Tag Archives: adolescents

Use of screening tools for depression in adolescents: An evidence-based systematic review

Depression  in adolescents is a growing health concern. Signs and symptoms (S/S) of depression in adolescents tend to be overlooked by parents and primary care practitioners (PCPs), including nurse practitioners, and are instead considered a normal part of growing up.  However, many adolescents do have clinical depression that is identifiable and treatable.1 Some adolescents are at a greater risk for developing depression than others. Risk factors for depression in this age group are listed in Table 1.2

Common S/S of depression are listed in Table 2.3 Adolescents may be particularly prone to experiencing sadness, hopelessness, poor sleep, decreased appetite or concentration, loss of pleasure in activities, irritability, anger, an social withdrawal.4In addition, adolescents with depression are at an increased risk for suicide.Instead of seeking help from a  healthcare practitioner, many adolescents with depression self-medicate by using alcohol or drugs and/or by participating in high-risk sexual behavior.5

The estimated prevalence of a major depressive disorder (MDD) in adolescents aged 13-18 is 5.6%,6 with MDD being slightly more common in girls than in boys (5.9% vs 4.6%). The rate is higher in members of minorities.7Despite increased awareness about depression in teens, this mental disorder continues to go unrecognized and untreated.7,8 About 75% of adolescents in the United States are seen routinely in a primary care setting, but only 16%-38% of PCPs correctly identify the presence of a mental health condition.4

The United States Preventive Services Task Force (USPSTF) recommends routine screening for depression in 12- to 18-year-olds in the primary care setting when appropriate mental health services, including confirmation of diagnosis, psychotherapy, and follow-up, are available.6,9 The recommendation statement also includes depression screening for any child or teen with one or more of these four risk factors: parental depression, a co-morbid mental health condition, a chronic health problem, or recent experience of a negative life event.

The study

The purpose of this systematic review was to critically evaluate current evidence regarding use of depression screening tools in the adolescent population. The search focused on use of the Center for Epidemiological Studies Depression Scale for Children (CES-DC) 10and the second revise Beck Depression Inventory (BDI-II).11 Because of the paucity of such studies conducted in the primary care setting, the author included studies done in an emergency department (ED) or a school.


Formulating a PICO question. This PICO (P, Population; I, Intervention; C, Comparison; and O, Outcome) question was written to guide the search: In adolescents aged 12-18 years (P), is use of a screening tool for depression (I), compared with the usual standard of care (C), more accurate in detecting depression (O)? The author’s goal in posing this PICO question was to determine whether enough evidence exists to support screening adolescents for depression using an appropriate screening tool. This PICO question itself facilitated the search strategy and guided the selection of key words.

Search strategy. The author searched multiple databases, including Medline, Cochrane Library, CINAHL, Eric, PsycINFO, Google Scholar, and the Agency for Healthcare Research and Quality. Key words were mental health, depression, depressive disorder, adolescents, teens, screening, CES-DC, and Beck or BDI-II. The author examined publishe and unpublished works and performed a complete hand search of reference lists of the systematic reviews and other relevant articles from 2005 to 2010. All articles examining use of a screening tool specific for depression in the adolescent population were included, regardless of whether the setting was a primary care practice, an ED, or a school. Thirteen studies met inclusion criteria. A 1999 study was added because it was one of the few conducted in a primary care setting.


The search revealed two systematic reviews on adolescent depression screening,6,12but no randomized controlled trials (RCTs). Five descriptive studies using the CES-DC or BDI-II were identified.13-17 Zuckerbrot et al18 also published guidelines delineating identification, assessment, and initial management of depression in adolescents. Six studies using the designated screening tools had cross-sectional, predictive, or correlational designs. 5,19-23Table 3 lists the results and recommendations of these studies.5,6,12-17,19-23

Systematic reviews. The most robust systematic review was conducted by Williams et al6 for the USPSTF. The search did not yield any data on health outcomes among screened versus unscreened populations or any studies examining the harms of screening. Although the literature was limited with regard to the use and accuracy of screening tools, several tools, including the Patient Health Questionnaire for Adolescents (PHQ-A),24 the Beck Depression Inventory for Primary Care (BDI-PC),25 and the CES-DC,10 all performed well.

In their systematic review, Zuckerbrot and Jensen12 aimed to determine existing evidence for the various methods used to identify adolescent depression in primary care and the identification practices that were in use a the time. The investigators concluded that self-report screening tools were available and that these tools had adequate psychometric properties and feasibility for use in primary care. They discussed two important findings: (1) self-report screening tools were more accurate than physician interviews in identifying depression; and (2) PCPs who relied on patients’ presenting chief complaints to detect depression would miss many teens with depression or depressive symptoms. In addition, they found that, with regard to the usual standard of care, physicians who received additional training improved their ability to detect depression, but not to the same level as that achieved with self-report tools. Although the HEADDSS (home, education, activities, drugs, depression,  safety, and sexuality)  assessment26 is widely used in adolescent health care, Zuckerbrot and Jensen12 did not find any studies examining its effectiveness in detecting depression. In addition, they found no studies that combined three essential elements: a screening component, an intervention, and an assessment of patient outcomes  at follow-up.

Randomized controlled trials. No RCTs examining the screening  process for MDD in adolescents  were identified in the  search. Hallfors et al5 used data from the National Longitudinal Study of Adolescent Health to determine whether gender-specific  patterns of substance use and sexual behavior predicted  depression or vice versa. They used the CES-DC to assess for depression. Overall findings showed that sex and drug behaviors predicted a higher likelihood of depressive S/S, especially among girls, but that depression did not predict high-risk behavior.

Descriptive studies. Scott et al21used the BDI-II to ascertain the prevalence of depressive S/S in 351 adolescents presenting to an ED in the Midwest. Significant differences were noted among certain groups of patients: Trauma patients were more likely to refuse screening; patients presenting with a psychiatric diagnosis were more likely to be hospitalized; and patients with a previous history of a mental illness reported significantly more depressive S/S. Rutman et al22 compared the CES-DC with a two-question screening tool in 121 adolescents presenting to an ED, and found that 37% had a positive screen on the CES-DC, with 21% being positive for suicidality, and 40% were positive on the two-question screen. Consistent with other reports, these researchers found higher rates of depressive symptoms in girls.

Lazaratou et al13 aimed to clarify the prevalence of depressive S/S in high school students in Athens, Greece, and to evaluate risk factors for these S/S using the CES-DC. A total of 713 students aged 15-18 years were enrolled. Depressive S/S were found to be linked to gender (girls had higher scores than boys), school record (students with better records had lower scores), and the interaction of gender a grade (males had higher scores as they grew older).

