social media, texting, and gaming become more common pastimes and sources of peer interaction (Li et al., 2013). Studies have shown that physical activity levels decrease significantly in early adolescence, espe-cially among girls (Dumith, Gigante, Domingues, & Kohl, 2011). Body image may be more of a concern in this age group, and negative mental health consequences associated with being overweight are more prevalent (Maggio et al., 2014; Marmorstein, Iacono, & Legrand, 2014; National Association of Pediatric Nurse Associates & Practitioners, 2006). E. Obesity in special populations 1. C hildren and adolescents with special healthcare needs (SHCN) Over the last decade there has been more awareness of the high prevalence of overweight in children with SHCN or developmental disabilities. Several factors may contribute to this issue (Bandini, Curtin, Hamad, Tybor, & Must, 2005; Murphy, Carbone, & American Academy of Pediatrics Council on Children with Disabilities, 2008; Reinehr, Dobe, Winkel, Schaefer, & Hoffmann, 2010; Rimmer & Rowland, 2008). Dietary restrictions or sensitive eating habits in some children with these conditions can provide challenges to caregivers' ability to consistently provide balanced and nutritious meals. Medications used to manage symptoms such as seizures or behavior concerns may cause weight gain. Children with physical impair-ments or significant cognitive deficits may have lim-ited ability to participate in sufficient physical activity. The need for intense cognitive therapies, which are more often sedentary in nature, may also take prece-dence over physical activity. 2. C hildren and adolescents with mental health concerns Proper prevention and management of childhood overweight must include the integration of physical and behavioral health considerations. Children with mental health conditions such as depression may have unique risk factors for overweight as well as par-ticular challenges in its prevention and management (Korczak, Lipman, Morrison, & Szatmari, 2013). Some psychotropic medications may exacerbate weight gain in an already overweight child (Cockerill, Biggs, Oesterle, & Croarkin, 2014; Mansoor et al., 2013). Especially when a mental health condition is exacerbated, a child's or teen's motivation and inter-est in physical activity may be negatively affected. The provider must also be aware of the potential for food and eating to be a significant source of 115 Database

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Stage 1 Prevention Plus Primary care office Target behavior Identify problem behaviors If no problem behavior s, praise current practice Patient/family counseling Review any ri sks (eg DM) Use patient-directedtechniques to encourage behavior change (seealgor ithm ta ble)1 Identification Calculate and plot BMI at every well child visit BMI 5th-84th percentile BMI 85th-94th percentile BMI ≥ 95th percentile Medical Risk Child history & ex am Child gr owth Parental obesity Family history Laborator y, as needed Child history & ex am Child gr owth Parental obesity Family history Laboratory2 Assessment Behav ior Risk Attitudes Stage 2 Structured Weight Management Primary care office with support Pediatric weight management cente r Stage 3 Comprehensive Multidisciplinary Intervention Tertiary care center Stage 4 Tertiary Care Intervention (select patients)(No evidence of health risk) (Evidence of health risk)Family and patient concern andmotivation Intervention for Treatment (Advance through stages based on age and BMI)Family and patientconcern andmotivation Family and patient concern andmotivation3 Prevention Child history & ex am Child gr owth Parental obesi ty Family history Sedentary time Eating Physical activity Sedentary time Eating Physical activity Sedentary time Eating Physical activity FIgure 16-1 assessment of obesity risk and steps to Prevention and tr eatment Reproduced from Barlow, S. E., & Expert Committee. (2007). Expert committee recommendations regarding the prevention, assessment, and treatment of child and adolescent overweight and obesity: Summary report. Pediatrics, 120(Suppl. 4), S164-S192. doi:120/Supplement _4/S164116 CHAPTER 16 | Childhood Overweight and Obesity

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d. I ntake of fast food or other food prepared outside the home e. F ruit and vegetable consumption f. S tarches low in fiber (made from white flour or rice, corn, etc. ) 4. P hysical activity and sedentary behavior a. M inutes per day spent engaged in moderate to vigorous physical activity (breathing hard, sweating, etc. ), and type of physical activity b. M inutes per day spent in screen-based activities (TV, computer, tablets, gaming, etc. ) c. P resence of a TV in the child's bedroom and frequency of eating in front of the TV d. Qua ntity and quality of sleep 5. E motional and social history a. H istory of mental/behavioral health conditions and management b. S creen for presence of active symptoms, for example, using a tool like the Pediatric Symptom Checklist (available at www. brightfutures. org) c. Di scuss family eating and activity patterns 6. Body im age and self-identified concerns about weight 7. P revious strategies for losing/maintaining weight 8. L evel of readiness, confidence, and motivation for lifestyle changes 9. Obe sity-focused review of systems a. Ge neral/constitutional: fatigue, unexplained weight gain/loss b. S kin: presence of dark patches around neck, abdomen, or under arm area that can't be “scrubbed off ” c. H ead, eyes, ears, nose, and throat (HEENT): snoring and/or gasping for air during sleep d. R espiratory: shortness of breath, cough, or wheeze with exercise e. C ardiac: history of elevated blood pressure f. G astrointestinal (GI): unexplained nausea or vomiting g. E ndocrine: irregular/absent menses, polydipsia, polyuria, polyphagia h. M usculoskeletal: joint pain, especially in the hips i. P sych/behavioral: moods, self-harm, suicidal ideation, stress, coping B. Objective 1. V ital signs Measure blood pressure at every visit for children over 3 years of age. Be sure that the appropriate cuff size is used, and if using an electronic sphygmoma-nometer, confirm elevated results with a manual cuff. Calculate blood pressure percentile for sex, age, and height percentile using a National Heart, Lung, and Blood Institute chart (National High Blood Pressure Education Program Working Group on High Blood Pressure in Children and Adolescents, 2004). 2. A nthropometric measurements Accurate weight and height should be measured at each visit. Calculate BMI, BMI percentile, and BMI z-score whenever possible. 3. P hysical exam a. Ge neral: observe overall appearance of health b. S kin: inspect posterior neck, axilla, and lower abdomen for evidence of acanthosis nigricans c. H EENT: inspect tonsils for hypertrophy d. N eck: palpate thyroid in older children and adolescents e. C hest: Auscultate breath and heart sounds f. GI: palpate for masses and hepatosplenomegaly g. Ge nitourinary: in males inspect for “buried penis” h. M usculoskeletal: observe range of motion in all extremities; if pain in the hips, perform appro-priate maneuvers to evaluate for acute slipped capital femoral epiphysis i. P sych/behavioral: note affect and mood 4. L aboratory testing The primary goal of laboratory analysis in the obese child is to evaluate for comorbid conditions, based on the presence of risk factors and/or any current symp-toms (Barlow & Expert Committee, 2007; Daniels, 2009). Elevated BMI can be a strong predictor of metabolic and cardiovascular disease risk (Daniels, 2009; de Onis et al., 2013; Friedemann et al., 2012; Harrington et al., 2013), and thus screening for these conditions should be considered. When deciding whether to perform laboratory analysis, it is important to consider whether the results will in any way alter the treatment plan. If the answer is no, then the provider should consider whether there is true justification for the use of resources and subjecting the patient to the trauma of venipuncture. It is possible that abnormal lab results can be useful in patient/family education, regardless of whether they will affect the overall management plan. An example is a lab report that demonstrates mildly elevated lipids, which would most often be treated with lifestyle modification, but could still be a powerful visual indicator for the family that the child's condition has had a negative physical impact. Consider risk-based screening for the following in children over 8-10 years of age and/or a child of any age with increased risk:a. Di abetes: Hgb A1c, fasting glucose (or if strong concerns about presence of hyperglycemia in clinic, perform a random fingerstick glucose)117 Database

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IV. Plan The foundation for the prevention or management of childhood overweight is lifestyle modification related to nutritional intake and physical activity, often by the entire family (Spear et al., 2007). The principal role of the primary care physician (PCP) is to provide the patient and family with sufficient education, counseling, and support to make and maintain these modifi-cations (National Association of Pediatric Nurse Associates & Practitioners, 2006; Rao, 2008). T able 16-1 illustrates a staged approach to treatment according to the child's age and BMI percentile (Barlow & Expert Committee, 2007). The following presents a complete plan for managing the child or adolescent with overweight in primary care. It is important to note that it may not be possible to cover everything in one visit, but rather the plan should include frequent follow-up to provide continuing educa-tion, review goal setting, and monitor progress. It is also pos-sible that the following would not be carried out by the PCP alone but in collaboration with other professionals. Ideally, holistic and comprehensive care for the overweight patient will involve an interdisciplinary team of clinicians that may include a registered dietician, behavioral health provider, and/or pediatric specialists as indicated. A. If secondary obesity, treat or refer for treatment of underlying cause. B. Provide family-centered education. 1. M ultifactorial etiology of obesity and associated health risks 2. I mportance of healthy nutrition and physical activity routines for all members of the family 3. N eed for support from all members involved in child/ adolescent's daily life 4. I mpact of weight and height changes on BMI for children who are still growing 5. R ealistic expectations for weight or BMI changes over time C. Encourage lifestyle modification where appropriate. 1. N utrition counseling a. U se “My Plate” (Figure 16-2) to encourage a balanced distribution of nutrients and healthy portion sizes b. E ncourage reduction/elimination of all SSBs c. R eview healthy eating behaviors, such as eating meals at the table as a family and not eating in front of the TV d. P rovide culturally tailored resources for grocery shopping and recipes for mealsb. N onalcoholic fatty liver disease (NAFLD): Aspartate aminotransferase (AST), alanine ami-notransferase (ALT) c. H yperlipidemia: Fasting lipid panel d. H ypertension: Complete metabolic panel or renal panel e. H ypovitaminosis D: 25-hydroxyvitamin D 5. Othe r diagnostics Other diagnostic evaluation may be useful in the diag-nosis of comorbid conditions, such as an ultrasound of the liver to confirm the diagnosis of NAFLD or a sleep study to confirm the diagnosis of obstructive sleep apnea or obesity hypoventilation syndrome. These conditions are generally comanaged with pedi-atric subspecialists, and thus it may be helpful to con-sult with such specialists prior to ordering additional studies to confirm what is needed. III. a ssessment A. Classification using BMI percentile BMI has been shown to be a reliable indicator of relative adiposity in children (Barlow & Expert Committee, 2007; Boeke et al., 2013) and as a noninvasive measure is com-monly used in screening for overweight. In the United States, childhood overweight and obesity are classified in youth 2 to 20 years of age according to percentile of BMI as reflected on either the CDC or World Health Organization (WHO) age-and sex-specific growth charts. Current cutoff measures define a BMI percentile of 85-94% as overweight, whereas a BMI percentile of 95% or above is considered obese (Barlow & Expert Committee, 2007). Although BMI is not calculated in infants and young toddlers, a weight for recumbent length of 95% (CDC) or 97. 7% (WHO) or above may be used as a foundation for overweight prevention counseling with families (National Association of Pediatric Nurse Associates & Practitioners, 2006; Ogden et al., 2014). B. Rule out physiologic origin (endocrine, medication, etc. ), particularly if weight gain is sudden over a brief period and/or not well explained by lifestyle or familial patterns C. Identify comorbid illnesses or conditions, including mental health concerns D. Motivation and confidence Use motivational interviewing methods to determine the patient's and family's perception of the child's weight, as well as level of motivation and confidence in the ability to make lifestyle changes (National Association of Pediatric Nurse Associates & Practitioners, 2006; Rao, 2008). 118 CHAPTER 16 | Childhood Overweight and Obesity

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Table 16-1 Staged T reatment of Obesity According to Age and BMI b MI Percentile a ge of 2-5 y a ge of 6-11 y a ge of 12-18 y 5th-85th (normal) Prevention stage Prevention stage Prevention stage 85th-94th (Overweight)a Start at Prevention Plus stage. Advance to structured weight management stage after 3-6 mo if increasing BMI percentile and persistent medical condition or parental obesity, weight goal is weight maintenance until BMI of <85th percentile or slowing of weight gain, as indicated by downward deflection in BMI curve. Start at Prevention Plus stage. Advance to structured weight management stage after 3-6 mo if increasing BMI percentile or persistent medical condition. Weight goal is weight maintenance until BMI of <85th percentile or slowing of weight gain, as indicated by downward deflection in BMI curve. Start at Prevention Plus stage. Advance to structured weight management stage after 3-6 mo if increasing BMI percentile or persistent medical condition. Weight goal is weight maintenance until BMI of <85th percentile or slowing of weight gain, as indicated by downward deflection in BMI curve. 95th-98th Start at Prevention Plus stage. Advance to structured weight management stage after 3-6 mo if not showing improvement. Weight goal is weight maintenance until BMI of <85th percentile, however, if weight loss occur with healthy, adequate-energy diet, it should not exceed 1 lb/mo, if greater loss is noted, monitor patient for causes of excessive weight loss. b Start at Prevention Plus stage. Advance to structured weight management stage depending on response to treatment, age, degree of obesity, health risks, and motivation. Advance from structured weight management stage to comprehensive multidisciplinary intervention stage after 3-6 mo if not showing improvement. Weight goal is weight maintenance until BMI of <85th percentile or gradual weight loss of ~1 lb/mo if greater loss is noted, monitor patient for causes of excessive weight loss. b Start at Prevention Plus or structured weight loss stage depending on age, degree of obesity, health risks, and motivation. Advance to more-intensive level of intervention depending on responses to treatment, age, health risks, and motivation. Weight goal is weight loss until BMI of <85th percentile, with no more than average of 2 lb/wk. If greater loss is noted, monitor patient for causes of excessive weight loss. b ≥99th Start at Prevention Plus stage. Advance to structured weight management stage after 3-6 mo if not showing improvement. Advance from structured weight management stage to comprehensive multidisciplinary intervention stage after 3-6 mo if not showing improvement and comorbidity or family history indicates. Weight goal is gradual weight loss, not to exceed 1lb/mo. If greater loss occurs, monitor patient for causes of excessive weight loss. b Start at Prevention Plus stage. Advance to structured weight management stage depending on responses to treatment, age, degree of obesity, health risks, and motivation. Advance from structured weight management stage to comprehensive multidisciplinary intervention stage after 3-6 mo if not showing improvement. After 3-6 mo with comorbidity present and patient not showing improvement. It may be appropriate for patient to receive evaluation in tertiary care center. Weight goal is weight loss not to exceed average of 2 lb/wk. If greater loss is noted, monitor patient for causes of excessive weight loss. b Start at stage 1, 2 or 3 of treatment depending on age, degree of obesity, health risks, and motivation. Advance to more-intensive levels of intervention depending on responses to treatment age, health risks, and motivation of patient and family. Advance from comprehensive multidisciplinary intervention stage to tertiary care stage after 3-6 mo with comorbidity present and patient not showing improvement. Patients may warrant tertiary care evaluation to determine next level of treatment. Weight goal is weight loss not to exceed average of 2 lb/wk. If greater loss is noted, monitor patient for causes of excessive weight loss. b In most circumstances, the general goal for all ages is for BMI to deflect downward until it is <85th percentile. Although long-term BMI monitoring is ideal, short-term (3<month) weight changes may be easier to measure. Resolution of comorbidities is also a goal. a Children in this BMI category whose BMI has tracked in the same percentile over time and who have no medical risks may have a low risk for excess body fat Clinicians can continue obesity prevention strategies and not advance treatment stages. b Because Youth Risk Behavior Surveillance Survey responses indicated that 15% of teens practice some unhealthy eating behaviors, all teens should be evaluated from these symptoms. Providers should be especially concerned if weight loss is >2 Ib/week in this age group and should evaluate patients for excessive energy restrictions by the parent or children or unhealthy forms of weight loss (meal skipping, purging fasting, excessive exercise, and/or use of fixatives, diet pills, or weight loss supplements). Reproduced from Barlow, S. E., & Expert Committee. (2007). Expert committee recommendations regarding the prevention, assessment, and treatment of child and adolescent overweight and obesity: Summary report. Pediatrics, 120 (Suppl 4), S164-92. doi:120/Supplement_4/S164119 Plan

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d. P rovide resources for low-cost, safe local activity options e. F or children with special needs, encourage participation in suitable physical activity when-ever possible 3. S et SMART (Specific, Measurable, Achievable, Realistic, Timely) goals for nutrition and activity, to be followed up at next visit. Write them on a 2. E xercise counseling a. R eview recommendations for at least 60 minutes (cumulative) of moderate to vigorous activity and less than 2 hours of screen time daily b. E ncourage turning off the TV during meals and removing the TV from the child's bedroom c. Di scuss creative ways to find enjoyable physical activities for the family Figure 16-2 “My Plate” Guide for Making Healthy Eating Choices Reproduced from the U. S. Department of Agriculture. Retrieved from http://www. choosemyplate. gov/print -materials-ordering/graphic-resources. html 120 CHAPTER 16 | Childhood Overweight and Obesity

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prescription pad for the family to take home and post in a visible location. D. Refer to specialty care as needed for management of comorbidities (otolaryngology, pulmonology, GI, endocrine, mental health, etc. ). E. Refer to tertiary obesity care if patient fails repeated attempts to control/lose weight. Tertiary interventions may include: 1. M edication management a. M etformin There is increasing evidence to suggest that the use of metformin may support weight loss in obese children with signs of insulin resistance (Adeyemo et al., 2014; Kendall et al., 2013; Yanovski et al., 2011). b. S ibutramine and Orlistat are the most com-monly studied antiobesity medications used for adolescents and have shown modest results in supporting weight loss, with increased side effects noted with the use of Orlistat (Viner, Hsia, T omsic, & Wong, 2010). 2. B ariatric surgery Adolescents who present with morbid obesity with either multiple comorbidities and/or the inability to lose weight via the methods described previously may progress to the need for surgical management. The types of surgery, course of recovery, and potential for complications vary from patient to patient but overall seem to be similar to that of adults (Levitsky, Misra, Boepple, & Hoppin, 2009). F. The encouragement of weight maintenance versus weight loss depends on the age and BMI percentile of the child as follows (Barlow & Expert Committee, 2007; Spear et al., 2007): 1. O verweight (BMI 85-94%) Children of any age should be encouraged to maintain weight and/or slow weight gain until a BMI of < 85% is achieved 2. Obe se (BMI 95-98%) a. C hildren under 12 should be encouraged to maintain weight or lose weight at a rate no greater than 1 lb per month. b. Ado lescents 12 and older should be encouraged to lose weight at a rate no greater than 2 lbs per week. 3. S everely obese (BMI > 98%) a. C hildren under 6 years old should be encouraged to lose weight at a rate no greater than 1 lb per month. b. C hildren 6 years and older should be encouraged to lose weight at a rate no greater than 2 lbs per week. G. Follow up with the patient at least every 3-6 months for weight/BMI monitoring and further support in lifestyle modification. V. h elpful online resources A. www. cdc. gov/obesity/childhood/ CDC website that provides statistics and facts about obesity in the United States, tools for BMI measurement and tracking, and strategies for obesity prevention B. http://ihcw. aap. org/ Website for the American Academy of Pediatrics Institute for Healthy Childhood Weight, which includes informa-tion about programs and practice resources aimed toward obesity prevention and treatment C. www. choosemyplate. gov U. S. Department of Agriculture-sponsored website that offers resources and tools for dietary assessment and nutrition education D. www. letsmove. gov Official website of the “Let's Move” campaign launched by first lady Michelle Obama; provides information about nutrition, physical activity, and advocacy around obesity prevention initiatives in communities and schools E. www. nchpad. org National Center on Health, Physical Activity and Disability website that provides information and resources to promote the health of people with disabilities through physical activity F. www. chopchopmag. org Website and print magazine developed by the nonprofit organization, Chop Chop Kids, whose mission is to pro-mote nutrition by teaching children and families to cook and eat together; offers a wide selection of easy recipes from a variety of cultural cuisines re Feren Ces Adeyemo, M. A., Mc Duffie, J. R., Kozlosky, M., Krakoff, J., Calis, K. A., Brady, S. M., et al. (2014). Effects of metformin on energy intake and satiety in obese children. Diabetes, Obesity & Metabolism, 17, 363-370. doi:10. 1111/dom. 12426 [doi] Bandini, L. G., Curtin, C., Hamad, C., Tybor, D. J., & Must, A. (2005). Prevalence of overweight in children with developmental disorders in the continuous national health and nutrition examination survey (NHANES) 1999-2002. Journal of Pediatrics, 146(6), 738-743. doi:10. 1016/j. jpeds. 2005. 01. 049 Barlow, S. E., & Expert Committee. (2007). Expert committee recommen-dations regarding the prevention, assessment, and treatment of child and adolescent overweight and obesity: Summary report. Pediatrics, 120(Suppl. 4), S164-S192. doi:120/Supplement_4/S164121 References

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Infant feeding practices and prevalence of obesity in eight European countries—the IDEFICS study. Public Health Nutrition, 16(2), 219-227. doi:10. 1017/S1368980012003850 Institute of Medicine (IOM). (2011). Early childhood obesity prevention policies. Washington, DC: National Academies Press. Jasik, C. B., & Lustig, R. H. (2008). Adolescent obesity and puberty: The “perfect storm. ” Annals of the New York Academy of Sciences, 1135, 265-279. doi:10. 1196/annals. 1429. 009 Kendall, D., Vail, A., Amin, R., Barrett, T., Dimitri, P., Ivison, F., et al. (2013). Metformin in obese children and adolescents: The MOCA trial. Journal of Clinical Endocrinology and Metabolism, 98(1), 322-329. doi:10. 1210 /jc. 2012-2710 Koontz, M. B., Gunzler, D. D., Presley, L., & Catalano, P. M. (2014). Longitudinal changes in infant body composition: Association with childhood obesity. Pediatric Obesity, 9(6), e141-e144. doi:10. 1111 /ijpo. 253122 CHAPTER 16 | Childhood Overweight and Obesity

