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Clinical Report—Identification and Management ofEating Disorders in Children and Adolescents

abstractThe incidence and prevalence of eating disorders in children and ado-lescents has increased significantly in recent decades, making it es-sential for pediatricians to consider these disorders in appropriateclinical settings, to evaluate patients suspected of having these disor-ders, and to manage (or refer) patients in whom eating disorders arediagnosed. This clinical report includes a discussion of diagnostic cri-teria and outlines the initial evaluation of the patient with disorderedeating. Medical complications of eating disordersmay affect any organsystem, and careful monitoring for these complications is required.The range of treatment options, including pharmacotherapy, is de-scribed in this report. Pediatricians are encouraged to advocate forlegislation and policies that ensure appropriate services for patientswith eating disorders, including medical care, nutritional intervention,mental health treatment, and care coordination. Pediatrics 2010;126:1240–1253

INTRODUCTIONIncreases in the incidence and prevalence of anorexia nervosa (AN),bulimia nervosa (BN), and other eating disorders in children and ado-lescentsmake it critically important that pediatricians be familiar withearly detection and appropriate management of these disorders. Re-sults of epidemiologic studies have indicated that the numbers of chil-dren and adolescents with eating disorders increased steadily fromthe 1950s onward.1–4 During the past decade, the prevalence of obesityin children and adolescents has also increased dramatically,5–9 accom-panied by further emphasis on dieting and weight loss among childrenand adolescents.10–15

The epidemiology of eating disorders has gradually changed; there isan increasing prevalence of eating disorders inmales16–19 andminoritypopulations in the United States20–23 as well as in countries in whicheating disorders had not been commonly seen.3,4,24,25 Of particular con-cern is the increasing prevalence of eating disorders at progressivelyyounger ages.19,26,27 A recent analysis by the Agency for HealthcareResearch and Quality revealed that from 1999 to 2006, hospitalizationsfor eating disorders increased most sharply—119%—for childrenyounger than 12 years.19

It is estimated that approximately 0.5% of adolescent girls in the UnitedStates have AN, that approximately 1% to 2% meet diagnostic criteriafor BN, and that up to 5% to 10% of all cases of eating disorders occurin males. A large number of people with eating disorders do not meetthe strict criteria set forth in the American Psychiatric Association’s

David S. Rosen, MD, MPH and THE COMMITTEE ONADOLESCENCE

KEY WORDSanorexia nervosa, bulimia nervosa, eating disorders

ABBREVIATIONSAN—anorexia nervosaBN—bulimia nervosaDSM-IV-TR—Diagnostic and Statistical Manual of MentalDisorders, Fourth Edition Text RevisionHPA—hypothalamic-pituitary-adrenalSSRI—selective serotonin-reuptake inhibitor

The guidance in this report does not indicate an exclusivecourse of treatment or serve as a standard of medical care.Variations, taking into account individual circumstances, may beappropriate.

This document is copyrighted and is property of the AmericanAcademy of Pediatrics and its Board of Directors. All authorshave filed conflict of interest statements with the AmericanAcademy of Pediatrics. Any conflicts have been resolved througha process approved by the Board of Directors. The AmericanAcademy of Pediatrics has neither solicited nor accepted anycommercial involvement in the development of the content ofthis publication.

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Diagnostic and Statistical Manual ofMental Disorders, Fourth Edition, TextRevision (DSM-IV-TR) for AN or BN andare labeled as having “partial syn-dromes” or “eating disorder not other-wise specified” (ED NOS).28 There aremany more patients with ED NOS thanthere are patients with AN or BN; theprevalence is estimated to be between0.8% and 14%, depending on the defini-tion used.29 These patients often expe-rience the same physical and psycho-logical consequences as do those whoreach the threshold for diagnosis of ANor BN.28–34 Athletes and performers,particularly those who participate insports and activities that reward alean body habitus (eg, gymnastics,running, wrestling, dance, modeling)may be at particular risk of developingpartial-syndrome eating disorders.35,36

The etiology of eating disorders is mul-tifactorial, and there is increasing evi-dence from both family and twin stud-ies for a strong genetic componentthat is shared between AN and BN.37,38

The mechanism(s) by which geneticfactors influence risk have not beenelucidated, but various hypotheseshave been proposed. Genetic predispo-sition to various trait disturbances suchas behavioral rigidity, perfectionism, orharm avoidance may be more salientthan genetic influences on eating, hun-ger, or satiety.39–41 Genetic effects seemto be “activated” by puberty,42–44 andthere is strong evidence for genetic-environment interactions.39,40

Dieting has also been implicated as apotent proximal risk factor in the de-velopment of disordered eating andeating disorders.45–47 In 1 community-based study, dieters at 5-yearfollow-up were at significantly higherrisk of disordered eating behaviors(eg, vomiting or using diet pills or lax-atives) than nondieters and were alsoat increased risk of obesity.47 In an-other large community cohort, dieterswere 5 times more likely to develop an

eating disorder and severe dieterswere 18 times more likely to developan eating disorder than nondieters.48

Neuroendocrine abnormalities havebeen implicated in the etiology of eat-ing disorders. Leptin is a circulatinghormone produced in adipose tissueand seems to have a significant role inmediating the neuroendocrine effectsof AN. Leptin concentrations are sensi-tive to the acute metabolic effects ofdecreased intake and energy deficits,and decreased circulating leptin con-centrations reflect depleted stores ofbody fat.49–51 Physical hyperactivity is acommon feature of AN and sometimesmanifests as restlessness, athleti-cism, or compulsive exercise. This hy-peractivity also seems to be mediatedby leptin.51

Physical hyperactivity associated withweight loss seems to occur in animalsas well, apparently mediated by hyper-activity of the hypothalamic-pituitary-adrenal (HPA) axis. Syndromes that re-semble AN, characterized by foodrefusal, physical overactivity, and ex-treme weight loss, occur in pigs,sheep, and goats bred for leanness.52

Caloric restriction coupled with envi-ronmental stress produces animalmodels for binge-eating.53 These ani-mals overeat dramatically despite nu-tritional satiety and normal energystatus, which strongly suggests thatreward circuits are being activatedrather than metabolic needs beingsatisfied.43,53

In community-based studies of adoles-cents, disturbances of body image andoverconcern about body shape arecommon, although the prevalence ofeating disorders remains low.54 Theseresults reinforce the likelihood of epi-genetic effects in which the develop-ment of eating disorders reflects theintersection between genetic predis-position, environmental triggers, andpersonal experience.