Using a school-based sample of more than 20,000 adolescents in grades 7-12, Rhee14 examined the race-specific prevalence of 10 physical symptoms (head – ache, stomachache, musculoskeletal pain, fatigue, sore throat, dizziness, feeling hot, chest pain, painful urination, cold sweat) in adolescents and the extent to which socioeconomic status and depressive S/S explained racial differences in those symptoms using the CESDC screening tool. Headache was the most common complaint in white students (32%). American Indians had greater complaints of musculoskeletal pain (35%), feeling hot (14%), and chest pain (10%), and blacks reported more urinary symptoms (4%). Differences between whites and blacks were significant for family income and depression. Overall depression scores were higher in blacks than in whites.

Robles-Pina et al 15 examined students held back one grade during the elementary school years (early school retention) as a predictor of depression in 191 Hispanic urban teens. No significant differences were found between males and females in selfconcept, rate of retention, past feelings of sadness, or gradepoint average (GPA). Females had higher mean scores on the CES-DC than did males, with the gender difference showing a low effect size. Thirty-six percent of Hispanic adolescents had CESDC scores indicating moderate to severe depression. Adolescents retained in school had lower self-concept, greater past feelings of depression, a lower GPA, and higher rates of depression than did non-retained adolescents. All results were significant. The highest predictor of depressionwas lower self-concept.

Chisolm et al16 used the CESDC and the PHQ-A single-question tool for detecting adolescent depression, and observed the use of mental health services following screening. In this population (N = 996), 24% screened positive for depression and 14% screened positive for suicidal thoughts. Only 16% of adolescents who screened positive for depression accessed mental healthcare services within the next 180 days (P <.01). However, adolescents who acknowledge having suicidal thoughts were 8 times more likely than those who screened negative for suicidal ideation to use behavioral health services. Overall findings showed that adolescents who were screened were more likely to seek physical or mental health services. One plausible explanation of this finding was that the screening process opened lines of communication between patients and practitioners.

Zuckerbrot et al17 conducted the first and only study examining the feasibility and acceptability of screening for adolescent depression in primary care. Average time for completion of a pencil-and-paper screening tool was 4.6 minutes; the refusal rate for screening was low. Practitioners and parents reported greater satisfaction than dissatisfaction with the screening process. The time burden was not significant.

Winter et al23  performed one of the few studies assessing screening for adolescent depression in the primary care setting using one of the most reliable screening tools, the BDI-PC. This report focused primarily on the BDI-PC’s psychometric properties. Although the sample size was small (50 females and 50 males), recruitment of subjects was halted because the effect size was so large. Eighty-nine adolescents screened negative and 11 screened positive for MDD. The mean BDI-PC score of the 11 adolescents with positive screens was about 9 times higher than that of the 89 negatively screened teens.


Strengths and limitations of the evidence. Research on adolescent depression has increased over the past 10 years, but few studies have evaluated the screening process in primary care or the use of specific screening tools. The two systematic reviews discussed previously contain the strongest evidence available (Level 1), according to the Rating System for Levels of Evidence.27 However, most of the research is Level VI—evidence from descriptive studies. Each study was also evaluated using the John Hopkins Nursing Evidence-Based Practice Research Evidence Appraisal, with the quality of the scientific evidence ranking as high, good, or low with major flaws.27Studies included in this review were deemed of good quality.

Studies varied in terms of validity, reliability, and applicability. Most were not conducted in a primary care setting. All but one was conducted in the U.S., which increases generalizability of the results. Despite their limitations, all the studies helped answer the PICO question and helped provide evidence for practice guidelines for screening for adolescent depression by PCPs. Guidelines set forth in the USPSTF are supported by the National Institute of Mental Health (NIMH),1,28 the American Academy of Pediatrics (AAP),29 and the National Association of Pediatric Nurse Practitioners (NAPNAP).3

A critical examination of available research studies regarding screening processes for adolescent depression reveals several gaps. Few RCTs investigated the screening process in primary care settings, and only one study assessed the feasibility of screening. 17  No studies examined all three critical elements—screening,treatment, and outcomes.

Two screening tools for primary  care use. The BDI-II is a widely accepted instrument for outpatient screening, performs consistently, and is linked to Diagnostic and Statistical Manual, Fourth Edition-Text Revision (DSMIV- TR) criteria.30 However, several disadvantages hamper its use in the primary care setting. Use of the tool incurs a fee, and practitioners must have additional training to use it. The BDI-II has high item difficulty and may require additional assistance in completing it. It appears more appropriate for use in intervention studies examining various treatment options in adolescent depression. The BDI-PC, by contrast, is a self-report instrument designed for primary care use in patients aged 13 years or older.

The CES-DC has not been used consistently in studies reported before 2005. This tool has gained greater popularity and been used more frequently in research  studies in the past few years. The CES-DC has been criticized for not being linked to DSM-IV-TR criteria.13,29On the plus side, this tool is readily available free of charge and does not require additional training for use. The CESDC’ reliability, validity, mean scores, and case rates of adolescent depression remain consistent across the literature. Therefore, the CES-DC is considered appropriate for use in screening adolescents for depression in the primary care setting.

Recommendations for practice

The USPSTF, in conjunction with the NIMH, has increased awareness of the need for screening for depression in adolescents and  has made practitioners more aware of the prevalence of this  mental illness in this population. 1,9 The AAP and NAPNAP have launched special tool kits and fellowship programs promoting  screening for mental  health problems in primary care.3,29Zuckerbrot et al17 found  that screening for depression in a primary care setting is quick, feasible, effective, and well accepted by patients and practitioners. Recommendations for practice include instituting a universal screening program for depression in adolescents aged 12-18 years when mental health services are available to aid in accuracy of the diagnosis, initiation of treatment, and follow-up.9

Primary care practices with available mental health support should begin screening adolescents annually for MDD at well-or acute-care visits. The CES-DC is free of charge and easy to use, and has adequate reliability and validity for use in primary care settings. Screening tools can be completed while patients are waiting to see their PCP. Partnering with a mental health practitioner to facilitate transitioning of adolescents from primary care depression screening to engagement in more in-depth psychiatry evaluation and treatment  could enhance the clinical utility of this screening endeavor.


Early identification of depression  in adolescents is a national health priority. PCPs, including primary care NPs, must learn to recognize the subtle S/S of this often-silent epidemic because most patients with undiagnosed depression present to their PCP first.8 PCPs must be aware of the common S/S of depression and how these S/S vary in different age groups. Many parents dismiss these S/S as a normal part of growing up. PCPs must be aware of current recommendations for screening, as outlined in the USPSTF 2009 statement.

More research is needed regarding screening for depression in primary care settings. In particular, studies examining the feasibility of screening, identifying efficient procedures for completing the screening and referral processes, and further testing of screening tools would be beneficial. PCPs will then be able to translate these research findings into practice. =

Sharolyn K. Dihigo is a clinical assistant professor and Interim Director of the DNP Program and Lead Teacher in the Primary Care Pediatric Nurse Practitioner  Program at The University of  Texas at Arlington. The author  states that she does not have a financial interest in or other relationship  with any commercial product named in this article.