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T anaka, C., Reilly, J. J., & Huang, W. Y. (2014). Longitudinal changes in objectively measured sedentary behaviour and their relationship with adiposity in children and adolescents: Systematic review and evidence appraisal. Obesity Reviews: An Official Journal of the International Association for the Study of Obesity, 15(10), 791-803. doi:10. 1111 /obr. 12195 van Geel, M., Vedder, P., & T anilon, J. (2014). Are overweight and obese youths more often bullied by their peers? A meta-analysis on the rela-tion between weight status and bullying. International Journal of Obesity, 38(10), 1263-1267. doi:10. 1038/ijo. 2014. 117 Viner, R. M., Hsia, Y., T omsic, T., & Wong, I. C. (2010). Efficacy and safety of anti-obesity drugs in children and adolescents: Systematic review and meta-analysis. Obesity Reviews: An Official Journal of the International Association for the Study of Obesity, 11(8), 593-602. doi:10. 1111/j. 1467-789X. 2009. 00651. x Yanovski, J. A., Krakoff, J., Salaita, C. G., Mc Duffie, J. R., Kozlosky, M., Sebring, N. G., et al. (2011). Effects of metformin on body weight and body composition in obese insulin-resistant children: A randomized clinical trial. Diabetes, 60(2), 477-485. doi:10. 2337/db10-1185Rao, G. (2008). Childhood obesity: Highlights of AMA expert committee recommendations. American Family Physician, 78(1), 56-63. Reinehr, T., Dobe, M., Winkel, K., Schaefer, A., & Hoffmann, D. (2010). Obesity in disabled children and adolescents: An overlooked group of patients. Deutsches Arzteblatt International, 107(15), 268-275. doi:10. 3238/arztebl. 2010. 0268 Rimmer, J. A., & Rowland, J. L. (2008). Physical activity for youth with disabilities: A critical need in an underserved population. Developmental Neurorehabilitation, 11(2), 141-148. doi:10. 1080 /17518420701688649 Rottenberg, J., Yaroslavsky, I., Carney, R. M., Freedland, K. E., George, C. J., Baji, I., et al. (2014). The association between major depressive disorder in childhood and risk factors for cardiovascular disease in adolescence. Psychosomatic Medicine, 76(2), 122-127. doi:10. 1097 /PSY. 0000000000000028 Spear, B. A., Barlow, S. E., Ervin, C., Ludwig, D. S., Saelens, B. E., Schetzina, K. E., et al. (2007). Recommendations for treatment of child and ado-lescent overweight and obesity. Pediatrics, 120(Suppl. 4), S254-S288. doi:120/Supplement_4/S254123 References

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management of both daytime and nighttime urinary inconti-nence (nocturnal enuresis) are discussed. There is also a brief review of the assessment and management of the common comorbid conditions associated with urinary incontinence including urinary tract infections (UTIs), stool retention, encopresis due to behavioral patterns (Feldman & Bauer, 2006; Franco, 2007a), and the psychological, social, and cultural impact on children with incontinence. As a child learns to contract the external sphincter muscle, the muscle inhibits both detrusor contraction and stool motility, which can affect both systems. This is now referred to as bladder and bowel dysfunction (BBD), when both lower urinary tract dysfunction and bowel dysfunction coex-ist (Austin et al., 2014). Chronic contraction of the sphincter muscle promotes further stool retention and distention and/or incomplete emptying of the bladder, potentially lead-ing to recurrent UTIs. In addition, a full rectum may exert pressure on the bladder, inducing bladder symptoms, such as sudden urgency or decreased bladder capacity, described as the “cross-talk” mechanism (Burgers et al., 2013; Franco, 2007a). Possible early childhood risk factors, such as develop-mental delays in motor, communication, and social skills, or even difficult temperament may contribute to a higher chance of daytime incontinence and soiling ( Joinson et al., 2008). Children with urinary incontinence have also been found to have social and psychological distress that must be addressed at the same time (Butler & Heron, 2008; Feldman & Bauer, 2006). Although correction of incontinence may not alter internalizing problems, such as anxiety or obses-sive-compulsive disorders, it does normalize the incidence of externalizing problems, such as conduct disorders (Glassberg & Combs, 2009). Our society has little tolerance for bladder and bowel incontinence; thus children with such symptoms are at risk for further embarrassment and psychologic and emotional distress (T obias, Mason, Lutkenhoff, Stoops, & Ferguson, 2008). Providers must handle both the initial work-up and routine follow-up with much sensitivity and respect for the child's self-esteem. I. Intr oduction and general background Urinary incontinence by definition is the involuntary loss of urine (Neveus et al., 2006). The bladder is responsible for the storage and emptying of urine. During infancy, this occurs as reflexive behavior by the complex pathway controlled by an “integration of sympathetic, parasympathetic, and somatic innervation that involves the lower urinary tract, the mic-turation center in the sacral spinal cord, the midbrain, and the higher cortical centers” (Hinds, 2005, p. 79). The infant also may not empty to completion (Feldman & Bauer, 2006). The cortical inhibitory pathway develops between 1 and 3 years of age, which inhibits bladder contraction and allows for voluntary control of the external sphincter (Feldman & Bauer, 2006). By age 4, a child has learned to control and coordinate the voiding process and can become dry between urination. The detrusor muscle (bladder wall muscle) is relaxed during the filling stage while the bladder neck remains closed to achieve continence. Once the bladder is full, the external sphincter relaxes while the detrusor muscle con-tracts during voiding to allow for complete emptying of the bladder. An estimated bladder capacity in m L for a child over 2 years of age is now defined as the child's age (in years) plus 1 × 30 m L up until puberty (Austin et al., 2014). The normal range of voiding is between 3 and 7 times per day for chil-dren between the ages of 7 and 15 years (Austin et al., 2014). However, a wide range of conditions or dysfunctions may cause either continuous or intermittent urinary incontinence in children. This chapter presents the latest standard terminology set forth by the International Children's Continence Society to standardize the language and avoid confusion among clinicians and researchers (Austin et al., 2014). Urinary incontinence is categorized as either continuous or intermittent. This chap-ter focuses on intermittent incontinence in children older than 5  years of age who are otherwise healthy and normal, both anatomically and neurologically. The assessment and Angel K. Chen Ur In Ary In Cont Inen Ce I n Ch I ldren© Eliks/Shutterstock; © donatas1205/Shutterstock 124 17Chapt Er

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e. B ladder and bowel dysfunction (BBD): combi-nation of both bladder and bowel dysfunction, without identifiable neurologic abnormality and potentially affecting the upper urinary tract sys-tem if severe. f. U nderactive bladder: low voiding frequency (three or less in 24-hour period) with need for intra-abdominal pressure (valsalva) to initiate, maintain, or complete voiding; caused by hypo-tonic detrusor muscle; large bladder volume with elevated PVR and increased risk for UTI. g. G iggle incontinence (enuresis risoria): a rare condition with complete involuntary emptying of bladder that occurs during or after laughter; bladder normal while not laughing; seen in girls. h. S tress incontinence: involuntary leakage of urine with physical exertion that increases abdominal pressure; on urodynamics the leakage is con-firmed by lack of a detrusor muscle contraction. i. E xtraordinary daytime urinary frequency or benign urinary frequency: frequent, small-vol-ume voiding during the day only (> 1 time per hour with voided volume of < 50% estimated bladder capacity). Generally self-limiting. 2. P revalence and incidence. Daytime urinary incontinence is generally consid-ered a problem after 4 years of age (Feldman & Bauer, 2006). It may account for up to 40% of the visits in a pediatric urology clinic. In addition, dysfunctional voiding is associated with increased risk of UTIs, stool retention and encopresis, vesicoureteral reflux, and psychologic distress (Feldman & Bauer, 2006). Emotional stressors, such as sexual abuse, may some-times trigger sudden dysfunctional voiding. B. Nighttime (intermittent) incontinence— nocturnal enuresis 1. D efinition and overview. a. N ighttime intermittent incontinence, also known as nocturnal enuresis, is the involuntary loss of urine in discrete episodes while asleep, occur-ring at least 2 nights per week (Butler, Heron, & The ALSPAC Study T eam, 2006; Neveus et al., 2006; Austin et al., 2014). Enuresis is thought to be caused by a lack of arousal during night-time with resultant bladder contractions and wetting, reduced nighttime bladder capacity, nighttime polyuria, bladder overactivity, or an elevated threshold for nighttime arousal (Butler et al., 2006; Neveus et al., 2010; Robson, 2009). T o better understand nighttime incontinence, it is important to divide the children into subgroups based on symptoms or by onset of enuresis:A. Daytime (intermittent) incontinence 1. D efinition and overview. Daytime urinary incontinence is the involuntary loss of urine while awake. It involves a wide array of clinical symptoms and causes, which differ in severity and reversibility. In addition, it may involve the maturation, functional, or behavioral process within the elimination cycle. Most commonly, children discover the power of controlling the exter-nal sphincter to postpone urination (by inhibiting the detrusor contraction) and thus eventually may reach a dyscoordination between the bladder and sphincter muscle control or have a delay in matura-tion of the bladder sphincter coordination (Franco, 2007a), both of which lead to daytime urinary leak-age. Furthermore, after repeated dyscoordination, the child may also have a difficult time relaxing the external sphincter muscle enough to void to comple-tion, thus increasing the risk of UTI and causing even more uninhibited contractions of the bladder (Austin & Ritchey, 2000). Some of the major causes of daytime incontinence include:a. V aginal reflux and postvoid dribbling: invol-untary leakage of urine immediately or within 10 minutes after voiding can be caused by urine trapped in the introitus during void or may occur with coughing, sneezing, or jumping; often due to voiding with adducted legs or presence of labial adhesions; may cause skin irritation. b. V oiding postponement: typically with classic post-poning maneuvers (“potty dance,” crossing legs fully, squatting with heel pressed into perineum, or penile grabbing) to externally contract the sphincter or compress urethra to temporarily relax the detrusor, postpone urination, or prevent uri-nary leakage, but followed by a sudden urge to void. c. O veractive bladder and urge incontinence: increased detrusor contractions that lead to pel-vic floor contraction, can be diagnosed by uro-dynamics or accurate voiding diary; may or may not involve urinary frequency; high association with UTIs; associated with strong desire to void with tendency to perform classic postponing maneuvers (see item b. ). d. D ysfunctional voiding: incomplete relaxation of external sphincter during voiding in an oth-erwise neurologically intact patient; may be verified by urodynamics or uroflow evaluation with staccato urinary flow pattern and prolonged voiding time potentially with incomplete emp-tying of the bladder (elevated postvoid residual [PVR]); associated with increased risk of UTI. 125 Introduction and general background

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for enuresis if left unresolved. The spontaneous cure rate in children is about 15% per year, depending on their culture. Approximately 2-3% of older ado-lescents and 1-2% of adults continue to experience nocturnal enuresis. This occurs more in boys than girls (Bogan, 2005; Robson, 2009). Although most children do outgrow enuresis, studies have shown reduced self-esteem in children with even just once per month enuresis. By providing treatment, self-esteem improves regardless of actual success of treat-ment (Robson, 2009). Another study by Butler and Heron (2008) reveals that 9-year-old children view enuresis as extremely stressful life events, even more stressful than physical illnesses. Insurance compa-nies may pay for bed alarm treatment for children over 7 years of age with monosymptomatic enuresis (Aetna, 2009), but daytime symptoms must be ruled out initially. The decision about when to start treat-ment depends on the child's degree of concern and motivation rather than the family's concerns and motivation (Robson, 2009). II. d atabase (may include but is not limited to) A. Subjective 1. D etailed voiding and elimination history: most useful and most important (see T able 17-1). a. H istory provides critical information. b. Dir ect questions at both child and parent because the child knows best what occurs during the day; parents have been found to be unreliable in stating the voiding and elimination history alone. 2. P ast health history. a. P renatal and birth history. b. M edical illnesses: significant congenital conditions especially of the genitourinary tract, heavy snoring. c. S urgical history: urologic or neurologic surgery. d. Obs tetric and gynecological history: recent pregnancy. e. Gr owth and development: developmental mile-stones and any challenges or delays especially in neuromuscular area; attention-deficit/hyperac-tivity disorder; and school performance. f. F amily history: renal or urologic diseases and history of enuresis. g. Die t: caffeine, soda, energy drinks, chocolate, or citrus intake (bladder irritants); fluid intake throughout the day and night; and fruit or fiber intake. i. M onosymptomatic enuresis: enuresis as the sole symptom, without any bladder dysfunc-tion or other lower urinary tract symptoms; the etiology is unclear but possible cause is thought to be related to immaturity of the brainstem, with fluctuation or decreased production of serum arginine vasopressin, which leads to increased nocturnal urine production (Glassberg & Combs, 2009). ii. N onmonosymptomatic enuresis: enuresis along with additional daytime lower urinary tract symptoms (e. g., daytime incontinence, frequency, and urgency); the cause is thought to be overactive bladder or stool retention, or a combination of both (Franco, 2007a, 2007b). iii. P rimary enuresis: child has never been dry at night—can be for either monosymptom-atic or nonmonosymptomatic enuresis. iv. S econdary enuresis: child has had dry nights for at least 6 consecutive months but now with recurrence of enuresis; may have similar presentation as primary enuresis with the difference in degree of constipation and age of toilet training. b. Add itional causes of enuresis may include genetic factors, maturational delay, upper airway obstruction (rare), psychologic factors, UTI, or decreased nighttime bladder capacity. Severe stool retention may also lead to decreased blad-der capacity. Secondary nonmonosymptomatic enuresis requires further work-up for neurologic involvement especially if unresponsive to tradi-tional treatments for enuresis or stool retention (Robson, 2009). 2. P revalence and incidence. Approximately 15-25% of 5-year-olds have noctur-nal enuresis despite cultural differences (Feldman & Bauer, 2006). A small percentage of this age group still wet two or more times per week (Robson, 2009). Recent studies have found more children with non-monosymptomatic enuresis than monosymptom-atic enuresis (Neveus et al., 2010; Robson, 2009), although the literature is mixed on actual prevalence. Children with nonmonosymptomatic enuresis tend to have higher rates of comorbidity, including both bladder and bowel dysfunction (Butler et al., 2006). In addition, they tend to have more severe symptoms including more wet episodes per night and more wet nights per week than those with monosymptomatic enuresis, because of persistent bladder overactivity throughout the night (Butler et al., 2006). The comorbid factors hinder the success of treatment 126 CHAPTER 17 | Urinary Incontinence in Children

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Table 17-1 Detailed V oiding and Elimination History from Child and Parent Daily Activities & Related Symptoms Information Gathering Voiding habits Potty training process (age, approach, and length of time) Number of voids throughout the day or at school (0-3 times)Postponing behavior (“potty dance”)Urgency or frequency (number of times per hour; can sit through a movie?)Intermittent versus smooth urine stream Use of abdominal pressure to void (Valsalva)Nocturnal wetting or polyuria Daytime incontinence Frequency: number of times wet per day or per week Amount and severity: dampness versus soaking accidents number of pads or liners used per day Pattern: morning versus afternoon weekday versus weekend Sudden wetting versus wet along the way to the bathroom Amount of time between voiding and wetting (immediately, 10 min, or 2 hr)Aware of wetting and change clothes independently?Previous treatment and results Nighttime incontinence Frequency: number of nights per week Amount and frequency: wet before or after midnight number of times per night (1 or > 1) soak through pull-ups or diapers Previous treatment and results; compliance or appropriate use?Age when initial nighttime wetting resolved (if applicable)Family history of delayed resolution of nighttime wetting Responsible for changing wet sheets or clothing History of urinary tract infection Bladder versus kidney infection Fever or other symptoms at presentation Symptoms after treatment Previous work-up Total number of infections, dates, and treatment Elimination habits Frequency of stooling in toilet Size, shape, and consistency of stool; clog the toilet?Staining on underwear versus complete soiling Postponing of stooling (withholding behavior)Chronic abdominal pain Water, fruit, and fiber intake per day; evaluate timing of fluid intake Prior treatment and results Family history of constipation or infrequent stooling Overall Skin breakdown or rashes in perineum Awareness before or right after accident (urine or stool)?Which occurred first: urinary wetting or stool retention or soiling?Which is worse: daytime or nighttime wetting, or stool retention or soiling?Which is the child more motivated to correct?Which is the family more motivated to correct?Assess child's and family's readiness to address the issues127 Database

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2. S upporting data from relevant diagnostic tests gathered from work-up and management plan (T able 17-3). III. Assessment A. Determine the diagnosis 1. D aytime (intermittent) urinary incontinence. 2. N ighttime (intermittent) urinary incontinence— nocturnal enuresis; monosymptomatic vs. nonmono-symptomatic; primary vs. secondary. h. P ersonal-social-psychologic history: trau-matic events or history of abuse, family and social support, reaction to accidents, recent major changes in the family; temperament in general. 3. R eview of systems a. Ge neral: self-esteem, mood, attitude, patterns of behavior, fatigue, weight loss. b. Musculoskeletal and neurologic: gait and chang-es in lower extremity sensation or control. B. Objective 1. P hysical examination findings (see T able 17-2). Table 17-2 Physical Examination System d etails General Assess self-esteem, attitude, and mood Abdomen Abdominal tenderness or distention Abdominal masses kidneys and bladder stool masses Genitourinary Overall hygiene Dampness or stool staining on underwear Tanner stage Anatomic abnormality Signs of skin breakdown or skin excoriation Signs of infection Male: urine pooled under foreskin, balanitis, or meatal stenosis Female: urine in introitus or perineum, discharge, or labial adhesion Active urine leakage at baseline versus with straining Rectum stool staining around rectum rectal fissures sphincter tone and sensation; anal wink If positive stool symptoms then consider digital rectal examination for assessment of rectal tone, presence of fecal or solid mass, or hemoccult testing Spine Sacral dimple, pit, or sinus tract Tuft of hair Hemangioma Subcutaneous lipoma Asymmetric gluteal crease Neurologic Gait Heel and toe walk Lower extremity muscle strength and tone Deep tendon reflexes Sensation in lower extremities128 CHAPTER 17 | Urinary Incontinence in Children

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Table 17-3 Common Urologic T ests Test Definition Clinical Implications Comments Urinalysis (UA) Analysis of the urine by urine dipstick and, when available, evaluation under the microscope with spun urine Specific gravity < 1. 000 may reveal concentrating defect > 1. 020 may reveal dehydration and insufficient fluid intake Positive glucose on dipstick: rule out diabetes mellitus Positive protein on dipstick: repeat and rule out renal disease Positive leukocytes or nitrites on dipstick: proceed with microscopic evaluation and culture and sensitivity to rule out UTIUTIs must be ruled out as they may be the cause of or the result of the incontinence Can exacerbate bladder symptoms Urine culture and sensitivity (urine C&S)Cultured urine specimen to evaluate organism causing UTI and sensitivity to panel of antibiotics Positive urine culture indicates UTI and requires treatment with antibiotics May follow with prophylactic antibiotics to prevent further infections until voiding dysfunction resolved Method of obtaining specimen is important Use a catheterized specimen if not fully toilet trained to avoid contamination Uroflowmetry (UF) Noninvasive test measuring urinary flow rate, voiding pattern (degree of external sphincter relaxation), voiding volume, and time Staccato flow (intermittent stream) indicates inability for sphincter to completely relax during voiding and may cause incomplete emptying in dysfunctional voiding Bell-shaped curve indicates proper sphincter relaxation during voiding Prolonged flow time with weak flow rate may indicate hypotonic bladder and detrusor contraction Best done with simultaneous pelvic floor electromyogram monitoring Need to have at least half of estimated bladder capacity in the bladder to be effective Can be evaluated by listening and observing the urine flow if machine is not available Bladder scan and PVR Ultrasound of the bladder after voiding to determine residual urine within the bladder; noninvasive Ideal goal of < 10% of expected bladder capacity Can detect bladder wall thickness (> 5 mm; caused by voiding dysfunction) and any masses within the bladder Useful as prognostic indicator Prevoid bladder volume is also helpful  Renal bladder ultrasound (RBUS)Ultrasound of the kidneys and bladder; noninvasive Assess renal size and parenchyma and any evidence of hydronephrosis Assess bladder volume, bladder wall thickness, and any masses within the bladder May see rectal distention (indicate stool retention)Normal renal bladder ultrasound can also be reassuring to both families and provider Kidneys, ureter, bladder radiograph (KUB)Plain film of kidneys, ureter, and bladder region Assess degree of stool retention Assess for any spinal deformity Complements clinical history and physical examination (continues)129 Assessment

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3. El iminate other conditions that may explain the patient's symptoms and presentation: a. U TIs b. C onstipation or stool retention; bladder and bowel dysfunction c. N eurogenic bladder d. Di abetes insipidus or diabetes mellitus e. E ctopic ureter (typically continuous incontinence) B. Severity Assess the severity of the disease (mild, moderate, severe, or debilitating). C. Significance Assess the significance of the problem to the child and family. D. Motivation and ability 1. D etermine the child's motivation, willingness, and ability to follow an individualized treatment plan. 2. P rovide individualized program and set realistic goals. 3. P rovide frequent follow-up to monitor progress and sustain motivation. IV. Goals of clinical management A. Screening or diagnosing 1. C hoose a cost-effective approach for screening or diagnosing daytime and nighttime urinary inconti-nence in children. Table 17-3 Common Urologic T ests Test Definition Clinical Implications Comments Urodynamics (UDS) Invasive study involving urethral catheter and filling of bladder for evaluation of bladder pressure, compliance, detrusor and uninhibited contractions, and bladder capacity Also evaluates pelvic floor muscle coordination and condition of bladder at time of urinary leakage (if any) Fluoroscopic urodynamics also is able to reveal VURReserved for those without improvement or concern for neurogenic cause Results may vary depending on how fast the bladder is filled and how cooperative is the patient Spinal MRI MRI of the spine to rule out tethered cord Consider for those suspected of neurogenic bladder Should be MRI of entire spine Children who require this work-up should also receive a full neurologic examination Voiding cystourethrogram (VCUG)Invasive fluoroscopic study with insertion of urinary catheter to fill the bladder and evaluate for signs of VUR; requires evaluation of voiding and PVRIndicated if positive history of febrile UTI to rule out VUR Also reveals bladder volume, bladder trabeculation, sphincter relaxation during voiding, urethra, and PVR Includes scout film (kidneys, ureter, bladder radiograph); reveals spinal deformity and degree of stool retention Incomplete relaxation of external sphincter during urination is seen as “spinning top urethra” in girls Consider fluoroscopic urodynamics rather than voiding cystourethrogram only if the child has a history of incontinence and pyelonephritis Abbreviations: UTI, urinary tract infection; PVR, postvoid residual; VUR, vesicourethral reflux; MRI, magnetic resonance imaging. (Continued)130 CHAPTER 17 | Urinary Incontinence in Children