SCREENING FOR EATINGDISORDERS IN PRACTICE

Primary care providers are in a uniqueposition to detect the onset of eatingdisorders at the earliest stages and tostop their progression.32,33 Pediatri-cians should screen for eating disor-ders as part of annual health supervi-sion or during preparticipation sportsexaminations by monitoring weightand height longitudinally and payingcareful attention to potential signs andsymptoms of disordered eating.

Screening questions about eating pat-terns and body image should be askedof all preteens and adolescents. TheBright Futures guidelines provide ex-amples for addressing this issue withadolescents of different ages.55 TheSCOFF questionnaire, although vali-dated only in adults, can provide aframework for screening (Table 1).56

Weight, height, and BMI should be de-termined regularly and plotted on ap-propriate growth charts. Deviationsfromnormal are easier to identify visu-ally, because nutritional insufficiencymay be manifest by falloff in eitherheight or weight percentiles ratherthan actual weight loss. Growth chartsare available for plotting changes inweight, height, and BMI over time andfor comparing individual measure-ments with age-appropriate popula-tion norms.

Any evidence of excessive weight con-cern, inappropriate dieting, or a pat-tern of weight loss requires further at-tention, as does primary or secondary

TABLE 1 The SCOFF Questionnaire56

1. Do you make yourself sick because you feeluncomfortably full?2. Do you worry you have lost control over howmuch you eat?3. Have you recently lost>1 stone (6.3 kg or 14lb) in a 3-mo period?4. Do you believe yourself to be fat when otherssay you are too thin?5. Would you say that food dominates your life?

One point should be given for every “yes” answer; a scoreof�2 indicates a likelihood of AN or BN.

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amenorrhea or a failure to achieveappropriate increases in weight orheight in growing children. In each ofthese situations, careful assessmentfor the possibility of an eating disorderand close monitoring at intervals asfrequent as every 1 to 2 weeks may beneeded until the situation is clarified.Adolescent girls who seek physiciancare for weight, shape, or eating con-cerns have been shown to be at signif-icantly higher risk of a subsequent di-agnosis of AN.57

A number of studies have shown thatmost adolescent girls express con-cerns about being overweight, andmany may diet inappropriately.10–12,14

Most of these children and adoles-cents do not have an eating disorder.On the other hand, it is known that pa-tients with eating disorders often tryto hide their illness, so simple denialsby the adolescent do not exclude thepossibility of an eating disorder. Ob-taining collateral history from a par-ent may help identify abnormal eatingattitudes or behaviors, although par-ents may, at times, be unaware or indenial as well. When an adolescent isreferred to a pediatrician becauseparents, friends, or school personnelsuspect the possibility of an eating dis-order, it is likely that disordered eatingis present. Pediatricians must, there-fore, not be lulled into a false sense ofsecurity if the adolescent denies allsymptoms. Table 2 outlines questionsthat are useful in eliciting a history ofeating disorders, and Table 3 delin-eates possible physical findings inchildren and adolescents with eatingdisorders.

DSM-IV-TR criteria28 for the diagnosis ofAN and BN are outlined in Table 4. Thesecriteria focus on the weight loss, atti-tudes and behaviors, and amenorrheadisplayed by patients with eating dis-orders. Limitations of these criteria,especially as they relate to childrenand adolescents, have been discussed

extensively in the literature,54,58–61 andrevisions to these criteria have beenproposed for the fifth edition of themanual.60,61 Alternative schema for theclassification of eating disorders inchildren have been described to betterreflect the range of eating issuesseen.58,62

Younger patients (�13 years of age)with eating disorders are more likely tohave premorbid psychopathology (de-pression, obsessive-compulsive disor-der, or other anxiety disorders) and areless likely to havebinge/purgebehaviorsassociated with their illness. The pre-dominance of females is far less; amongthe youngest patients with eating disor-ders, males and females may be equallyaffected. Weight loss often occurs at afaster rate than in older patients. Still,studies have shown that more than half

TABLE 2 History

Specific historyWhat is the most you ever weighed? How tall were you then? When was that?What is the least you ever weighed in the past year? How tall were you then? When was that?What do you think is your healthy weight?What would you like to weigh?Exercise: how much, how often, level of intensity? How stressed are you if you miss exercising?Current eating habits: adequacy of intake, portion sizes, food restrictions, picky eating, fluid intake,ritualized eating habits? Recent vegetarianism? Excessive noncaloric fluid intake?24-h diet history?Calorie-counting? Fat gram–counting? Carbohydrate-counting?Any binge-eating? Frequency? Triggers?Purging history?Use of diuretics, laxatives, diet pills, or ipecac? Ask about elimination pattern, constipation, diarrhea.Any vomiting? Frequency? Timing in relation to meals?Any previous therapy? What kind and how long? What was and was not helpful?Symptoms of hyperthyroidism, diabetes, malignancy, infection, inflammatory bowel disease?Family history: obesity, eating disorders, depression, other mental illness (especially anxiety disordersand obsessive-compulsive disorder), substance abuse by parents or other family members?Menstrual history: age at menarche? Regularity of cycles? Last menstrual period?Use of cigarettes, drugs, alcohol?Use of anabolic steroids (especially in boys)?Use of stimulants?Involvement with proanorexia (“pro-ana”) or probulimia (“pro-mia”) Web sitesHistory of physical or sexual abuse?Review of symptomsDizziness, presyncope, syncope, fatigue?Pallor, easy bruising or bleeding?Cold intolerance? Cold extremities?Palpitations, chest pain, shortness of breath? Exercise intolerance?Hair loss, lanugo, dry skin?Fullness, bloating, abdominal pain, epigastric burning?Vomiting, symptoms of gastroesophageal reflux?Change in bowel habits? Diarrhea, constipation, rectal bleeding?Weakness, muscle cramps?Menstrual irregularities?

