Eating Disorders Dr Bert Laszlo Consultant Psychiatrist HALDON Eating Disorders Service Devon Partnership NHS Trust November 2009
What are we doing today? • Discussion of major eating disorders – Dr. Laszlo • Break • Etiology and psychological aspects – Elisa Rivera • Break • Vignette discussions x 3 – Everyone • Dietetic aspects of ED – Tanya Sturley
The term was first used 130 yrs ago, only more recently that the diagnostic criteria have become medical knowledge. • Due to an increase in incidence and diagnosis the impression may well be that the disorder is a fairly “new” one however a 1000 year old legend exists which suggests that the illness was known to the ecclesiastical authorities of the time.
According to the legend, St Wilgefortis was the 7th daughter of the King of Portugal. The King was known to be tyrannical and cruel and their relationship was poor and possibly incestuous. The relationship further deteriorated upon her discovery of her father’s plans to marry her to the King of Sicily. She had already made a vow of virginity and planned to give her life to God and not man. She therefore prayed to God to help her avoid the proposed marriage. The intensity of her prayers impressed others and she overcame her appetite as an expression of her selfless love of God and to enhance her spiritual development. “She begged the Lord to deprive her of all her beauty and God granted her prayer” by causing her to develop a hairy body and grow a beard. The King of Sicily withdrew his offer, and her enraged father had her crucified. She claimed that she had been liberated from “worldly care”.
The legend is one of a saintly, virgin martyr who avoided her sexuality by growing hair. She was seen to have divested herself of female “care” or problems. It spread throughout Europe and a cult developed.
Driven, striving females • High ethical and moral standards • Higher social classes • Arises during early adolescence • Inability to cope with demands • Fears of adult sexuality • History of Abuse • Personality structure
Traditionally in medicine, both food avoidance and overeating have been looked upon as symptoms of gastrointestinal disorders. Preoccupations with body weight and shape have only acquired medical attention in the last part of the 20th century and only in westernised countries. Therefore they appear to be relatively “modern” clinical entities.
For centuries extreme fasting was part of the penitential or ascetic practice of pious Christians. Later forms of long-lasting food refusal not accompanied by symptoms of well known diseases e.g. tuberculosis were likely to stir up speculation about supernatural powers or demonic influences.
Morbid self-starvation only became recognised as a distinct clinical entity in the second half of the 19th century. In 1873 Lasegue (French) and Gull (English) both provided independently the first explicit description of anorexia nervosa. • It was in the context of anorexia nervosa that the modern notion of bulimia nervosa emerged. In 1979 Gerald Russell coined the term “bulimia nervosa”
ICD 10 – Anorexia Nervosa • Weight < 85% expected (BMI <17.5) • Intense fear of gaining weight • Body image disturbance • Amenorrhoea (hypogonadotrophic hypogonadism) • Restrictive vs binge-eating / purging subtype in the DSM IV criteria(very helpful)
ICD 10- Bulimia Nervosa • Recurrent episodes of binge eating –both of: • Large amount, discreet time period,craving • Sense of lack of control • Recurrent compensatory behaviour – to avoid wt gain • Eg;purging activities,periods of starvation,medication • At least twice a week X 3months • Self evaluation unduly influenced by body shape and weight • Usually in normal weight range
1. Incidence and prevalence rates: • Incidence = number of new cases presenting in a given time • Prevalence = total number of cases in the population at one time • AN :incidence = 4-10/100 000/yr • prevalence = 10-30/100 000 • BN:incidence = 5-15+/100 000/yr • prevalence = 50 -150/100 000
2. Course and prognosis: • AN: long time for recovery to occur • Recovery rates increase with time as chronicity rates decrease • 10 yr follow up: 47% recover • 33% improved • 20 -25 % chronic course • High rates of relapse in the first year following treatment. • BN: course and outcome is more favourable. • 50% - 74% recover completely therefore a significant number still have clinically significant symptoms.