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2. El iminate other possible conditions causing urinary incontinence, which require referral to a specialty service. B. Treatment 1. I mprove the patient's bladder and bowel health, including skin integrity. 2. P roperly treat conditions with minimal use of medication (both in dose and length of treatment). 3. D ecrease the prevalence of UTIs. 4. I mprove the quality of life for both patient and family. 5. P revent psychological and emotional trauma caused by incontinence. 6. F oster a healthy and active lifestyle. 7. E mpower the patient and family to manage bladder and bowel health. C. Patient adherence 1. S elect an approach that maximizes patient and family adherence, including positive reinforcement. 2. P rovide close follow-up to maximize patient and family adherence. V. Plan A. Screening 1. U rinalysis or urine culture and sensitivities, if indicated, to rule out UTI and other abnormalities in the urine (T able 17-3). 2. D ysfunctional Voiding Scoring System (DVSS) Questionnaire—a 10-item questionnaire to quantify severity of symptoms (Farhat et al., 2000). 3. Add itional psychological questionnaires may be used to determine behavioral comorbidities. B. Diagnostic tests (Table 17-3) 1. V oiding or elimination diary as both a diagnostic tool and treatment via urotherapy—the timed voiding and elimination process (Figure 17-1). 2. U roflowmetry (parents can watch child void and listen to urine flow for interruption or smooth flow); review past history and bladder scan (if available); evaluate patient's voiding pattern and PVR. 3. R enal bladder ultrasound if positive for UTI or severe wetting (see Figures 17-2, 17-3). 4. A bdominal plain film if there is stool retention or unclear history of constipation5. V oiding cystourethrogram if positive history of febrile UTI; or video urodynamics study, which includes fluoroscopic voiding cystourethrogram in addition to the urodynamics study of the bladder (see Figures 17-2, 17-3). 6. U rodynamics study and spinal magnetic resonance imaging if suspicion of neurogenic bladder for both day and nighttime incontinence or no improvement with initial treatment regimen of nonmonosymp-tomatic enuresis. C. Management including treatment, consultation, referral, and follow-up care (see Tables 17-4, 17-5 and Figures 17-2, 17-3) (Burgers et al., 2013; Austin et al., 2014; Maternik, Krzeminska, & Zurowska, 2015) 1. D aytime incontinence. a. B ladder and bowel dysfunction: adhere to strict urotherapy, including education on normal blad-der function, regular voiding and elimination hab-its and posture, fluid intake, prevention of stool retention, and instruction on the use of voiding and elimination diaries. Of note, not enough data exist regarding benefits of fiber or probiotics for them to be recommended routinely. b. V aginal reflux and postvoid dribbling: sit on toilet with underwear all the way down by the ankles or sit backward on toilet to allow full abduction of legs during urination to prevent urine from backflowing into the vagina. c. G iggle incontinence and enuresis risoria: meth-ylphenidate, 0. 2-0. 5 mg/kg orally daily for 2 months for trial. i. C hildren less than 10 years of age: short-acting (4-hr) form used midmorning ii. C hildren more than 10 years of age: intermediate-acting (8-hr) form used before school (Berry, Zderic, & Carr, 2009) d. V alsalva voiding habits should be referred to pediatric urology for consultation and work-up. 2. N ighttime incontinence. a. N onmonosymptomatic: start with treatment for daytime incontinence and address any other comorbid factors (e. g., stooling) before achieving nighttime continence. b. M onosymptomatic primary nocturnal enuresis: following daytime urotherapy and ruling out of stool retention, choice of bed alarm or medica-tion if appropriate. c. S econdary nonmonosymptomatic nocturnal enuresis: following daytime urotherapy and ruling out stool retention, if unresponsive, refer 131 Plan

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FIGUre 17-1 V oiding and e limination d iary Date Mon T ues W ed Thurs Fri Sat Sun When you wake up Mid AM recess Lunch Mid PM (before leaving school) Dinner Bedtime Poop Dry Days Dry Nights Date Mon T ues W ed Thurs Fri Sat Sun When you wake up Mid AM recess Lunch Mid PM (before leaving school) Dinner Bedtime Poop Dry Days Dry Nights Date Mon T ues W ed Thurs Fri Sat Sun When you wake up Mid AM recess Lunch Mid PM (before leaving school) Dinner Bedtime Poop Dry Days Dry Nights 132 CHAPTER 17 | Urinary Incontinence in Children

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Figure 17-2 Algorithm for Diagnosis, Evaluation, and T reatment for Urinary Incontinence to pediatric urology for full work-up possibly with renal bladder ultrasound, urodynamics, and/or spinal magnetic resonance imaging to rule out neurogenic bladder caused by possible tethered cord or other etiologies. D. Client education 1. I nformation. Provide verbal and, preferably, written information regarding:a. N ormal bladder and bowel functions, coordina-tion of detrusor muscle with external sphincter muscle, and relationship between bladder and bowel functions. b. The d isease process, including but not limited to signs and symptoms and underlying etiologies. Emphasize that this condition is neither the child's nor parent's fault and that the healthcare provider will work together with family to resolve issues. Provide encourage-ment and motivation throughout the recovery process (average 3-6 months or as long as the length of dysfunction). c. Di agnostic tests that include a discussion about preparation, cost, the actual procedures, and aftercare. d. M anagement (rationale, action, use, side effects, associated risks, and cost of therapeutic 2. Hx of UTI 4. Nighttime Wetting3. Daily soft BM1. Daytime Wetting Yes Yes Yes Proceed to #3 5. Behavioral Modification Proceed to #4 Proceed to #5No No No Timed voiding Double voiding** F/U in 1-2 mo Timed stooling-Daily sit for stool after meals Use of Bladder/Bowel Diary for Rewards/Incentives * Consider work-up and management accordingly; see Tables 17-3, 17-4, and 17-5. Stool retention must be addressed/resolved. **Void every 1-2 hr; double void if elevated postvoid residual. Fluid limitation after dinner* Increase fluids & fruits/veggies Identify barriers and potential solutions Antibiotic Prophylaxis* (Optional) Polyethylene glycol (Miralax)- CLEAN OUT then daily MAINTENANCE*133 Plan

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Figure 17-3 Algorithm for Follow-Up of Urinary Incontinence in terventions; and the need for adhering to long-term treatment plans). 2. C ounseling. a. R ecommended if symptoms have contributed to emotional distress or social isolation. b. I f underlying issues contribute to the incon-tinence and encopresis, counseling or other psychotherapy may assist in addressing and cor-recting the issues. VI. r esources A. Provider resources 1. A n umber of validated tools are available to measure the psychologic and behavioral effects of incontinence, such as the Child Behavioral Check List (CBCL), or Pin Q, a cross-cultural continence-specific pediatric quality-of-life measurement tool (Bower et al., 2006). 2. Hx of UTI 3. Daily soft BM1. Improved Daytime Symptoms 4. Improved Nighttime Wetting Yes No Yes Yes Yes Proceed to #3Proceed to #2 5. Behavioral Modification Proceed to #4 Proceed to #5No No No Timed voiding Double voiding** F/U in 1-2 mo Timed stooling-Daily sit for stool after meals Use of Bladder/Bowel Diary for Rewards/Incentives * Consider work-up and management accordingly; see Tables 17-3, 17-4, and 17-5. Stool retention must be addressed/resolved. **Void every 1-2 hr; double void if elevated postvoid residual. ***Consider anticholinergics only if (+) symptoms despite adherence to excellent behavioral modification. Continue with behavioral regiment Consider bed alarm system or DDAVP only if NO BBD symptoms Consider: Anticholinergics only if no GI symptoms*** Referral to Pediatric Urology*** Increase fluids & fruits/veggies Identify barriers and potential solutions Continue with behavioral regimen Work up with RBUS and PVR, +/-VCUGConsider referral to Pediatric Urology Consider GI referral if only GI symptoms Polyethylene glycol (Miralax)- CLEAN OUT then daily MAINTENANCE*134 CHAPTER 17 | Urinary Incontinence in Children

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Table 17-4 Management of Daytime and Nighttime Urinary Incontinence* Step Recommendation Comments Step 1: Initial work-up or treatment Antibiotic prophylaxis if needed (see Table 17-5)If positive for recurrent urinary tract infection or incomplete emptying, consider daily low-dose prophylactic antibiotics at the same time as timed voiding and stooling May consider trimethoprim-sulfamethoxazole nitrofurantoin   Timed voiding and double voiding Initiate voiding every 1-2 hours during the day whether or not the child “feels the need”; approximately 6 times per day: first thing in the morning, midmorning recess, lunch, midafternoon before coming home, dinner, and bedtime. If elevated postvoid residual (> 10% estimated bladder capacity), perform double voiding by returning to void a few minutes after initial voiding; may consider antibiotic prophylaxis AVOID POSTPONING BEHAVIOR!   Timed stooling After a meal, typically dinner, sit on toilet for 10 minutes to attempt to have a bowel movement, and as needed Avoid rushing through the attempt Use of footstool to help with best posture in stooling   Voiding and elimination diary (see Figure 17-1)Document every voiding and elimination attempt each day, along with any dry days and nights May do a frequency-volume chart of shorter duration (i. e., 2-day diary) that includes fluid intake and volume voided Make note of size, shape, and consistency of stool   Rewards system Use the results on voiding-elimination diary to provide positive reinforcement Small treats, stickers, stamps, and privileges for voiding and elimination attempts rather than just for accident-free days and nights   Dietary adjustments Encourage fluids throughout the day (water best); avoid sodas and caffeinated beverages Increase fruit intake; natural best   Stool retention and encopresis management (see Table 17-5)If initial presentation with significant stool retention or encopresis, or on return with symptoms despite behavioral regimen, consider polyethylene glycol (Miralax) for cleanout and maintenance regimen May consider footstool to achieve best posture to relax external sphincter for stooling and voiding Refer to pediatric gastrointestinal service for further work-up if no improvement or gastrointestinal symptoms more severe than genitourinary symptoms Instruct families to expect 6-12 months of treatment, then wean therapy   Fluid restriction (for nocturnal enuresis)Avoid large amounts of fluids ingested at dinner and beyond Caution: children in afterschool sports activities require sufficient rehydration, thus significant fluid restriction may cause further dehydration Encourage fluid intake throughout the day   Follow-up Return to clinic in 1 month for close follow-up; best to maintain frequent contact especially if minor adjustments are necessary to behavior regimen Step 2: Follow-up evaluation or treatment Reevaluate On return, review voiding-elimination diary and symptoms since last visit Repeat uroflowmetry and postvoid residual check (if available)If failed to comply with behavioral regimen, discuss barriers and possible ways to resolve barriers Continue with timed voiding, timed stooling, use of diary, and reward system (continues)135 Resources

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Table 17-4 Management of Daytime and Nighttime Urinary Incontinence* Step Recommendation Comments   Anticholinergic and antispasmodic medication (daytime incontinence or nonmonosymptomatic enuresis despite timed voiding) (see Table 17-5)Use as adjunct to strict timed voiding for those with uninhibited bladder spasms and potentially increased functional bladder capacity May consider: oxybutynin tolterodine Second line of treatment for monosymptomatic enuresis or in conjunction with desmopressin acetate (DDAVP)   Bed alarm system (monosymptomatic enuresis)Consider for children greater than 6 years of age Choose loud sensor (sound/lights/vibration) to wake child up at the beginning of accident at night; not the same as setting an alarm at a specific time of the night Sensor is attached to underwear and is activated by the wetting of the underwear Child needs to get up (or to be woken up) at the time of alarm activation to void, then reattach alarm Should follow-up on results in 2-3 weeks; overall regimen for 2-3 months. If not effective, can consider pharmacologic regimen Pro: conditioning regimen; effective when used correctly in a motivated child and family (80%) Con: wakes up entire family with the loud sound; if soft then does not wake child up to void; relapse may occur after discontinuation   Antidiuretic: desmopressin acetate (DDAVP) (monosymptomatic enuresis) (see Table 17-5)First line of pharmacologic treatment for monosymptomatic enuresis   Tricyclic antidepressant: imipramine (Tofranil) (see Table 17-5)Third line of pharmacologic treatment for enuresis related to safety concerns   Additional modalities: biofeedback Consider biofeedback therapy to learn to relax sphincter and empty to completion; limited by child's ability to cooperate and follow directions (Franco, 2007b); “bladder stretching” exercises are not useful   Other modalities (less evidence in the literature)Alpha blocker therapy for overactive bladder Hypnosis Acupuncture Chiropractor Extracorporeal magnetic innervation therapy Botulinum A toxin for overactive bladder or sphincter dyssynergia   Timed voiding and stooling regimen Continue strict timed voiding and stooling along with medication trial   Follow-up Return in 1-2 months for follow-up and minor adjustments Continued support for patient and family Provide motivation in compliance with regimen Reminder regarding length of time required for full recovery Step 3: Without improvement despite treatment compliance Referral for further work-up Pediatric gastroenterology if severe encopresis or stool retention Pediatric urology if recurrent urinary tract infection, persistent daytime or nighttime wetting, or suspicion of neurogenic bladder (require full work-up of renal bladder ultrasound, urodynamic study, spinal magnetic resonance imaging) Psychotherapy for emotional stressors to be assessed and treated * Includes treatment, consultation, referral, and follow-up care. (Continued)136 CHAPTER 17 | Urinary Incontinence in Children

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Table 17-5 Common Urologic and Bowel Regimen Medication* Category Indication/Mechanism of Action Name Dosage Side Effects Comments Anticholinergic 1. T reat daytime incontinence caused by bladder overactivity (uninhibited contractions) 2. Second line of treatment for monosymptomatic enuresis or in conjunction with desmopressin acetate (DDA VP)—must rule out constipation and daytime voiding dysfunction first Oxybutynin Daytime: 5 mg PO BID or TID dosing; or XL 10 mg PO daily Nighttime wetting:5 mg PO QHSImmediate release, extended release, and transdermal forms available. Max dose 0. 4 mg/kg Dry mouth, constipation, occasional initial drowsiness; do not use in hot weather because of reduced perspiration, which leads to facial flushing; possible mood changes Contraindication: incomplete emptying Tolterodine 2 mg PO QHS or 1 mg PO BID Antidiuretic Synthetic antidiuretic hormone to reduce urine output at night Consider for children > 6 years of age 30% respond fully; 40% partial response May use only for sleepovers or camp Desmopressin acetate (DDAVP)Dose: 0. 2-mg tablet 1-3 tablets PO QHS (1 hour before bedtime); may use higher dose then taper down Risk of hyponatremia (rare) with mostly nasal spray formulation (longer half-life); limit fluids after dinner Contraindication: excessive fluid intake in evening, (+) headache, nausea, or vomiting Antidepressant Mechanism unknown; used rarely; 50% response rate Imipramine 0. 5-1. 5 mg/kg/d given 1-2 hours before bedtime OR 25-50 mg PO QHS (50 mg for children > 9 years of age)Daytime sedation, anxiety, insomnia, dry mouth, nausea, and personality changes Overdose can cause fatal cardiac arrhythmias, hypotension, respiratory distress, and convulsions (continues)137 Resources

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Table 17-5 Common Urologic and Bowel Regimen Medication* Category Indication/Mechanism of Action Name Dosage Side Effects Comments Osmotic laxative Induce catharsis by strong electrolyte and osmotic effect Polyethylene glycol (Miralax)Clean-out: 1. 5 g/kg/d for 3 days (may split to BID dose) followed by daily maintenance dose and daily sit Maintenance:2-11 years of age: 8. 5 g (1/2 cap) in 4 oz. of water per day > 12 years of age: 17 g (1 cap) in 8 oz. of water per day; or 0. 26-0. 84 g/kg/d(titrate accordingly for daily soft stool)Nausea, vomiting, cramps If no stooling, return to cleanout procedure and then maintenance Parents will titrate depending on stool output, consistency, and staining Antibiotic Treatment of UTI; daily low-dose prophylaxis for prevention of UTIs Trimethoprim (TMP)-sulfamethoxazole UTI prophylaxis: 2 mg/kg/dose of TMP daily Nausea, vomiting, Stevens-Johnson syndrome, rash Contraindication: hypersensitivity to sulfa drug, trimethoprim, or components     Nitrofurantoin UTI prophylaxis: 1-2 mg/kg/d as single daily dose; maximum 100 mg/d Nausea, vomiting, anorexia, Stevens-Johnson syndrome, rash Avoid suspension; use capsule instead and sprinkle onto yogurt or ice cream Administer with food or milk  Abbreviation: UTI = urinary tract infection. Data from Walia, R., Mahajan, L., & Steffen, R. (2009). Recent advances in chronic constipation. Current Opinion in Pediatrics, 21, 661-666. (Continued)138 CHAPTER 17 | Urinary Incontinence in Children

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Butler, R., & Heron, J. (2008). An exploration of children's views of bedwetting at 9 years. Child Care, Health and Development, 34(1), 65-70. Butler, R., Heron, J., & The ALSPAC Study T eam. (2006). Exploring the differences between mono-and polysymptomatic nocturnal enuresis. Scandinavian Journal of Urology and Nephrology, 40(4), 313-319. Farhat, W., Bagli, D. J., Capolicchio, G., O'Reilly, S., Merguerian, P. A., Khoury, A., et al. (2000). The dysfunctional voiding scoring system: Quantitative standardization of dysfunctional voiding symptoms in children. Journal of Urology, 164(3), 1011-1015. Feldman, A. S., & Bauer, S. B. (2006). Diagnosis and management of dysfunctional voiding. Current Opinion in Pediatrics, 18(2), 139-147. Franco, I. (2007a). Overactive bladder in children. Part 1: Pathophysiology. Journal of Urology, 178(3), 761-768. Franco, I. (2007b). Overactive bladder in children. Part 2: Management. Journal of Urology, 178(3), 769-774. Glassberg, K. I., & Combs, A. J. (2009). Nonneurogenic voiding disorders: What's new? Current Opinions in Urology, 19, 412-418. Hinds, A. (2005). Daytime urinary incontinence (in the otherwise healthy child). In L. Baskin & B. Kogan (Eds. ), Handbook of Pediatric Urology (2nd ed., pp. 79-91). Philadelphia, PA: Lippincott Williams & Wilkins. Joinson, C., Heron, J., von Gontard, A., Butler, U., Golding, J., & Emond, A. (2008). Early childhood risk factors associated with daytime wetting and soiling in school-age children. Journal of Pediatric Psychology, 33(7), 739-750. Maternik, M., Krzeminska, K., & Zurowska, A. (2015). The management of childhood urinary incontinence. Pediatric Nephrology, 30(1), 41-50. Neveus, T., Eggert, P., Evans, J., Macedo, A., Rittig, S., T ekgül, S., et al. (2010). Evaluation of and treatment for monosymptomatic enuresis: A standardization document from the International Children's Continence Society. Journal of Urology, 183(2), 441-447. Neveus, T., von Gontard, A., Hoebeke, P., Hjälmås, K., Bauer, S., Bower, W., et al. (2006). The standardization of terminology of lower urinary tract function in children and adolescents: Report from the Standardization Committee of the International Children's Continence Society. Journal of Urology, 176(1), 314-324. Robson, W. L. (2009). Clinical practice. Evaluation and management of enuresis. New England Journal of Medicine, 360(14), 1429-1436. Steers, W. D. (1997). Physiology and pharmacology of the bladder and urethra. In P. C. Walsh, A. B. Retol, E. D. Vaughan, A. J. Wein (Eds. ), Campbell's urology (7th ed., pp. 870-916). Philadelphia: WB Saunders. T obias, N., Mason, D., Lutkenhoff, M., Stoops, M., & Ferguson, D. (2008). Management principles of organic causes of childhood constipation. Journal of Pediatric Health Care, 22(1), 12-23. Walia, R., Mahajan, L., & Steffen, R. (2009). Recent advances in chronic constipation. Current Opinion in Pediatrics, 21, 661-666. B. Patient and client education websites 1. w ww. Kidshealth. org Part of Nemours Foundation's Center for Children's Health Media, Kidhealth. org is a website dedicated to providing health and safety information and helpful tips, in both English and Spanish. Content is designed to specifically address parents, kids, and teenagers. Search “bedwetting” to retrieve helpful information. 2. w ww. Healthychildren. org Sponsored by American Academy of Pediatrics. Contains health topics ranging from regular develop-ment to conditions such as enuresis and constipation. 3. w ww. i-c-c-s. org International Children's Continence Society official website. Includes resources for providers and patients on bladder and bowel dysfunction. 4. w ww. Bedwettingstore. com Offers both resources and products to help manage daytime and nighttime urinary incontinence. re Feren Ce S Aetna, Inc. (2009). Clinical policy bulletin: Nocturnal enuresis treatments. Retrieved from http://www. aetna. com/cpb/medical/data/400_499/0431. html. Austin, P. F., & Ritchey, M. L. (2000). Dysfunctional voiding. Pediatrics in Review, 21(10), 336-341. Austin, P. F., Bauer, S. B., Bower, W., Chase, J., Franco, I., Hoebeke, P., et al. (2014) The standardization of terminology of lower urinary tract function in children and adolescents: Update report from the Standardization Committee of the International Children's Continence Society. Journal of Urology, 191, 1863-1865. Berry, A. K., Zderic, S., & Carr, M. (2009). Methylphenidate for giggle incontinence. Journal of Urology, 182(Suppl. 4), 2028-2032. Bogan, P. A. (2005). Nocturnal enuresis. In L. Baskin & B. Kogan (Eds. ), Handbook of Pediatric Urology (2nd ed., pp. 92-97). Philadelphia, PA: Lippincott Williams & Wilkins. Bower, W. F., Sit, F. K., Bluyssen, N., et al. (2006). Pin Q: A valid, reliable and reproducible quality-of-life measure in children with bladder dysfunction. Journal of Pediatric Urology, 2(3), 185-189. Burgers, R. E., Mugie, S. M., Chase, J., Cooper, C. S., von Gontard, A., Rittig, C. S., et al. (2013). Management of functional constipation in children with lower urinary tract symptoms: Report from the Standardization Committee of the International Children's Continence Society. Journal of Urology, 190, 29-36. 139 References

