Transcript OVERVIEW OF EATING DISORDERS

OVERVIEW OF EATING
DISORDERS
Dr. Gillian Baksh
Monday Meeting
February 2011
USE OF TERMS
FEEDING
DISORDER
EATING
DIFFICULTY
EATING
DISTRESS
FEEDING
PROBLEM
EATING
PROBLEM
FEEDING
DISTURBANCE
EATING
DISORDER
EATING
EATING
DISTURBANCE
DISTURBANCE
FEEDING
DIFFICULTY
DIAGNOSIS AND
CLASSIFICATION
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‘True Eating Disorder’ – grossly disordered or
chaotic eating behaviour associated with
morbid preoccupation with body weight and
shape (irrespective of weight)
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Eating difficulty / problem – not associated with
clinically significant functional or developmental
impairment
TRUE EATING DISORDERS
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AN
▪ Restricting or binge-purge subtypes
(DSM 1V)
BN
▪ Purging and non-purging subtypes
(DSM 1V)
Related atypical or not otherwise specified forms
▪ EDNOS
(DSM 1V)
▪ Atypical AN and atypical BN
(ICD 10)
OTHER EATING DISORDERS
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Selective eating
Restricted / minimal eating
Phobia associated with limited intake
Functional dysphagia
Food avoidance emotional disorder
(FAED)
Food refusal
?Pervasive food refusal syndrome
Overeating associated with obesity
EATING DISORDERS IN
CHILDREN
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Not developmentally
sensitive
Do not consider parental
observed behaviours
FAED = Non-fat phobic ED
– not classifiable in DSM as
an ED
Mismatch between
diagnostic categories and
clinical presentations
DSM V and ICD 11
EDNOS or
ATYPICAL
FAED
AN
BN
DSM ΙV vs ICD10 CLINICAL
EATING DISORDERS
DSM ΙV (Amer Psych Assoc1994)
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AN restricting and binge-purge
subtypes
BN purging and non-purging
subtypes
EDNOS (clinically severe but does
not meet criteria for AN, BN)
Feeding disorder of infancy or
early childhood (onset before 6
years)
Pica
Rumination disorder
ICD 10 (WHO 1992)
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AN
BN
Atypical AN and atypical BN
Other :
- Overeating associated with other
psychological disturbances
- Vomiting associated with other
psychological disturbances
- Other eating disorders
- Eating disorder, unspecified
Feeding disorder of infancy and
childhood
Pica of infancy and childhood
ANOREXIA NERVOSA IN CHILDREN
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First described in late 19th century
Defined from (6 –) 8 years
Weight loss at least 15% below normal weight for age
and height
Weight control behaviours mainly dietary restriction and
exercise, laxatives, vomiting
Older patients binge-purge (20-30% BN past history of
AN)
Abnormal cognitions regarding weight and / or shape
Sometimes difficult to elicit explicit weight / shape
psychopathology
Food preoccupations, guilt around eating, concern
about eating with others, low self esteem common
In boys (10-25%) often concern around fitness and
health – shape more than weight – excessive exercise
more common - OCD commonly associated
BULIMIA NERVOSA
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Requires degree of psychological maturation including capacity
for self evaluation often manifest as shame or guilt
Rare under 13 years
Abnormal cognitions regarding weight and / or shape
Can arise out of anorexia or secondary to repeated dieting
behaviour
Recurrent binging and inappropriate compensatory behaviours
occur at least x2 per week for 3 months
Compensatory behaviours- purges, food restriction, excessive
exercise– laxative/enema/appetite suppressant misuse more
common in older adolescents
Sense of lack of control & chaos
May be associated with other teenage problem behaviours –
drinking, self harm, casual sex, drugs
DIFFERENTIAL DIAGNOSIS
Endocrine
Diabetes Mellitus, Hyperthyroidism,
Glucocorticoid Insufficiency
Gastrointestinal Coeliac Disease, IBD, Peptic Ulcer
Disease
Oncological
Lymphoma, Leukaemia,Intracranial
Tumours
Infections
TB
Psychiatric
Depression, Conversion Disorder
EPIDEMIOLOGY
BN
AN
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Incidence
- 4.2 – 8.3 / 100 000 (Currin et al,Hoek et al)
- 40% between 14 – 19 years
- 1.2/ 100 000 hospitalised
Stable over time ? except young