TABLE 3 Physical Examination FindingsSometimes Seen in Children andAdolescents With Eating Disorders

Sinus bradycardia; other cardiac arrhythmiasOrthostatic changes in pulse (�20 beats per min)or blood pressure (�10 mm Hg)HypothermiaCachexia; facial wastingCardiac murmur (one-third with mitral valveprolapse)Dull, thinning scalp hairSialoadenitis (parotitis most frequently reported)Angular stomatitis; palatal scratches; oralulcerations; dental enamel erosionsDry, sallow skin; lanugoBruising/abrasions over the spine related toexcessive exerciseDelayed or interrupted pubertal developmentAtrophic breasts; atrophic vaginitis(postpubertal)Russell sign (callous on knuckles from self-induced emesis)Cold extremities; acrocyanosis; poor perfusionCarotenemia (orange discoloration of the skin,particularly palms and soles)Edema of the extremitiesFlat or anxious affect


of all children and adolescents with eat-ing disordersmaynot fullymeet all DSM-IV-TR criteria for AN or BN because theydonot articulate body-imagedissatisfac-tion or because their inadequate nutri-tion is manifest by growth failure ratherthan weight loss to less than 85% of ex-pected weight.63,64 These patients experi-ence the same medical and psychologi-cal consequences of their disorders asdo patients who meet criteria for AN orBN. Indeed, because the sequelae ofweight loss (or failure to gain weight ap-propriately) may have even more worri-some implications for younger patients,relaxation of the diagnostic criteria forchildren and adolescents has been pro-posed in the development of the fifth edi-tion of the Diagnostic and Statistical

Manual of Mental Disorders to facilitateearlier diagnosis and treatment.61

INITIAL EVALUATION OF THEPATIENT WITH DISORDERED EATING

When screening raises suspicion of aneating disorder, initial evaluation in-cludes establishing the diagnosis,evaluating medical and nutritional sta-tus, determining severity, and per-forming an initial psychosocial evalua-tion. This comprehensive evaluation isoften performed in the pediatric pri-mary care setting, and primary careclinicians who feel competent andcomfortable in performing this as-sessment are encouraged to do so.Others should refer to appropriatemedical subspecialists and mental

health personnel to ensure that a com-plete evaluation is performed. A differ-ential diagnosis for the adolescentwith symptoms of an eating disordercan be found in Table 5.

Because eating disorders can affectevery organ system and the medicalcomplications can be serious or evenlife-threatening, a comprehensive his-tory should be taken and a comprehen-sive physical examination should beperformed. The most frequently seenmedical complications are listed in Ta-ble 6 and are detailed in the followingsection.

Most laboratory results will be nor-mal in patients with eating disor-ders; however, normal laboratory re-sults do not exclude serious illnessor medical instability in these pa-tients. Still, an initial laboratory as-sessment should include a completeblood cell count; measurement of se-rum electrolytes, calcium, magne-sium, and glucose; liver functiontests; urinalysis; and measurementof thyrotropin level. Additional stud-ies (eg, urine pregnancy test, serumluteinizing and follicle-stimulatinghormones, serum prolactin, and se-

TABLE 4 Diagnosis of AN, BN, and Eating Disorders Not Otherwise Specified, From DSM-IV-TR28

AN1. Refusal to maintain body weight at or above a minimally normal weight for age and height (ie,weight loss that leads to maintenance of body weight 85% of that expected or failure to makeexpected weight gain during period of growth and leads to a body weight of 85% of that expected).2. Intense fear of gaining weight or becoming fat, even though underweight3. Disturbance in the way in which one’s body weight or shape is experienced, undue influence of bodyweight or shape on self-evaluation, or denial of the seriousness of current body weight4. In postmenarcheal females, amenorrhea (ie, the absence of at least 3 consecutive menstrual cycles)Types

● Restricting type: no regular bingeing or purging (self-induced vomiting or use of laxatives anddiuretics)

● Binge-eating/purging type: regular bingeing or purging behaviorBN1. Recurrent episodes of binge-eating characterized by (a) eating, in a discrete period of time, anamount of food that is definitely larger than most people would eat in a similar period of time andunder similar circumstances and (b) a sense of lack of control over eating during the episode2. Recurrent inappropriate compensatory behavior to prevent weight gain, such as self-inducedvomiting, misuse of laxatives, diuretics, enemas, or other medications; fasting; or excessive exercise3. The binge-eating and inappropriate compensatory behaviors both occur, on average, at least twiceper week for 3 mo4. Self-evaluation unduly influenced by body shape or weight5. The disturbance does not occur exclusively during episodes of ANTypes

● Purging type: the person has regularly engaged in self-induced vomiting or misuse of laxatives,diuretics, or enemas

● Nonpurging type: the person has used other inappropriate compensatory behaviors, such asfasting or excessive exercise, but has not regularly engaged in self-induced vomiting or themisuse of laxatives, diuretics, or enemas

Eating disorder not otherwise specifiedDisorders of eating that do not meet the criteria for either AN or BN; examples include

● All criteria for AN are met except the patient has regular menses● All criteria for AN are met except that despite significant weight loss, weight remains in thenormal range

● All criteria for BN are met except that binge-eating and inappropriate compensatory behaviorsoccur less frequently than twice per week or for a duration of�3 mo

● A patient with normal body weight who regularly engages in inappropriate compensatorybehavior after eating small amounts of food (eg, self-induced vomiting after eating 2 cookies)

TABLE 5 Differential Diagnosis of EatingDisorders

Gastrointestinal disordersInflammatory bowel diseaseCeliac diseaseInfectious diseasesChronic infections (human immunodeficiencyvirus infection, tuberculosis, others)

Endocrine disordersHyperthyroidism (hypothyroidism)Diabetes mellitusOther endocrine disorders (eg,hypopituitarism, Addison disease)

Other psychiatric disordersObsessive-compulsive disorder and anxietydisordersSubstance abuseOther disordersCentral nervous system lesions (includingmalignancies)Other cancersSuperior mesenteric artery syndrome (morecommonly a consequence of severe weightloss)




rum estradiol) may be indicated forpatients with amenorrhea. Bone den-sitometry, using age-appropriatesoftware, should also be considered for

those with amenorrhea for more than 6to 12 months. Other studies includingerythrocyte-sedimentation rate, screen-ing for celiac disease, or radiographicimaging, such as computed tomographyor MRI of the brain or studies of the up-per or lower gastrointestinal system,should be considered if there are uncer-tainties about the diagnosis. An electro-cardiogram should be performed forany patient with cardiovascular signs orsymptoms, for any patient with electro-lyte abnormalities, or for any patientwith significant purging or weight loss.