  1. National Institute of Mental Health. Depression in children and adolescents. Updated January 29, 2013. www.nimh.nih.gov/health/ topics/depression/depression-inchildren-and-adolescents.shtml

  2. Mayo Clinic. Teen depression: Risk factors. Updated 2011. www.mayoclinic.com/health/teendepression/DS01188/DSECTION=risk-factors.

  3. Melnyk BM, Moldenhauer Z. Child and Adolescent Mental Health Fellowship Guide to Child and Adolescent Mental Health Screening, Early Intervention and Health Promotion. Kyss Fellowship ed. New Jersey: Joint Special Initiative of The National Association of Pediatric Nurse Practitioners (NAPNAP) and the NAPNAP Foundation; 2006.

  4. Melnyk BM, ed. Assessment & Evidenced-based Management o Mood Disorders in Children and Teens: Part 1. Kyss Program ed. New Jersey: Joint Special Initiative of The National Association of Pediatric Nurse Practitioners (NAPNAP) and the NAPNAP Foundation; 2009.

  5. Hallfors DD, Waller MW, Bauer D, et al. Which comes first in adolescence— sex and drugs or depression? Am J Prev Med.  2005;29(3):163-170.

  6. Williams SB, O’Connor EA, Eder M, Whitlock EP. Screening for child and adolescent depression in primary care settings: a systematic evidence review for the US Preventive Services Task Force. Pediatrics. 2009;123(4):e716-e735.

  7. Barclay L. Managing child and adolescent depression: an expert interview with Bernadette Melnyk, PhD, RN, CPNP/PMHNP, FNAP, FAAN. Medscape Med News. April 28, 2010. www.medscape.com/viewarticle/720910

  8. Melnyk BM, ed. Nuts and bolts of child and adolescent mental health screening and assessment: Part 1. Kyss Fellowship ed. New Jersey: Joint Special Initiative of The National Association of Pediatric Nurse Practitioners (NAPNAP) and the NAPNAP Foundation; 2006.

  9. US Preventive Services Task Force. Screening and treatment for major depressive disorder in children and adolescents: US Preventive Services Task Force recommendation statement. Pediatrics. 2009;123(4):1223-1228. http://www.ncbi.nlm.nih.gov/pubmed/19336383

  10. Radloff LS. The use of the Center for Epidemiologic Studies Depression Scale in adolescents and young adults. J Youth Adolesc. 1991;20(2):149-166.

  11. Beck AT, Steer RA, Brown GK. Beck Depression Inventory (BDI-II). San Antonio, TX: The Psychological Corporation; 1996.
  12. Zuckerbrot RA, Jensen PS. Improving recognition of adolescent depression in primary care. Arch Pediatr Adolesc Med. 2006;160:694-704.

  13. Lazaratou H, Dikeos D, Anagnostopoulos D, Soldatos C. Depressive symptomatology in high school students: the role of age, gender, and academic pressure. Comm Mental Health J. 2010;46:289-295.

  14. Rhee H. Racial/Ethnic differences in adolescents’ physical symptoms. J Pediatr Nurs. 2005;20(3):153-162.

  15. Robles-Pina RA, DeFrance E, Cox DL. Self-concept, early childhood depression and school retention as predictors of adolescent depression in urban Hispanic adolescents. School Psychology Int. 2008;29:426-441.

  16. Chisolm DJ, Lima J, Gardner W, Kelleher KJ. Adolescent behavioral risk screening and use of health services. Adm Polichy Ment Health. 2009;36:374-380.

  17. Zuckerbrot RA, Maxon L, Pagar D, et al. Adolescent depression screening in primary care: feasibility and acceptability. Pediatrics. 2007;119(1):101-108.

  18. Zuckerbrot RA, Cheung AH, Jensen PS, et al. Guidelines for Adolescent Depression in Primary Care (GLAD-PC): I. identification, assessment, and initial management. Pediatrics. 2007;120:1299-1312.

  19. Perreira KM, Deeb-Sossa N, Harris KM, Bollen K. What are we measuring? An evaluation of the CES-D across race/ethnicity and immigrant generation. Social Forces. 2005;83(4):1567-1602.

  20. Phillips GA, Shadish WR, Murray  DM, et al. The Center for Epidemiologic  Studies Depression Scale with a  young adolescent populations: a confirmatory factor analysis. Multivar Behav Res. 2006;41(2):147-163.

  21. Scott EG, Luximore B, Alexander H, et al. Screening for adolescent depression in a pediatric emergency department. Soc Acad Emerg Med. 2006;13(5):537-542.

  22. Rutman MS, Shenassa E, Becker BM. Brief screening for adolescent depressive symptoms in the emergency department. Acad Emerg Med. 2008;18(1):17-22.

  23. Winter LB, Steer RA, Jones-Hicks L. Beck AT. Screening for major depression disorder in adolescent medical outpatients with the Beck Depression Inventory for primary care. J Adolesc Health. 1999(24):389-394.

  24. Johnson JG, Harris ES, Spitzer RL, Williams JB. The patient health questionnaire for adolescents. J Adolesc Health. 2002;30(3):196-204.

  25. Beck AT, Steer RA, Ball R, et al. Use of the Beck Anxiety and Beck Depression Inventories for Primary Care with medical outpatients. Assessment. 1997;4:211-219.

  26. Stephans M. Preventative health counseling for adolescents. Am Fam Physician. 2006;74(7):1151-1156.

  27. Melnyk BM, Fineout-Overton E. Evidenced-Based Practice in Nursing and Healthcare.  Philadelphia, PA Lippincott; 2005.
  28. National Institute of Mental Health. Depression in boys and adolescent males. Updated January 22, 2013. www.nimh.nih.gov/health/publications/men-and-depression/depression-in-boys-and-adolescentmales.shtml

  29. American Academy of Pediatrics. Enhancing pediatric mental health care: Report from the American Academy of Pediatrics Task Force on Mental Health. Pediatrics.2010;125(suppl 3):S69-S160.

  30. American Psychological Association. Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition-Text Revision. Arlington, VA:American Psychiatric Publishing; 2000.


The adolescent with irregular menses

NM is a 16-year-old female who presents to the clinic with concerns about irregular periods. She tells the nurse practitioner (NP) that she had her first period when she was 14 and that her cycles have never been regular, ranging from 1 to 3 months. Her last menstrual period was about 2 months ago and she thinks that she has had only four or five periods over the past year. In addition, NM is interested in discussing contraception.

What else is helpful to know about NM?

Because NM has come to the clinic for the first time, the NP takes a comprehensive health history. Given NM’s report of irregular periods, the NP obtains a thorough gynecologic, sexual, endocrine, medication, and lifestyle history. The NP also takes a family history to discern any relevant endocrine disorders.

The NP learns that most of NM’s periods are light, with no cramping. On occasion, she has a heavy period that requires a super tampon change every hour and that is associated with moderate cramps. She says she can predict a heavy period because she has breast tenderness and feels moody right before it starts.

