dr. richard l. levine professor of pediatrics and psychiatry chief, division of adolescent medicine...
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Dr. Richard L. LevineProfessor of Pediatrics and PsychiatryChief, Division of Adolescent Medicine and Eating DisordersPenn State Hershey Children’s Hospital
Case Example
K is a 22 y.o. female college student, track star at a local university.
Asked to leave track team this semester because of malnutrition, referred to student health center for evaluation.
Transferred to HMC for severe malnutrition and medical instability.
Evaluated and admitted to MIMC.
Case Example
History of severe restriction of food intake and more than 50 lbs.weight loss over 6-9 months. Seen by Internist during summer and cleared for return to school. Asked to “eat better.”
Significant exercise with running, even the day of admission.
No vomiting or laxative use, but history of diet pill use.
Amenorrhea, and fatigue.
Case Example
On examination: Ht. 5’11’’, Wt. 109 lbs. Vital Signs: pulse 32 bpm, BP 88/56. Laboratories demonstrated
hyponatremia, hypokalemia, hypophosphatemia, abnormal LFT and abnormal renal function tests.
Abnormal EKG with heart block and prolonged QTc.
Abnormal echo with dilated RV, LV, low systolic function, MVP and mitral regurgitation.
Case Example
Patient did well in MIMC. Treated with IV fluids, electrolyte
replacement including phosphate replacement.
Nutrition slowly improved. However- found exercising in bed- which was discouraged.
Transferred to medical floor bed and then to inpatient eating disorder facility close to family’s home.
Diagnostic Criteria
Established in DSM IV Useful in setting the diagnostic
standard But should not be applied too strictly
in determining who is to be treated, especially in adolescents
Diagnostic Criteria
Anorexia Nervosa Refusal to maintain a normal weight
for height, leading to a weight which is less than 85% expected
This may include weight loss or failure to make expected weight gains during a period of growth
Diagnostic Criteria
Anorexia Nervosa An intense fear of gaining weight or
becoming fat A disturbance in the perception of
body weight or shape In post-menarchal females- the
presence of secondary amenorrhea for three consecutive menstrual cycles
Diagnostic Criteria
Anorexia Nervosa Two subtypes described: Restricting
and Binge eating/Purging Many adolescents with eating
disorders do not fulfill all of these criteria
One should not deny treatment to these “sub-clinical” patients
Case 2-Bulimia Nervosa
A.M. was a 16 year old female seen on the GI inpatient service with a history of chronic intractable vomiting. Negative w/u. Symptoms did not improve after cholocystectomy.
Eventually admitted to bulimic symptoms History of sexual activity without
contraception Positive testing for chlamydia and herpes History of substance use,depression and
cutting behavior
Diagnostic Criteria
Bulimia Nervosa Recurrent episodes of binge eating
followed by some recurrent inappropriate compensatory behavior
Binges characterized by eating a very large amount of food over a short period of time and feeling a lack of control over eating
Diagnostic Criteria
Bulimia Nervosa The compensatory behavior can
include self-induced vomiting, laxatives, enemas, diuretics or compulsive exercise
This behavior must occur on average twice a week for three months
Also demonstrate over-concern with weight and body shape
Diagnostic Criteria
Bulimia Nervosa Two subtypes described:Purging and
Non-purging who use fasting and exercise as the compensatory behavior
Also category of Eating Disorder-Not Otherwise Specified
Diagnostic Criteria
Significant controversies regarding the diagnostic criteria and possible modifications for DSM V. Cutoff weight for AN Amenorrhea for AN BED Role of EDNOS ED in children
Epidemiology
Incidence increased 2-5x in past 30 years
Prevalence of AN is about 1/120 adolescent females
Female to male ratio is 10-1
AN demonstrates a bimodal age range with peaks at 14,18
Bulimia nervosa has prevalence of 1-5%
Increased in older teens
Female to male ratio of 5-1 to 20-1
Must consider Dx of AN, BN in males
All social, economic, cultural classes
Epidemiology
Statistics underestimate prevalence of disturbed body image and eating behavior in teens
50%-67% of adolescent females are dissatisfied with wt, body shape
Majority of female teens have dieted
Many use unhealthy wt control methods such as fasting, diet pills and vomiting
Studies correlate abnormal eating attitudes and behavior with other risk-taking behavior
Etiology
Etiology is multifactorial Biological vulnerability and genetic
role Psychological factors Cultural influences
Etiology
Neuroendocrine dysfunction Serotonin dysregulation According to family studies the risk of
AN or BN is 7- 20 times more common among a female relative of a patient with an ED than the general population.