The initial mental health assessmentshould include an evaluation of the pa-tient’s obsession with food and weight,his or her understanding of the diag-nosis, and his or her willingness to re-ceive help. The patient’s social func-tioning at home, in school, and withfriends should be assessed. Psychiat-ric comorbidity is common with eatingdisorders and is often previously undi-agnosed.34,65 The pediatrician shouldidentify other potential psychiatric di-agnoses (such as depression, anxiety,or obsessive-compulsive disorder),which may be a cause or consequenceof disordered eating. Use of tobacco,alcohol, or illicit drugs or misuse ofprescription or over-the-counter med-ications may also complicate the man-agement of eating disorders. Suicidalideation and history of physical or sex-ual abuse or violence should also beassessed. Suicide attempts and com-pleted suicide are relatively common,particularly for patients who havebinge/purge or purging behavior andare a major contributor to eating dis-order–associated mortality. Deathfrom suicide is 50 times more likely inpatients with AN,66 and 25% to 35% ofpatients with BN report a history of at-tempted suicide.34

The parents’ reaction to the illnessshould also be assessed. Parental in-difference or denial of the problem orinconsistent views about treatment

may affect the course of the illness andrecovery.

Determining where and by whom thepatient will be treated is an importantand practical component of the initialevaluation. Patients with limited nutri-tional, medical, and psychological dys-function can be managed in the pedia-trician’s office in conjunction withoutpatient nutrition and mental healthsupport. Patients who are more ill of-ten require more intensive services,ideally delivered by a specialized mul-tidisciplinary team, and sometimes inday-treatment, hospital, or residentialsettings.

MEDICAL COMPLICATIONS INPATIENTS WITH EATING DISORDERS

Medical complications associatedwitheating disorders are listed in Table 5,and details of these complicationshave been described in many re-views.32,33,67–74 Significant complica-tions are seen in both outpatients andinpatients.75 Most of the medical com-plications of eating disorders resolvewith refeeding and/or resolution ofpurging.70 However, there is increasingconcern that some complications—particularly growth retardation, struc-tural brain changes, and low bone min-eral density—may, with time, becomeirreversible.72 Malnutrition underliesmany of the somatic symptoms seen ini-tially, and these changes are often adap-tive to the associated energy deficits.Over time, adaptation fails and signs andsymptoms reflect the inability to com-pensate for inadequate nutrition. Meta-bolic rate decreases, body temperaturecan no longer be maintained, andnearly every organ system iscompromised.70,75,76

Common cardiovascular signs andsymptoms include orthostasis withblood pressure and/or pulse changes,bradycardia, and poor peripheral perfu-sion characterized by cold extremities,delayed capillary refill, and sometimes

TABLE 6 Medical Complications That ResultFrom Eating Disorders

GeneralDehydrationHypokalemiaHypomagnesemiaHyponatremiaIrreversible cardiomyopathy and myositis(ipecac toxicity)Amenorrhea and menstrual irregularitiesLow bone mineral density; osteoporosisCognitive deficitsMood symptomsObsessive/compulsive symptomsSuicideCaloric restriction and weight lossInability to maintain body temperatureProlonged corrected QT interval or increasedQT dispersion (uncommon but maypredispose patient to sudden death)Dysrhythmias (including supraventricularbeats and ventricular tachycardia, with orwithout exercise)Other electrocardiographic abnormalitiesMitral valve prolapsePericardial effusionsDelayed gastric emptying and impairedgastrointestinal tract motilityConstipationBloating; postprandial fullnessHypoglycemiaHypercholesterolemiaAbnormal liver function test resultsSterile pyuriaAnemia, leukopenia; thrombocytopeniaSick-euthyroid syndromeGrowth retardationCortical atrophyVomiting-relatedHypochloremic metabolic alkalosis (vomiting)EsophagitisGastroesophageal refluxDental erosionsMallory-Weiss tearsEsophageal or gastric rupture (rare)Aspiration pneumonia (rare)Laxative-relatedHyperchloremic metabolic acidosis (laxativeabuse)HyperuricemiaHypocalcemiaFluid retention (may gain up to 10 lb in 24 h)with laxative withdrawal

RefeedingDiaphoresis and night sweatsPolyuria and nocturiaPeripheral edemaRefeeding syndrome


acrocyanosis. Conduction abnormalitiesmay occur as a result of myocardial at-rophy and are thought to be the mostcommon proximal cause of death withAN. Repolarization abnormalities, char-acterized by QTc prolongation and/or in-creased QT dispersion, are reportedwith widely variable prevalence andseem to be more frequent in older pa-tients andwith increasing duration of ill-ness.77 Repolarization abnormalities arepotentially life-threatening and shouldbemanaged aggressively. Pericardial ef-fusion, a functional mitral valve pro-lapse, myocardial dysfunction, and eme-tine (ipecac-related) cardiomyopathyare all seen less frequently. Congestiveheart failure canoccurduring refeeding,particularly in the setting of electrolyteabnormalities.72,73,78