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Section iii co MMon Wo Men'S He ALt H PR e S ent Ation Sluteal phase progresses, the corpus luteum continues to enlarge, producing greater levels of progesterone and estrogen, and the endometrium becomes more organized in preparation for implantation. If conception does not occur, the corpus luteum regresses spontaneously on a predictable and stable timetable. With this regression, estrogen and progesterone levels drop rapidly and menstruation begins again. According to Fritz and Speroff (2011), “The sequence of events is so controlling that most ovulatory women have a pattern, volume, and duration of menstrual flow they recognize as their own and come to expect, very often accompanied by an equally consistent and predict-able pattern of premenstrual molimina (bloating, breast ten-derness, and mood swings)” (p. 593). New terminology is being adapted to define clinical pre-sentations of abnormal uterine bleeding (Munro, Critchley, & Fraser, 2012). Definitions such as menorrhagia and metrorrhagia have been replaced by heavy or prolonged men-strual bleeding for the former and irregular bleeding for the latter (see T able 18-1 for a description of new terminology as well as the characteristic of the normal limits of the menstrual cycle/bleeding). Etiologies of AUB have been recently classified as related or unrelated to uterine structural abnormalities, categorized with the acronym PALM-COEIN (Munro et al., 2011). Structural abnormalities (PALM) are polyps, adenomyosis, leiomyoma, and malignancy/hyperplasia; and nonstructural abnormalities (COEIN) are coagulopathy, ovulatory dysfunc-tion, endometrial, iatrogenic, and not otherwise classified (see T able 18-2). Abnormal uterine bleeding can manifest as acute or chronic. Acute refers to “an episode of bleeding in a woman of reproductive age, who is not pregnant, that, in the opinion of the provider is of sufficient quantity to require immediate intervention to prevent further blood loss” (Munro, Critchley, & Fraser, 2012, p. 3). A woman's perception of menstrual blood loss may differ significantly from the measured amount of blood loss (Hallberg, Högdahl, Nilsson, & Rybo, 1966); as such, a better description that addresses women's concerns is that from the National Institute for Health and Health Care I. Intr oduction and general background Abnormal uterine bleeding (AUB) is one of the most com-mon presenting healthcare complaints of women. Most commonly the origin of genital bleeding is from the uterus; however, other genital track bleeding etiologies are discussed in this chapter as the evaluation is very similar. AUB is respon-sible for 25% of all gynecological surgical procedures in the United States ( Jain & Santoro, 2005). Menorrhagia (heavy or prolonged menstrual bleeding) alone has been noted as the primary cause for 12% of referrals to gynecological specialty practices (Mohan, Page, & Higham, 2007). Changes in the menstrual cycle accounted for 19. 1% of the 20. 1 million visits to healthcare providers for gynecological conditions observed in a 2-year study (Nicholson, Ellison, Grason, & Powe, 2001). Menstruation, ovulation, and the coordinated sequence of endocrine signals that distinguish the menstrual cycle are the foundation for the regularity, predictability, and consistency of menstrual bleeding (Fritz & Speroff, 2011). Although an extensive review of the endocrinology of the menstrual cycle is beyond the scope of this chapter, an overview of the normal menstrual cycle provides important background and context for understanding AUB. There are essentially three phases to a normal menstrual cycle: (1) the follicular phase, (2) ovulation, and (3) the luteal phase, all of which are managed by the hypothalamic-pituitary-ovarian (HPO) axis, a complicated system of feed-back between the hypothalamus, the pituitary, and the ovary (Fritz & Speroff, 2011). During the follicular phase, increas-ing levels of follicle-stimulating hormone cause the develop-ment and maturation of the dominant ovarian follicle, which in turn leads to increased production of estrogen and the pro-liferation of the endometrium. Increasing levels of estrogen also stimulate a surge of luteinizing hormone and ovulation occurs in response. After ovulation, the corpus luteum, which develops from the dominant ovarian follicle, continues to pro-duce estrogen and also begins to produce progesterone. As this Pilar Bernal de Pheils ABnorm Al Uter Ine Bleed I ng© eliks/shutterstock; © donatas1205/shutterstock 14018Chapter

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A. PALM (structural) etiologies: Polyps, adenomyosis, leiomyomas, malignancy 1. D efinition and overview: a. P olyps are focal outgrowths of the endome-trium, found in the endometrial cavity or in the cervical canal; often seen in association with uterine bleeding in premenopausal and post-menopausal women. Polyps are often asymp-tomatic and most frequently benign. Bleeding from polyps is uncommon and most likely will present as intermenstrual bleeding. b. A denomyosis is a benign condition in which the endometrium invades the myometrium, producing a diffusely enlarged uterus. It causes heavy bleeding and dysmenorrhea, although it may also be asymptomatic. Definite diagnosis is made via uterine pathology after hysterectomy. c. L eiomyomas are benign tumors originating mainly from myometrium (smooth muscles of the uterus). They are also called myomas and fibroids. Depending on their location in the uterus, they may be subserous (originating at the serosal surface of the uterus), intramural (developing from within the uterine wall), or submucosal (originating from the myometrial cells just underneath the endometrium and may Excellence Clinical Guideline, which defines heavy menstrual bleeding as “excessive menstrual blood loss which interferes with the woman's physical, emotional, social and material quality of life, and which can occur alone, or in combination with other symptoms” (National Collaborating Centre for Women's and Children's Health, 2007, p. 35). Acute uterine bleeding can present without prior occurrences or within the context of chronic abnormal uterine bleeding. Chronic AUB is defined as being present for most of the last 6 months and not needing urgent attention (Munro, Critchley, & Fraser, 2012). Some episodes of AUB can occur during the women's reproductive years as a result of alterations in the menstrual cycle (frequently seen in perimenopause) or can be superim-posed over a regular menstrual cycle. Other less common sites of bleeding are the vagina and vulva or, rarely, the fallopian tubes or ovaries. When abnormal bleeding occurs before menarche or after menopause, malignancy is a primary concern. Pregnancy should always be considered in women with AUB who are in the reproductive years, as bleeding in early pregnancy can lead to severe health consequences like a ruptured ecto-pic pregnancy. The reader is referred to an obstetric book for a discussion of the work-up and management of abnormal bleeding in a pregnant patient. This chapter addresses both acute and chronic AUB in hemodynamically stable patients. Table 18-1 Clinical Presentations of Abnormal Uterine Bleeding Clinical presentation Descriptive terms—New terminology: International Federation of Gynecology and Obstetrics (FIGO) (Munro, Critchley, & Fraser, 2012)Descriptive terms— Old terminology Frequency of menses Normal limits (5th to 95th percentiles) Frequency of menses   Normal   Normal 24-38 days Frequent Polymenorrhea < 21-24 days Infrequent Oligomenorrhea > 38 days Absent Amenorrhea No menses × 3 regular cycles or < 9 cycles × year Regularity of menses, cycle-to-cycle variation over 12 months (timing)  Regular Regular (2-20 days, FIGO)(±5 days) Irregular Metrorrhagia Variation > 20 days acyclical Duration of flow  Prolonged Menorrhagia > 8. 0 days Normal   4. 5-8 days Shortened Hypomenorrhea < 4. 5 (2 days) Volume of monthly blood loss  Heavy Menorrhagia > 80 cc Normal Normal 5-80 cc Light Hypomenorrhea < 5 cc Data from Munro, M G, Critchley, H O, & Fraser, I S. (2012). American journal of obstetrics and gynecology, 207(4), 259-265. 141 Introduction and general background

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Table 18-2 Abnormal Uterine Bleeding Etiologies Outside of Pregnancy Classification l ikely e tiology PALM (structural-organic and pelvic tract pathology) Polyps, AUB-P Can be found in the cervix or the endometrium. Adenomyosis: AUB-A, benign lesion in the endometrium Leiomyomata: AUB-LSM for submucosal myoma or AUB-LO for myomas in other layers of the muscle. This distinction is important as the submucosal leiomyomas are the most likely to contribute to the origin of AUB (Munro et al., 2011). Malignancy: is preceded by endometrial hyperplasia, which also causes abnormal bleeding. ‰ ‰Other malignant etiologies to consider are: - Premalignant lesions: cervical dysplasia - Malignant lesions: cervical squamous cell carcinoma, endometrial adenocarcinoma, estrogen-or testosterone-producing ovarian tumors, leiomyosarcoma COEIN (nonstructural-systemic pathology) Coagulation disor ders: Encompasses a spectrum of systemic disorders of hemostasis, most commonly von Willebrand disease. Other conditions to consider are idiopathic thrombocytopenia purpura, coagulation factor deficiencies and other thrombophilias, dysfibrogenemias, disorders like leukemia that produce platelet deficiency, severe sepsis, hypersplenism, severe hepatic or renal disease, and rarely HIV-related thrombocytopenia Ovulatory dysfunction: may be due to endocrinopathies (thyroid dysfunction, polycystic ovary syndrome, obesity) and ovulatory disorders that frequently occur at either end of the reproductive age: adolescence and the menopause transition ‰ ‰ Other endocrine disorders can produce abnormal uterine bleeding; however, one is more likely to see amenorrhea or oligomenorrhea with: - Hypothalamic dysfunction—habit changes, stress, anxiety, eating disorders, excessive weight loss, aggressive exercise, organic disease - Pituitary diseases—hyperprolactinemia, acromegaly, pituitary adenoma; adrenal diseases—Cushing syndrome, Addison disease, tumors, congenital adrenal hyperplasia Endometrial: local endometrial disorders due to homeostasis problems, which are difficult to diagnose (previously called idiopathic AUB), or secondary to local inflammation or infection, most commonly seen with subclinical infection with Chlamydia trachomatis. In such cases, bleeding is superimposed on a normal menstrual cycle. If no infection is identified, consider as a diagnosis of exclusion. ‰ ‰Other pelvic tract etiology of abnormal bleeding may include: - Infections: salpingitis, cervicitis, endometritis, myometritis, pelvic inflammatory disease, tubo-ovarian abscess - V ulvovaginal trauma: foreign body, abrasions, lacerations, sexual abuse or assault Iatrogenic (see under pharmacologic). 142 CHAPTER 18 | Abnormal Uterine Bleeding

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Pharmacologic (the “I” for iatrogenic in the COEIN etiologies) Combined estrogen-progestin contraceptives (unscheduled breakthrough bleeding) Progestin-only contraceptives (prolonged and spotting, but many develop amenorrhea) Intrauterine devices: Nonhormonal (most likely heavy menstrual bleeding, may have spotting); levonorgestrel IUD (most likely spotting, absent bleeding in up to 40% of women at 2 years of use). Hormonal therapy: unscheduled postmenopausal bleeding with hormonal treatment ‰ ‰Medications interfering with coagulation - Anticoagulants - Aspirin and other prostaglandin synthetase inhibitors ‰ ‰Medications causing dopamine receptor blockade (see Chapter 19) ‰ ‰Others - Anabolic steroid use - Chemotherapeutic medications - Herbal and other supplements: ginseng, ginkgo biloba, garlic, ginger, soy - Tamoxifen - Thyroid replacement hormone Not yet classified Conditions not demonstrated conclusively to contribute to AUB or others not yet identified by current diagnostic assays Data from American College of Obstetrics and Gynecology (ACOG). (2013). Committee opinion no. 557: Management of acute abnormal uterine bleeding in nonpregnant reproductive-aged women. Obstetrics and Gynecology, 121(4), 891-896; Munro, M. G., Critchley, H. O., Broder, M. S., et al. (2011). FIGO classification system (PALM-COEIN) for causes of abnormal uterine bleeding in nongravid women of reproductive age. International Journal of Gynecology and Obstetrics, 113(1), 3-13. 143 Introduction and general background

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fibrin function defects. The most common coag-ulopathy is von Willebrand disease, which is classified as mild, moderate, or severe. Diagnosis occurs usually at menarche, although clinical symptoms can present at any age, with heavy menstrual bleeding being one of the most sig-nificant morbidities (ACOG, 2013b; Ng, Motto, & Di Paola, 2015). b. O vulatory disorders commonly present with changes in frequency and flow of menses (see T able 18-1). Previously called dysfunctional uterine bleeding, the new term is ovulatory dysfunction. Menstrual bleeding is considered abnormal if it persists for longer than 7 days (prolonged or menorrhagia) or less than 2 days (light or hypomenorrhea); occurs more often than every 21 days (frequent or polymenor-rhea); or exceeds a total blood loss of 80 m L (heavy or menorrhagia) (see T able 18-2). Women with anovulatory cycles undergo dis-rupted and unpredictable patterns of hormonal production that result in irregular and variable menstrual bleeding. These women are essen-tially in a continuous follicular phase because there is no stimulus for ovulation or subsequent luteal phase development. As a result, the endo-metrium is continually exposed to estrogen, with resulting proliferation. Ultimately, without the organizing support of progesterone pro-duced during the luteal phase, focal areas of the structurally fragile endometrium begin to break down, leading to a pattern of heavy (menorrha-gia) and/or irregular heavy menstrual bleeding (menometrorrhagia) (Fritz & Speroff, 2011). c. E ndometrial etiologies of AUB present as heavy menstrual bleeding in the context of regular pre-dictable menstrual cycles when no other etiology is identified, previously called idiopathic menorrhagia. It is primarily a disorder of the endometrium either due to problems of homeo-stasis, which currently are difficult to diagnose, or may be secondary to endometrial inflamma-tion or infection (Munro et al., 2011). d. I atrogenic etiologies include anticoagulants (such as warfarin and heparin), anticonvul-sants, or certain antibiotics (e. g., rifampin and griseofulvin) or medications that influence ovulation, like hormonal medications (estrogens, progestins, or androgens). Because of enhanced hepatic metabolism, cigarette smoking can increase the incidence of breakthrough bleed-ing in women on hormonal combined contra-ceptive (Rosenberg, Waugh, & Stevens, 1996). protrude in different degrees into the uterine cavity). Leiomyomas may be asymptomatic, although chronic pelvic pain and heavy and prolonged menstrual bleeding is the most common pre-sentation (Khan, Shehmar, & Gupta, 2014). Submucosal leiomyomas are thought to cause AUB although bleeding can be significant regard-less of location and size (Doherty, Mutlu, Sinclair, & T aylor, 2014). On physical exam, the uterus can be enlarged and irregular. Growth of leiomy-omas is associated with exposure to circulating estrogen; thus, these lesions can grow rapidly in the premenopausal years. Growth of leiomyomas is greater earlier in pregnancy, but early elevation of hormones alone does not sufficiently explain this rapid growth (Benaglia et al., 2014). d. Ma lignancy and endometrial hyperplasia must be considered in nearly all women of reproduc-tive age when presenting with abnormal vaginal bleeding (AVB) or AUB. Endometrial hyperpla-sia is the result of endometrial gland proliferation by unopposed chronic estrogen stimulation. It is classified as simple or complex, and both can be seen with or without atypia. Atypical endome-trial hyperplasia can progress to adenocarcinoma if left untreated (Fritz & Speroff, 2011; Horn, Meinel, Handzel, & Einenkel, 2007). 2. P revalence and incidence Polyps are detected in an estimated 20-40% of women with abnormal uterine bleeding (Lasmar et al., 2008) but are not always the source of bleeding. During the reproductive years, uterine leiomyomas are the most common solid pelvic tumor. They are rarely observed before menarche and significantly decrease in size in the postmeno-pausal years. The prevalence of these lesions can be up to 70% in Caucasians and 80% in women of African ancestry (Day Baird, Dunson, Hill, Cousins, & Schectman, 2003). Prevalence of adenomyosis varies widely, ranging from 5% to 70% (Dueholm, 2006). Endometrial cancer (EC) is the most common malignancy of the female genital tract in the Western world with an estimated incidence of 39,080 annual new cases in the United States ( Jemal, 2007). B. COEIN etiologies (nonstructural anomalies): coagulopathy, ovulatory, endometrial, iatrogenic, not yet classified 1. D efinition and overview a. C oagulopathy encompasses a variety of sys-temic disorders of hemostasis that include clot-ting defects, thrombocytopenia, or platelet/144 CHAPTER 18 | Abnormal Uterine Bleeding

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Systemic medications that interfere with dopa-mine metabolism resulting in inhibition of prolactin released (e. g., tricyclic antidepressants and phenothiazines) may lead to absent or infre-quent menses. See Chapter 19, “ Amenorrhea and Polycystic Ovary Syndrome,” for a list of medica-tions causing amenorrhea and oligomenorrhea. Hormonal contraceptive agents result in regular withdrawal bleeding when provided in a cyclical manner, although it can be normal for bleeding not to occur in some cycles. Unscheduled bleeding (also called breakthrough bleeding) may be related to missed, delayed, or improper use of hormonal contraceptive methods. Women using progestin-only contraceptives such as levonorgestrel IUS (intrauterine system), the progestin-only pill, or the implant may have unscheduled bleeding. Women on the copper intrauterine device (IUD) may have increased menstrual flow after insertion. e. N ot yet classified etiologies are those condi-tions that have not been demonstrated conclu-sively to contribute to AUB or other disorders that have not yet been identified by current diagnostic assays. 2. P revalence and incidence: As many as 20% of women with AUB have an underlying coagulation disorder (AGOG, 2013a); a large majority of these women have a variant of von Willebrand disease (VWD). This condition is the most common coagulation disorder in American women (ACOG, 2013b). Anovulation results in sustained high levels of estrogen, which manifest with heavy and/or irregular bleeding. Examples of this phenomenon are polycystic ovary syndrome (PCOS), obesity, postmenarchal adolescents, and women in their perimenopausal period (Fritz & Speroff, 2011). Anovulation occurs most often at the extremes of reproductive life: soon after menarche due to imma-turity of the hypothalamic-pituitary axis and in the years before menopause due to declining ovarian function. AUB is more frequent in the first 18 months postmenarche, particularly in obese teens, whereas AUB in perimenopausal women is a result of intermittent anovulation (ACOG, 2013c). In both scenarios, bleeding patterns are noncyclic and the flow may be heavy or light, with few if any molimi-nal symptoms (Fritz & Speroff, 2011). After all the underlying problems resulting in AUB are evalu-ated and addressed, medical treatment to reestablish cycle regularity and provide endometrial protection should be instituted (ACOG, 2013c). II. d atabase (may include but is not limited to) A. Subjective 1. P ast medical history (Fritz & Speroff, 2011) a. Obs tetric history i. H istory of postpartum hemorrhage ii. H istory of pregnancy complicated by leiomyoma iii. R ecent history of pregnancy ending in miscarriage or abortion b. G ynecological history i. G ynecological disorders and surgeries including evaluation, findings, and treatment ii. P revious episodes of AUB including work-up and treatments iii. P ap smear history including last Pap smear iv. S exually transmitted infections or upper reproductive tract infection (i. e., pelvic inflammatory disease, tubo-ovarian abscess) Note dates and treatments. v. M enstrual cycle history a. A ge at menarche b. L ast normal menstrual period c. P revious normal menstrual periods (preferably the previous three men-ses): usual cycle duration, flow, interval length, molimina symptoms (breast tenderness, bloating, mood changes, and dysmenorrhea, which suggest ovulatory cycles) d. D ate of onset of change in menses: rapid or gradual change e. A mount of flow: number of pads or tampons used and degree of saturation. Numerous studies to clarify amounts of blood lost have not been successful or practical, and evaluation ultimately depends on the woman's perception of her blood loss (Hallberg et al., 1996). f. P resence of intermenstrual bleeding, premenstrual or postmenstrual bleed-ing, and postcoital bleeding vi. C ontraception history: methods, complica-tions, and adverse outcomes vii. F uture fertility concerns viii. S exual history: number of lifetime sexual partners, and sexual practices c. M edical history: medical illnesses (see T able 18-2); general medical health; complete history of any and all medical problems including evaluation and treatments, ongoing and previous145 Database