Most likely not related, however, to one particular gene or chromosome but rather a “multi- hit” process.
Etiology
Psychological factors Individual problems and family
dynamics Patients with AN demonstrate low
self esteem and pervasive sense of ineffectiveness
Depressed, anxious, obsessive, perfectionistic.
BN- problems with impulse control
Etiology
Cultural Influences are important
Emphasis on thinness in society
Exacerbated by media
Increase in nutrition and fitness articles
Female body shape of models
Role of excessive exercise
Females in gymnastics and ballet
Males in wrestling
Differential Diagnosis
Diagnosis usually self-evident
Must consider other conditions
Eating Disorders can present in patients with another chronic disease
Endocrine Gastroenterlogical Neurological Malignancies Chronic Infection Connective Tissue
Diseases Other
Psychological Conditions
Evaluation
Screen yearly Assess with
complete H/P Assess eating
behavior, weight history, body image, bingeing/purging, exercise, etc.
Complete PE with vital signs, accurate ht. and wt.
Examine looking for physical sequelae of disease and other diagnoses.
Limited laboratory evaluation.
In the office
“Red Flags” on Physical Exam Bradycardia Hypotension BMI Hypothermia Parotid enlargement Enamel Erosion Acrocyanosis Russel’s sign- abrasions of knuckles of the
hand
Medical Complications
Serious medical conditions that require early and aggressive treatment
Affect every organ of the body Some are reversible, but concerns about
long-term, irreversible complications 4% mortality associated with anorexia Causes of death include suicide, severe
electrolyte disturbances, and arrhythmias
Metabolism
Patients with Anorexia have an abnormal metabolism with reduced energy expenditures- demonstrated by indirect calorimetry.
Fat and lean body mass are reduced and extra cellular water volume is expanded.
Physiological adaptation to severe malnutrition.
Concept of “Autocannibalization.”
Case - Fluids and Electrolytes CH is 18 year old female with Anorexia
Nervosa with purging features. Long history of eating disorder behavior
with restricting and purging via vomiting.
Presents to the emergency room with syncope.
Ht. 65”, Wt. 76 lbs., BP- 93/65, P-60 Labs included Na 132, CL 84, K 1.4,
CO2 36
Fluids and Electrolytes
Patients with Bulimia or Anorexia with purging features can present with significant abnormalities in fluids and electrolytes.
With vomiting this takes the form of a hypokalemic, hypochloremic metabolic alkalosis.
Fluids and Electrolytes
Patients with laxative abuse develop metabolic acidosis due to bicarbonate losses in the stool.
Patients with anorexia can present with dehydration if fluid restricting.
Patients can also demonstrate symptomatic hypoglycemia.
Case One - GI Complications J is a 19 year old female presenting
with a restricting/bingeing/purging cycle. Diagnosis- Bulimia Nervosa.
History of depression, self-mutilation treated with medication. History of substance abuse including “huffing”.
History of abdominal pain, hematemesis, involuntary vomiting.
Case One -GI Complications On PE- Ht. 5’4’’, Wt. 139 lbs.,
epigastic tenderness Endoscopy revealed esophagitis. Patient treated with PPI, sucralfate,
and metoclopramide. Poor compliance with medications-
symptoms persist at the present time.
Currently in ED-PHP
Case Two-GI Complications MM is 16 year old female who
presented with restricting and weight loss, and amemorrhea. Significant family problems.
On PE- Ht. 5’9’, wt. 94.5 lbs.- emaciated appearance.
Started to eat with treatment but began bingeing. Developed abdominal pain and constipation with laxative abuse.
Case Two- GI Complications Gained a large amount of weight
quickly- now up to 150 lbs. Abdominal pain increased. Saw local
GI specialist. Had normal barium enema.
Required colace, lactulose, mineral oil for bowel movements.
Condition has currently stabilized but continues to over eat
Gastrointestinal Complications Depend on the nature of the eating
disorder. With Anorexia Nervosa-
complications of decreased gastric and small intestinal motility
Early satiety Gastroparesis Chronic constipation
Gastrointestinal Complications With Bulimia Nervosa- complications
from the purging behavior. Can develop chronic constipation
from laxative abuse. Cathartic colon syndrome
Gastrointestinal Complications With Bulimia Nervosa significant
complications from chronic vomiting Complications include involuntary
regurgitation from weakening of the gastroesophageal sphincter.
