To Eat or not to Eat: That is the Question. Update on the Medical

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Transcript To Eat or not to Eat: That is the Question. Update on the Medical

UPDATE ON THE MEDICAL
MANAGEMENT OF EATING DISORDERS
Dr. Richard L. Levine
Professor of Pediatrics and Psychiatry
Chief, Division of Adolescent Medicine and Eating Disorders
Penn 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
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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
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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 selfevident
 Must consider other
conditions
 Eating Disorders can
present in patients
with another chronic
disease
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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
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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 expendituresdemonstrated 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. DiagnosisBulimia 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
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tenderness
Endoscopy revealed esophagitis.
Patient treated with PPI, sucralfate, and
metoclopramide.
Poor compliance with medicationssymptoms 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 OneCardiac 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 TwoCardiac 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 ThreeCardiac 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 stimulantsephedra-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 lifelong 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
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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 osteoporosisdefined 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
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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
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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-Anticonvulsants
Topiramate
 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
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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