Prevalence
- average 0.3% ( 0-0.9%)
- 0.4 % adolescent girls
- lifetime 1.4 – 2.2 %
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Incidence
- 6.6 – 13.5 / 100 000
More sensitive to global environmental
changes - possibly decreasing from
peak in 1990’s (Currin et al, BJ Psych 2005)
Prevalence
- average 1% (similar to
schizophrenia)
- lifetime 4 -7%
3-12% of adolescents experience some form of eating
disorder – most EDNOS (Machado 2007; Slice et al 2009)
-
PROGNOSIS AND OUTCOME
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Predictors of outcome of EDs – mixed results
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Fair degree of association of morbid family functioning
and poor prognosis in AN regardless of age
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At 2 years – 33% fully recovered, 27% still full AN
(Toucan
study)
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Adolescents do slightly better than adults – 75% or
more fully recover
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Children < 11years may do worse – only 2 studies
RECOVERY AN
? 30 %
11 – 27 %
CHILDHOOD ADOLESCENT ONSET ADULT ONSET
ED
ONSET ED
ED
Halvorsen et al 2003
Raastam et al 2003
Patton et al 2003
Depression / OCD/
Other axis 1
diagnosis
MORTALITY
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Mortality AN 0% – 22 % depending on follow up period
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Crude mortality: 4% AN, 3.9% BN, 5.2% EDNOS
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3x more likely to die of a childhood or adolescent ED
than any other causes
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AN – 12x annual death rate from all causes in 15 – 24
year females (physical complications &suicide)
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Highest mortality (2%) in the first year after
presentation in females and in the first 2 years (5%)
after presentation in males
EATING DISORDERS
ARE SERIOUS
AND NEED TO BE
TAKEN SERIOUSLY
HELPFUL SITES
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B-EAT
http://www.youtube.com/watch?v=K5WZv8Pr
TRo
http://sites.google.com/site/marsipannini
www.rcpsych.ac.uk/files/pdfversion/CR162.pd
f
GENES
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Family studies- female relatives of someone with an
ED are >x4 risk of BN and >x11 risk AN than
someone with no family history (probably higher for
subclinical and partial syndromes)
Twin studies – (MZ:DZ concordance) – AN has
estimated heritability of 58 -76 %, BN from 31 – 83%
Puberty may activate some aspect of genetic
heritability (Klump et al)
A 7% increased incidence in first degree relatives
may be related to area on chromosome 1p at the
DF1153721 locus (Grice et al 2002)
BIOPSYCHOSOCIAL MODELS OF
RISK AND MAINTENANCE
•Physical and nutritional status
•Temperament
•Self esteem,values,personal identity
•Emotional processing and literacy
SOCIAL
INDIVIDUAL
•Life events
•Peer relationships
•Media influence
Predisposing
Precipitating
Perpetuating
SYSTEMIC
•Genetic
•Family beliefs re weight,shape,
eating
MALNUTRITION
IS A MEDICAL
EMERGENCY
MEDICAL COMPLICATIONS
Underweight
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CVS: ECG (low voltage;sinus bradycardia;T wave inversions:ST depression-electrolyte
imbalance:prolonged QTc), dysrhythmias(SV ectopics, VT), pericardial effusions – all
reversible except following ipecac use
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Growth and development: pubertal and growth delay, 1˚ amenorrhoea, delayed bone
mineral accretion
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Dietary deficiencies: calcium, vit D , folate, B12
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GIT: delayed gastric emptying, ↓gastric motility, constipation, bloating, fullness, abnormal
LFTs, hypercholesterolaemia, pancreatitis,abnormal LFTs(fatty infiltration):superior
mesenteric artery syndrome– all reversible
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Renal: dehydration, ↓GFR, stones, polyuria, total body Na and K depletion; peripheral
edema with refeeding
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Haematologic: leukopoenia, anaemia, thrombocytopoenia, iron deficiency