NM and her boyfriend started to have sex 6 months ago and have been consistently using condoms. She has never been pregnant but has never been tested for a sexually transmitted infection (STI). She has not noticed any unusual vaginal discharge or pelvic pain. She has completed the HPV vaccination series.

NM does not smoke, drink alcohol, or use illicit drugs. She denies food binging or food-restricting behaviors. Her exercise is limited to participating in gym class twice a week. She sleeps 7-8 hours each night without problem. She has no major stressors at school, at home, or with peers.

The patient takes no medications other than occasional over-the-counter (OTC) pain remedies for menstrual cramps or head aches. NM reports that the headaches occur only prior to her heavy periods, are sometimes severe enough to keep her from her usual activities, and are relieved by rest and OTC medications. The headaches are not preceded by an aura or other neurologic signs or symptoms (S/S). NM relates an additional concern—acne—which has been worsening over the past 4-6 months. OTC acne medications have provided only minimal improvement.

In a review of systems, the NP further explores any S/S that might suggest that an endocrine disorder is causing or contributing to NM’s menstrual irregularity. NM denies hair loss, unusual hair growth, weight changes, heat or cold intolerance, fatigue, change in headaches, visual changes, breast nipple discharge, or bowel function changes. Her family history is positive for hypothyroidism and type 2 diabetes in her mother and infertility in an older sister.

Which differential diagnoses are you considering at this point?

NM is experiencing infrequent periods that are most likely anovulatory. Ovulatory cycles are typically characterized by regular intervals (28-32 days) and cramping and are often preceded by moliminal symptoms such as breast tenderness and moodiness. Menstrual irregularities in adolescents are usually related to aberrations in the hypothalamic–ovarian–pituitary axis and fall into one of two distinct categories, hypothalamic menstrual disorders or endocrinopathies. Hypothalamic menstrual disorders are usually associated with alterations in stress, diet, exercise, and/or body weight. Endocrinopathies associated with menstrual irregularities include thyroid disorders, hyperprolactinemia, hyperandrogenic anovulation or polycystic ovary syndrome (PCOS), adult-onset congenital adrenal hyperplasia (CAH), and Cushing syndrome.1

Based on NM’s history, her menstrual irregularity cannot be ascribed to changes in stress, diet, exercise, or body weight. She has no S/S of a thyroid disorder or hyperprolactinemia other than the menstrual irregularity. The combination of menstrual irregularity and acne, albeit common in adolescents, alerts the NP to possible hyperandrogenism associated with PCOS. As such, the NP will look for physical examination findings and choose laboratory tests in consideration of possible hyperandrogenism. Adrenal disorders such as CAH and Cushing syndrome are uncommon but will be explored if indicated.

Which elements do you include in your physical examination?

NM’s blood pressure is 128/78 mm Hg and her body mass index (BMI) is 26.3 kg/m2. A urine hCG is negative. She has moderate inflammatory acne with a combination of comedones, papules, pustules, and some faint scars along the jaw line and upper back. Scalp and body hair distribution is normal. She has no signs of hirsutism. The thyroid is normal sized with no tenderness or nodularity. Breasts are Tanner stage 5. Palpation of the abdomen indicates no tenderness, masses, or hepatosplenomegaly. An external genital exam shows no clitoromegaly or lesions. Pubic hair distribution is Tanner stage 5, with no expanded escutcheon. No speculum or bimanual exam is indicated.2 A self-collected vaginal swab specimen is obtained for chlamydia and gonorrhea testing.3 

Based on the history and physical examination findings, what are your working diagnoses?

Infrequent menses, or oligomenorrhea, is defined as cycles longer than 38 days. Irregular menses is defined as a variation of cycle length greater than 20 days.Many adolescents have menses that meet these criteria in the first 1-2 years postmenarche. About 75% of adolescents have an average menstrual cycle of 21-45 days within 1 year postmenarche and about 90% are in this range within 4 years postmenarche.NM reached menarche 2 years ago. Her cycles range from 1 to 3 months. Most adolescents become ovulatory over time, but half of girls with infrequent menses or secondary amenorrhea have a permanent ovulatory disorder.6

Moderate to severe acne affects 15%-20% of 15- to 17-year-olds.The exact cause of acne is unknown. Genetic influences may determine acne susceptibility and severity. Main contributory factors are excessive sebum production, hyperkeratinization of pilosebaceous follicles causing blockage and mixing dead skin cells with sebum, and proliferation of the bacterium Propionibacterium acnes. Inflammatory acne develops when the wall of these follicles ruptures and sebum enters the surrounding dermis. Pustules form when inflammation is close to the surface, and papules and cystic nodules form when inflammation is deeper, causing mild to severe scarring.Although most cases of acne regress spontaneously during later adolescence, some may persist into adulthood.

Production of adrenal androgen increases in early puberty in girls, contributing not only to pubic and axillary hair growth but also to increased sebum production and acne. However, acne in adolescent girls should be evaluated not in isolation but, rather, in the context of each patient’s family history and menstrual history and in the absence or presence of hirsutism.

Which laboratory tests are indicated?

Because infrequent menses or amenorrhea may be the only presenting sign in adolescents with thyroid dysfunction or hyperprolactinemia, laboratory testing for these disorders is indicated. Normal serum thyroid-stimulating hormone (TSH) and prolactin levels rule out these two conditions. After PCOS, non-classic CAH is the second most common cause of hyperandrogenic anovulation.Non-classic CAH can be excluded with a carefully timed 17-hydroxyprogesterone measure, which is checked in the early morning, during the follicular phase or an anovulatory cycle.

Although a diagnosis of hyperandrogenism can be made clinically in typical presentations of adult PCOS, adolescents should undergo a serologic evaluation because of the prevalence of acne in teens with normal androgen levels.  About 50% of adolescents with acne have no biochemical evidence or other clinical findings associated with hyperandrogenism.10 If a lab can assure accuracy in females, a total testosterone level, best drawn in the morning, can be checked as a cost-effective test for hyperandrogenemia. If rapid-onset or severe hirsutism is noted, the level of dehydroepiandrosterone sulfate is measured to detect adrenal hyperandrogenism caused by unusual virilizing disorders. Absence of serologic hyperandrogenism in an adolescent can exclude a diagnosis of PCOS.

NM’s lab findings include TSH, 2.4 mIU/L (normal range, 0.4-4.0 mIU/L); prolactin, 16 ng/mL (normal range in nonpregnant females, 2-29 ng/mL; normal range in pregnant females, 10-209 ng/mL); and total testosterone, 84 ng/dL (normal range for girls aged 12-16 years, <7-75 ng/dL).

Which additional study or studies can help make the diagnosis?

Ultrasonography (USG) of the ovaries is needed in NM’s case. The presence of clinically insignificant polycystic ovaries is high in the general adolescent population,11 suggesting that multifollicular ovaries may be a normal developmental variant. Overall ovarian volume may be a stronger determinant of PCOS in adolescents than subjective qualities of the ovary, which are often limited by the transabdominal USG technique frequently used in adolescent girls.12

NM’s USG shows bilaterally enlarged ovaries with numerous follicles, and a mean ovarian volume of 11.3 cm3. Based on the constellation of infrequent menses, serologic evidence of hyperandrogenism, absence of other endocrinopathies, and the USG findings, a diagnosis of PCOS is made.