Peptic ulcer disease, gastroesophageal reflux with resulting esophagitis, Mallory-Weiss esophageal tears and even esophageal rupture.
Dental caries and loss of enamel- lingual surfaces
Gastrointestinal Complications Medications options- Proton pump
inhibitors, Histamine Blockers Prokinetic agents such as
metoclopramide. Polyethylene Glycol for chronic
constipation.
Case One- Cardiac Complications
J is a 12 year old female with a history of weight loss for several months.
Ht. 64” and wt. 72 lbs. Her pulse rate was 38 bpm in clinic (18 bpm on the ward) and BP was 74/40 with orthostatic changes.
Her EKG demonstrated borderline QTc abnormality.
Echocardiogram demonstrated a pericardial effusion.
Case Two- Cardiac Complications
E is a 18 year old female also with at history of significant weight loss and eating disorder symptoms for 2 years.
History of food restriction and purging. Ht. 65”and Wt. 83 lbs. Echocardiogram revealed abnormal
thinning of anterior and lateral left ventricular walls.
Cardiac Complications
Patients with Anorexia demonstrate significant bradycardia and hypotension.
Demonstrate EKG abnormalities and arrhythmias.
Right axis deviations, ST-T wave abnormalities, concerns regarding prolonged QT interval.
Cardiac Complications
Changes in myocardial function have been shown including decrease in myocardial tissue mass.
Risk of CHF with too rapid hydration and refeeding.
Case Three-Cardiac Complications
KK is a 16 year old female admitted for muscle weakness and dyspnea.
Significant muscle weakness on exam.
QTc abnormality on EKG. Dilated left ventricle and poor
cardiac contractility on echocardiogram
Cardiac Complications
Admitted to daily purging with self-induced vomiting via ipecac use for several months.
Significant risk of cardiac damage from abuse of Ipecac. Contains toxic alkaloid- emetine.
Rate of excretion is slow and ingestion of regular doses can accumulate.
Leads to a reversible myopathy. Significant cardiac toxicity including
arrhythmias and cardiomyopathy.
Cardiac Complications
Significant risk from OTC diet pill use and abuse.
Most compounds contain stimulants- ephedra-like compounds
Herbal stimulants These drugs can cause cardiac
arrhythmias, cardiac ischemia, myocardial infarctions and strokes.
Neurological Complications Alterations in neurotransmitter levels
including serotonin and others. Significant role in the etiology and
persistence of the condition. Associated with psychiatric co-
morbidities. Neuropsychiatric abnormalities include
impaired attention, concentration, learning and behavior.- Could be associated with resistance seen in treatment
Neurological Complications In severe Anorexia, CT scans have
demonstrated cortical atrophy and ventricular dilatation.
These changes have been shown to reversible on CT with refeeding and improved nutrition.
However, abnormalities have been shown to persist on MRI scans even after treatment and weight recovery.
Neurological Complications The most recent study is by
Wagner et al in Biological Psychiatry in 2006.
This study looked at MRI scans in 40 recovered patients with AN, AN B/P and BN.
Average length of recovery ranged from 29.8-39.5 months
Case One- Endocrine Complications
A is a 24 year old female who presented at age 12 with malnutrition and lack of weight gain. +preoccupation with food and wt and distorted body image.
Ht 59.5” and wt. 76.2 lbs. Patient diagnosed with AN and treated in
outpatient program. She lost more wt. and required 3 inpatient hospitalizations.
Now recovered. Ht. 61” and wt. 120 lbs.
Case One- Endocrine Complications
Patient has not reached and will not reach her genetic potential for height.
Patient has had primary amenorrhea and demonstrates osteopenia on DEXA scan.
Patient has had 5 stress fractures associated with running.
Endocrine Complications
This case demonstrates several of the potential complications- short stature, amenorrhea, and the risk of osteoporosis.
Endocrine Complications
Risk of irreversible short stature in patients that develop AN and malnutrition during their adolescent growth spurt.
A recent study demonstrated that the longer the duration of illness at this time, the more disturbance in growth and increased risk of short stature.