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woman complaining of AUB. The following is appro-priate for both AUB of structural and nonstructural etiologies. 1. V ital signs (VS): orthostatic VS, temperature, body mass index 2. Ge neral: body habitus, posture, stature, motor activity, gait, mood, affect, dress, grooming, and personal hygiene 3. H air: texture, hirsutism, pattern of loss if present (axillary, pubic, and scalp hair) 4. E yes and ears: stare, lid lag, exophthalmos, and visual field abnormalities 5. N eck: thyroid nodules or enlargement and lymph nodes 6. S kin: pallor, jaundice, petechiae, ecchymosis, hematomas, palmar erythema, spider hemangiomata, rough or velvety, striae, acanthosis nigricans, acne, color of nail beds 7. E xtremities: edema, perfusion, and wasting 8. C ardiovascular: tachycardia and murmurs 9. L ungs: hypoxia and accessory muscle use 10. A bdomen: striae, ascites, hepatomegaly, spleno-megaly, tenderness, inguinal nodes, uterine height if palpable 11. Ge nital/anal a. E xternal genitalia: pubic hair distribution and developmental stage, clitoromegaly, lesions, edema, cysts, bruising, trauma, urethral prolapse, and atrophy b. V agina: traumatic lesions, bruising, erythema, type of discharge, foreign bodies, prolapse, and atrophy c. C ervix: polyps, eversion, ectopy, lesions, inflam-mation, erythema, mucopurulent discharge, cer-vical motion tenderness, atrophy d. U terus: enlargement, contour, mobility, shape, consistency, tenderness, and masses e. Adnex ae: masses and tenderness f. A nus/rectum: masses and bleeding C. Assessment 1. D etermine the appropriate diagnosis. a. Es tablish if acute or chronic. b. A ssess for conditions that may underlie AUB— PALM (structural) or COEIN (nonstructural) etiologies (see T able 18-2). c. R ule out complications of pregnancy in repro-ductive-age women. d. R ule out malignancies as indicated. 2. A ssess severity of AUB and associated conditions. d. M edication history: medications, vitamins, and supplements (see T able 18-2) e. T rauma: sexual assault or sexual abuse f. E xposure history: radiation (e. g., breast cancer, thyroid cancer, pelvic malignancies and associ-ated treatments) 2. F amily history a. G ynecological problems: Family history of excessive menstrual blood loss; uterine, breast, and ovarian malignancies, endometriosis, leio-myomata, and diethylstilbestrol exposure b. M edical diseases: endocrine dysfunction, blood clotting disorders 3. O ccupational hazards: e. g., pelvic trauma (motor vehicle accident) or straddle injuries 4. P ersonal and social history a. E ducation, occupation, social and family sup-port systems, situational life stress, social and personal anxiety level, and cultural influences b. H abits: tobacco c. N utrition: dietary history (weight loss or gain) d. I mpact of AVB/AUB on lifestyle (sexual prac-tices, deterrence of exercise, work time loss) 5. R eview of systems a. C onstitutional signs: fatigue, weight gain or loss, weakness, malaise, hot or cold sensitivity, appetite change, headaches, obesity, and edema. Suspect hemodynamic instability when patient reports shortness of breath, dizziness, and/or loss of consciousness b. S kin, hair, and nails: hair loss or unwanted hair growth, petechiae, bruising, jaundice, acne, acan-thosis nigricans, and sweating c. C ardiac: palpitations d. A bdomen: nausea and bloating e. Ge nitourinary: pelvic pain, dyspareunia, dysmen-orrhea, hot flashes, night sweats, vaginal dryness, vaginal discharge. Precipitating factors associated with abnormal bleeding (i. e., coitus, trauma, douch-ing, diaphragm use, and the presence of a pessary) f. H ematologic: suspect bleeding disorder (par-ticularly VWD) when the patient reports heavy menstrual bleeding since menarche; one of the following conditions: excessive blood loss with dental work, postpartum hemorrhage, or surgery-related bleeding; or two or more of the following conditions: epistaxis one to two times per month, frequent gum bleeding, or family history of bleeding symptoms (ACOG, 2013b) B. Objective (physical examination) A complete physical examination and assessment of the following systems is essential in the evaluation of a 146 CHAPTER 18 | Abnormal Uterine Bleeding

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test, warrant urgent referral to gynecology. Clinical evaluation and management of such patients are beyond the scope of this discussion. b. Ac ute heavy bleeding in the hemodynamically stable womani. H ormonal management (combined oral contraceptives and progestins) is in most cases sufficient (ACOG, 2013a). For non-pregnant women of reproductive age, the goal of initial therapy is to stabilize the endometrial lining, prevent recurrence, and establish regular, orderly, and synchronous bleeding patterns. Hormonal therapies are equally effective in most cases for the man-agement of acute heavy menstrual bleeding. The following regimens have been studied and found to be effective (Munro, Mainor, Basu, Brisinger, & Barreda, 2006):a. 35 e thinyl estradiol/1 mg norethin-drone combined oral contraceptive (COC) taken by mouth daily three times a day for 7 days followed by 35  ethinyl estradiol/1 mg norethin-drone daily for the next 3 weeks. b. M edroxyprogesterone acetate (MPA) 20 mg taken by mouth 3 times daily for 7 days followed by MPA 20 mg daily for 3 weeks. Compliance was higher in MPA than COC group. All of the MPA group and 95% of COC group avoid-ed emergency surgical procedures. Eighty-eight percent of the COC group and 76% of MPA group achieved cessation of bleeding. The median time to bleeding cessation was 3 days for both groups. Compliance was higher in the MPA than in the COC group. (Munro et al., 2006). c. A thir d alternative treatment can also be considered: MPA 20 mg taken by mouth 3 times daily for 3 days plus depo medroxyprogesterone acetate (DMPA) 150 mg intramuscular, once. All patients stopped bleeding within 5  days, with a mean time to bleeding cessation of 2. 6 days, with infrequent side effects and high patient satisfaction (Ammerman & Nelson, 2013). If desired, the patient may continue with COC to prevent anovulatory bleeding; otherwise the women will experience regular COC withdrawal. 3. A ssess significance of AUB to the patient and to family and significant others. 4. E valuate the ability of the patient to adhere to a treatment plan and follow-up. D. Goals of clinical management 1. C hoose a cost-effective approach for screening and evaluating AVB/AUB. 2. D evelop a treatment plan that addresses AUB and associated conditions and returns the patient to stability and optimal health in a safe and effective manner. 3. W ork with patient to ensure that the plan enables adherence to treatment and follow-up and that is designed to reduce long-term complications AUB such as anemia and endometrial hyperplasia. E. Plan 1. Di agnostic tests As a general rule, the patient's age, reproductive status, and data from the history and physical examination guide decision making regarding the appropriate diag-nostic tests. Diagnostic testing is generally organized into three categories: (1) diagnostic tools, (2) initial testing, and (3) secondary or specialty-based testing. a. Di agnostic tools. i. F or patients presenting with a history of irregular cycles, menstrual calendars can be very helpful to establish bleeding pat-terns. Several online sites are available but may include product advertisements and potentially biased information (e. g., www. My Monthly Cycles. com). Number of pads or tampons and degree of saturation are of limited use in evaluation of blood loss (Hallberg et al., 1996). b. I nitial testing (T able 18-3a). c. S econdary and specialty-based testing (T able 18-3b). These tests are often done by or in consultation with gynecology and women's health specialists. 2. T reatment and management Therapeutic management of AUB depends on the acuity, chronicity, and etiology of the disorder along with the goals of the woman, including her desire for pregnancy and the long-term consequences of any underlying medical conditions. a. Ac ute hemorrhagic bleeding Patients with acute hemorrhagic bleeding who are hemodynamically unstable (signs of hypovo-lemia, including orthostatic changes on physical examination) or who have a positive pregnancy 147 Database

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Table 18-3a Essential Initial T esting in the Investigation of Abnormal Uterine Bleeding test d efinition Clinical Implications Comments Urine pregnancy test (urine h CG)Measures the beta subunit of human chorionic gonadotropin hormone (B-h CG). Urine h CG is a qualitative measurement of B-h CG and gives negative or positive results. A positive urine pregnancy test (qualitative) warrants ordering a pelvic sonogram. If intrauterine sac is not visible, a quantitative serum B-h CG should be ordered and guide referral to an obstetrics specialty clinic (Fritz & Speroff, 2011; Levine, 2006)Urine pregnancy test should be ordered in all sexually active women in their reproductive years, even those who have had a tubal ligation (ACOG, 2013a) Complete blood count (CBC) with platelets To assess the presence of significant anemia and bleeding disorders Excessive vaginal bleeding can lead to iron deficiency anemia. CBC and platelet count are some of the initial tests in the investigation of von Willebrand disease. Because the prevalence of blood dyscrasias (particularly von Willebrand diseases) in adolescents can be quite high (5-20%), and may present with heavy menstrual bleeding at menarche, routine screening for coagulation disorders is appropriate (ACOG, 2013b). Highly sensitive thyroid-stimulating hormone (TSH)Measurement of thyroid-stimulating hormone: an anterior pituitary hormone that stimulates growth and function of thyroid cells An elevated TSH is diagnostic of primary hypothyroidism; a low TSH indicates hyperthyroidism (both can be implicated in AUB)Thyroid disease is common in women. See Chapter 69 for more information on diagnostic testing and treatment. Pap smear To screen for cervical cancer Early cervical cancer is frequently asymptomatic. Late cervical cancer may manifest as irregular, heavy, or postcoital bleeding (Monk & Tewari, 2007). Endocervical and ectocervical sampling required for accuracy. See Chapter 20 for more discussion. Testing for Neisseria gonorrhoeae (GC) and Chlamydia trachomatis (CT)Gold standard method to test for GC and CT is nucleic acid amplification test (NAAT)Cervicitis, caused by GC or CT, can cause postcoital or intermenstrual bleeding As indicated for sexually active women. It can be collected in the endocervix or in the vagina. First-catch urine (no clean catch) can also be submitted to NAAT testing. Wet mount of vaginal secretions with normal saline and potassium hydroxide Evaluate for vaginal infections: trichomoniasis, bacterial vaginosis, and vulvovaginal candidiasis Severe trichomoniasis, vulvovaginal candida, bacterial vaginosis, and may present with postcoital bleeding Useful only if the woman is not bleeding heavily and vaginitis is suspected148 CHAPTER 18 | Abnormal Uterine Bleeding

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Transvaginal ultrasonography of the pelvis (TVS)Ultrasound imaging (most important, transvaginal) plays a pivotal role in the evaluation of AUBa. Indicated to rule out anatomical lesions (endometrial polyps, leiomyomas, or adenomyosis), women with regular cycles but heavy menstrual bleeding or long duration or intermenstrual bleeding (Dueholm, 2006; V alentin, 2014), and when medical management has failed (Fritz & Speroff, 2011). b. T o measure the thickness of the endometrial lining in the postmenopausal woman. If the lining is 4 mm or less, endometrial cancer is very unlikely (Giannella et al., 2014). c. In the evaluation of AUB in pregnancy. d. In the evaluation of adnexal and ovarian masses. Leiomyomas are very common beginning in the third decade of life, and heavy menstrual bleeding is the most common symptom of leiomyoma (most commonly of submucosal origin), thus altering the endometrial lining. However, most leiomyomas are not the major cause of abnormal uterine bleeding, and the evaluation of abnormal uterine bleeding should not necessarily cease with this finding. In the case of asymptomatic leiomyomas, treatment is not mandatory (Bignardi, Van den Bosch, & Condous, 2009; Fritz & Speroff, 2011). For women on cyclic hormone therapy, do TVS after the progestin withdrawal bleed (Bignardi et al., 2009). Endometrial biopsy (EMB)Office sampling of the endometrium with low-pressure cannula (e. g., Pipelle), evaluates for the presence of endometrial hyperplasia and cancer All women > 35 years of age with suspected anovulatory bleeding should be evaluated for endometrial hyperplasia and cancer (after excluding pregnancy). Endometrial cancer is more common in older women. However abnormal endometrial histology in premenopausal woman with irregular bleeding is relatively high—14%; or at any age if the duration of unopposed estrogen is significant (Fritz & Speroff, 2011). EMB is indicated in obese women who have prolonged bleeding. EMB is also indicated in postmenopausal women who are not on hormone therapy or in those who have been on hormone therapy for 6 months or more with unpredicted and unscheduled bleeding episodes (Fritz & Speroff, 2011)Incidence of endometrial carcinoma in women ages 40-54 years is 17. 8%, increasing to 34. 2% (the highest incidence) at ages 55-64. Obesity, high blood pressure, and diabetes mellitus may increase the risk of endometrial cancer (http://seer. cancer. gov/statfacts/). 149 Database

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Table 18-3b Second-Line T esting in the Investigation of AUB, Including Tests Where Consultation or Referral Is Suggested test d efinition Clinical Implications Comments Coagulation panel: prothrombin time, partial thromboplastin time, bleeding time Second-line testing when coagulation disorder is suspected Abnormal coagulation panel tests indicate coagulopathies Abnormalities warrant a referral to hematology (ACOG, 2013b) Ristocetin cofactor assay Measures the ability of a patient's plasma to agglutinate in the presence of the antibiotic Ristocetin. Related to the concentration and functional activity of the von Willebrand factor Evaluation for von Willebrand disease is appropriate in adolescents, women with a worrisome family history, and in the case of unexplained menorrhagia. These tests should be ordered and interpreted in conjunction with hematology (ACOG, 2013b). Magnetic resonance imaging (MRI)MRI is a noninvasive imaging technology Should be reserved for those women in whom adenomyosis diagnosis by TVS is inconclusive (Dueholm, 2006). MRI can help evaluate masses, adenomyosis, and the presence of endometrial polyps MRI has a greater cost than TVS. Consult with physician. Saline infusion sonography (sonohysterography)Visualizes the contours of the uterine cavity Indicated when polyps are not clearly identified with TVSSafe and highly sensitive. Specific imaging used for the diagnosis of endometrial polyps (Radwan, Radwan, Kozarzewski, Polac, & Wilczyński, 2014). Hysteroscopy A small lighted scope is inserted via cervix into the uterus to visualize the endometrial cavity. Also allows for instrumentation as described in next column. Usually performed by gynecologist. Direct visualization of the endometrium allows for: Assessment of intrauterine adhesions Assessment and removal of submucosal fibroids or endometrial polyps Removal of embedded intrauterine devices (IUDs) Assessment and biopsy of any lesions for pathologic evaluation (Farquhar, Ekeroma, Furness, & Arroll, 2003; Bignardi et al., 2009)This instrumentation can be performed in the office setting by MD specialist to remove small endometrial lesions. Biopsy   Indicated for suspicious vulvar, vaginal, or cervical lesion.   Dilatation and curettage (D&C)  Indicated for severe acute bleeding events where hypovolemia is present or where suspicion of malignancy is high. It is valuable for the removal of endometrial polyps and for histologic diagnosis when endometrial sampling has been unsuccessful or inadequate. This instrumentation can be performed in the office setting by gynecology specialist, often in conjunction with hysteroscopy. D&C can also be a curative treatment for AUB. 150 CHAPTER 18 | Abnormal Uterine Bleeding

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High-dose estrogen therapy and COC are both contraindicated in any woman at risk of or with a personal or family his-tory of thromboembolic events. c. C hronic bleeding While the acute bleeding is being controlled, the clinician should initiate a diagnostic investigation to determine the underlying etiology. T able 18-3a will promptly assist the clinician in evaluation and long-term management of AUB. If pregnancy is desired, the clinician should promptly consult or refer the woman to an infertility specialist as AUB etiologies and their management may prevent or complicate pregnancy. Otherwise, some of the PALM etiologies (structural: adenomyosis and leiomyomas) and intractable heavy bleeding may ultimately be treated with surgery; however, phar-macologic management can be attempted as the initial treatment and, if successful, as a long-term treatment. Management of chronic bleeding is addressed in three sections:i. C ommon long-term pharmacology thera-pies for the management of heavy menstrual bleeding (addressing medical therapies for AUB in patients diagnosed with adenomyo-sis, leiomyomas, coagulation disorders, and idiopathic endometrial conditions): after includes progestin IUS, combined hormonal contraceptives, depo-medroxyprogesterone acetate, nonsteroidal anti-inflammatory drugs (NSAIDs), and gonadotropin-releasing hormone agonists. a. L evonorgestrel-releasing IUD (Mirena®). LNG20-IUS has been observed to reduce heavy menstrual bleeding by 75-95% after 3 to 12 months of use (Doherty et al., 2014; Lethaby, Irvine, & Cameron, 2003). LNG20-IUS is very cost effective compared to hys-terectomies for the management of heavy menstrual blood loss (Edlund, 2011; Ganz et al., 2013). In women with a maximum 12-week-size uterus without cavity distortion, LNG-IUS is a safe and effective treatment option for heavy menstrual bleeding charac-teristic of leiomyomas (Doherty et al., 2014). This IUD has been shown to work well in larger uteruses with cav-ity distortion; however, placement by an experienced clinician under sono-gram guidance is advised. Limited data suggest that the LNG-IUS is equally effective in women with adenomyosis (Bitzer, Heikinheimo, Fraser, Calaf-Alsina, & Fraser, 2015). b. C ombined oral contraceptives (COC): COC may reduce heavy menstrual flow by promoting the development of an atrophic endometrium and can increase levels of factor VIII and von Willebrand factor, combating potential underlying coagulopathies (ACOG, 2013c). Oral contraceptive pills will not improve symptoms related to fibroid size. However, they are inex-pensive and may be used as first-line therapy in patients with fibroids and heavy menstrual bleeding (Doherty et al., 2014). Daily cyclic use (withdrawal every 28 days), sequential withdrawal (every 90 days), or continuous use may be considered as treatment strategies and is particularly helpful for patients with anemia. Sequential withdrawal and continuous use require careful counseling to improve adherence. c. P rogestin-only treatment of leiomyo-mas with depo-medroxyprogesterone acetate (DMPA) may improve bleeding parameters and increase hemoglobin with a modest reduction in leiomyoma volume (Doherty et al., 2014). d. N SAIDS have been observed to reduce heavy menstrual flow in several stud-ies, possibly by reducing prostaglandin levels in the endometrium by enzyme (cyclo-oxygenase) inhibition (Lethaby, Augood, Duckitt, & Farquhar, 2007; Fritz & Speroff, 2011). Efficacy of NSAIDs in women with leiomyomas with heavy bleeding is limited (Bitzer et al., 2015). NSAIDS do not appear to reduce blood loss in women with myomas but can help to decrease painful menses. Counseling regarding the potential for gastrointestinal side effects should be provided. Options include:i. I buprofen: 600 mg orally three times a day for the first 3 days of menses, or longer as needed. ii. N aproxen sodium: 500 mg at onset and followed 3 to 5 hours later. Then 250 to 500 mg twice a day 151 Database

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for the first 3 days. May continue throughout the menstrual cycle. iii. M efenamic acid: 500 mg by mouth 3 times daily for the first 3 days of menses or for the dura-tion of the cycle, as needed. e. Gon adotropin-releasing hormone ago-nists, such as depo leuprolide (Lupron®), 3. 75 mg intramuscularly monthly or 11. 25 mg every 90 days, or nafarelin, 0. 2-0. 4 mg intranasally twice a day, can be useful for short-term manage-ment of heavy menstrual bleeding, par-ticularly in the setting of leiomyoma or adenomyosis, as they reduce fibroid and uterine volume (Doherty et al., 2014). However, this therapy is limited to short-term use because of its expense and unpleasant side effects (menopausal vasomotor symptoms and bone loss), which resolve after discontinuation of therapy. Therefore, these medications are most often used as a preoperative adjunctive therapy for women intending conservative (myomectomy or endo-metrial ablation) or definitive (hyster-ectomy) surgery for abnormal bleeding and should be done in close collabora-tion with a gynecologist. For perimenopausal women, the methods listed previously are all appropriate. ii. The rapeutic management of ovulatory dys-function and the management of simple endometrial hyperplasia without atypia. The goals for management of ovulatory dysfunction are to eliminate acute bleeding and its complications, to prevent future epi-sodes, and to reduce the patient's lifetime risk of complications arising from long-term anovulation (endometrial hyperplasia and cancer). T reatment should induce or rees-tablish regular patterns of menstrual bleed-ing (ACOG, 2013c). Adherence issues may complicate treatment, because heavy bleed-ing may continue for several cycles after one of the treatment strategies for acute presen-tation has been initiated. Counseling the patient regarding treatment approaches and long-term goals improves adherence. T reatment options include hormonal medications with and without contracep-tive effects. a. C ombined estrogen and progestin contraceptive options include:i. L ow-dose, monophasic COC, the contraceptive vaginal ring, or transdermal contraceptive patch: this treatment is contraindicated for women over 35 who smoke, women with evidence of vascular disease, or those with a personal or family history of thromboem-bolic events (ACOG, 2013c). b. P rogestin-only medications include: i. L evonorgestrel 20 IUS. T reat-ment of endometrial hyperplasia is generally more effective than with systemic progesterone treat-ments, and should be offered as a first line treatment (Abu Hashim, Ghayaty, & El Rakhawy, 2015). Management should be done in consultation with MD, and close follow-up is advisable (Bitzer et al., 2015). ii. S ubdermal implant releasing etonogestrel 68 mg over a 3-year period (Nexplanon®). Indicated for women with ovulatory dys-function. Not studied for the management of endometrial hyperplasia. iii. D epo-MPA (Depo-Provera®), 150 mg intramuscularly every 12  weeks. Indicated for women with ovula-tory dysfunction. c. P rogestins without contraceptive activity i. M edroxyprogesterone acetate (MPA), 10 mg by mouth daily for the first 10-14 days of each month for three to six cycles, with careful follow-up. Alternatively, continuing monthly cyclic MPA induces regular withdrawal and reduces the likelihood for long-term complications of anovu-lation. However, it does not provide pregnancy protection (Fritz & Speroff, 2011). ii. N orethindrone acetate, 5-10 mg orally once to three times a day for the first 10-14 days of each month. iii. M icronized progesterone, 200 mg orally twice a day for the first 152 CHAPTER 18 | Abnormal Uterine Bleeding

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10-14 days of each month (Hickey, Higham, & Fraser, 2009). iii. S urgical options managed by the gynecolo-gist. Complex endometrial hyperplasia, hyperplasia with atypia, or cancer is man-aged by the gynecologist and is beyond the scope of this chapter. a. P olyps: best managed with removal, most likely with hysteroscopy. b. L eiomyoma: myomectomy; uterine fibroid: embolization or hysterectomy. c. D&C i s most commonly considered in the acute care setting. d. C onservative management with endo-metrial ablation can be done with hys-teroscopic guidance or with newer “blind” techniques. In all cases the goal is to prevent further menorrhagia by eliminating the endometrium. Not indicated for women who desire further childbearing, who are menopausal, or who are at high risk of endometrial can-cer. Because endometrial ablation can be done in the office or an outpatient surgical unit, it is less costly than hys-terectomy, involves less risk of surgical complications, and requires less recov-ery time. It is appropriate for women with conditions that make them poor candidates for major surgery (Fritz & Speroff, 2011; Lethaby, Hickey, Garry, & Penninx, 2009). e. H ysterectomy remains the defini-tive treatment for menorrhagia and all abnormal bleeding patterns. It is appropriate for cases where treatment has failed or has been too noxious to tolerate, and where childbearing is no longer desired. iv. P ostmenopausal bleeding Both endometrial biopsy and D&C provide information regarding the state of the endometrium, including evaluation for the presence of endometrial carcinoma. The pathologic examination of the sample identifies the presence of hyperplasia, atypia, polyps, and other endometrial lesions. The presence of atypia is of particular importance in determining an appropriate treatment plan (Fritz & Speroff, 2011). An initial transvaginal ultrasound (TVUS) finding of an endometrial lining less than or equal to 4 mm may reduce the need for endometrial sampling in some cases, but EMB together with TVUS establishes the most precise diagnosis (Farquhar et al., 2003). If atypia is not present, cyclic or daily progestin therapy with MPA or norethindrone acetate every month for 3  months may be considered, followed by resampling. Close follow-up is strongly recommended and evaluation should be accelerated if abnormal bleed-ing patterns recur. The presence of atypia mandates specialty consultation for further evaluation, and hysterectomy is gener-ally recommended. For postmenopausal women on hormone therapy, EMB findings can guide dose adjustments once endome-trial pathology has been excluded. F. Additional considerations and follow-up 1. A ll patients should be evaluated for anemia and treated as needed. Specialty referral should be instituted for: a. P atients with suspected coagulation disorders b. W hen medical treatment fails or AUB is persis-tent or recurrent 2. P atients with acute bleeding require follow-up soon after initiation of therapy to evaluate for further bleeding or to evaluate for success of treatment. a. The s chedule of follow-up care varies depending on the etiology (PALM or COEIN) and treat-ment of AUB and associated conditions. b. A ssessment at regular intervals should be established as warranted (i. e., 3-6 months, or as needed). c. F or leiomyomas, evaluation for symptoms and growth may be done every year, although TVUS may not be required if symptoms remain unchanged. G. Client education 1. I nformation: ACOG provides many educational pamphlets available online: http://www. acog. org /Resources-And-Publications/Patient-Education- FAQs-List 2. C ounseling: detailed explanation of the etiologies of AUB, essential diagnostic tests, and treatment plans is imperative for patient understanding and adherence. Patient involvement in the decision-making process, inclusion of family members when desired, and consideration of cultural issues are essential for promoting adherence. The clinician should: a. Di scuss medication side effects, risks versus benefits, and expected outcomes (e. g., with-drawal bleeding after progestin therapy). 153 Database

