OVERVIEW OF EATING DISORDERS

Dr. Gillian Baksh

Monday Meeting

February 2011

USE OF TERMS

EATINGDISTURBANCEEATING

DISTURBANCE

FEEDINGPROBLEM

EATINGPROBLEM

FEEDINGDISTURBANCE

EATINGDISORDER

FEEDING DISORDER

EATINGDIFFICULTY

EATINGDISTRESS

FEEDINGDIFFICULTY

DIAGNOSIS AND CLASSIFICATION

‘True Eating Disorder’ – grossly disordered or chaotic eating behaviour associated with morbid preoccupation with body weight and shape (irrespective of weight)

Eating difficulty / problem – not associated with clinically significant functional or developmental impairment

TRUE EATING DISORDERS 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

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

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

BNAN

FAED

EDNOS orATYPICAL

DSM ΙV vs ICD10 CLINICAL EATING DISORDERS

DSM ΙV (Amer Psych Assoc1994)

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)

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 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

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

EPIDEMIOLOGYAN 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 %

3-12% of adolescents experience some form of eating disorder – most EDNOS (Machado 2007; Slice et al 2009)

-

BN 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%

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

Children < 11years may do worse – only 2 studies

RECOVERY AN

ADOLESCENT ONSETED

CHILDHOODONSET ED

ADULT ONSETED

Depression / OCD/Other axis 1 diagnosis

Halvorsen et al 2003Raastam et al 2003Patton et al 2003

? 30 % 11 – 27 %

MORTALITY Mortality AN 0% – 22 % depending on follow up period

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

EATING DISORDERS ARE SERIOUS

AND NEED TO BE TAKEN SERIOUSLY

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.p

df

GENES 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

INDIVIDUAL

SYSTEMIC

SOCIAL

•Physical and nutritional status•Temperament•Self esteem,values,personal identity•Emotional processing and literacy

•Genetic•Family beliefs re weight,shape,eating

•Life events•Peer relationships•Media influence

PredisposingPrecipitatingPerpetuating

MALNUTRITION IS A MEDICAL EMERGENCY

MEDICAL COMPLICATIONSUnderweight

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

Growth and development: pubertal and growth delay, 1˚ amenorrhoea, delayed bone mineral accretion

Dietary deficiencies: calcium, vit D , folate, B12

GIT: delayed gastric emptying, ↓gastric motility, constipation, bloating, fullness, abnormal LFTs, hypercholesterolaemia, pancreatitis,abnormal LFTs(fatty infiltration):superior mesenteric artery syndrome– all reversible

Renal: dehydration, ↓GFR, stones, polyuria, total body Na and K depletion; peripheral edema with refeeding

Haematologic: leukopoenia, anaemia, thrombocytopoenia, iron deficiency

Endocrine: sick euthyroid syndrome, amenorrhoea, osteopoenia

Neurologic: cortical atrophy, seizures

MEDICAL COMPLICATIONS

Purging / Binging

Fluid and electrolyte imbalance: ↓K and Na, hypochloremic alkalosis

Use of ipecac: irreversible myocardial damage and diffuse myositis

Chronic vomiting: esophagitis, dental erosions, parotitis, Mallory-Weiss tears, oesophageal or gastric rupture, aspiration pneumonia

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

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

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

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 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 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 Weight loss – loss fat and muscle

A low BMI more strongly correlated with lean muscle mass than fat mass (Cole et al BMJ 2007)

BMI:

- Adults concern if BMI < 17.5- Adults severe malnutrition cut off BMI =13

WFH : % Median BMI= Actual BMI / Median BMI (50th percentile for age & sex) x 100

WFH 100% = BMI 50th centile

WFH

Be concerned if WFH < 90% = BMI < 9th centile – stop exercise

Be very concerned WFH 80% = BMI < 2nd centile (definition of underweight) –

stop school

Consider hospitalisation if WFH < 75%

DIAGNOSTIC DECISION TREE

UNDERWEIGHT?

FEAR OF WEIGHT GAIN?

BINGES?

ANOTHER

EMOTIONAL DISORDER?

FAEDEXCLUDE PHYSICAL ILLNESS

LIMITED RANGEOF FOODS?

PURGES?