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Endocrine: sick euthyroid syndrome, amenorrhoea, osteopoenia
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Neurologic: cortical atrophy, seizures
MEDICAL COMPLICATIONS
Purging / Binging
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Fluid and electrolyte imbalance: ↓K and Na, hypochloremic alkalosis
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Use of ipecac: irreversible myocardial damage and diffuse myositis
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Chronic vomiting: esophagitis, dental erosions, parotitis, Mallory-Weiss
tears, oesophageal or gastric rupture, aspiration pneumonia
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Use of laxatives: dehydration, renal stones, metabolic acidosis, ↓Ca
and Mg, ↑uric acid – withdrawal may get fluid retention (up to 4 kg in 24
hours)
Amenorrhoea (may see in normal or overweight with BN): menstrual
irregularities, osteopoenia
CARDIOVASCULAR
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Cardiac death – 1/3 all deaths in adults
Cardiac deaths unknown in paediatrics
↓ PR- ↓ vagal tone, ↓ BMR- aim to ↓cardiac output and
preserve energy and reduce demand on malnourished
heart
↓ BP – myocardial atrophy
Orthostatic changes – leg and heart muscles
ECG – electrolytes
Changes reversible with weight restoration
Caution with fluids – boluses often unnecessary and
can be dangerous
HISTORY
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Detailed feeding history
Duration eating concerns
Rapidity weight loss - > 1 kg/week serious risk
Current intake & pattern including fluids
Use laxatives, diuretics etc
Weight / shape cognitions
Sleep pattern
Menstrual history / pubertal progression
Co-morbid mental illness (anxiety, phobia, OCD, depression)
Personality description from relatives
Suicidal ideation, DSH, overdose
Symptoms of hyperthyroidism, diabetes, malignancy, IBD,
tumour etc
Symptoms related to complications – acute and chronic
HISTORY
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Family and social history – ED , mental
illness
Female relative of someone with an ED is
> x4 likely to have BN and > x11 likely to
have AN than someone with no family
history
Activities / exercise
School attendance
Relationships
MEDICAL ASSESSMENT
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History
WFH / BMI
Temp
Urine
Examination:
-haemodynamic stability – lying / standing BP & PR
-pubertal status
-signs of malnutrition
-signs of possible underlying medical condition
SUSS Test – stand up sit up test
Investigations
EXAMINATION
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Oversized clothes
Muscle wasting / lack subcutaneous fat
Cold extremities, cyanosis
Anaemia
Dehydration
Murmurs, arrythmias, weak pulse
Lanugo, dull thin scalp hair
Signs binging / purging: Russell’s sign, palatal scratches /
petechiae, dental erosions, parotitis
Signs of vitamin and mineral deficiency: anaemia, dry/sallow
skin, carotenaemia , glossitis, lip fissures, bleeding gums, brittle
nails, Chvostek’s sign, Trousseau’s sign
Look for signs to help rule out possible underlying medical
condition
BMI AND WEIGHT FOR HEIGHT
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Weight loss – loss fat and muscle
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A low BMI more strongly correlated with lean muscle mass than
fat mass (Cole et al BMJ 2007)
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BMI:
- Adults concern if
- Adults severe malnutrition cut off
BMI < 17.5
BMI =13
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WFH : % Median BMI= Actual BMI / Median BMI (50th
percentile for age & sex) x 100
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WFH 100% = BMI 50th centile
WFH
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Be concerned if WFH < 90% = BMI < 9th
centile – stop exercise
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Be very concerned WFH 80% = BMI < 2nd
centile (definition of underweight) –
stop school
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Consider hospitalisation if WFH < 75%
DIAGNOSTIC DECISION TREE
UNDERWEIGHT?
YES
NO
FEAR OF
WEIGHT GAIN?
YES
BINGES?
NO
OTHER
EMOTIONAL
DISORDER?
AN
YES
FAED
YES
NO
LIMITED RANGE
OF FOODS?