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Doherty, L., Mutlu, L., Sinclair, D., & T aylor, H. (2014). Uterine fibroids: clinical manifestations and contemporary management. Reproductive Sciences, 21(9), 1067-1092. Dueholm, M. (2006). T ransvaginal ultrasound for diagnosis of adenomyo-sis: A review. Best Practice Research Clinical Obstetrics & Gynecology, 20(4), 569-582. Edlund, M. (2011). Nonhormonal treatments for heavy menstrual bleeding. Journal of Women's Health, 20, 1645-1653. Farquhar, C., Ekeroma, A., Furness, S., & Arroll, B. (2003). A systematic review of transvaginal ultrasonography, sonohysterography and hysteroscopy for the investigation of abnormal uterine bleeding in premenopausal women. Acta Obstetricia et Gynecologica Scandinavica, 82, 493-504. Fritz, M. A., & Speroff, L. (2011). Abnormal uterine bleeding. In Clinical gynecologic endocrinology and infertility (8th ed., pp. 591-620). Philadelphia, PA: Wolters Kluwer/Lippincott Williams & Wilkins. Ganz, M. L., Shah, D., Gidwani, R., Filonenko, A., Su, W., Pocoski, J., et al. (2013). The cost-effectiveness of the levonorgestrel-releasing intrauter-ine system for the treatment of idiopathic heavy menstrual bleeding in the United States. Value in Health, 16(2), 325-333. Giannella, L., Mfuta, K., Setti, T., Cerami, L. B., Bergamini, E., et al. (2014). A risk-scoring model for the prediction of endometrial cancer among symptomatic postmenopausal women with endometrial thickness > 4 mm. Bio Med Research International. dx. doi. org/10. 1155/2014/130569 Hallberg, L., Högdahl, A. M., Nilsson, L., & Rybo, G. (1966). Menstrual blood loss—a population study. Variation at different ages and attempts to define normality. Acta Obstetricia et Gynecologica Scandinavica, 45(3), 320-351. Hickey, M., Higham, J. M., & Fraser, I. (2009). Progestogens versus oestro-gens and progestogens for irregular uterine bleeding associated with anovulation (review). Cochrane Database System Review, 4, CD001895. Horn, L., Meinel, A., Handzel, R., & Einenkel, J. (2007). Histopathology of endometrial hyperplasia and endometrial carcinoma: An update. Annals of Diagnostic Pathology, 11(4), 297-311. Jain, A., & Santoro, N. (2005). Endocrine mechanisms and management of abnormal bleeding due to perimenopausal changes. Clinical Obstetrics and Gynecology, 48(2), 295-311. Jemal A., Siegel, R., Ward, E., Murray, T., Xu, J., & Thun, M. J. (2007). Cancer statistics, 2007. CA: A Cancer Journal for Clinicians, 57, 43-66. Khan, A. T., Shehmar, M., & Gupta, J. K. (2014). Uterine fibroids: Current perspectives. International Journal of Women's Health, 6, 95-114. Lasmar, R. B., Dias, R., Barrozo, P. R., Oliveira, M. A., Coutinho, E. S., & da Rosa, D. B. (2008). Prevalence of hysteroscopic findings and histologic diagnoses in patients with abnormal uterine bleeding. Fertility & Sterility, 89, 1803-1807. Lethaby, A., Augood, C., Duckitt, K., & Farquhar, C. (2007). Nonsteroidal anti-inflammatory drugs for heavy menstrual bleeding (review). Cochrane Database of Systematic Reviews, 4, CD000400. Lethaby, A., Hickey, M., Garry, R., & Penninx, J. (2009). Endometrial resection/ablation techniques for heavy menstrual bleeding. Cochrane Database Systematic Reviews, CD001501. Lethaby, A., Irvine, G., & Cameron, I. (2003). Cyclical progestogens for heavy menstrual bleeding (review). Cochrane Database of Systematic Reviews, CD001016. Levine, S. (2006). Dysfunctional uterine bleeding in adolescents. Journal of Pediatric Adolescent Gynecology, 19, 49-51. Mohan, S., Page, L. M., & Higham, J. M. (2007). Diagnosis of abnormal uterine bleeding. Best Practice & Research in Clinical Obstetrics and Gynecology, 21(6), 891-903. b. Di scuss all treatment options (medical versus surgical) and initiate referrals to specialists or surgeons. c. C onsider associated issues, such as weight management, interference with exercise, stress management, and management of chronic dis-orders. Referral for psychologic support may be necessary. 3. S elf-management resources and tools a. The mos t important tool for the patient is the menstrual calendar. Selected resources include:i. A merican Society for Reproductive Medi-cine (http://www. asrm. org/) ii. H arvard Women's Health Watch is a monthly publication providing information regard-ing issues in women's health written by the researchers and clinicians at Harvard Medical School (www. harvardwomenshealthwatch. org/) referen Ces Abu Hashim, H., Ghayaty, E., & El Rakhawy, M. (2015). Levonorgestrel-releasing intrauterine system vs oral progestins for non-atypical endometrial hyperplasia: A systematic review and metaanalysis of randomized trials. American Journal of Obstetrics and Gynecology. Epub ahead of print. American College of Obstetricians and Gynecologists (ACOG). (2013a). Committee opinion no. 557: Management of acute abnormal uterine bleeding in nonpregnant reproductive-aged women. Obstetrics and Gynecology, 121(4), 891-896. American College of Obstetricians and Gynecologists (ACOG). (2013b). Committee Opinion No. 580: von Willebrand disease in women. Obstetrics and Gynecology, 122(6), 1368-1373. American College of Obstetricians and Gynecologists (ACOG). (2013c). Practice bulletin no. 136: management of abnormal uterine bleed-ing associated with ovulatory dysfunction. Obstetrics and Gynecology, 122(1), 176-185. Ammerman, S. R., & Nelson, A L. (2013). A new progestogen-only medical therapy for outpatient management of acute, abnormal uterine bleeding: A pilot study. American Journal of Obstetrics and Gynecology, 208(6), 499-500. Benaglia, L., Cardellicchio, L., Filippi, F., Paffoni, A., Vercellini, P., Somigliana, E., et al. (2014). The rapid growth of fibroids during early pregnancy. PLo S ONE, 9(1), e85933. Bignardi, T., Van den Bosch, T., & Condous, G. (2009). Abnormal uterine bleeding and post-menopausal bleeding in the acute gynaecology unit. Best Practice and Research Clinical Obstetrics and Gynecology, 23, 595-607. Bitzer, J., Heikinheimo, O., Nelson, A. L., Calaf-Alsina, J., & Fraser I. S. (2015). Medical management of heavy menstrual bleeding: A com-prehensive review of the literature. Obstetrical & Gynecological Survey, 70(2), 115-130. Day Baird, D., Dunson, D. B., Hill, M. C., Cousins, D., & Schectman, J. M. (2003). High cumulative incidence of uterine leiomyoma in black and white women: Ultrasound evidence. American Journal of Obstetrics & Gynecology, 188(1), 100-107. 154 CHAPTER 18 | Abnormal Uterine Bleeding

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London: RCOG Press, Retrieved from http://www. ncbi. nlm. nih . gov/books/NBK56536/. Ng, C., Motto, D. G., & Di Paola, J. (2015). Diagnostic approach to von Willebrand disease. Blood, 125(13), 2029-2037. Nicholson, W. K., Ellison, S. A., Grason, H., & Powe, N. R. (2001). Patterns of ambulatory care use for gynecologic conditions: A national study. American Journal of Obstetrics and Gynecology, 184(4), 523-530. Radwan, P., Radwan, M., Kozarzewski, M., Polac, I., & Wilczyński, J. (2014). Evaluation of sonohysterography in detecting endometrial polyps—241 cases followed with office hysteroscopies combined with histopathological examination. Wideochirurgia i Inne Techniki Maloinwazyjne, 9(3), 344-350. Rosenberg, M. J., Waugh, M. S., & Stevens, C. M. (1996). Smoking and cycle control among oral contraceptive users. American Journal of Obstetrics & Gynecology, 174(2), 628-632. Valentin, L. (2014). Imaging techniques in the management of abnormal vag-inal bleeding in non-pregnant women before and after menopause. Best practice & research. Clinical Obstetrics & Gynecology, 28(5), 637-654. Monk, B. J., & T ewari, K. S. (2007). Invasive cervical cancer. In P. J. Di Saia & W. T. Creasman (Eds. ), Clinical gynecologic oncology (7th ed., pp. 55-124). Philadelphia, PA: Mosby. Munro, M. G., Critchley, H. O., & Fraser, I. S. (2012). The FIGO systems for nomenclature and classification of causes of abnormal uterine bleeding in the reproductive years: Who needs them? American Journal of Obstetrics and Gynecology, 207(4), 259-265. Munro, M. G., Critchley, H. O., Broder, M. S., Fraser, I. S., & FIGO Working Group on Menstrual Disorders. (2011). FIGO classification system (PALM-COEIN) for causes of abnormal uterine bleeding in nongravid women of reproductive age. International Journal of Gynecology and Obstetrics, 113(1), 3-13. Munro, M. G., Mainor, N., Basu, R., Brisinger, M., & Barreda, L. (2006). Oral medroxyprogesterone acetate and combination oral contraceptives for acute uterine bleeding: A randomized controlled trial. Obstetrics & Gynecology, 108, 924-929. National Collaborating Centre for Women's and Children's Health. Heavy menstrual bleeding (NICE Clinical Guidelines, No. 44). 155 References

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midcycle surges in luteinizing hormone secretion, failure to ovulate, and low serum estradiol concentra-tions. Low estrogen levels place the woman at risk for osteopenia and osteoporosis. Factors contributing to FHA include nutritional deficiencies, such as marked weight loss, malnutrition, eating disorders (anorexia and bulimia), excessive exercise, and severe physical or emotional stress. In many women with FHA, no obvi-ous precipitating factor is evident. Untreated primary hypothyroidism can lead to hypothalamic amenorrhea (primary or secondary) by decreasing the hypothalamic content of dopa-mine and increasing prolactin levels with or with-out resulting galactorrhea (Khawaja et al., 2006). Dopaminergic drugs (e. g., phenothiazines, antipsy-chotics, and antiemetic-gastrointestinal agents) may also be responsible for hypothalamic amenorrhea. Menses usually return to normal after discontinuation of medications. Rarely, hypothalamic amenorrhea may be associated with congenital Gn RH deficiency, called Kallmann syndrome, if there is associated anos-mia or hyposmia (Fritz & Speroff, 2011). 2. P revalence and incidence Prevalence of adult-onset hypothalamic amenorrhea is 35%, representing 20% of primary amenorrhea cases (Reindollar, Byrd, & Mc Donough, 1981; Reindollar, Novak, Tho, & Mc Donough, 1986). The “female ath-lete triad” is defined as amenorrhea, disordered eating, and osteoporosis or osteopenia. This syndrome is especially common in amenorrhea associated with ballet dancing. It is also prevalent in high school (Hoch et al., 2009) and college athletes (Beals & Hill, 2006). B. Amenorrhea associated with pituitary dysfunction 1. D efinition and overview Prolactin-secreting tumors are responsible for most cases of amenorrhea attributed to the pituitary gland. Increased prolactin levels lead to anovulation and low ovarian estradiol levels, causing the same problems as I. Intr oduction and general background Amenorrhea is classified as primary or secondary. Primary amenorrhea is defined as the lack of initiation of menses by age  13 with concomitant lack of growth of secondary sexual characteristics, such as breast development. If growth of sec-ondary sexual characteristics is present, this diagnosis may be delayed until age 15, or within 5 years of breast development, if this happens before age 10 (Practice Committee of the American Society for Reproductive Medicine, 2008). Secondary amenor-rhea is defined as menstrual cessation after three previous regu-lar menstrual cycles or irregular menses (oligomenorrhea) or less than nine menstrual cycles per year (Practice Committee of the American Society for Reproductive Medicine, 2008). Distinguishing primary and secondary amenorrhea is important because the former encompasses a more extensive differential diagnosis that includes genetic or anatomic abnor-malities. As the most likely diagnosis is constitutional delay, early categorization may lead to an unnecessary work-up (Fritz & Speroff, 2011). Amenorrhea may result from disturbances at the level of the hypothalamus, pituitary, ovaries, uterus, or outflow tract or may result from chronic illness or other endocrine abnormali-ties. Polycystic ovarian syndrome (PCOS) is one of the most common causes of amenorrhea, with disturbances that involve the hypothalamic-pituitary-ovarian (HPO) axis. Amenorrhea is physiologic during pregnancy, menopause, and in the post-partum period in lactating women. It can also be iatrogenic caused by hormonal contraception, exogenous androgens, or medications blocking dopamine receptors. A. Hypothalamic amenorrhea 1. D efinition and overview Hypothalamic amenorrhea is often used interchange-ably with functional hypothalamic amenorrhea (FHA), the most common cause of amenorrhea in this category. In FHA, there is a decrease in gonadotropin-releasing hormone pulsatile secretion causing absent Pilar Bernal de Pheils Amenorrhe A And Polycyst Ic ov A ry s yndrome© Eliks/Shutterstock; © donatas1205/Shutterstock 156 19Chapt Er

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fragile X  premutations; and idiopathic causes. Radiation therapy and chemotherapy can also cause ovarian failure. c. Gon adal dysgenesis (karyotypic abnormalities as described previously) can present with primary or secondary amenorrhea. 2. P revalence and incidence Premature ovarian insufficiency develops in approxi-mately 1% of women before age 40 (Fritz & Speroff, 2011). Chromosomal abnormalities and gonadal dys-genesis are more common causes of primary amen-orrhea than secondary amenorrhea (Fritz & Speroff, 2011; Reindollar et al., 1981). D. Amenorrhea originating from disorders of the outflow tract or uterus 1. D efinition and overview End-organ abnormalities are rare in secondary amen-orrhea. If present, the etiology is usually caused by Asherman syndrome, manifested clinically by very scant menstrual bleeding or amenorrhea. In almost all cases, there is a history of uterine manipulation, such as a dilatation and curettage, other surgical procedures resulting in uterine scarring, or miscarriage. Congenital anomalies can lead to anatomic altera-tions in the genital tract, causing primary amenorrhea. These abnormalities include congenital developmen-tal anomalies (imperforate hymen, vaginal septum, or cervical atresia) and müllerian agenesis (absence of the uterus and upper vagina). Ovaries are present as are secondary sex characteristics. Androgen insensitivity is another etiology of primary amenorrhea. These patients are phenotypic females with some breast development, minimal axillary and pubic hair, external genitalia, blind vaginal canal, and absent uterus; however, they are genotypic males with testes, XY karyotype, and unre-sponsive androgen receptors but normal to high range of male testosterone levels. 2. P revalence and incidence Prevalence of Asherman syndrome is unknown because it is difficult to define the denominator (Berman, 2008). Müllerian abnormalities and com-plete androgen sensitivity are, with gonadal dysgen-esis described previously, the most common causes of primary amenorrhea; androgen insensitivity is rare (Fritz & Speroff, 2011). E. PCOS 1. D efinition and overview PCOS is one of the most common causes of anovula-tion. It is a syndrome, not a disease, reflecting multiple potential etiologies with variable clinical expression. seen in FHA. Hyperprolactinemia can cause galac-torrhea. Most prolactinomas are small (< 10 mm in diameter), called microadenomas, and maintain nor-mal pituitary function. Macroadenomas are 10 mm or larger and can exert mass effects causing headaches and vision changes. Prolactin-secreting tumors can occur in the premenarchal female and present as pri-mary amenorrhea. Pituitary functional tumors should be suspected when patients have acromegaly caused by exces-sive secretion of growth hormone, Cushing's disease caused by excessive secretion of adrenocorticotropic hormone, or secondary hyperthyroidism caused by a thyroid-stimulating hormone secreting tumor. These tumors are rare but potential causes of amenorrhea. Most of these tumors are associated with headaches and visual changes (bitemporal hemianopsia/blurred vision) (Fritz & Speroff, 2011). Hyperprolactinemia can also be caused by decreased clearance of dopamine in patients with chronic renal or liver impairment. Other causes of pituitary amenorrhea are Sheehan syndrome (severe postpartum hemorrhage causing acute infarction and necrosis of the pituitary gland) and empty sella syndrome. Hyperprolactinemia may be functional (idiopathic), found in about one-third of women (Fritz & Speroff, 2011). 2. P revalence and incidence Prolactin-secreting pituitary tumor (prolactinoma) is responsible for almost 20% of cases of second-ary amenorrhea and is the most common pituitary etiology of amenorrhea (Reindollar et al., 1986). Pituitary disease is less common in primary amen-orrhea, accounting for 5% of cases (Reindollar et al., 1981). C. Amenorrhea originating from disorders of the ovaries 1. D efinition and overview a. P olycystic ovarian syndrome (PCOS) (dis-cussed later as a separate category). b. P rimary ovarian insufficiency (POI), also known as premature ovarian failure, is defined as menopause before the age of 40. The average age of menopause is 51 with a range from 47-55. Ovarian insufficiency is more accepted as this condition may have periods of follicular devel-opment, ovulation, and menstrual bleeding followed by periods of hypoestrogenemia and anovulation. Causes of POI include autoimmune disorders, such as hypothyroidism, diabetes, and adrenal insufficiency; karyotypic abnor-malities (Turner syndrome and mosaicism); 157 Introduction and general background

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ii. Obs tetric and gynecological: recent his-tory of severe postpartum hemorrhage or oophorectomy (should also ask about mis-carriages and postpartum course). Recent history of dilatation and curettage iii. E xposure history: radiation or chemotherapy directed to the pelvic organs iv. M edication history: dopamine adrenergic drugs or hormonal contraceptives (particu-larly progestin-only contraceptives and psy-chiatric medication) (T able 19-1) b. F amily history i. D elayed or absent puberty ii. POI iii. F ragile X syndrome, developmental or intellectual disabilities iv. C ongenital abnormalities (e. g., Turner syn-drome) v. Aut oimmune disorders c. O ccupational and environmental history i. W ork-related exposures: radiation d. P ersonal and social history i. S evere stress, malnutrition, crash dieting, excessive exercise e. R eview of systems i. C onstitutional symptoms: hot flushes or night sweats ii. S kin, hair, and nails: lanugo (anorexia) iii. N ose: anosmia (Kallmann syndrome) iv. E yes: blurred vision if pituitary tumor (may be a late symptom in patients with macroadenomas) v. B reast: galactorrhea (hyperprolactinemia) vi. Ge nitourinary: oligomenorrhea (may precede amenorrhea), vaginal dryness if hypoestro-genic state, cyclical pelvic pain in primary amenorrhea (imperforated hymen, transverse septum, cervical atresia) vii. E ndocrine: hot or cold sensitivity (suspect thyroid disease); fatigue, polydipsia, poly-phagia (pituitary disease) viii. N eurologic: headaches (may be a late symp-tom in patients with macroadenomas and other pituitary lesions) particularly asso-ciated with blurred vision; change in per-sonality, report of marked mood changes (infiltrative pituitary lesions) 2. P COS a. E thnicity Consider congenital adrenal hyperplasia in women of Ashkenazi Jewish descent, Hispanics, Yugoslavs, Native American Inuits, Alaskans, or Italians (ACOG, 2009). Hallmarks of the syndrome are chronic anovulation, insulin resistance, and hyperandrogenism. Women with PCOS are frequently overweight (Vrbikova & Hainer, 2009). Regardless of obesity, insulin resis-tance is present, which poses risks for long-term metabolic sequelae and cardiovascular disease. Up to 30% of patients with PCOS also have metabolic syndrome (American College of Obstetricians and Gynecologists [ACOG], 2009). Depression, anxiety, and obstructive sleep apnea are seen more frequently in women with PCOS, independent of obesity ( Jedel et al., 2010; T asali, Van Cauter, & Ehrmann, 2008; Vrbikova & Hainer, 2009). Endometrial cancer may also be increased in women with PCOS because anovulation, central obesity, and diabetes are all risk factors for this cancer. The 2003 Rotterdam ESHRE/ASRM-Sponsored PCOS Consensus Workshop Group (2004) rede-fined the diagnosis of PCOS as the presentation of two of the following three criteria (ACOG, 2004b): (1) oligo-ovulation or anovulation (irregular cycles), (2) clinical or biochemical markers of hyperan-drogenism, and (3) polycystic ovaries on ultraso-nography and exclusion of other etiologies. The Androgen Society considers hyperandrogenism as essential to this diagnosis (ACOG, 2009). PCOS remains a diagnosis of exclusion and can be diagnosed clinically meeting the criteria just described, including clinical or biochemical markers of hyperandrogenism. Other conditions to be ruled out are hypothyroidism, hyperprolactinemia, ovarian or adrenal tumors, late-onset adrenal hyperplasia, and Cushing syndrome. Women with PCOS are at risk for infertility. If they become pregnant, they are at an increased risk for gestational diabetes and hyperten-sion (Altieri et al., 2010). 2. P revalence and incidence PCOS is frequently undiagnosed in the community. Prevalence varies from a high of 17. 8 ± 2. 8% to a low of 10. 2 ± 2. 2% (March et al., 2010; Rotterdam ESHRE/ASRM-Sponsored PCOS Consensus Workshop Group, 2004). II. d atabase (may include but is not limited to) A. Subjective 1. A menorrhea a. P ast health history i. M edical illnesses (T able 19-1)158 CHAPTER 19 | Amenorrhea and Polycystic Ovary Syndrome