Gastrointestinal complaints are com-mon and sometimes precede diagno-sis of the eating disorder. Delayed gas-tric emptying and increased intestinaltransit time often contribute to subjec-tive descriptions of bloating and post-prandial fullness, which can furthercompromise nutritional restoration. Inpatients who vomit, symptoms of gas-troesophageal reflux are common, andupper gastrointestinal bleeding some-times occurs. Severe bleeding second-ary to Mallory-Weiss tears of theesophagus is rare. Constipation iscommon and often difficult to manage.Nutritional strategies, stool softeners,or polyethylene glycol 3350 (Miralax)are the treatments of choice; stimulantlaxatives should be avoided. Rectalprolapse sometimes occurs in the set-ting of constipation and/or laxativeabuse. Hepatic transaminase levelsare often elevated as a consequence ofmalnutrition and are not usually indic-ative of viral hepatitis. Hypertrophy ofthe salivary glands often occurs andmay be a clue to binge-eating and/orvomiting. Esophageal or gastric rup-ture are catastrophic but rare compli-

cations that usually occur duringrefeeding.73

Fluid and electrolyte abnormalitiesmay occur as a result of purging orwith increasing cachexia. Dehydrationcan be seen in any patient with an eat-ing disorder and can sometimes leadto orthostatic symptoms, presyncope,or syncope. Chronic dehydration andthe body’s effort to conserve watermay induce a pseudohyperaldosteron-ism, which also leads to hypokalemia.However, significant deficits in totalbody potassium and the associatedrisk of arrhythmia may exist even witha normal serum potassium level. Pa-tients with vomiting may have a hypo-chloremic metabolic alkalosis be-cause of chronic loss of hydrochloricacid. Patients who abuse laxatives mayhave a hyperchloremic metabolic aci-dosis related to bicarbonate wasting.Dilutional hyponatremia can be seen inpatients who “water load” instead ofeating or to misrepresent their weightat outpatient visits. Hypomagnesemiathat results from inadequate intake isassociated with sudden cardiac death,may interfere with potassium reple-tion in patients who are hypokalemic,and sometimes contributes to refeed-ing syndrome.70 Edema, sometimessignificant, may be seen as a result ofhypoproteinemia, during refeeding, orin association with laxative abuse.70

Endocrine dysfunction is common andincludes hypothyroidism, hypercorti-solism, and disturbances of the HPAaxis, which result in hypogonadotropichypogonadism, luteal phase abnor-malities, and anovulation. Euthyroid-sick syndrome (low free thyroxine,normal thyrotropin) is the most com-mon thyroid abnormality and is re-versible with refeeding. Supplementalthyroid hormone is not indicated. Acti-vation of the HPA axis has been clearlydemonstrated. In addition to its delete-rious effects on growth, thyroid func-tion, and the reproductive system, HPA

hyperactivity also contributes to theappetite suppression and physicaloveractivity that characterize eatingdisorders.79 Hypothalamic suppres-sion causing amenorrhea is attribut-able not only to weight loss but alsoto physical overactivity, emotionalstress, and the metabolic changesassociated with acute energy defi-cits70,75; it sometimes precedesweight loss.70 Hypothalamic secre-tion of gonadotropins reverts to aprepubertal pattern that reverseswith refeeding.70 Amenorrhea is animportant marker for increased riskof low bone mineral density and os-teoporosis (discussed in a laterparagraph),80–83 and an intriguing re-cent report suggested that amenor-rhea is also associated with the cogni-tive impairments seen with AN.84

Common skin changes include lanugo,dry scaly skin, and yellow discolora-tion related to carotenemia. Acrocya-nosis can be seen when perfusion ispoor. Hair and nail changes are oftenseen as well, and angular stomatitismay be related to either vomiting orvitamin deficiencies.70

Growth retardation, short stature, andpubertal delay may all be seen in pre-pubertal and peripubertal childrenand adolescents with eating disor-ders.75,85 Many endocrine abnormali-ties contribute to this growth failure;abnormal thyroid function, abnormaladrenal function, low levels of sex ste-roids, and uncoupling of growth hor-mone from insulin-like growth factor 1(IGF-1) have all been implicated.72

Catch-up growth has been inconsis-tently reported in the literature;younger patients may have greaterand more permanent effects ongrowth.72,86

Low bone mineral density is a frequentcomplication of eating disorders inboth male and female patients. It isworrisome not only because of the in-creased risk of pathologic fractures




but also because of its potential to beirreversible and compromise skeletalhealth across the entire life span. Thepathophysiology of abnormal bonemineralization in the eating disordersis likely to be multifactorial; proposedmechanisms include deficiencies ofgonadal steroids (estrogen and/or tes-tosterone), deficiencies of calcium andvitamin D, reduction in lean musclemass and its mechanical effects onbone, and excesses of endogenous glu-cocorticoids related to hyperactivity ofthe HPA axis. The reversibility of skele-tal changes is unclear and probablyvaries on the basis of disease severity,the timing of illness and recovery, andperhaps genetic factors. Because ado-lescence is a critical period for bonemineralization, younger patients withAN are at higher risk of skeletalchanges than are older patients. Treat-ment strategies, such as supplementalestrogen, bisphosphonates, calcium,and vitamin D replacement, have notbeen shown to be consistently effec-tive, are not a substitute for nutritionalrecovery, and are not recommendedfor routine use.72,87,88

Volume deficits in both gray and whitematter of the brain and associated in-creases in the cerebrospinal fluidspace occur with weight loss in AN andare proportional to weight loss. Brainchanges may be associated with ele-vated cortisol concentrations relatedto HPA-axis dysfunction, analogous tochanges now being reported in otherpsychiatric disorders such as post-traumatic stress disorder.89 Cognitiveimpairment has been demonstratedacross the wide range of neuropsycho-logical domains but does not seem tobe directly proportional to structuralbrain changes.84 Functional imagingstudies of the brain show decreases inboth global and localized brain activity,but it is unknown whether these de-creases precede or are a consequenceof weight loss or whether they are re-

versible.90 Normalization of whitematter occurs with refeeding; how-ever, gray matter changes seem topersist despite weight recovery.84,89

TREATMENT CONTINUUM FORCHILDREN AND ADOLESCENTS WITHEATING DISORDERS

Most adolescent patients with eatingdisorders will be treated in outpatientsettings. Pediatricians play an impor-tant role in the management ofthese patients, assessing treatmentprogress, screening for and managingmedical complications, and coordinat-ing care with nutrition and mentalhealth colleagues. Some pediatriciansin primary care practice will feel com-fortable in coordinating care; otherswill choose to refer some or all pa-tients with eating disorders to thosewith special expertise. Depending onthe availability of local resources,these providersmay be a specialty eat-ing disorders program, an adolescentmedicine specialist, a psychiatrist, oranother mental health provider.32,91

Collaborative Outpatient Care

Most children and adolescents witheating disorders will bemanaged in anoutpatient setting by a multidisci-plinary team coordinated by a pediatri-cian or medical subspecialist with ex-pertise in the care of children andadolescents with eating disorders. Pe-diatricians generally work with nurs-ing, nutrition, and mental health col-leagues in provision of the medical,nutrition, and mental health care re-quired by these patients.