NO
EXCLUDE
PHYSICAL
ILLNESS
YES
SELECTIVE
EATING
PURGES?
YES
BN
NO
BINGE
EATING
DISORDER
INVESTIGATIONS
Baseline bloods including clotting, Ca, PO4, Mg, HCO3, iron
studies, folate, B12, Vit D, amylase, ESR, CRP,TFTs, lipids,
glucose
 ECG
 Urinalysis
 Wrist Xray - Bone age and density
 Pelvic USS
Consider:
 DEXA scan
 CXR
 Abdominal Xray
 MRI / CT scan
 Autoimmune, coeliac screen
 Cardiac ECHO
DON’T BE FALSELY REASSURED BY NORMAL BLOOD
RESULTS
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MEDICAL TREATMENT
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When to hospitalise / inpatient treatment?
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Weight recovery usually 2 – 3 kg per month
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Target weight : WFH 95 – 110%
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Resumption of growth and / or menses
are better indicators of recovery than
targets
EDs and GUIDELINES/ EVIDENCE
BASE
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Clinical guidelines (e.g. NICE 2004) mostly based on consensus
views
NICE guidelines developed to advise on the identification, treatment
and management of AN, BN, and related conditions in those 8 years
and over
EDNOS may not be same as in adults
Guidelines do not cover other eating disturbances
Evidence for effectiveness of treatments weak across age range
(5RCT : 3 AN, 2 BN)
No large scale randomised controlled drug trials for AN
MARSIPAN (2010) and Junior MARSIPAN(2011)
http://www.rcpsych.ac.uk/files/pdfversion/CR162.pdf
Nicholls D, Hudson L, Mohamed f. Arch Dis Child. 2010 Oct 7. (Epub) Managing
anorexia nervosa
INPATIENT TREATMANT
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1 in 4 AN will be hospitalised
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The need for inpatient treatment for AN and the
need for urgent weight restoration should be
balanced alongside the educational and social
needs of the young person (NICE)
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Admit locally and in age appropriate setting (NICE)
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Do not isolate
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Attend school
INDICATIONS FOR HOSPITALISATION IN AN
ADOLESCENT WITH AN EATING DISORDER
(Society for Adolescent Medicine position paper Dec 2003)
One or more of the following:
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Wt for ht ≤ 75%
Dehydration
Electrolyte disturbance (hypokalaemia, hyponatremia,
hypophosphataemia, hypomagnesemia)
Cardiac dysrhythmia
Physiological instability
Severe bradycardia (< 50 b/min day; < 45 b/min night)
Hypotension (< 80/50 mm Hg)
Hypothermia (< 35 ˚C)
INDICATIONS FOR HOSPITALISATION IN AN
ADOLESCENT WITH AN EATING DISORDER
(Society for Adolescent Medicine position paper Dec 2003)
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Orthostatic changes in pulse (↑> 20 b/min) or ↓ BP (> 10
mm Hg systolic) from lying to standing
Arrested growth and development
Failure of outpatient treatment
Acute food refusal
Uncontrollable binging and purging
Acute medical complications of malnutrition ( e.g.
syncope, seizures, cardiac failure, pancreatitis etc.)