3. Mortality rates: • AN: MR = 6% overall, 0.5% per year. • Higher MR than for BN – highest MR for any functional psychiatric illness • Reasons: the illness,comorbidity,suicide • BN: lower MR than for AN – 0.3% -1% overall
4. Treatment options: Anorexia • Limited evidence base from which to recommend the most effective treatment • NICE Guidelines – January 2004: • Outpatient , psychological treatment for at least 6 months • Family therapy > Ind.Th. (child and adolescents) • Dietary counselling should not be provided as sole treatment • Limited evidence base for the use of medication in AN
BN: NICE Guidelines – January 2004: • First step = evidence based self-help programme • CBT-BN + IPT > BT (CBT-BN to be 16-20 sessions over 4-5 months) • IPT is alternative to CBT-BN (8-12 months to achieve results – improvement occurs 4 months after treatment ends. • May be offered trial of antidepressant – 1st choice :SSRI’s esp. Fluoxetine
Aetiology of eating disorders Predisposing Precipitating Perpetuating
Predisposing factors - AN • Personality traits: low self-esteem, perfectionism seek ‘compliance’ • Depression & anxiety disorders (OCD) • Pre-morbid obesity: 7 - 20% anorectics • Female • Feeding/GI problems –early child • ? Over concerned parenting
Predisposing factors -BN • Female • Childhood obesity • Sexual abuse/adversity • Parental depression, alcohol or drug abuse • Parental obesity, weight/shape criticism • Adverse family experiences
The discovery of past abusive experiences should be the beginning of further thought for the clinician. It should not be the occasion for premature closure around the notion that all is now explained
Family Psychiatric History • Lifetime risk of AN and depression in 1st degree relative 3 times greater than controls • Genetic vulnerability: • ? to anorexia nervosa • ? to pre-morbid obesity • ? to predisposing personality traits
Family dynamics Speculative research driven by dogma, but : • ?More rigid family systems • “Consensus sensitive” • Family intervention particularly useful for younger anorectics
Sociocultural factors • Sociocultural factors may better explain body image dysphoria among Western women in general than AN in particular • Contiguity between thin female beauty ideal and increased prevalence of eating disorders
Precipitating factors • Dieting : - intentional • positive reinforcement (social, psychological, physiological) • Major life events • (puberty, loss events, trauma)
Perpetuating factors • Cognitive distortions • Interpersonal factors • Physiology
Is it Anorexia Nervosa? • Usually the history from self or informants is clear • 20%-30% atypical cases do occur • Differential diagnosis: examine over time (can they gain weight? – “watchfulwaiting” over a few weeks) ESR, platelets, TFT, albumin are useful screening tests.
Risk factors in History: • Excessive exercise with low weight • Blood in vomit • Inadequate fluid intake in combination with poor eating – young patients tend to do this • Rapid weight loss = 1kg/wk over a few months. • Factors which may have interfered with ritualized eating patterns e.g. holiday, • exams,times of being evaluated etc.
Monitoring: • Weigh at each weekly therapy/review appointment • Make sure that environment is conducive • More detailed risk assessment if there are concerns regarding nutritional and metabolic safety. • If medical risk becomes high then: (a)other professional and carers need to be involved (b)intensity of care increased with family work, day or inpatient care. • Estimate of calories needed for weight gain • Estimate time needed for sufficient weight gain to occur to reduce risk
Medical risk assessment: • on assessment, with weight loss and if previous risk • Weight, height and BMI • Tanner stage and height centile if premenarchal • Stand up from squat test (SUSS) or sit up test • BP, HR/sitting and standing • Look for signs of peripheral shutdown, skin breakdown • Core temp –tympanic membrane(electronic) • Blood tests – FBC, U&E, LFT, glucose, phosphate, magnesium, zinc • ECG
Muscle power: patient is asked to squat down on haunches and is asked to stand up without using arms as levers if at all possible. • Sit up test: patient lies flat on a firm surface such as the floor and has to sit up without, if possible using her hands.