It is generally accepted that medicalstabilization and nutritional rehabilita-tion are the most important determi-nants of short-term outcomes and areessential for correcting cognitive defi-cits to allow for effective mental healthinterventions. Components of nutri-tional rehabilitation required in themanagement of patients with eating

disorders have been presented in sev-eral reviews.32,33,92–95 In the UnitedStates, oral refeeding is clearly thepreferred modality for nutritional re-habilitation. However, for patients whoare unwilling or unable to eat, supple-ments or nasogastric feeding may belife-saving.

Meals and snacks generally are rein-troduced or improved in a stepwisemanner for those with AN, which leads,in most cases, to an eventual intake of2000 to 3000 kcal (or more) per dayand a weight gain of 0.25 to 1 kg perweek. Smaller, more frequent meals;increasing the caloric density of foods;and substituting nutrient fluids (eg,fruit juice) for water can sometimeshelp patients overcome the postpran-dial fullness and psychological barri-ers associated with the substantialincrease in caloric intake that is re-quired. Patients with abdominal com-plaints from acquired nutritionallyme-diated lactase deficiency may benefitfrom supplemental lactase. Meals arechanged to ensure ingestion of 2 to 3servings of protein per day. Daily fatintake should be slowly shifted towarda goal of 30 to 50 g per day. The stereo-typical and obsessional eating habitsfavored by many patients with eatingdisorders and the observation thatsimilar levels of weight loss and mal-nutrition can lead to dramatically dif-ferent medical consequences suggestthat deficiencies of specific micronu-trients may share responsibility withprotein-calorie malnutrition for themedical consequences in eating disor-ders.70 Food variety should be encour-aged, and a multivitamin should berecommended. Behavioral interven-tions are often required to encouragereluctant (and often resistant) pa-tients to meet necessary caloric intakeand weight-gain goals.96–99

Ranges for treatment goal weightshould be individualized and based onage, height, pubertal stage, premorbid


weight, and previous growth trajec-tory. Furthermore, for growing chil-dren or adolescents, the goal weightrange should be reevaluated at regu-lar intervals (eg, every 3 to 6 months)on the basis of changing age andheight. In postmenarcheal girls, re-sumption of menses provides an ob-jective measure of biological health100;in 1 recent study, resumption of men-ses occurred at a mean BMI percentileof 27; 75% of the girls resumed men-struating once they had achieved andsustained approximately the 40th per-centile for BMI.101 Resumption of men-ses can also be used to refine the treat-ment goal weight.

Family-Based (“Maudsley”)Therapy

Over the past decade, specialized eat-ing disorder–focused family-based in-terventions, based on work originallyperformed at the Maudsley Hospital inLondon, have gained attention in thetreatment of adolescent AN because ofpromising short-term and long-termoutcomes. Although the etiologic un-derpinnings of this treatment ap-proach have lostmuch of their supportover time (ie, it is no longer believedthat eating disorders are causedmainly by family dysfunction), family-based interventions, nevertheless, re-main an effective and evidence-basedtreatment strategy for adolescent ANin both open trials and randomizedcontrolled studies.102–105 Family-basedinterventions are typically describedas having 3 phases. In the first phase,parents, supported by the therapist,take responsibility to make certainthat their adolescent is eating ade-quately and limiting other pathologicweight-control behaviors. In the sec-ond phase, substantial weight recov-ery has already occurred, and the ad-olescent is helped to gradually resumeresponsibility for his or her own eat-ing. In the final phase of treatment,weight has been restored, and the

therapy shifts to address the moregeneral issues of adolescent develop-ment and how they may have been de-railed by the eating disorder.102 A man-ual for providers106 and a family-support manual107 are now available.Unfortunately, family-based treatmentby experienced providers is not avail-able in all communities. Nevertheless,the essential principles of family-based treatment can still be encour-aged by community providers in theirwork with patients and families.105

Family-based treatment may not besuitable for all patients; caution hasbeen advised for families in whichthere is parental psychopathology orhostility toward the affected child, forolder patients, or for patients who arethe most medically compromised.102,104

Additional randomized controlledstudies of family-based treatment, in-cluding studies of long-term out-comes, are still needed. Family-basedapproaches are now being evaluatedfor the treatment of BN as well.108

Treatment of BN in adolescents hasbeen poorly studied, and there is littleevidence to guide treatment recom-mendations. For adults, BN-focusedcognitive behavioral therapy is thetreatment of choice. Pharmacotherapy(see “Pharmacotherapy”) has beenhelpful as well.