Acute psychiatric emergencies (e.g. suicidal ideation,
acute psychosis)
Co-morbid diagnosis that interferes with the treatment of
the eating disorder (e.g. severe depression, OCD,
severe family dysfunction)
MEDICAL INPATIENT TREATMENT
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Difference between stabilisation and refeeding
Food= medicine therefore need to be helped to eat
Support for nurses
Admission may give the wrong message to patient
and family
Autistic spectrum disorder patients fare badly when
admitted
Studies on outcome following admission – patients
admitted are very ill or don’t do very well
REFEEDING
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Parents helped to take responsibility
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Establish parental control of food and fluid
intake
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Patient encouraged to negotiate the “how” of
food intake and not the “whether”
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Consistency of approach
REFEEDING
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Aim for 0.5 -1.0 kg weight gain per week
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At least 500 – 1000 Kcals above basic requirement
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Inpatients may need 3000 Kcals /d
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Start at 15 – 20 Kcal/kg/d
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Avoid underfeeding syndrome
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NICE: refeeding is a necessary component but is not
sufficient
- refeeding against the will of a patient is a highly
specialised procedure requiring expertise – Mental Health Act
1983, Children Act 1989, (Mental Capacity Act 2007)
REFEEDING SYNDROME
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Oral, enteral, parenteral route
Refeeding: → insulin surge → extracellular to intracellular
phosphate, magnesium, potassium, glucose, water
Cardiovascular, neurologic, haematologic complications
Can cause prolonged QTc or variable QTc
Can be associated with significant morbidity and mortality
Usuallly 4-6 days after refeeding started
Highest risk : WfH <75%, BMI < 13,laxative use, diabetics,
too rapid feeding, abnormal electrolytes (Glucose, Na, K,
PO4, Ca at start)
Start Thiamine 50 – 200mg bd (necessary for utilisation glucose
in Krebs cycle)
Daily bloods and ECG for 1 week then alternate days for 1
week
Daily physical assessments and weights
INPATIENT TREATMENT - AN
Short term
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Physical evaluation and
stabilisation
Long term
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Establish healthy body weight
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Identify and manage emotions
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Develop new coping skills
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Develop communication skills
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Develop peer relationships
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Learn to use help
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Reintegrate to home or other
environment
Reestablishment of food intake
Risk assessment
Relief of patient, parent,
professional anxiety
Assessment of treatment
needs
INPATIENT TREATMENT - BN
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Not used in adults as a rule
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Means of breaking cycles of binge / purge
and establishing regular eating patterns
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Related to risks of other self-harming
behaviours
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Related to severity of other co-morbid illness
PSYCHOLOGY
AN
 Avoidance, anxiety,
obsessionality
 Vicious circle of restraint
 Need for control is central
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Egosyntonic – rarely seek
voluntary treatment
BN
 Impulsivity, emotionality,
chaos
 Vicious circle of failed
restraint
 Need for control is central
 Depressed by behaviour
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Egodystonic – more
motivated but ambivalent
about weight gain
PHYSICAL EFFECTS OF AN ON
BRAIN
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Cortical atrophy and
ventricular enlargement
Secondary to starvation
Reverse with
restoration of adequate
nutrition
FUNCTIONAL EFFECTS OF AN
ON BRAIN
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Significantly reduced activity in
antero-medial temporal region
(insula)
Correlates with
neuropsychological findings
Does not correlate with BMI,
mood, length of illness nor
cerebral dominance
No reversal with nutritional
restoration
Gordon et al 1997, Chowdhury et al 2003,
Key et al 2004, Lask et al 2005,
Agrawal and Lask 2009, Brewerton et
al 2009, Frampton et al 2010
FUNCTIONS OF THE INSULA
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Regulates the ANS (anxiety)
Regulates appetite and eating
Monitors the gut (sense of fullness /
emptiness)
Monitors body image
Reception, perception and integration
of taste
Perception and integration of disgust
Perception of pain
Integrates thoughts and feelings
Awarenass of illness
Social awarenaee
Global processing
Motivation
BRAIN FUNCTION
IN AN
SOMATO
SENSORY
CORTEX DISTORTED BODY
IMAGE
PARIETAL LOBEVISUOSPATIAL
DEFECITS
FRONTALEXECUTIVE
DEFICITS
INSULA
BASAL GANGLIAOBSESSIONAL
DRIVE
NUCLEUS
ACCUMBENSREWARD
HIPPOCAMPUSMEMORY
AMYGDALAEXTREME
ANXIAETY
UNLIKELY THAT EACH OF THESE IS NOT FUNCTIONING CORRECTLY
THERAPY
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Family therapy