Amenorrhea
Primary: Absence of menses:
By age 16 years with normal pubertal development
By 2 years after completion of sexual maturity
By age 14 without secondary sexual characteristics
Secondary: Absence of 3-6 consecutive menstrual
cycles after menarche
Endocrine Complications
Amenorrhea related to dysfunction of the hypothalamic- pituitary- ovarian axis.
Evidence suggests a dysregulation of the hypothalamic secretion of GnRH.
Still under debate if due to primary neuroendocrine dysfunction or secondary to malnutrition with decreased energy availability.
Endocrine Complications
Amenorrhea typically occurs when 10-15% of body weight is lost but can occur before significant weight loss.
Resumption of menses (ROM) usually occurs at about 90% of IBW with approximately 20% body fat.
Case One- Osteoporosis
JJ is a 25 year old female with a long history of AN and primary amenorrhea.
Medical complications have included hypoglycemic seizures, abnormal renal function tests and osteoporosis.
Bone mineral density on DEXA scan of lumbar spine is 0.598 gm/sq..cm. With a T score of -3.76.
Patient treated with hormonal replacement
Osteoporosis:Bone Development
Bone is a living tissue. It is metabolically active and
constantly being turned over and remodeled.
Osteoblasts- Bone forming cells. Osteoclasts- Bone resorbing cells
Osteoporosis- Bone Development There are three phases to bone
mineral development: growth, consolidation and senescence.
Adolescence represents a critical window of opportunity for the development of peak bone mass.
Bone Mineral Density
NIH consensus statement—bone mass acquired early in life “most important determinant of life-long skeletal health” National Institutes of Health Consensus Statement, 2000
Critical years in bone acquisition between ages 10-14 years
About 90% of peak bone mass is attained by age 18 Bonjour JP, Theinz G, Buchs B, et al. J Bone Mineral
Research, 1991
Osteoporosis- Bone Development There is a linear increase of BMD until
early puberty which is accelerated in the perimenarchal years.
The majority of bone mineral accretion occurs by the middle of the second decade. A small fraction is gained in the third decade.
Concept of “bone bank” in relation to calcium and bone mineral metabolism.
Bone Density over the lifespan
Osteoporosis- Bone Development Bone mineral acquisition is influenced
by nutrition, exercise, and the overall hormonal milieu.
Imbalances in any of these factors can lead to insufficient deposition of calcium in the bone bank and/ or increased loss of calcium from the bone bank.
This can result in osteopenia and osteoporosis- defined by abnormal results on DEXA Scan.
Osteoporosis
The majority of women with AN show evidence of bone loss.
At least 50% have evidence of osteoporosis.
This is true even for adolescents with AN.
Two studies have suggested that this is not true for BN.
Osteoporosis
The pathogenesis of osteoporosis in patients with AN is not completely known.
Involves both decreased bone formation and increased bone resorption.
Factors include: severe malnutrition, poor calcium intake, excessive exercise, hypoestrogenemia, increased serum cortisol, and other hormonal imbalances.
Osteoporosis
There are significant concerns about the lasting impact and possible irreversibility of the osteoporosis in these young patients.
Consider bone density evaluation with a DEXA scan.
Currently recommend central DEXA scan T score vs. Z score Other modalities being studied including
quantitative CT and ultrasound
Osteoporosis
Treat risk with nutritional rehabilitation.
Bone density correlates with BMI. Addition of calcium of 1500 mg/day
with vitamin D. Lifestyle counseling. Issue of exercise.
Osteoporosis
Controversial issue of medication with hormonal replacement with OCP.
Some studies have demonstrated improvement while others have not.
Important not to make patient complacent about nutrition with OCP.
Other experimental treatments include bisphosphonates, DHEA, IGF-1.
Refeeding Syndrome
Nutritional rehabilitation is usually done orally but sometimes NG feeds are done.
HAL seen in literature but ? indication. Initial intake between 800-1500 Kcal/day. Gradual increases of 200-300 Kcal/day. Often takes several days of equilibration
before the patient will start to gain weight. Expect inpt.weight gain of 1/4-1/2 lbs./day
Refeeding Syndrome
Significant risk of refeeding syndrome in malnourished patients with AN.
Patients are in somewhat of an homeostatic state. Too rapid hydration and/or refeeding can upset this balance.
Risk of edema and CHF. Often develop abdominal pain and
bloating due to decreased gastric emptying.