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Table 19-1 Amenorrhea and PCOS: Important Etiologies classification e tiology Hypothalamic amenorrhea Functional hypothalamic amenorrhea (common etiology for primary or secondary amenorrhea) Anorexia Stress Rapid weight loss Excessive exercise Idiopathic Most likely presenting with primary amenorrhea Gonadotropin-releasing hormone deficiency, Kallmann syndrome if associated with anosmia Infiltrative lesions of the hypothalamus Amenorrhea associated with pituitary dysfunction Physiologic: breastfeeding Pathologic (pituitary): Pituitary adenomas: functional prolactin-secreting hormone (most common) Other nonfunctional adenomas Adrenocorticotropic hormone-secreting tumor causing Cushing syndrome Thyroid-stimulating hormone-secreting tumor causing hyperthyroidism Somatotroph adenomas secreting growth hormone and causing acromegaly Other masses (cyst, tuberculosis, sarcoidosis, fat deposits) Renal failure Cirrhosis Sheehan syndrome Empty sella syndrome Drugs Amenorrhea originating from disorders of the ovaries Physiologic: menopause, constitutional delay Pathologic: Polycystic ovary syndrome (caused by internal-external sources)—most likely explanation of secondary amenorrhea Premature ovarian failure (common); supply of oocytes is depleted before age 40; consider autoimmune disorders, karyotype abnormalities Other conditions: Local disturbance of ovarian conditions: History of infection (tuberculosis, mumps) History of radiation therapy or cytotoxic drugs Problems in gonadal development that can present either with primary or secondary amenorrhea Turner syndrome Mosaicism (continues)159 Database

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Table 19-1 Amenorrhea and PCOS: Important Etiologies classification e tiology Amenorrhea originating from disorders of the outflow tract Abnormalities in the first compartment are rare in secondary amenorrhea If present, is caused by destruction of the endometrium, from dilatation and curettage or other surgery or miscarriage resulting in uterine scarring (Asherman syndrome) Congenital anomalies can lead to anatomic alterations in the genital tract mostly causing primary amenorrhea Imperforate hymen, transverse vaginal septum, or cervical atresia Müllerian agenesis (ovaries are present because they are not müllerian structures) Complete androgen insensitivity (testicular feminization) Pharmacologic Medications causing dopamine receptor blockade: Tranquilizers (phenothiazine derivatives) Antipsychotics (risperidone) Antidepressants (desipramine, monoamine oxidase) Antihypertensive (methyldopa, reserpine, verapamil) Narcotics: opiates and heroin Gastrointestinal medications: metoclopramide (Reglan), cimetidine, domperidone Hormonal contraceptives (high-dose progestin) Danazol (androgen-like medication for endometriosis treatment) Polycystic ovary syndrome Unknown etiology. It is a syndrome, not a disease, reflecting multiple potential etiologies with variable clinical expression comprised of anovulation, hyperandrogenism, and insulin resistance(Continued)160 CHAPTER 19 | Amenorrhea and Polycystic Ovary Syndrome

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b. P ast health history i. M edical illnesses: metabolic syndrome may be present concomitantly or be the result of PCOS ii. Obs tetric and gynecological history: men-strual irregularities and infertility or preg-nancy complications (gestational diabetes and pregnancy-induced hypertension), obstructive sleep apnea. iii. M ental illness: depression or anxiety c. F amily history i. PC OS or other endocrinopathies d. P ersonal and social history e. R eview of systems i. C onstitutional signs and symptoms: fatigue ii. S kin and hair: acne, oily skin, acanthosis nigricans (neck, axilla, under breast, or groin), hirsutism, and androgenic alopecia iii. Ge nitourinary: irregular menses or amen-orrhea, cyclical pelvic pain in primary amenorrhea (anatomical defects cause accu-mulation of blood behind the obstruction) iv. N eurologic: depressive symptoms B. Objective 1. P hysical examination findings (T able 19-2). Patient may also have a benign examination. 2. S upporting data from relevant diagnostic tests (T ables 19-3A-19-3C). III. Assessment A. Diagnosis Diagnosis of amenorrhea is determined by its onset (primary or secondary); significant findings from the history, physical examination; and diagnostic tests (see T ables 19-3A-19-3C). Most common etiologies encoun-tered in primary care are as follows: 1. P rimary amenorrhea caused mainly by constitutional delay 2. P rimary or secondary amenorrhea caused by: a. H ypothalamic etiology, most likely functional hypothalamic. b. P ituitary etiology, most likely hyperprolac-tinemia or prolactinoma c. O varian disorders, most likely premature ovarian failure (POF) in secondary amenorrhea or ovar-ian dysgenesis in primary amenorrhea (Turner syndrome and mosaicism). d. Di sorders of the outflow tract, most likely Asherman syndrome in secondary amenorrhea (precipitated by an insult to the endometrium) or müllerian agenesis or complete androgen insensitivity in primary amenorrhea e. P COS 3. Othe r conditions that may explain the patient's amenorrhea or oligomenorrhea and need to be ruled out in the investigation of PCOS are: a. Th yroid disease (most likely primary hypothyroidism) b. H yperprolactinemia c. L ate-onset adrenal hyperplasia Iv. Goals of clinical management Select a treatment plan that helps the patient restore nor-malcy of her menstrual cycle and fertility, if she desires, and reduces risk from hypoestrogenic state or unopposed estro-gen stimulation of the endometrium. v. Plan A. Diagnostic tests T ables 19-3A-19-3C provide descriptions of relevant diagnostic studies. 1. A ll women late for their menses or with oligomenorrhea should have a urine pregnancy test to rule out pregnancy. 2. L aboratory testing: prolactin, TSH, and FSH (T able 19-3A). 3. S ome clinicians perform a progesterone withdrawal test in the initial evaluation of amenorrhea to determine endogenous estrogen status; others do not advocate for this test arguing poor sensitivity and specificity (ACOG, 2004a; Fritz & Speroff, 2011). 4. Di agnostic work-up in the adolescent with primary amenorrhea is based on the presence of breast development; secondary sexual characteristics; and the presence of the uterus and an intact outflow tract, likely determined with an ultrasound. If all are present and FSH is normal, the work-up should focus on the etiology of secondary amenorrhea. If there is no breast development and the FSH level is elevated, the probable diagnosis is gonadal dysgenesis. A karyotype should then be ordered. If the uterus or outflow tract is not present and the FSH values are normal, then the diagnostic test should be directed to diagnose müllerian agenesis or androgen insensitivity syndrome. In the latter, circulating testosterone is in the male range and a karyotype confirms the presence of a Y chromosome. 161 Plan

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5. S econd-line diagnostic tests in the investigation of amenorrhea include tests where consultation and referral are suggested (T able 19-3B). 6. M agnetic resonance imaging (MRI) or computerized tomography scanning (not as sensitive but less expensive) for the evaluation of a pituitary tumor in the setting of hyperprolactinemia, galactorrhea, or headaches and vision field changes. 7. K aryotype, including fragile X testing, in any woman younger than 30 years of age diagnosed with POF (Fritz & Speroff, 2011), or for women presenting with primary amenorrhea with no uterus on ultrasound. Table 19-2 Physical Examination Findings and Likely Etiologies in Amenorrhea and PCOS* organ or system e xamination Findings l ikely e tiologies Vitals Increased blood pressure High blood pressure may be present in pituitary diseases (e. g., Cushing disease); karyotype abnormalities (e. g., Turner syndrome); or associated with PCOS Anthropometric measurements Body mass index< 18. 5 kg/m 2—underweight or25. 0-29. 9 kg/m 2—overweight and > 30 kg/m2—obesity Underweight may be present in functional hypothalamic amenorrhea (e. g., anorexia) Overweight or obesity may be present in PCOSWaist circumference > 80 cm (311/2 in) is predictive of PCOS (Chen, Xu, & Zhang, 2014) or waist-hip ratio > 0. 85 (Fritz & Speroff, 2011). Height Short stature: less than 60 inches—152. 40 cm (Fritz & Speroff, 2011)Consistent with Turner syndrome General appearance Mood/affect (depression, anxiety) Change in personality, marked mood changes Depression associated with PCOS Rare hypothalamic lesions Hair Excess terminal (thick, pigmented) body hair in a male distribution, as seen in upper lip, sideburn area, chin, chest, inner thighs, lower back, lower abdomen, and buttocks Thinning of hair Absent axillary and pubic hair Lanugo PCOSAndrogen-secreting tumor Thyroid disease Androgen insensitivity Anorexia Eyes Visual field defects Stare, lid lag, exophthalmos Pituitary tumor Hypothyroidism Neck Thyroid enlargement Webbed neck Thyroid disease Turner syndrome Breast Secretions and galactorrhea expressed from multiple ducts Undeveloped breast in primary amenorrhea Occurs in 80% of patients with hyperprolactinemia Primary amenorrhea likely caused by karyotype abnormalities Pelvic examination Scant/absent hair on mons pubis Vulvar or vaginal atrophy Clitoromegaly Imperforate hymen, transverse vaginal septum Cervical atresia Vaginal pouch (blind or absent vagina), no uterus Enlarged ovaries Androgen insensitivity Hypoestrogenic state as in premature ovarian failure Virilizing effect as in androgen tumor Congenital developmental abnormalities (primary amenorrhea) Müllerian agenesis (primary amenorrhea)May be palpable if PCOS Abbreviation: PCOS = polycystic ovary syndrome. * Directed to organs and systems based on subjective information; examination may be benign. 162 CHAPTER 19 | Amenorrhea and Polycystic Ovary Syndrome

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Table 19-3 a Essential T esting in the Investigation of Amenorrhea test d efinition c linical Implications c omments Urine pregnancy test Measures the beta subunit of human chorionic gonadotropin hormone (HCG)Pregnancy is the most common cause of amenorrhea. This diagnosis must be ruled out in sexually active women before embarking on any additional work-up. Pregnancy detection by urine HCG relative to the expected first day of menses: Two days before (79%) Seven days after (97%) Eleven days after (100%) (Wilcox, Baird, Dunson, Mc Chesney, & Weinberg, 2001) Prolactin Prolactin is produced by the lactotrophs of the anterior pituitary. Serum prolactin elevation causes amenorrhea by inhibiting pulsatile gonadotropin-releasing hormone secretion. This inhibits FSH and LH secretion resulting in anovulation and low ovarian estrogen production. Normal prolactin varies from 15 to 20 mcg. Prolactin levels measured > 50 ng/m L (or galactorrhea, or visual disturbances) deserve consultation to order a magnetic resonance imaging (MRI) to rule out pituitary tumors or lesions (some practitioners would say 100 ng/m L). Prolactin < 100 mcg may be caused by dopamine agonist drugs, polycystic ovary syndrome, hypothyroidism, or functional (idiopathic); or may be caused by a microadenoma. Prolactin > 150 most likely indicates a prolactinoma (Casanueva et al., 2006)Prolactin is best drawn fasting, early in the morning. Pregnancy, stress, intercourse, breast stimulation, and meals can increase levels. Prolactin may be mildly elevated in patients with polycystic ovary syndrome (Casanueva et al., 2006) or with long-standing hypothyroidism (Fritz & Speroff, 2011). If prolactin elevations are mild, repeat on a different day (Casanueva et al., 2006). Drugs are a common cause of elevated prolactin, primarily psychotropic medications. Highly sensitive thyroid-stimulating hormone (TSH)Measurement of TSH: anterior pituitary hormone that stimulates growth and function of thyroid cells An elevated TSH accompanying prolactin levels < 100 ng/m L is diagnostic of primary hypothyroidism (Fritz & Speroff, 2011)Very few patients with amenorrhea or galactorrhea may have subclinical hypothyroidism that is not clinically apparent (Fritz & Speroff, 2011). Follicle-stimulating hormone (FSH)Measures the amount of follicle-stimulating hormone produced by the anterior pituitary FSH ≥ 30 IU/L (found persistently) points to premature ovarian failure or insufficiency or gonadal dysgenesis in primary amenorrhea (with absent breast development in the latter case) a. Normal or low FSH concentrations indicate anovulation likely caused by hypothalamic or pituitary etiology in secondary amenorrhea, or polycystic ovary syndrome Intermittent follicular development and normalization of FSH values may occur in premature ovarian failure Progesterone challenge test Useful in evaluating the status of estrogen production. Administer progestins for 3-10 days. Bleeding is expected 2-7 days after discontinuation of the progestin (may bleed as late as 15 days later if ovulation triggered). Oral progestins available: Provera, 10 mg daily for 5-10 days, or micronized progesterone, 200 mcg at bedtime for 3-5 days Progesterone challenge test is negative in patients who do not bleed after progestin withdrawal, which indicates lack of estrogen or end-organ problems (Asherman syndrome). Progesterone challenge test is positive in patients who bleed 2-7 days after progestin withdrawal. This indicates that estrogen is being produced by the ovaries. If a progesterone challenge test is negative, you can give combined oral contraceptives to ensure that Asherman syndrome is not present. Some clinicians advocate for the progesterone challenge test to help in the interpretation of FSH values, and to assist in therapy decision making; need for estrogen therapy for prevention of bone loss (Fritz & Speroff, 2011). Other clinicians do not advocate for the progesterone challenge test due to high rates of false-positive and false-negative results. 163 Plan

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Table 19-3 b Second-Line T esting in the Investigation of Amenorrhea, Including Tests Where Consultation or Referral Is Suggested test d efinition c linical Implications c omments Abdominal-pelvic ultrasound Ultrasound imaging to evaluate internal organs if unable to perform a pelvic examination, particularly in the case of primary amenorrhea. Absent uterus, vaginal septum, or congenital absence of the vagina. May be useful to confirm the presence of a uterus and ovaries. Absent uterus and vagina is likely caused by müllerian agenesis or androgen insensitivity in primary amenorrhea. If absent uterus, then karyotype and renal ultrasound indicated. Abnormalities of the urinary tract frequently accompany müllerian anomalies. Referral to a specialist is indicated. MRI of the sella turcica to evaluate for prolactinomas (prolactin-secreting tumors) or other rare pituitary-hypothalamic tumors The goal of imaging is to evaluate the possibility of a hypothalamic or pituitary lesion. In the case of a prolactinoma, the image allows determination of a microadenoma or a macroadenoma (≤ 1 or > 1 cm, respectively). Abnormal imaging (or hyperprolactinemia) requires referral to a specialist. All women with high serum prolactin values (≥ 50 mcg/L; some practitioners would say > 100 mcg/L) should have imaging of the sella turcica (MRI). MRI is also indicated if galactorrhea, headaches, or visual field disturbances are present in the evaluation of amenorrhea. MRI is indicated for delayed puberty and hypogonadism. Karyotype evaluation To evaluate for abnormal XY chromosomes in any woman diagnosed with premature ovarian failure, if younger than 30 years of age, or in women older than 30 years with short stature or family history of early menopause (Fritz & Speroff, 2011). Mosaicism with a Y chromosome requires excision of gonads. Malignant tumor formation is highly possible with the presence of any testicular component within the gonad. Most gonadal tumors appear before 20 years of age. A significant number of cases appear between ages 20 and 30. None have been found above age 30 (Fritz & Speroff, 2011). Fragile X premutations To evaluate fragile X syndrome premutation carriers who are at risk for having a fragile X syndrome (Fritz & Speroff, 2011)Premutation of fragile X syndrome can result in premature ovarian failure (POF) or POI. Indicated when diagnosis of POF/POI is made. The mechanism by which a premutation causes ovarian failure is not known. Antiadrenal and anti thyroid antibodies, fasting blood sugar (FBS), and electrolytes To evaluate autoimmune disorders involved in POF/POI. Abnormal values for these tests are indicated in the work-up for autoimmune disorders causing POF/POI. Autoimmune abnormalities (AA) are common in women with POF. Addison's disease has the strongest association with POF (Fritz & Speroff, 2011). Saline-infusion hysterography or hysterosalpingogram Imaging procedure allows for confirmation of Asherman syndrome. Presence of intrauterine synechiae. Hysteroscopy is used for the final diagnosis and treatment. Hysteroscopic lysis of adhesions is the main method of treatment. Abbreviations: MRI, magnetic resonance imaging; mcg, micrograms; ng, nanograms; IU, international units. 164 CHAPTER 19 | Amenorrhea and Polycystic Ovary Syndrome

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Conditions that can mimic PCOS must first be excluded. 11. W omen diagnosed with PCOS should have testing for the investigation of insulin resistance and metabolic abnormalities, including 2-hour oral glucose tolerance test and fasting lipids. Hemoglobin A1C can be used if unable or unwilling to do the 2-hour glucose tolerance test (GTT) (Legro et al., 2013). In addition they should be screened for mood disorders and obstructive sleep apnea (Legro et al., 2013) 12. Add itional testing to consider may be found in T able 19-3C. 8. S aline infusion hysterography or hysterosalpingogram, for the confirmation of intrauterine synechiae pres-ent in Asherman syndrome. Initial investigation of Asherman syndrome, in the setting of secondary amen-orrhea and history of instrumentation, is performed by “priming” the uterus with 1 month of any low-dose combined oral contraceptive. Lack of withdrawal bleeding is highly suspicious of Asherman syndrome (Fritz & Speroff, 2011). 9. A bdominal and pelvic ultrasound to confirm the presence of the uterus. 10. The re are no specific tests for the diagnosis of PCOS. Table 19-3c Additional T ests in the Investigation of Polycystic Ovary Syndrome* test d efinition c linical Implications c omments Total and free testosterone Serum testosterone provides the best estimate of androgen production. Total testosterone is more widely available and better standardized than free testosterone (free testosterone is the best estimate of bioavailable testosterone). Testosterone values may be normal in women with PCOS. Testosterone in the male range is seen in women with androgen insensitivity. Total testosterone may be elevated (> 60 ng/d L), but is not required for the diagnosis of PCOS. Testosterone twice the upper limit is most likely caused by androgen-producing tumors. If testosterone levels are normal in a woman with high suspicion of PCOs, consider repeating testosterone and order sex hormone binding globulin (SHBG) in a specialized center. Low SHBG indicates PCOS (Conway et al., 2014). Be aware that local laboratory values for free testosterone vary greatly and the sensitivity and reliability are poor (ACOG, 2009). Dehydroepiandrosterone sulfate A direct measurement of adrenal androgen activity. This test may be ordered to rule out androgen-secreting tumor. Upper limit of normal is 350 ng/d L. It may vary by laboratory. It may also be mildly elevated in PCOS. It is most useful in the evaluation of rapid virilization, not as useful in common hirsutism (ACOG, 2009). 17-Hydroxy-progesterone Serum blood test that evaluates adult-onset adrenal hyperplasia (caused by 21-hydroxylase deficiency). Fasting, in the follicular phase: < 200 ng/d L excludes adult-onset adrenal hyperplasia Limit test to high-risk women with hirsutism (Fritz & Speroff, 2011). Pelvic ultrasound To evaluate for presence of polycystic ovaries, perform sonogram ideally on days 3-5 of the menstrual cycle. Polycystic ovaries are present when 12 or more follicles are seen in one of the ovaries. Recent studies raised the number to ≥ 19 in one of the ovaries (Conway et al., 2014). Follicles measure 2-9 mm in diameter Increase in ovarian volume > 10 m LThe appearance of polycystic ovaries is nonspecific. It can also be seen in women with normal hormonal function or with other androgen excess disorders. Hence it is not recommended solely for the evaluation of PCOS. If done, patients should not be on oral contraceptives because these medications can change the ovarian morphology. Abbreviation: PCOS = polycystic ovary syndrome; ng = nanograms. * PCOS is a diagnosis of exclusion. If initial testing for the investigation of amenorrhea and oligomenorrhea is unrevealing, other conditions are advised to rule out other hyperandrogenic conditions. 165 Plan