Day-Treatment Programs

Day-treatment programs (day hospi-talization, partial hospitalization) havebeen developed to provide an interme-diate level of care for patients with eat-ing disorders who require more thanoutpatient care but less than 24-hourhospitalization.109–112 These programshave been used in an attempt to pre-vent the need for hospitalization; insome cases, they are used as a “step-down” from inpatient to outpatientcare. Day-treatment programs areless costly and more accessible thantraditional hospitalization. In addition,

they allow for more family and socialsupport and for recovery to occur in amore naturalistic environment thatmay be more generalizable.109 Daytreatment typically involves 8 to 10hours of care (including meals, ther-apy, groups, and other activities) by amultidisciplinary staff 5 days/week.Evaluation of day-treatment programshas been characterized by small sam-ples and the difficulty in undertakingrandomized controlled trials.113 Still,short-term outcomes have generallybeen reported to be good.110,113,114 A re-cent study that used a range of out-come measures, including BMI andmeasurement of binge-purge behav-ior, demonstrated day treatment to behighly effective in the treatment ofboth restrictive and binge-purge ANand BN. Furthermore, these resultswere sustained or improved over 18months of follow-up.113

Hospital-Based Treatment

Hospital-based treatment for eatingdisorders is less common when inten-sive outpatient or day-treatment pro-grams are available. Hospitalization ismuchmore frequently required for ad-olescent patients with AN than for pa-tients with BN. Criteria for hospitaliza-tion of children and adolescents witheating disorders have been enumer-ated by the Society for AdolescentMed-icine and are listed in Table 7.32 Similarcriteria are endorsed in the AmericanPsychiatric Association’s practiceguideline for the treatment of patientswith eating disorders33 and by otherorganizations.115 These criteria ac-knowledge that hospitalization may berequired because ofmedical or psychi-atric needs or when there is failure ofoutpatient treatment to achieve medi-cal, nutritional, or psychiatric goals.Unfortunately, many third-party pay-ers in the United States do not adhereto these criteria and make it difficultfor some children and adolescentswith eating disorders to receive the




recommended level of care.116,117 Chil-dren and adolescents have the bestprognosis if their disease is treatedrapidly and aggressively (an approachthat may not be as effective for adultswith a more long-term, protractedcourse).91 Hospitalization, when indi-cated, allows for medical stabilization,adequate weight gain, and establish-ment of safe and healthy eating habitsand improves the prognosis for chil-dren and adolescents. Discharge ofhospitalized patients too soon often re-sults in medical complications, aworse clinical course, and readmis-sion. In 1 study, patients with AN whowere discharged while still under-weight had a 50% readmission ratecompared with a rate of less than 10%for patients who had reached at least90% of their recommended averagebody weight before discharge.118

The pediatrician involved in the treat-ment of hospitalized patients must beprepared to provide nutrition via a na-sogastric tube or even intravenouslywhen necessary. In hospitalized maleadolescents, supplemental nighttime

nasogastric feedings have been shownto significantly increase both weightgain and improvement in BMI com-pared with oral refeeding alone.119

Refeeding syndrome may occur in se-verely malnourished patients, particu-larly in the setting of aggressivenutritional rehabilitation. Refeedingsyndrome refers to a constellation ofmetabolic, cardiovascular, neurologic,and hematologic complications pri-marily related to shifts of phosphatefrom extracellular to intracellularspaces in the setting of total bodyphosphorus depletion. The syndromeis most common in hospitalized pa-tients during the first week of hospital-ization and patients who are receivingsupplemental enteral or parenteral nu-trition. Cautious refeeding, careful mon-itoringof serumelectrolyte,magnesium,phosphorus, and glucose levels, and alow threshold for phosphorus supple-mentation prevent the development ofrefeeding syndrome.71,72,120–123 Refeedingsyndrome is unusual after the first 2weeks of nutritional rehabilitation orin patients being treated in the outpa-tient setting.

Pharmacotherapy

Nomedications have been approved bythe US Food and Drug Administrationfor the treatment of AN.124 Pharmaco-therapy is sometimes prescribed butis typically targeted at comorbidsymptoms of depression and anxiety.Selective serotonin-reuptake inhibi-tors (SSRIs) are most often used butmay not be effective in severely mal-nourished patients. There is also lim-ited evidence for the use of SSRIs forrelapse prevention in AN.125 In recentcase reports and open-label trials,atypical neuroleptic agents, predomi-nantly olanzapine (Zyprexa), have beennoted to improve both weight gain anddysfunctional thinking in patients withAN.126 A recently completed random-ized, double-blind, placebo-controlled

trial in adults showed a significant in-crease in weight gain in those whowere taking olanzapine and a concom-itant decrease in obsessive symptoms,although the effect size was modest.127

Further evaluation of the effectivenessof these agents is underway, and cau-tion is warranted because of the riskof developing insulin resistance andmetabolic syndrome.

In contrast to AN, several pharmaco-logic agents have been demonstratedto be effective for the treatment of BN.Although only fluoxetine has beenapproved by the Food and Drug Admin-istration, other SSRIs, serotonin/norepinephrine-reuptake inhibitors (eg,venlafaxine), and tricyclic antidepres-sants have also been shown to decreasebinge-eating and purging in BN.124,128

Topiramate has been shown to signifi-cantly decreasebinge-eatingandmaybean option for patients who do not re-spond to or are not able to tolerate SS-RIs.129 Other drugs, including naltrexoneand ondansetron (Zofran), are beingused with some success in BN, althoughdataare lacking to recommend their usemore broadly.130

Hormonal supplementation, althoughcapable of restoring menstruation,has not been shown to reliably im-prove bone mineral density and is nota substitute for nutritional rehabilita-tion and restoration of positive energybalance.

PROGNOSIS

The prognosis of eating disorders inadolescents has varied widely in theliterature, and outcomes have de-pended on methodology, definitions ofrecovery, and duration of follow-up inthe studies reported.131 Adolescentoutcomes are significantly better thanthe outcomes reported in adults. Lon-gitudinal reports reflect a more opti-mistic and less hopeless outcome; fol-lowed over time, the majority ofpatients fully recover, and an even

TABLE 7 Criteria for Hospital Admission forChildren, Adolescents, and YoungAdults With Eating Disorders32

AN�75% ideal body weight or ongoing weightloss despite intensive managementRefusal to eatBody fat� 10%Heart rate� 50 beats per min daytime;�45beats per min nighttimeSystolic pressure� 90 mm HgOrthostatic changes in pulse (�20 beats permin) or blood pressure (�10 mm Hg)Temperature� 96°FArrhythmiaBNSyncopeSerum potassium concentration� 3.2 mmol/LSerum chloride concentration� 88 mmol/LEsophageal tearsCardiac arrhythmias including prolonged QTcHypothermiaSuicide riskIntractable vomitingHematemesisFailure to respond to outpatient treatment


larger proportion have a behavioralcure (normal eating, normal weight,and resumption of menses). However,these results accrue only after morethan 10 years of follow-up; therefore,patients, their families, and cliniciansmust be prepared to remain engagedin what may sometimes be a pro-tracted treatment process.132–134