What are the official diagnostic criteria for PCOS in adolescents?

The diagnostic criteria for PCOS have not been firmly established. The National Institutes of Health calls for evidence of hyperandrogenism and oligoamenorrhea; ovarian USG is not needed to make the diagnosis.13 The Rotterdam criteria consider various phenotypes of PCOS based on a combination of any two of these three findings: hyperandrogen ism, menstrual irregularity, and polycystic ovaries on USG.14 The Androgen Excess and the PCOS Society emphasize hyperandrogenism, with additional findings of menstrual irregularity and/or polycystic ovaries on USG being diagnostic.15

Whereas the diagnostic criteria for PCOS may have broadened for women, inclusion of adolescents is problematic. Transitory findings of clinical hyperandrogenism (i.e., acne) and perimenarchal menstrual irregularity may lead to a premature diagnosis of PCOS in adolescents. Such a diagnosis can contribute to unnecessary treatment, psychological distress, body image concerns, and undue worry about future fertility. However, true PCOS in adolescents is a marker for future metabolic syndrome and should be treated and monitored accordingly.16

The 2012 consensus report of the two largest fertility societies, the European Society of Human Reproduction and Embryology and the American Society for Reproductive Medicine suggests that all three Rotterdam criteria, with stipulations specific to adolescents, be present to accurately diagnose PCOS in this population10:

• Hyperandrogenism, defined by serologic testing;

• Oligoamenorrhea, present for at least 2 years; and

• Polycystic ovaries by USG, with an ovarian volume >10 cm3.

The Figure provides an algorithm designed by the author that is based on these diagnostic criteria.

What are NM’s treatment options?

Treatment of PCOS is judged appropriate in NM’s case. Goals of her treatment include S/S management and prevention and detection of subsequent chronic conditions for which she is at higher risk. These conditions include metabolic syndrome, infertility, and endometrial cancer. NM should have an annual assessment of her lipid levels, HbA1C or glucose tolerance, BMI, and BP.

The NP and NM discuss treatment options related to NM’s goals. NM wants to have regular periods—or no periods—and reduced acne, and she wants to start using an effective contraceptive. She may be able to reach all these goals with one pharmacologic agent, a combined hormonal contraceptive (CHC). No contraceptive method is specifically contraindicated in patients with PCOS.17 Correction of NM’s hyperandrogenism through use of a CHC, specifically a combined oral contraceptive (COC), may be the most effective treatment for her acne, while offering reliable contraception and endometrial cancer protection at the same time. By suppressing ovarian production of testosterone, COCs reduce free or circulating androgens. All COCs can help improve acne.18 Little research is available on the effectiveness of transdermal or vaginal CHCs in this regard.19 COCs containing drospirenone (DRSP), relative to those containing other progestins, may have superior efficacy against acne because of DRSP’s antiandrogenic, spironolactone-like effect.

For many women, the spironolactone equivalent of 25 mg of DRSP contained in COCs is not a high enough dose to adequately control acne. One study found that adding 100 mg of spironolactone to a DRSP-containing COC was well tolerated and resulted in near-resolution of acne in 85% of subjects.20 Although DRSP has androgen-blocking potential, NPs must be cautious in prescribing DRSP-containing COCs for obese women because of a potentially increased risk for venous thromboembolism.21

Long-acting reversible contraceptives (LARC) such as intrauterine devices (IUDs) and implantable progestin rods are first-line contraceptive choices for adolescents.22 Although both the levonorgestrel-containing intrauterine system (LNG-IUS) and the progestin implant offer endometrial cancer protection, neither produces reliable androgen suppression. Some studies of the LNG-IUS and the progestin implant show improvement of baseline acne, whereas others show onset or worsening of acne.23-25 If a LARC method is deemed the most acceptable contraceptive for a given patient, it can be paired with spironolactone to treat hyperandrogenic acne. Because of its potentially teratogenic effects, spironolactone is contraindicated in sexually active women who are not using a reliable contraceptive. LNG-IUS and progestin implant users may experience irregular bleeding during the first several months of use and possibly amenorrhea after 6 months to 2 years of use.26

NM decides to take a COC in a continuous regimen so as to avoid having her period and perhaps her menstrual headaches as well. The NP encourages NM to continue condom use along with the COC for STI risk reduction. In addition, because COCs can take 3-6 months to control acne,27 NM is started on a regimen of topical clindamycin and tretinoin. Topical tretinoins are vitamin A derivatives that act by normalizing keratinocyte development, decreasing sebum production, and reducing inflammation. Their use in combination with topical antibiotics such as clindamycin is more effective for moderate acne than either agent used alone.28

The NP refers NM to an online guide about PCOS for teens provided by the Center for Young Women’s Health of Boston Children’s Hospital.29 She gives NM a prescription for regular exercise and nutrition counseling, with a goal of keeping her BMI below 26.


Irregular menses and acne are common findings in adolescent girls; NPs need to use evidence-based guidelines to aid these girls by distinguishing PCOS from normal physiologic variants. In NM’s case, the findings of oligomenorrhea, serologic hyperandrogenism, and polycystic, enlarged ovaries confirm a diagnosis of PCOS. Once the diagnosis is made, treatment is focused on the adolescent’s goals and need for S/S management. Long-term monitoring for associated chronic diseases is included in the ongoing plan of care. With appropriate monitoring and lifestyle modifications, PCOS can be effectively managed with minimal longterm complications.

Beth A. Kutler is Director of Women’s and Sexual Health Services, Gannett Health Services, at Cornell University in Ithaca, New York. The author states that she does not have a financial interest in or other relationship with any commercial product named in this article. The author also acknowledges that she has discussed off-label use of medications and/or devices in this article.