SELECTIVEEATING

BNBINGE

EATING DISORDER

YES NO

YES NO NO YES

YESNO YES

YES NO

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 USSConsider: DEXA scan CXR Abdominal Xray MRI / CT scan Autoimmune, coeliac screen Cardiac ECHODON’T BE FALSELY REASSURED BY NORMAL BLOOD

RESULTS

MEDICAL TREATMENT When to hospitalise / inpatient treatment?

Weight recovery usually 2 – 3 kg per month

Target weight : WFH 95 – 110%

Resumption of growth and / or menses are better indicators of recovery than targets

EDs and GUIDELINES/ EVIDENCE BASE

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.pdfNicholls D, Hudson L, Mohamed f. Arch Dis Child. 2010 Oct 7. (Epub) Managing anorexia nervosa

INPATIENT TREATMANT

1 in 4 AN will be hospitalised

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)

Admit locally and in age appropriate setting (NICE)

Do not isolate

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:

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)

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

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 Parents helped to take responsibility

Establish parental control of food and fluid intake

Patient encouraged to negotiate the “how” of food intake and not the “whether”

Consistency of approach

REFEEDING Aim for 0.5 -1.0 kg weight gain per week

At least 500 – 1000 Kcals above basic requirement

Inpatients may need 3000 Kcals /d

Start at 15 – 20 Kcal/kg/d

Avoid underfeeding syndrome

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 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

Physical evaluation and stabilisation

Reestablishment of food intake

Risk assessment

Relief of patient, parent, professional anxiety

Assessment of treatment needs

Long term

Establish healthy body weight

Identify and manage emotions

Develop new coping skills

Develop communication skills

Develop peer relationships

Learn to use help

Reintegrate to home or other environment

INPATIENT TREATMENT - BN

Not used in adults as a rule

Means of breaking cycles of binge / purge and establishing regular eating patterns

Related to risks of other self-harming behaviours

Related to severity of other co-morbid illness

PSYCHOLOGY

AN Avoidance, anxiety,

obsessionality Vicious circle of restraint Need for control is central

Egosyntonic – rarely seek voluntary treatment

BN Impulsivity, emotionality,

chaos Vicious circle of failed

restraint Need for control is central Depressed by behaviour

Egodystonic – more motivated but ambivalent about weight gain

PHYSICAL EFFECTS OF AN ON BRAIN

Cortical atrophy and ventricular enlargement

Secondary to starvation Reverse with

restoration of adequate nutrition

FUNCTIONAL EFFECTS OF AN ON BRAIN

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

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

FRONTAL-EXECUTIVE DEFICITS

NUCLEUSACCUMBENS-

REWARD

HIPPOCAMPUS-MEMORY

AMYGDALA-EXTREMEANXIAETY

BASAL GANGLIA-OBSESSIONAL

DRIVE

PARIETAL LOBE-VISUOSPATIAL

DEFECITS

SOMATOSENSORY CORTEX -

DISTORTED BODYIMAGE

INSULA

UNLIKELY THAT EACH OF THESE IS NOT FUNCTIONING CORRECTLY

BRAIN FUNCTIONIN AN

THERAPY 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

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

Parent & patient relieved of anxietyPatient relieved of internal conflict

Reinforces parents’ sense of failure

LONG TERM PHYSICAL SEQUELAE

Growth

Bone density

Puberty

GROWTH

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

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

Changes start early in disease Impaired bone formation and increased absorption Factors: low oestrogen & IGF1

high cortisolpoor nutrition, low BMIlow Ca and Vit D

Greatest risk: > 12 months onset AN> 6months amenorrhoealow BMIlow Ca intakelow physical activity (Castro et al 2000)

BONE DENSITY

Mainstay treatment – weight gain, nutritional rehabilitation, spontaneous resumption menses

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)

Ca and Vit D supplements may be prescribed

Full recovery unlikely – osteopoenia in 1/3 recovered AN

Long term fracture risk around x3 –x7 of general population

PUBERTYMenses:

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

Response to treatment – difficult to distinguish from natural course as treatment almost invariably ensues and limited on untreated cases

Remission

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

Children < 11years may do worse – only 2 studies

POOR OUTCOME

Continuing illness associated with functional impairment or death

Lower body fat at presentation (Mayer et al. Am J Psych 2007)

Longer duration illness

Hospitalised (Gowers et al. B J Psych 2007)

Readmitted (up to 45%) (Steinhausen 2007)

MORTALITY Mortality AN 0% – 22 % depending on follow up period

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.p

df