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more effective in reduction of prolactin levels when used up to 2 years (Dekkers et al., 2010). Bromocriptine, however, has been used for many more years and is less expensive. i. I f cost is an issue start with bromocriptine tablets, 2. 5 mg at bedtime or half a pill twice a day, increasing levels weekly to the lowest possible that maintains normal prolactin levels, generally twice or occasionally three times a day dosing (Fritz & Speroff, 2011). ii. S ide effects of bromocriptine are nausea, constipation, faintness caused by ortho-static hypotension, headache, and nasal stuffiness. Side effects can be minimized by taking the pill at bedtime along with a snack, by increasing the dose slowly as described previously, or by administering the 2. 5-mg tablet high into the vagina at bedtime avoiding the first pass through the liver and achieving therapeutic results at lower doses (Fritz & Speroff, 2011). iii. C abergoline can be started at a dose of 0. 5 mg, one-half to one tablet administered once or twice weekly. The dose is increased monthly until prolactin levels normalize. The lowest dose to normalize prolactin should be attempted as well as medication discontinuation when prolactin levels have been normal for 2 years or more to prevent valvular heart disease, which can occur with doses > 3 mg daily (Fritz & Speroff, 2011). Doses over 3 mg per week are rarely neces-sary (Casanueva et al., 2006). iv. I n a considerable proportion of patients, discontinuation of dopamine agonist medi-cation results in resumption of symptoms, the tumor, and hyperprolactinemia. c. D opaminergic treatment may reestablish ovula-tion, even before the first normal menstruation. The woman needs contraception if she wants to prevent pregnancy (Casanueva et al., 2006). d. V ery few patients with microadenomas prog-ress to larger tumors. Amenorrheic women with microadenomas do not need to be treated with dopamine agonists unless they want to become pregnant or they have bothersome galactorrhea. However, they need to be treated with estrogen and should have annual evaluations of serum prolactin. Request an MRI when prolactin rises significantly (or symptoms of tumor expansion ensue (Casanueva et al., 2006). Estrogen should be provided with progestins. Any low-dose oral hormonal contraception can be recommended (Fritz & Speroff, 2011). B. Management Therapeutic management of amenorrhea depends on the etiology, the goals of the woman including her desire for pregnancy, and the long-term consequences of her condition. 1. H ypothalamic amenorrhea a. Addr ess the underlying condition and issues related to hypothalamic amenorrhea (e. g., eating disorders or excessive exercise) that may nega-tively affect ovulation and normal menstrual cycle. Cognitive behavioral therapy, designed to identify maladaptive attitudes toward eating and weight, and problem-solving strategies and coping skills to improve healthy eating behaviors have demonstrated improvement of hypotha-lamic function (Berga et al., 2003). b. Be gin oral replacement with estrogen to prevent osteoporosis. Any low-dose oral contraceptive method provides the necessary estrogen replace-ment in a woman during the reproductive years, in addition to providing contraception. OCPs are preferable to estrogen alone as these women need the higher doses of estrogens. c. S upplement with calcium and vitamin D to strengthen bone health. d. R efer to reproductive endocrinology if preg-nancy is desired. Some women may respond to clomiphene citrate; most require gonadotropin-releasing hormone. 2. A menorrhea associated with pituitary dysfunction a. I n hyperprolactinemia with pituitary mac-roadenomas, the treatment goal is to establish normal estrogen secretion, menstrual function, and tumor reduction. Therapy is indicated for all patients with macroadenoma and in most patients with microadenomas, particularly if there are bothersome symptoms and desired fertility and for the prevention of osteoporosis (Casanueva et al., 2006). Women with mac-roadenomas may need transsphenoidal surgery or radiation therapy (Casanueva et al., 2006). Women desiring fertility may need induction of ovulation, although in many cases pharmaco-logic management of hyperprolactinemia estab-lishes ovulatory cycles. b. D opamine agonists, such as bromocriptine and cabergoline, are the drugs of choice for women with hyperprolactinemia and prolactinomas. These medications decrease the size of the pro-lactinomas, restore menstrual function and prolactin levels to normal, and ameliorate galac-torrhea. Cabergoline is better tolerated, is more convenient, and has been demonstrated to be 166 CHAPTER 19 | Amenorrhea and Polycystic Ovary Syndrome

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e. C alcium and vitamin D supplementation is advised in the amenorrheic patient for the pre-vention of osteoporosis. f. C orrect hypothyroidism. g. Addr ess hyperprolactinemia induced by medi-cations. Review the patient medication profile for drugs that cause hyperprolactinemia and amenorrhea, such as dopamine agonist drugs and estrogen or danazol. Withdrawal of the drug for 72 hours, if able to do this safely, helps elucidate if the drug is responsible for hyperp-rolactinemia. MRI should be considered if this alternative is not feasible, particularly in patients with neurologic symptoms to rule out a pitu-itary lesion (Casanueva et al., 2006). 3. O varian disorders a. P rimary amenorrhea: refer patients diagnosed with Turner syndrome or mosaicism to a phy-sician. Patients with Turner syndrome need a multidisciplinary approach for management including the approach for primary or second-ary amenorrhea. It is critical to review with the woman in a sensitive manner the consequences of POF and the need for early estrogen to induce pubertal development in the case of primary amenorrhea and to protect bone health during the adult life (Bondy, 2007). b. S econdary amenorrhea caused by POF i. Or der a karyotype if woman is 30 years old or younger. Refer if the karyotype is abnormal. Malignant tumor formation with-in the gonad is associated in mosaicism with a Y chromosome. Removal of the gonadal areas is required (Fritz & Speroff, 2011). ii. I n women younger than 35 consider an evaluation of autoimmune disorders. iii. Adv ise all women with POF to establish standard hormonal therapy with estrogen. Advised at least until age 50 to prevent osteoporosis (Kalantaridou & Nelson, 2000; Ostberg et al., 2007). Progestin should be added to estrogen to protect the endometrium if there is an intact uterus. Hormonal treatment also reduces meno-pausal symptoms. iv. W omen with POF commonly experience unpredictable and intermittent ovarian function (Rebar & Connolly, 1990). For women who wish to avoid pregnancy, offer any low-dose combined oral contraception instead of hormonal therapy because the estrogen doses in the hormonal therapy are not high enough to prevent pregnancy. The possibility of vasomotor symptoms during the cyclical hormone-free pill inter-val should be addressed. v. R efer women who desire pregnancy to an infertility specialist. Women with POF are candidates for ovum donation or adoption. Although rare, these women may become pregnant spontaneously (Check & Katsoff, 2006). 4. Di sorders of the outflow tract a. P rimary amenorrhea i. R efer patients suspected of or diagnosed with androgen insensitivity to a specialist. Patients with this condition need removal of gonads to prevent the development of gonadal neoplasia. Gonadectomy is usu-ally delayed until puberty in patients with complete androgen insensitivity syndrome. These patients have a normal pubertal growth spurt and feminize at the time of expected puberty; tumors do not usually develop until after this time. These patients require psychological counseling given that they have female phenotype and male karyotype (Fritz & Speroff, 2011). ii. R efer patients diagnosed with müllerian abnormalities or agenesis to a specialist. Surgery is needed if there is vaginal outlet obstruction to allow passage of menstrual blood. Creation of a neovagina for patients with müllerian agenesis is usually delayed until the woman is emotionally mature and ready to participate in the postoperative care required to maintain vaginal patency (Fritz & Speroff, 2011). b. S econdary amenorrhea: refer patients to a spe-cialist if Asherman syndrome is suspected. Final diagnosis is made with hysteroscopy performed by lysis of adhesions during the diagnostic procedure (Fritz & Speroff, 2011). 5. P COS T reatment goals should be directed to control menstrual irregularities, management of hyper-androgenic manifestations (acne and hirsutism), infertility issues, and the long-term consequences of hyperinsulinemia. a. Adv ise weight loss (via caloric restricted diet) and regular exercise. Although the best treat-ment approach in obese PCOS patients remains to be defined, weight loss is the first-choice rec-ommendation for the treatment of the clinical manifestations of PCOS, such as menstrual cycle irregularities, infertility, and hirsutism (Conway 167 Plan

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ii. A ntiandrogen medications: consult with a specialist for the prescription of these medications (ACOG, 2009). For spirono-lactone the usual dosage is 25-100 mg, twice a day. It may take up to 6 months to observe full clinical effect. One-fifth of women on this medication may experience metrorrhagia if the dose is in the upper limit (Helfer, Miller, & Rose, 1988). Use cautiously in women with renal impair-ment because of hyperkalemia. Rarely, exposure has resulted in ambiguous geni-talia in male infants. Offer mechanical hair removal (laser treatment). Eflornithine is a topical option. d. S creen and treat to reduce risk of cardiovascular disease and diabetes. i. Ado lescents and women with PCOS should be screened for impaired glucose tolerance every 3-5 years, or earlier if clinical suspi-cion of diabetes with a 2-hour glucose level using a 75-g oral glucose load (Legro et al., 2013; Salley et al., 2007) ii. S creen women for cardiovascular risk fac-tors: smoking, obesity (central), hyperten-sion, dyslipidemia, diabetes, obstructive sleep apnea, family history of early cardio-vascular disease e. M edical therapy for women with PCOS desir-ing pregnancy: the antiestrogen clomiphene citrate remains the drug of choice for ovulation induction. Recent data suggest that an aroma-tase inhibitor is more effective, particularly when BMI > 30 (Franik, Kremer, Nelen, & Farquhar, 2014). Discussion of ovulation induction is beyond the scope of this chapter. C. Client education 1. I nformation: provide verbal and, preferably, written information regarding: a. R isk-reduction strategies and screening for osteoporosis in women with hypothalamic and pituitary amenorrhea and for metabolic syn-drome and endometrial hyperplasia in women with PCOS. b. The d isease process: signs and symptoms and underlying etiologies. c. Di agnostic tests: preparation, cost, the proce-dures, and aftercare. d. M edication management: rationale, action, use, side effects, associated risks, cost of therapeutic interventions, and the need for adhering to long-term treatment plans. et al., 2014; Vrbikova & Hainer, 2009). A 5% weight loss has shown improvement in ovula-tory cycles (ACOG, 2009). Bariatric surgery is now recommended for morbidly obese women (central obesity), as it may restore the HPO axis function, prevent or even reverse the metabolic syndrome and its consequences, and improve pregnancy outcomes (Conway et al., 2014). b. P harmacologic treatment for menstrual irregu-larities and hyperandrogenic manifestations include:i. I f no contraindication for combined hor-monal contraception use any low-dose oral contraceptives in order to decrease bio-available testosterone levels (ACOG, 2009; Sheehan, 2004). Contraceptive patch and vaginal ring are also alternatives (Legro et al., 2013). Cyclic progestin is a good choice for menstrual regulation if contraception is not needed (200 mg daily micronized progestin or10 mg medroxyprogesterone acetate 10-14 days/month if contraception is not needed for menstrual regulation) (Conway et al., 2014). ii. M etformin, although not approved by the Food and Drug Administration for PCOS management, is widely used for its anti-insulinic effects. It is recommended as a second-line treatment for the prevention of diabetes when lifestyle modifications have not been successful (Legro et al., 2013). The dose suggested to treat women with PCOS is 1,500-2,000 mg per day given in divided doses (De  Leo et al., 2009). Metformin is preferred over other classes of anti-insulinic drugs because the medication tends to decrease weight (ACOG, 2009). Metformin has limited effect in treating hirsutism, acne, and infertility and has a higher incidence of gastrointestinal side effects ( Johnson, 2014). iii. Di scuss contraception in women who do not desire pregnancy and are taking met-formin because ovulation rates can improve with metformin. c. M anagement of hirsutism can be additionally accomplished by:i. Or al contraceptives: although the Food and Drug Administration has not approved them for the management of hirsutism, observational and nonrandomized studies have shown some benefit (ACOG, 2009). OCPs help with hirsutism by increasing SHBG and reducing free testosterone. 168 CHAPTER 19 | Amenorrhea and Polycystic Ovary Syndrome

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2. C ounseling Women interested in becoming pregnant should be counseled on possible therapeutic options and possi-ble referral to reproductive endocrinology specialists. v I. s elf-management resources and tools A. Patient and client education The Mayo Clinic website also has excellent patient infor-mation at www. mayoclinic. org. Resources are found under “Patient Care & Health Information”; click on “Diseases and Conditions” and search for “amenorrhea. ” B. Community support groups Women with POF can consult the Premature Ovarian Failure Support group at www. posupport. org, created by the nonprofit organization The International Premature Ovarian Failure Support Group, Alexandria, VA (email: info@pofsupport. org; telephone: 703-913-4787). re Ferences Altieri, P., Gambineri, A., Prontera, O., Cionci, G., Franchina, M., & Pasquali, R. (2010). Maternal polycystic ovary syndrome may be associated with adverse pregnancy outcomes. European Journal of Obstetrics, Gynecology and Reproductive Biology, 149(1), 31-36. American College of Obstetrics and Gynecology. (2004a). Current evaluation of amenorrhea. Fertility and Sterility, 82(Suppl. 1), 266-272. American College of Obstetrics and Gynecology. (2004b). Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome. Fertility and Sterility, 81(1), 19-25. American College of Obstetricians and Gynecologists. (2009). ACOG Practice Bulletin No. 108: Polycystic ovary syndrome. Obstetrics and Gynecology, 114(4), 936-949. Beals, K. A., & Hill, A. K. (2006). The prevalence of disordered eating, menstrual dysfunction, and low bone mineral density among US collegiate athletes. International Journal of Sport Nutrition and Exercise Metabolism, 16(1), 1-23. Berga, S. L., Marcus, M. D., Loucks, T. L., Hlastala, S., Ringham, R., & Krohn, M. A. (2003). Recovery of ovarian activity in women with functional hypothalamic amenorrhea who were treated with cognitive behavior therapy. Fertility and Sterility, 80(4), 976-981. Berman, J. M. (2008). Intrauterine adhesions. Seminars in Reproductive Medicine, 26(4), 349-355. Bondy, C. A. (2007). Care of girls and women with Turner syndrome: A guideline of the Turner Syndrome Study Group. Journal of Clinical Endocrinology and Metabolism, 92(1), 10-25. Casanueva, F., Molitch, M. E., Schlechte, J. A., Abs, R., Bonert, V., Bronstein, M. D., et al. (2006). Guidelines of the Pituitary Society for the diagnosis and management of prolactinomas. Clinical Endocrinology, 65(2), 265-273. Check, J. H., & Katsoff, B. (2006). Successful pregnancy with spontaneous ovulation in a woman with apparent premature ovarian failure who failed to conceive despite four transfers of embryos derived from donated oocytes. Clinical and Experimental Obstetrics & Gynecology, 33(1), 13-15. Chen, L., Xu, W. M., Zhang, D. (2014). The association of abdominal obesity, insulin resistance, and oxidative stress in adipose tissue in women with polycystic ovary syndrome. Fertility & Sterility, 102(4), 1167-1174. Conway, G., Dewailly, D., Diamanti-Kandarakis, E., Escobar-Morreale, H. F., Franks, S., Gambineri, A., et al. (2014). The polycystic ovary syndrome: A position statement from the European Society of Endocrinology. European Journal of Endocrinology, 171(4), P1-P29. De Leo, V., Musacchio, M. C., Palermo, V., Di Sabatino, A., Morgante, G., & Petraglia, F. (2009). Polycystic ovary syndrome and metabolic comorbidities: Therapeutic options. Drugs T oday, 45(10), 763-775. Dekkers, O. M., Lagro, J., Burman, P., Jørgensen, J. O., Romijn, J. A.,  & Pereira, A. M. (2010). Recurrence of hyperprolactinemia after withdrawal of dopamine agonists: Systematic review and meta-analysis. Journal of Clinical Endocrinology and Metabolism, 95(1), 43-51. Franik, S., Kremer, J. A. M., Nelen, W. L. D. M., & Farquhar, C. (2014) Aromatase inhibitors for subfertile women with polycystic ovary syndrome. Cochrane Database of Systematic Reviews, 2. Fritz, M. A., & Speroff, L. (2011). Clinical gynecologic endocrinology and infertility (8th ed. ). Philadelphia, PA: Lippincott Williams & Wilkins. Helfer, E. L., Miller, J. L., & Rose, L. I. (1988). Side-effects of spironolactone therapy in the hirsute woman. Journal of Clinical Endocrinology and Metabolism, 66(1), 208-211. Hoch, A. Z., Pajewski, N. M., Moraski, L., Carrera, G. F., Wilson, C. R., Hoffmann, R. G., et al. (2009). Prevalence of the female athlete triad in high school athletes and sedentary students. Clinical Journal of Sport Medicine, 19(5), 421-428. Jedel, E., Waern, M., Gustafson, D., Landén, M., Eriksson, E., Holm, G., et al. (2010). Anxiety and depression symptoms in women with polycystic ovary syndrome compared with controls matched for body mass index. Human Reproduction, 25(2), 450-456. Johnson, N. P. (2014). Metformin use in women with polycystic ovary syndrome. Annals of Translational Medicine, 2(6), 56. doi:10. 3978 /j. issn. 2305-5839. 2014. 04. 15. Kalantaridou, S. N., & Nelson, L. M. (2000). Premature ovarian failure is not premature menopause. Annals of the New York Academy of Sciences, 900, 393-402. Khawaja, N. M., T aher, B. M., Barham, M. E., Naser, A. A., Hadidy, A. M., Ahmad, A. T., et al. (2006). Pituitary enlargement in patients with primary hypothyroidism. Endocrine Practice, 12(1), 29-34. Legro, R. S., Arslanian, S. A., Ehrmann, D. A., Hoeger, K. M., Murad, M. H., Pasquali, R., et al. (2013). Diagnosis and treatment of polycystic ovary syndrome: An Endocrine Society clinical practice guideline. Journal of Clinical Endocrinology and Metabolism, 98(12), 4565-4592. March, W. A., Moore, V. M., Willson, K. J., Phillips, D. I., Norman, R. J., & Davies, M. J. (2010). The prevalence of polycystic ovary syndrome in a community sample assessed under contrasting diagnostic criteria. Human Reproduction, 25(2), 544-551. Ostberg, J. E., Storry, C., Donald, A. E., Attar, M. J., Halcox, J. P., & Conway, G. S. (2007). A dose-response study of hormone replacement in young hypogonadal women: Effects on intima media thickness and metabolism. Clinical Endocrinology, 66(4), 557-564. Practice Committee of the American Society for Reproductive Medicine. (2008). Current evaluation of amenorrhea. Fertility and Sterility, 90(5), S219-S225. 169 References

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

Salley, K. E., Wickham, E. P., Cheang, K. I., Essah, P. A., Karjane, N. W., & Nestler, J. E. (2007). Glucose intolerance in polycystic ovary syndrome— a position statement of the Androgen Excess Society. Journal of Clinical Endocrinology and Metabolism, 92(12), 4546-4556. Sheehan, M. T. (2004). Polycystic ovarian syndrome: Diagnosis and man-agement. Clinical Medicine & Research, 2(1), 13-27. T asali, E., Van Cauter, E., & Ehrmann, D. A. (2008). Polycystic ovary syn-drome and obstructive sleep apnea. Sleep Medicine clinics, 3(1), 37-46. Vrbikova, J., & Hainer, V. (2009). Obesity and polycystic ovary syndrome. Obesity Facts, 2(1), 26-35. Wilcox, A. J., Baird, D. D., Dunson, D., Mc Chesney, R., & Weinberg, C. R. (2001). Natural limits of pregnancy testing in relation to the expected menstrual period. JAMA, 286(14), 1759-1761. Rebar, R. W., & Connolly, H. V. (1990). Clinical features of young women with hypergonadotropic amenorrhea. Fertility and Sterility, 53(5), 804-810. Reindollar, R. H., Byrd, J. R., & Mc Donough, P. G. (1981). Delayed sexual development: A study of 252 patients. American Journal of Obstetrics and Gynecology, 140(4), 371-380. Reindollar, R. H., Novak, M., Tho, S. P., & Mc Donough, P. G. (1986). Adult-onset amenorrhea: A study of 262 patients. American Journal of Obstetrics and Gynecology, 155(3), 531-543. Rotterdam ESHRE/ASRM-Sponsored PCOS Consensus Workshop Group (2004). Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome. Fertility and Sterility, 81(1), 19-25. 170 CHAPTER 19 | Amenorrhea and Polycystic Ovary Syndrome

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf

[ACOG], 2012; Saslow et al., 2012; U. S. Preventive Services T ask Force [USPSTF], 2012). The Pap test remains an important modality in determining the health of a woman's cervix, whether it is obtained by using the conventional Pap test or the liquid-based test. It screens for both glandular and squamous cell abnormalities. The use of HPV testing in combination with cervical cytology was approved for screening women 30 years of age or older and as a reflex test in younger women who have atypical cells of undetermined significance reported on their results. Reflex testing involves test-ing the cervical sample for the presence of high-risk HPV types. It is not necessary to test for low-risk types because they lack the potential for oncogenic transformation. HPV testing should not be used in women younger than 21 years. In April 2014, the Food and Drug Administration (FDA) approved Roche Diagnostics' cobas® HPV test as a primary screening test for cervical cancer. This action received unanimous support from an FDA advisory committee (Huh et al., 2015). 2. Ac cording to all three guidelines—ACOG (2012), American Cancer Society (Saslow et al., 2012), and USPSTF (2012), the recommendations for initiation, frequency, and cessation of cervical screening are: a. Be gin Pap test screening at age 21 and continue every 3 years through age 29. b. W omen age 30 and older may continue to be screened with cytology alone every 3 years or with HPV testing plus cytology every 5 years. c. Di scontinuation of cervical cancer screening can be at age 65 in women who have had three or more consecutive negative cytology test results or two consecutive negative cytology plus HPV tests within 10 years before cessa-tion of screening, with the most recent test per-formed within 5 years. Women with a history of CIN 2 or greater should continue routine I. Intr oduction and general background A. Abnormal cytology 1. I ntraepithelial neoplasia (IN), often referred to as dysplasia, is an abnormal precancerous change in cells as they mature. This abnormality can be found in multicentric areas of the lower genital tract, such as the cervix (CIN), vagina (VAIN), vulva (VIN), anus (AIN), and perianal epithelium (PAIN). The natural history of the disease is unpredictable. Mediated by the immune system, the abnormality can regress, persist at the same level, or progress to malignancy. 2. The etiology of the condition is multifactorial, but the dominant agent is human papillomavirus (HPV). Over 100 different HPV types exist, but 14  types are considered oncogenic (Markowitz et al., 2014). Worldwide, types 16 and 18 are responsible for 70% of cervical cancers (Li, Franceschi, Howell-Jones, Snijders, & Clifford, 2010). HPV is necessary for malignant cellular transformation, but other cofactors, such as age of first intercourse, number of sexual partners, other sexually transmitted infections (STIs), smoking, diet, stress, and host immunologic status all play a role (Winer et al., 2003). Persistence of high-risk HPV types is also required for progression to high-grade lesions (Kosiol et al., 2008; Kjaer, Frederiksen, Munk, & Iftner, 2010). The virus is for the most part sexually transmitted and is responsible for other noncancerous conditions, such as genital warts (condyloma acuminata). B. Screening guidelines 1. G uidelines for the use of cytology for cervical cancer screening (Pap tests) have undergone major revision (American College of Obstetrics and Gynecology Mary M. Rubin and Lynn Hanson Sc Reen Ing fo R Int Raep It He LIa L n eop L a SI a and c ance R of t H e Lowe R g en I ta L t R act© Eliks/Shutterstock; © donatas1205/Shutterstock 17120Chapt Er

Clinical Guidelines for Advanced Practice Nursing-1 1.pdf