  1. Gibbs R, Karlan B, Haney A, Nygaard I. Danforth’s Obstetrics and Gynecology. 10th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2008.
  2. American Congress of Obstetricians and Gynecologists. Well-Woman Recommendations. 2016.
  3. Centers for Disease Control and Prevention (CDC). Sexually Transmitted Diseases Treatment Guidelines, 2015. MMWR Morb Mortal Wkly Rep. 2015;64(RR3):1-137.
  4. Fraser IS, Critchley HO, Broder M, Munro MG. The FIGO recommendations on terminologies and definitions for normal and abnormal uterine bleeding. Sem Reprod Med. 2011;29(5):383-390.
  5. Rosenfield R. Adolescent anovulation: maturational mechanisms and implications. J Clin Endocrinol Metab. 2013;98(9):3572-3583.
  6. Wiksten-Almströmer M, Hirschberg A, Hagenfeldt K. Prospective follow-up of menstrual disorders in adolescence and prognostic factors. Acta Obstet Gynecol Scand. 2008;87(11):1162-1168.
  7. Williams H, Dellavalle R, Garner S. Acne vulgaris. Lancet. 2012;379(9813):361-372.
  8. McCance KL, Huether SE. Pathophysiology: The Biologic Basis for Disease in Adults and Children. 7th ed. Atlanta, GA: Elsevier, Inc; 2014.
  9. Trapp C, Oberfield S. Recommendations for treatment of nonclassic congenital adrenal hyperplasia (NCCAH): an update. Steroids. 2012;77(4):342-346.
  10. Fauser B, Tarlatzis B, Rebar R, et al. Consensus on women’s health aspects of polycystic ovary syndrome (PCOS): the Amsterdam ESHRE/ASRM-Sponsored 3rd PCOS Consensus Workshop Group. Fertil Steril. 2012;97(1):28-38.
  11. Mortensen M, Rosenfield R, Littlejohn E. Functional significance of polycystic-size ovaries in healthy adolescents. J Clin Endocrinol Metab. 2006;91(10):3786-3790.
  12. Carmina E, Oberfield S, Lobo R. The diagnosis of polycystic ovary syndrome in adolescents. Am J Obstet Gynecol. 2010;203(3):201.e1-201.e5.
  13. Zawadzki JK, Dunaif A. Diagnostic criteria for polycystic ovary syndrome: towards a rationale approach. In: Dunaif A, Givens JR, Haseltine F, Merriam GR, eds. Polycystic Ovary Syndrome. Boston, MA: Blackwell Scientific Publications; 1992:377-384.
  14. Rotterdam ESHRE/ASRM-Sponsored PCOS Consensus Workshop Group. Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome (PCOS). Hum Reprod. 2004;19(1):41-47.
  15. Azziz R, Carmina E, Dewailly D, et al. Criteria for defining polycystic ovary syndrome as a predominantly hyperandrogenic syndrome: an Androgen Excess Society Guideline. J Clin Endocrinol Metab. 2006;91(11):4237-4245.
  16. Roe A, Prochaska E, Smith M, et al. Using the Androgen Excess–PCOS Society Criteria to Diagnose polycystic ovary syndrome and the risk of metabolic syndrome in adolescents. J Pediatr. 2013;162(5):937-941.
  17. U.S. Medical Eligibility Criteria for Contraceptive Use, 2010. 2016.
  18. Arowojolu A, Gallo M, Lopez L, Grimes D. Combined oral contraceptive pills for treatment of acne. Cochrane Database Syst Rev. 2012;7:CD004425.
  19. Zaenglein A, Pathy A, Schlosser B, et al. Guidelines of care for the management of acne vulgaris. J Am Acad Dermatol. 2016;74(5):945-973.
  20. Krunic A, Ciurea A, Scheman A. Efficacy and tolerance of acne treatment using both spironolactone and a combined contraceptive containing drospirenone. J Am Acad Dermatol. 2008;58(1):60-62.
  21. Jick S, Hernandez R. Risk of non-fatal venous thromboembolism in women using oral contraceptives containing drospirenone compared with women using oral contraceptives containing levonorgestrel: case-control study using United States claims data. BMJ. 2011;342:d2151.
  22. Adolescents and long-acting reversible contraception: implants and intrauterine devices. Committee Opinion No. 539. Obstet Gynecol. 2012;120(4):983-988.
  23. Urbancsek J. An integrated analysis of nonmenstrual adverse events with Implanon®. Contraception. 1998;58(6):109S-115S.

Dying to be thin: Recognizing and treating anorexia in adolescents

Ubiquitous images of waiflike models and other females in the media prompt many adolescent girls in the United States to curb their caloric intake and lose weight, even to a perilously low level. The authors provide up-to-date information regarding identification, assessment, and management of anorexia in adolescent girls so that nurse practitioners can intervene before this illness threatens these patients’ lives.

For most girls and women in the United States, images of extremely thin models and other females in the media do not greatly influence their own body image or their eating or exercise habits. For other girls and women, however, the focus on thinness becomes distorted, obsessive, and extreme, and contributes to the development of an eating disorder that can have catastrophic consequences.1 The reasons for this body image disturbance are likely related to a combination of psychological, environmental, and biologic factors; adolescent females seem to be among the most vulnerable. When adolescent girls, as opposed to women, develop an eating disorder, they present with greater emotional distress, functional impairment, and suicide risk; a dangerously lower body mass index (BMI); and an increased need for mental health assessment and treatment.2 Females with eating disorders, versus those with other psychiatric disorders, are more likely to attempt suicide and to undergo inpatient treatment.2,3

According to a recent cross-sectional survey, about 3% of girls aged 13-18 years have some form of eating disorder: 0.3% have anorexia, 0.9% have bulimia, and 1.6% have a binge eating disorder.4 In this study, although most teens with an eating disorder reported seeking some form of treatment, only a minority received treatment specifically for their eating or weight problems. To increase the likelihood that adolescent girls with anorexia, the most common eating disorder, receive the help they need from nurse practitioners (NPs) who see them for primary care, the authors provide background information about anorexia and then discuss its signs and symptoms (S/S), screening, diagnosis, and treatment.

Background information

Anorexia nervosa, an eating disorder characterized by immoderate food restriction, inappropriate eating habits or rituals, obsession with having a thin figure, and an irrational fear of weight gain, as well as a distorted body-image, tends to develop during adolescence, with peaks in onset at ages 14 and 18.5 Fear of gaining weight is the driving force behind anorexia; afflicted individuals refuse to sustain a minimally normal weight.6 To achieve their goal of losing weight, these individuals restrict their food intake and may exercise excessively. Some of them may use laxatives, diuretics, and enemas to accelerate weight loss.

Individuals with anorexia view themselves as fat despite being thin or even emaciated. They judge their self-worth by their weight, and they tend to have a greatly distorted body-image and cognitive thought process.6 Driven by perfectionism, even after receiving therapy, these girls find that they can never quite achieve their “ideal” weight.5

Signs and symptoms

The most obvious sign of anorexia is extreme thinness or emacia­tion.7 Other S/S related to body weight and body-image include a relentless pursuit of thinness, an unwillingness to maintain a normal or healthy weight, an intense fear of gaining weight, a distorted body-image, low self-esteem, and a denial of the danger of low body weight. Over time, anorexia takes a toll on the body; common physical manifestations of anorexia include dry skin, brittle hair and nails, lanugo (fine downy hair) all over the body, decreased blood pressure and heart rate, cold extremities, severe constipation, and mild anemia.5-8

Anorexia can have severe adverse effects on many body systems as well. It is associated with a reduction in bone density,1 which may lead to an increased risk for fractures. Some young patients with anorexia fail to reach their full adult growth potential. Anorexia can cause muscle weakness and wasting, and damage to the structure and function of the heart.7 In addition, anorexia can lead to cerebral atrophy and delayed neurocognitive development. When anorexia is untreated or inadequately treated, patients can die, usually of medical complications (e.g., arrhythmia, multi-organ failure) or from suicide.9

View: Eating disorders


One commonly used tool is the SCOFF screen,10 which asks patients with suspected eating disorders these questions:

  • Do you make yourself Sick because you feel uncomfortably full?
  • Do you worry you have lost Control over how much you eat?
  • Have you recently lost Over 15 pounds in a three-month
  • Do you believe yourself to be Fat when others say you are too thin?
  • Would you say that Food dominates your life?