- family members including siblings should normally be included in the
treatment of children and adolescents with EDs (NICE)
Multi- family therapy
Individual therapy
- child should be offered individual sessions with professional separate from
family worker (NICE)
Adolescent focussed therapy
Interpersonal therapy
Directed behaviour therapy
Group therapy
CBT –
- adolescents with BN may be treated with CBT, adapted as needed to suit
their age, circumstances and level of development (NICE)
- some suggest if WFH < 80% should avoid
Motivational enhancement therapy
Cognitive remediation therapy – focuses on the process (how) rather than
the content (what) of thought and perception
PARENTS
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Sense of guilt, self-blame
Sense of failure
Mistrust for professionals
May reject child in response to ED
View ED as a personal attack on them as
parents
No empirical evidence to suggest that
families cause EDs, but no doubt that families
becomes dysfunctional in response to ED
Engaging parents as important as engaging
child
THERAPY
DOCTOR
Parent & patient relieved
of anxiety
Patient relieved of internal conflict
Reinforces parents’ sense of failure
PARENT
PATIENT
LONG TERM PHYSICAL
SEQUELAE
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Growth
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Bone density
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Puberty
GROWTH
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Important in boys and prepubertal girls
Slows / stops in starvation
No weight gain = weight loss
‘Catch-up growth’- may be first sign of a
healthy weight
The ‘dose’ of starvation needed to have a
permanent effect on height is 4 years before
completion of growth
LINEAR GROWTH
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Retardation may be related to –
- ↓ T4, T3
- ↑ cortisol
- ↓ sex hormones
- relative resistance to GH
Catch up growth with weight restoration
Variable reports of effect on final height
versus height potential
BONE MINERAL DENSITY
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Changes start early in disease
Impaired bone formation and increased absorption
Factors: low oestrogen & IGF1
high cortisol
poor nutrition, low BMI
low Ca and Vit D
Greatest risk: > 12 months onset AN
> 6months amenorrhoea
low BMI
low Ca intake
low physical activity (Castro et al 2000)
BONE DENSITY
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Mainstay treatment – weight gain, nutritional
rehabilitation, spontaneous resumption menses
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Oestrogen administration should not be used to treat
bone density problems in children and adolescents as
this may lead to premature fusion of the epiphyses
(NICE)
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Ca and Vit D supplements may be prescribed
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Full recovery unlikely – osteopoenia in 1/3 recovered AN
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Long term fracture risk around x3 –x7 of general
population
PUBERTY
Menses:
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Clearest marker of adequate endocrine function
Pubertal delay / arrest almost inevitable with WFH < 90%
Pelvic USS more sensitive than other hormone markers
and not susceptible to diurnal variation
- regression in size uterus and ovarian activity
- experienced ultrasonographer
- can be used to guide weight restoration and determine
onset of menses
No use in boys!
May not return until 6 months after achieving appropriate
weight (about 95% WFH)
OUTCOME
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Response to treatment – difficult to distinguish from
natural course as treatment almost invariably
ensues and limited on untreated cases
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Remission
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Recovery
Remission and recovery similar for AN since relapse
rare
PROGNOSIS AND OUTCOME

Predictors of outcome of EDs – mixed results

Fair degree of association of morbid family functioning
and poor prognosis in AN regardless of age

At 2 years – 33% fully recovered, 27% still full AN
(Toucan study)

Adolescents do slightly better than adults – 75% or more
fully recover
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Children < 11years may do worse – only 2 studies
POOR OUTCOME
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Continuing illness associated with functional
impairment or death
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Lower body fat at presentation (Mayer et al. Am J Psych
2007)
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Longer duration illness
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Hospitalised (Gowers et al. B J Psych 2007)
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Readmitted (up to 45%) (Steinhausen 2007)
MORTALITY
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Mortality AN 0% – 22 % depending on follow up period
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Crude mortality: 4% AN, 3.9% BN, 5.2% EDNOS

3x more likely to die of a childhood or adolescent ED
than any other causes

AN – 12x annual death rate from all causes in 15 – 24
year females (physical complications &suicide)

Highest mortality (2%) in the first year after
presentation in females and in the first 2 years (5%)
after presentation in males
HELPFUL SITES




B-EAT
http://www.youtube.com/watch?v=K5WZv8Pr
TRo
http://sites.google.com/site/marsipannini
www.rcpsych.ac.uk/files/pdfversion/CR162.pd
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