Refeeding Syndrome
Patients are total body phosphate depleted but in relative homeostasis with low normal serum phosphate.
With overly rapid refeeding, (either enteral or parenteral), glucose rapidly enters the cells, followed by phosphate- stimulated by insulin.
This can lead to rapid reduction of serum phosphate.
Thus risk of significant hyophosphatemia if patients receive IV, NG or PO nutrition too rapidly.
Refeeding Syndrome
Studies have documented potentially life- threatening arrhythmias as well as mental status changes associated with this hypophosphatemia.
Recent study demonstrated that phosphorus reaches its lowest point during the first week of treatment.
Refeeding Syndrome
Monitor weight carefully and serum electrolytes, phosphate frequently.
Prevent/ treat with oral phosphate replacement. IV phosphate replacement if life-threatening.
Treatment
Goals of treatment include medical stabilization, nutritional rehabilitation, control of abnormal eating behavior, psychological treatment, and prevention of relapse.
Employ an biopsychosocial model for treatment with a multidisciplinary team.
Treatment options differ sometimes with AN, BN, and EDNOS.
APA Guidelines published as supplement to American Journal of Psychiatry, Jan 2006.
Treatment
Medical stabilization and some nutritional rehabilitation must occur before significant psychological progress can be made.
Some psychiatric abnormalities such as depression and food obsession can be starvation induced.
Treatment
Indications for hospitalization include: Severe malnutrition- less that 75% Ideal body weight, dehydration and electrolyte disturbances,arrhythmias, other medical complications, acute food refusal, uncontrollable bingeing and purging, acute psychiatric emergency, failure of outpatient treatment
Treatment
Inpatient treatment options. Medical monitoring. Contracts/Approach. Discharge criteria.- Study using
normalization of vital sign instability as discharge criteria.
Insurance issues.
Treatment
Outpatient treatment options. Multidisciplinary team. Group therapy. Individual therapy. Family therapy Day treatment programs
Treatment
Approximate goal weight of set at 90% of IBW using NCHS tables for teens and “rule of thumb rule” for adults.
Used for medical evaluation and follow- up. Usually do not discuss goal weight with patients. Expect wt. gain of 1-2 lbs./week.
Use goal of resumption of menses. It is clear that the treatment must be
long-term and that there is no quick fix.
Treatment- Pharmacotherapy Many studies indicate that fluoxetine
is efficacious in treatment of BN especially in conjunction with therapy.
Usual dose is 60 mg per day. Studies demonstrate that medication
plus therapy more efficacious than either alone.
However, therapy more efficacious than medication alone.
Treatment-AnticonvulsantsTopiramate Effective in eliminating binging and
purging behavior Improved self-esteem, eating attitudes,
anxiety, and body image Can see cognitive and peripheral
nervous system side effects—slow titration of drug may limit effect
Treatment - Pharmacotherapy Fluoxetine also shown in one study to be
helpful in preventing relapse in AN. No medication clearly shown to help in AN
when patient is malnourished. Other medication options- Olanzapine etc. Recent trials- Significant reduction in
depression, anxiety and core eating disorder disturbances. Significant increase in weight.
Need for more controlled medication trials.
Prognosis
Prognosis in adolescents with anorexia is much better than that reported in adult literature.
Studies indicate a 71-86% satisfactory outcome on long-term follow-up
Many of the subjects,however, still did had concerns about weight and eating and one study showed some crossover to bulimic symptoms
Prognosis
14-29% of patients had a poor outcome Factors associated with a poor
prognosis included: later onset, longer duration of disease, lower minimum weight, failed previous treatment, greater social and family difficulties, more disturbed personality, increased obsessive somatic concerns, and bulimic subtype
Prognosis
Long term prognosis is not as clear with BN, often a history of recovery and relapse.
Study- “Outcome in BN” from AM J Psych Analysis of 5-10 year outcome studies 50 % patients recovered 20% met full criteria for BN 30% had experienced relapse
Conclusion
We live in a culture preoccupied with thinness, reflected in the media
This places an enormous burden on adolescent females in our society
In a vulnerable teen, these pressures can interact with other biological, psychological, and familial factors to lead to an eating disorder
Conclusion
Anorexia Nervosa and Bulimia Nervosa are serious illnesses that can have significant, sometimes irreversible medical complications
The prognosis with early recognition and aggressive treatment is very favorable
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