A “yes” answer to two or more of these questions indicates that an eating disorder may be present. The Eating Disorder Examination, an interview of the patient by the healthcare provider (HCP),11 and the self-reported Eating Disorders Examination-Questionnaire12 are both considered valid screens for eating disorders and for determining specific features of a person’s condition (e.g., vomiting, laxative use).


New diagnostic criteria

The American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Health Disorders, Fifth Edition (DSM-5) states that anorexia, which primarily affects adolescent girls and young women, is characterized by distorted body image and excessive dieting that leads to severe weight loss, with a pathologic fear of becoming fat.9 The DSM-5 lists three diagnostic criteria for anorexia:

A. Restriction of energy intake relative to requirements, leading to a significantly low body weight in the context of age, sex, developmental trajectory, and physical health. Significantly low weight is defined as a weight that is less than minimally normal or, for children and adolescents, less than that minimally expected.

B. Intense fear of gaining weight or of becoming fat, or persistent behavior that interferes with weight gain, even though at a significantly low weight.

C. Disturbance in the way in which one’s body weight or shape is experienced, undue influence of body weight or shape on self-evaluation, or persistent lack of recognition of the seriousness of the current low body weight.

The new diagnostic criteria have several minor but important changes from previous editions. Criterion A focuses on behaviors such as restricting caloric intake, and no longer includes the word refusal in terms of weight maintenance because that implies intention on the part of the patient and can be difficult to assess.13 In the DSM-5, Criterion B is expanded to include not only overtly expressed fear of weight gain but also persistent behavior that interferes with weight gain.14 The DSM-IV-TR Criterion D15 requiring amenorrhea, or the absence of at least three menstrual cycles, has been deleted from the DSM-5. This criterion cannot be applied to males, pre-menarchal females, females taking oral contraceptives, or postmenopausal females. In some cases, individuals exhibit all other S/S of anorexia but still report some menstrual activity.

Diagnostic tests

Early detection of anorexia is important. As patients approach the 5-year mark of living with the illness, recovery becomes increasingly less likely.16 NPs should ask all female patients about their self-perception, self-image, and overall satisfaction with their body appearance. Height, weight, and BMI should be monitored at every visit. Additional testing is considered on a case-by-case basis. Laboratory tests such as complete blood count, electrolytes, liver function tests, serum albumin, urinalysis, and thyroid-stimulating hormone level are considered as part of the initial workup.17

Poor nutrition and extremely low caloric intake take a toll on the body not only in terms of appearance but also in terms of overall function. The hypovolemia that occurs in relation to anorexia can result in an atrophic heart and decreased cardiac output. An electrocardiogram and perhaps an echocardiogram should be included as part of the standard workup because of the high likelihood that arrhythmias will occur; arrhythmia is the most common cause of death in patients with anorexia. Prolonged QTc interval, bradycardia, heart block, and hypovolemia are just a few of the likely end points related to the atro­phic heart and the electrolyte imbalances.18Differential diagnosis

Many other diagnoses can contribute to, coexist with, or be solely responsible for extreme weight loss. When working up a patient with a suspected eating disorder, NPs must consider other diagnoses such as HIV/AIDS, major depression, anxiety disorder, post-traumatic stress disorder, sexual abuse, substance abuse, brain tumor, inflammatory bowel disease, malabsorption syndrome, lupus, cancer, and esophageal motility disorders.

Because isolated cases of anorexia—without other co-morbid conditions—are rare, NPs should screen patients with anorexia for depression, anxiety, and other mental health disorders. Monitoring for suicidal ideation and ascertaining a patient’s risk for suicide are vitally important.


Nurse practitioners are key members of the healthcare team that formulates a comprehensive treatment plan for patients with anorexia. Despite treatment offered, relapse risk remains high. Thirty percent to 50% of treated individuals relapse after an inpatient stay, especially during the first 2 years post-discharge.8Pharmacotherapy

No drugs have been approved by the FDA for treatment of anorexia nervosa, and no research supports the use of medications to cure the disorder.6 However, once patients reach their maintenance weight, selective serotonin reuptake inhibitors may help reduce obsessive-compulsive behaviors.6 Several randomized controlled trials are currently assessing the possible benefit of olanzapine, aripiprazole, and quetiapine.19 The results of these studies are not yet available. Many patients in whom atypical antipsychotics are indicated will not take these medications because of their association with weight gain.6Non-pharmacologic approaches

Cognitive behavioral therapy (CBT) is the gold standard for treating patients with anorexia.20 CBT assists patients, who view their body with unrealistic scrutiny and resist gaining any weight, in changing their unhealthy body-image. A recent Cochrane review evaluated the efficacy of family-based therapy (FBT), also known as the Maudsley Approach, in treating anorexia.21 In this intensive outpatient treatment approach, parents play a major role in (1) helping restore their adolescent child’s weight to a normal level for her age and height, (2) returning control over eating to the child, and (3) encouraging normal adolescent development through an in-depth discussion of these crucial developmental issues as they pertain to their child.21 The review showed that FBT was slightly superior to usual care (i.e. patient-based care) in treating adolescents with anorexia. In a more recent comparative trial, FBT, with its focus on facilitation of weight gain, was as effective as systemic family therapy, which addresses general family processes, and could be delivered at lower cost.22Hospitalization

Because of the life-threatening effect of starvation on the body, many patients with anorexia require hospitalization.3 If a patient is experiencing an extreme electrolyte imbalance or weighs below 75% of ideal body weight, the treatment is immediate inpatient unit treatment with medical stabilization. Because of the urgent need to reintroduce food in patients with anorexia, a rare but potentially fatal condition called refeeding syndrome may occur. This syndrome, attributed to a metabolic alteration in serum electrolytes, sodium retention, and vitamin deficiencies, taxes the patient’s system by overburdening the body with fluids too quickly.6Treatment at a psychiatric facility

Many patients with anorexia are admitted to an inpatient psychiatric facility in a crisis state. A comprehensive assessment is necessary, and symptoms such as suicidal ideation must be managed immediately. Some inpatient psychiatric facilities such as the Remuda Ranch at the Meadows, in Wickenburg, Arizona,23 specialize in the treatment of eating disorders in females. At this facility, treatment duration is flexible; some patients stay 1-2 weeks, whereas others with more severe illness may remain in treatment for 30 days or longer. Each patient has an individualized treatment plan implemented by a team of HCPs that includes a psychiatric and primary care provider, a registered dietician, a licensed master’s or doctoral-level therapist, a psychologist, and registered nurses. Along with treating the patient’s eating disorder, the team treats coexisting problems such as depression, anxiety, substance abuse, and trauma.