In the management of these patients good practice involves discussions of issues of confidentiality and necessary involvement of other parties.
Examination: • BMI • Height centile (for stunting) • BP lie and stand • HR • Temperature • Sit up and squat test • Look for signs of peripheral shutdown • Skin breakdown
Investigations: • HB, WCC, FBC –platelets • U&E, renal function, LFT (if abnormal check clotting profile) • Glucose • Mg, Ca, Phosph • ECG
Moderate risk: • See table (for guidance) • Priority should be given to physical examination • Weekly monitoring • Good practice – actively encourage involvement of carers
High risk: • See table (for guidance) • Priority should be given to physical examination • CONSIDER URGENT MEDICAL ADMISSION • Consult specialist
Indication for Admission • Very low weight or rapid weight loss • Serious physical complications • Severe psychiatric co-morbidity • Failure of outpatient treatment • Need for separation from family
IF VOLUNTARY ADMISSION REFUSED: ASSESS CAPACITY • Understand the nature of the health risk • To assess the risks and benefits of treatment /no treatment • Able to weigh up the information rationally • Make a fully informed choice with full capacity • Consider use of the Mental Health Act
TreatmentThe Mental Health Act • Anorexia may be treated under Mental Health Act • Anorexia Nervosa may affect capacity to make decisions about treatment due to starvation effects and psychopathology • Should be last resort • In life-threatening circumstances, compulsory feeding (e.g. naso-gastric) under Section 3 of MHA is lawful
Mouth, face and skin provide diagnostic clues… • “Russell’s sign” – biting down on the hand to induce repeated vomiting • Dental erosion due to repeated exposure of teeth to gastric acid • Parotid or submandibular salivary gland enlargement due to repeated vomiting • Lanugo hair • Dry skin • Carotenoderma – high levels of betacarotene • Cold blue hands, nose and feet.
Gastrointestinal complications… • Constipation, esp with laxative abuse, atonic bowel with sustained laxative abuse. • Delayed gastric emptying • Abnormal liver function tests • Upper gastrointestinal bleeding - Mallory –Weiss tear (oesophageal mucosa) • oesophagitis (acid reflux) • Very rare – acute pancreatitis, acute gastric dilatation, volvulus, rectal prolapse, oesophageal or gastric perforation.
Cardiovascular complications… • Account for ~ 50% of deaths in AN • Occur frequently in eating disorder patients, esp low weight AN and BN patients with electrolyte abnormalities. • Bradycardia • Hypotension • Poor peripheral circulation • ECG abnormalities – sinus bradycardia - ST and T wave changes - reduced size of QRS complex - prolonged QT/QTc interval (normal QTc<450 msec)
Arrhythmias –serious in patients with disturbed electrolyte balance • ECG changes are compounded by electrolyte disturbances, partic K+ • Reduced oral intake (dehydration) = low BP + sinus bradycardia. • Sinus bradycardia and sinus arrhythmia are both common in low weight patients with AN but do not pose an increased risk of death. • Ventricular arrhythmias cause sudden death. • Reduced cardiac mass • Mitral valve prolapse • Cardiac failure – most likely on refeeding, parenteral feeding esp dangerous, hypophosphataemia may be a factor. • Refeeding oedema not due to cardiac failure but? due to low serum proteins (albumin) but can occur with normal albumin. Also occurs with previous heavy laxative abuse.
Neurological complications … • myopathies – generalised weakness and muscle wasting commonest, usually improves on weight restoration. Raised CK (Creatine Kinase), very high if exercising • peripheral neuropathies – may be due to mechanical pressure on nerve from loss of fat and subcutaneous tissue, may be due to nutritional deficit or metabolic disturbance, peroneal nerve palsy (foot drop) commonest. • Brain changes – loss of volume and some functional changes. Generally reversible on weight restoration.