Treatment of Eating Disorders

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Transcript Treatment of Eating Disorders

Dr Jackie Hoare
Liaison Psychiatry GSH
 is an illness characterised by extreme concern about
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body weight
with serious disturbances in eating behavior
leading to a self-imposed starvation state
Severe weight loss.
Body image becomes the predominant measure of selfworth
denial of the seriousness of the illness.
 (a) refusal to maintain weight within the normal
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range for height and age
(b) fear of weight gain;
(c) body image disturbance
(d) absence of menstrual cycles or
amenorrhea in women (and loss of sexual interest
in men).
 Criterion A focuses on behaviors, like restricting
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calorie intake
But no longer includes the word ‘refusal’
in terms of weight maintenance since that implies
intention on the part of the patient
The DSM-IV Criterion requiring amenorrhea, is
deleted.
This criterion cannot be applied to males, children,
OC, and post-menopausal females.
exhibit all other symptoms and signs of anorexia
nervosa but still report some menstrual activity
 All 3 of the following:
 Energy restriction leading to significantly low body
weight
 Fear of weight gain or behavior interfering with weight
gain
 Disturbance in self perceived weight or shape
 Restricting type
 Binge eating /purging type; recurrent episodes of
bingeing or purging in the last 3 months
 Mild BMI>17 kg/m2
 Moderate 16-16.9
 Severe 15-15.9
 Extreme <15
 Few controlled trials to guide treatment
 Weight restoration, family therapy and structured
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psychotherapy
Improve nutritional health – refeeding
Drugs can be used to treat co-morbid conditions
Limited role in weight restoration
Phosphate, K+, thiamine, Mg, Ca2+ supplementation in
oral form
 results in a decrease in the serum levels of phosphate,
potassium, and magnesium, all of which are already
depleted.
 hormonal and metabolic changes are aimed at preventing
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protein and muscle breakdown.
use fatty acids as the main energy source.
increase in blood levels of ketone bodies
brain to switch from glucose to ketone bodies as its main
energy source.
The liver decreases its rate of gluconeogenesis, thus
preserving muscle protein.
several intracellular minerals become severely depleted
serum concentrations of these minerals (including
phosphate) may remain normal.
reduction in renal excretion.
 During refeeding, glycaemia leads to increased insulin and
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decreased secretion of glucagon.
Insulin stimulates glycogen, fat, and protein synthesis.
Insulin stimulates the absorption of potassium into the
cells through the sodium-potassium ATPase symporter,
which also transports glucose into the cells.
Magnesium and phosphate are also taken up into the cells.
Water follows by osmosis.
These processes result in a decrease in the serum levels of
phosphate, potassium, and magnesium
The clinical features of the refeeding syndrome occur as a
result of the functional deficits of these electrolytes and the
rapid change in basal metabolic rate.
 rate of feeding should be slowed down and essential
electrolytes should be replenished.
 Fluid repletion should be carefully controlled to avoid fluid
overload
 Bone loss complication serious consequences
 Hormonal treatment with oestrogen or
dehydroepiandrosterone (DHEA) no positive effect on
bone density
 Oestrogen not recommended in children and
adolescents – risk premature fusion of bones
 2009 Cochrane review: no evidence from 4 placebo
controlled trials
 On weight gain, eating disorder or associated
psychopathology
 Suggested neurochemical abnormalities in starvation
may explain non-response
 Co-prescribing supplementation incl. tryptophan with
fluoxetine does not increase efficacy
 Olanzapine, benzodiazepines or promethazine to
reduce anxiety with refeeding
 1 RCT showed 88% of patients given olanzapine
achieved weight restoration (55% placebo)
 Quetiapine may improve psychological symptoms but
few data
 Small trial suggested that fluoxetine useful in
improving outcome and preventing relapse after
weight restoration
 Other studies found no benefit
 Antidepressants often used to treat co-morbid
depression and OCD
 However these conditions may resolve with weight
gain alone
 Significant disturbance in eating manifested by
persistent failure to meet nutritional/energy
requirement associated with 1 of:
 Significant weight loss
 Significant nutritional deficiency
 Dependence on enteral feeding or supplements
 Interference with psychosocial functioning
 NOT due to lack of food or body image disturbance
 Avoidant/Restrictive Food Intake Disorder (ARFID) has
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replaced Feeding Disorder of Infancy and Early Childhood
and EDNOS which was described in the DSM-IV.
While few data on ARFID have been published, it appears
that it usually presents in infancy or childhood, but it can
also present or persist into adulthood.
The course of illness for individuals relatively unknown.
Avoidance due to sensory characteristics of food, emotional
difficulties, food beliefs etc.
ARFID may be associated with impaired social functioning
and affect family functioning, especially if there is great
stress surrounding mealtimes.
 The presence of other psychological disorders may be risk
factors for ARFID, such as anxiety disorders, obsessivecompulsive disorders, attention deficit disorders, and
autism spectrum disorders
 If an individual presents with one of these illnesses and an
eating problem, a diagnosis of ARFID should be given only
when the feeding disturbance itself is causing significant
clinical impairment
 individuals with a history of gastrointestinal conditions
such as gastroesophageal reflux may develop feeding
disturbances, but a diagnosis of ARFID should be assigned
only when the feeding disturbances require significant
treatment beyond that needed for the gastrointestinal
problems.
 Little is currently known about effective treatment
interventions for individuals presenting with ARFID
 given the prominent avoidance behaviors, it seems
likely that behavioral interventions, such as forms of
exposure therapy
 depression or anxiety that affects feeding, cognitive
behavioral therapy and other treatments for the
underlying condition
 Bulimia nervosa is characterized by recurrent and
frequent episodes of eating unusually large amounts of
food
 feeling a lack of control over the eating.
 purging (e.g., vomiting, excessive use of laxatives or
diuretics), fasting and/or excessive exercise
 DSM-5 criteria reduce the frequency of binge eating
and compensatory behaviors to once a week from
twice weekly as specified in DSM-IV.
 Psychological treatments first choice
 Adults mat be offered antidepressants
 SSRI’s esp fluoxetine
 60mg effective dose
 Can reduce frequency of binge eating and purging
 Long term effects unknown
 Early response at 3 weeks strong indicator of response
overall
 Used off licensed in adolescents
 Some evidence for topiramate, duloxetine, lamotrigine and
sertraline reduce binges
 Binge eating disorder will now have its own category as an
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eating disorder.
In the DSM-IV, under the category Eating Disorder Not
Otherwise Specified
“recurring episodes of eating significantly more food in a
short period of time than most people would eat under
similar circumstances, with episodes accompanied by
feelings of lack of control.”
eat quickly and uncontrollably, despite hunger signals or
feelings of fullness.
feelings of guilt, shame, or disgust
behavior will have typically taken place at least once a week
over a period of three months.
 NICE recommends
 Evidenced based self help programme of CBT as first
line
 Trial of SSRI as an alternative or additional first step
 Although AN is not a common condition
 its morbidity and mortality are amongst the highest
psychiatric disorders
 due to malnutrition, purging
 behavior and suicide.
 18-fold increase in mortality in patients with AN
 Over 7 years, the majority of women with anorexia
nervosa experienced diagnostic crossover: more than
half crossed between the restricting and binge
eating/purging anorexia nervosa subtypes over time;
one-third crossed over to bulimia nervosa but were
likely to relapse into anorexia nervosa. Women with
bulimia nervosa were unlikely to cross over to anorexia
nervosa
 Key is MDT
 Dietician, psychology, medicine, psychiatry, OT and
social worker
 Clearly defined case manager , roles of team members
in case defined