Strober et al132 conducted an impor-tant study in which 95 people who hadbeen hospitalized for AN as adoles-cents were followed for 10 to 15 years.By the end of follow-up, 86.3% hadachieved partial or complete recovery,and there were no deaths. However,the median time to partial recoverywas 57.4 months, and the median timeto full recovery (met by �75% of thestudy population) was 79.1 months. Astudy from Germany produced similarfindings; at 10-year follow-up, 69% ofthe patients (including 7 boys) hadachieved full recovery, and there wereno deaths. Again, however, the coursewas protracted and the authorspointed out a high rate of residual psy-chiatric disorders even after full re-covery from AN.135

Patients with an earlier age of onsetseem to have a better prognosis.85,134

Other characteristics associated witha better prognosis include shorter du-ration of symptoms and a betterparent-child relationship. Purging be-havior, physical hyperactivity, moresignificant weight loss, and diseasechronicity are all associated with aless favorable prognosis.134 Even afterrecovery, therearehighratesof residualpsychiatric illness—predominantly de-pression and anxiety—that per-sist.133,136,137 A meta-analysis of 119 ANoutcome studies showed little im-provement in the success of treatmentover the 5 decades reviewed.133

Mortality rates for adolescents withboth AN and BN are lower than thosethat have historically been report-ed.133,134 In a recent meta-analysis, the

mortality rate among adolescents withAN was reported to be 1.8% comparedwith a mortality rate of 5.9% whenadults and adolescents were consid-ered together.134 Mortality, when itdoes occur, is most often attributableto the complications of starvation or tosuicide.66

PEDIATRICIANS’ ROLE INPREVENTION AND ADVOCACY

Efforts to prevent eating disorders cantake place both in practice and com-munity settings, such as schools. Pri-mary care pediatricians can help fam-ilies and children learn to apply theprinciples of proper nutrition andphysical activity and to avoid an un-healthy emphasis on weight and diet-ing.138 In addition, pediatricians canscreen to detect the early onset ofdisordered eating and be careful toavoid seemingly innocuous statements(such as “you could stand to lose a lit-tle weight”) that are sometimes re-ported by patients to have triggeredthe onset of their eating disorder. Atthe community level, there is generalagreement that changes in the culturalapproaches to weight, dieting, andbody image will be required to de-crease the growing numbers of chil-dren and adolescents at risk of devel-oping eating disorders. This culturalshift is made more challenging by theincreasing prevalence of obesity andthe competing responsibility to ad-dress its health risks as well.15

A variety of successful programs forpreventing eating pathology have beendeveloped for various settings.139 Thelargest effect sizes were seen in pro-grams targeted at high-risk popula-tions, in programs that were interac-tive rather than didactic, and inprograms aimed at older adolescents.Content varied even in the most suc-cessful programs, which suggests thata variety of approaches may be effec-tive. Multisession programs were more

effective than single-session pro-grams,140 and there has even been someconcern that single-session programsmay be counterproductive.141–146 An im-portant question currently beingasked is whether we can work simul-taneously toward the prevention ofeating disorders and obesity.15

Reimbursement issues continue tolimit the access of many patients witheating disorders to appropriate ser-vices. Availability of mental health ser-vices, lack of mental health parity, andservice “carve-outs” all have been bar-riers to patients and families who seekclinically necessary treatment andseem to be disproportionately prob-lematic for patients with eating disor-ders. Despite evidence of its effective-ness, family-based treatment is notavailable in many communities.Through advocacy, pediatricians canhelp support health care reform ef-forts that will ensure that children andadolescents with eating disorders areable to receive necessary care.

GUIDANCE FOR PEDIATRICIANS

1. Pediatricians need to be knowl-edgeable about the risk factorsand early signs and symptomsof disordered eating and eatingdisorders.

2. When counseling families on prevent-ing obesity, pediatricians should fo-cus on healthy eating and buildingself-esteem while still addressingweight concerns. Care needs to betaken not to inadvertently enable ex-cessive dieting, compulsive exercise,or other potentially unhealthyweight-management strategies.

3. Pediatricians should be encour-aged to calculate and plot weight,height, and BMI by using age- andgender-appropriate charts and as-sessmenstrual status in girls at an-nual health supervision visits.

4. Pediatricians should screen pa-tients for disordered eating




and related behaviors and beprepared to intervene whennecessary.

5. Pediatricians should monitor orrefer patients with eating disor-ders for medical and nutritionalcomplications.

6. Pediatricians need to be familiarwith treatment resources in theircommunities so that they can coor-dinate or facilitate multidisci-plinary care.

7. Pediatricians can play a role in pri-mary prevention during office visitsand through school-based and com-munity interventions with a focus

on education, early screening, andadvocacy.

8. Pediatricians are encouraged to ad-vocate for legislation and policychanges that ensure appropriateservices for patients with eatingdisorders, including medical care,nutritional intervention, mentalhealth treatment, and care coordi-nation, in settings that are appro-priate for the severity of the illness.

LEAD AUTHORDavid S. Rosen, MD, MPH

COMMITTEE ON ADOLESCENCE,2009–2010Margaret J. Blythe, MD, ChairpersonPaula K. Braverman, MD

Cora C. Breuner, MD, MPHDavid A. Levine, MDPamela J. Murray, MD, MPHRebecca F. O’Brien, MDWarren M. Seigel, MD

PAST COMMITTEE MEMBERSDavid S. Rosen, MD, MPHMichelle S. Barratt, MD, MPHCharles J. Wibbelsman, MD

LIAISONSLesley Breech, MD – American College ofObstetricians and GynecologistsJorge L. Pinzon, MD – Canadian PaediatricSocietyBenjamin Shain, MD, PhD – American Academyof Child and Adolescent Psychiatry

STAFFKaren [email protected] Del Monte, JD

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