Nurse practitioner role

Because NPs may be the first HCPs to come into contact with an adolescent with anorexia, they must be able to recognize the S/S of an eating disorder, screen for and diagnose the disorder, and treat or refer the patient to prevent further harm. Treatment may entail prescribing medications, which, although not curative, can lessen S/S. Pharmacotherapy for patients with eating disorders targets three domains: (1) remission of presenting S/S during acute treatment, (2) prevention of relapse in the post-acute phase, and (3) diversion of recurrences over the lifetime course.24 The treatment plan will also likely include CBT to enhance the patient’s self-image. If the NP is not well versed in providing CBT, a referral to a mental health specialist is advisable. FBT is also a reasonable therapeutic approach. In all cases, education of family members regarding anorexia and its treatment is vital. The Box lists useful resources for NPs and their patients.

Those NPs who are treating patients with anorexia should initially see these patients weekly to monitor their weight and to check their laboratory values. Frequency of weight monitoring and lab testing will decrease over time as patients demonstrate the ability to maintain a maximum tolerable weight. Reactions of patients with anorexia to requests to step on a scale range from reluctance to resistance to outright refusal. Refusal to be weighed is a patient’s right, and should be viewed as a protective mechanism in which the patient is avoiding a perceived negative stimulus, as opposed to a demonstration of defiance. In some instances, obtaining an accurate weight and completing certain tests are essential to rule out complications such as heart failure. Although most life-threatening sequelae that occur in the acute phase of anorexia subside in the post-acute phase, ongoing monitoring can help ensure that liver and kidney function have stabilized, that electrolyte and vitamin deficiencies have corrected, and that BMI remains at an acceptable level.

Nurse practitioners caring for patients with anorexia are members of a team of HCPs, which
usually includes a dietician, a counseling psychologist, and a psychia­trist. Some patients engage in only limited treatment with their NP, and periodically engage in more intensive treatment with a mental health specialist when their illness becomes more severe. Understanding that the treatment phase is often characterized by remissions and exacerbations helps NPs know what to expect. At the very least, NPs will play an integral part in keeping patients engaged in the treatment process. Supporting patients from their entry into treatment and through recovery can help them endure the extensive rehabilitative process and ultimately save their lives.

Erik Southard is the Director of the DNP Program, Department of Advanced Practice Nursing; Renee N. Bauer is Director of 2nd Degree Track, Department of Baccalaureate Nursing; and Andreas M. Kummerow is Director RN to BS Track, Department of Baccalaureate Nursing Completion, all at Indiana State University in Terre Haute. The authors state that they do not have a financial interest in or other relationship with any commercial product named in this article.

Useful Resources


1. Hudson LD, Court AJ. What pediatricians should know about eating disorders in children and young people. J Paediatr Child Health. 2012;48(10):869-875.

2. Stice E, Marti CN, Rohde P. Prevalence, incidence, impairment, and course of the proposed DSM-5 eating disorder diagnosis in an 8-year prospective community study of young women. Abnorm Psychol. 2013;122(2):445-457.

3. Dooley-Hash S, Banker JD, Walton MA, et al. The prevalence and correlates of eating disorders among emergency department patients aged 14-20 years. Int J Eat Disord. 2012;45(7):883-890.

4. Swanson SA, Crow SJ, Le Grange D, et al. Prevalence and correlates of eating disorders in adolescents. Results from the national comorbidity survey replication adolescent supplement. Arch Gen Psychiatry. 2011;68(7):714-723.

5. Fursland A, Byrne S, Watson H, et al. Enhanced cognitive behavior therapy: a single treatment for all eating disorders. J Couns Dev. 2012; 90(3):319-329.

6. Halter MJ. Foundations of Psychiatric Mental Health Nursing: A Clinical Approach. 7th ed. St. Louis, MO: Saunders; 2014.

7. National Institute of Mental Health. What Are Eating Disorders? www.nimh.nih.gov/health/topics/

8. Berends T, van Meijel B, van Eldburg A. The Anorexia Relapse Prevention Guidelines in practice: a case report. Perspect Psychiatr Care. 2012;48(3):149-155.

9. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Health Disorders: Fifth Edition. Washington, DC: American Psychiatric Publishing; 2014.

10. Morgan JF, Reid F, Lacey JH. The SCOFF questionnaire, a new screening tool for eating disorders. West J Med. 2000;172(3):164-165.

11. Fairburn CG, Cooper Z, O’Connor M. Eating disorder examination. In: Fairburn CG. Cognitive Behavior Therapy and Eating Disorders. New York, NY; Guilford Press; 2008. http://rcpsych.ac.uk/pdf/EDE_16.0.pdf

12. Fairburn CG, Beglin S. Eating disorder examination-questionnaire. Appendix in: Fairburn CG. Cognitive Behavior Therapy and Eating Disorders. New York, NY: Guilford Press; 2008. https://www.rcpsych.ac.uk/

13. Mannix M. DSM-5 updates for eating disorders: implications for diagnosis and clinical practice. Brown Univ
Child Adolesc Behav Letter. 2012;28(12):3.

14. American Psychiatric Association. Highlights of Changes from DSM-IV-TR to DSM-5. 2013. www.

15. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Health Disorders: Fourth Edition-Text Revision. Washington, DC: American Psychiatric Publishing; 2000.

16. Ben-Tovim D. Clinical eating disorders: outcome, prevention and treatment of eating disorders. Curr Opin
Psychiatry. 2003;16(1):65-69.

17. Richardson B. Pediatric Primary Care, Practice Guidelines for Nurses. 2nd ed. Burlington, MA: Jones & Bartlett; 2013.

18. Casiero D, Frishman WH. Cardiovascular complications of eating disorders. Cardiol Rev. 2006;14(5):

19. Watson HJ, Bulik CM. Update on the treatment of anorexia nervosa: review of clinical trials, practice guidelines and emerging interventions. Psychol Med. 2013;43(12): 2477-2500.

20. Watson, HJ, Allen K, Fursland A, et al. Does enhanced cognitive behaviour therapy for eating disorders improve quality of life? Eur Eat Disord Rev. 2012;20(5):393-399.

21. Fisher C, Hetrick S, Rushford N, Family therapy for anorexia nervosa. Cochrane Database Syst Rev. 2010;

22. Agras SW, Lock J, Brandt H, et al. Comparison of 2 family therapies for adolescent anorexia nervosa. JAMA Psychiatry. 2014;71(11):1279-1286.

23. Remuda Ranch website. From the /Desk of the CEO. https://www

24. Kruger S, Kennedy SH. Psychopharmacotherapy of anorexia nervosa, bulimia nervosa and binge-eating disorder. J Psychiatry Neuro­sci. 2000;25(5):497-508.