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Eating Disorder Primary Care Workshop

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Presentation on theme: "Eating Disorder Primary Care Workshop"— Presentation transcript:

1 Eating Disorder Primary Care Workshop
Jaco Serfontein

2

3 What are Eating Disorders?
Complex psychological disorders Serious Physical complications Mortality increased Psychiatric co-morbidity People often ambivalent about treatment 3

4 AN in History Holy Anorexics St Catherine of Siena (14th Century)

5 Victorian Fasting Girls
Sarah Jacob – The Welsh fasting girl ( ) Mollie Fancher – The Brooklyn Enigma ( ) Josephine Marie Bedard – The Tingwick Girl Therese Neumann ( ) - Bavaria

6 Diagnostic Criteria - AN
DSM-5: Markedly low weight (Body weight < 85% of expected in DSM-IV) Intense fear of gaining weight or persistent behaviour to avoid weight gain Weight and shape disturbance (Amenorrhea in DSM-IV) Restricting type and binge-eating/purging type

7 BMI 20 - 25 Normal weight 17.5 - 20 Underweight 15 – 17.5
Anorexia nervosa Severe Anorexia nervosa 12 – 13.5 Critical Anorexia nervosa < 12 Life threatening anorexia nervosa

8 Bulimia Nervosa Recurrent episodes of binge eating once per week
Recurrent inappropriate compensatory behaviour in order to prevent weight gain Present for 3 months Self-evaluation unduly influenced by body weight and shape (morbid fear of fatness) Two subtypes Purging type Non-purging type

9 NoS-FED or atypical subthreshold cases partial syndromes
Disorders of eating or weight control: resembles AN or BN but do not reach their diagnostic criteria subthreshold cases partial syndromes

10 Binge-Eating Disorder (DSM-5)
Binge eating (once per week for 3/12) Binges associated with 3 of: Eating rapidly Uncomfortably full Large amounts when not hungry Alone because embarrassed Guilty, depressed, disgusted Marked distress No compensatory behaviour

11 Categories and movement between diagnoses
BN ED-NOS Fairburn & Harrison (2003). Lancet 361,

12 The patients Anorexia nervosa Bulimia nervosa
weight/shape related psychopathology not always present culturally influenced highly visible reluctant patients who deny their problems others concerned outcome poor mortality high (20% at 30 yrs; 1/3 = suicide) early-onset  shorter stature Bulimia nervosa weight/shape related psychopathology central strongly culture-bound invisible “shameful secret” ambivalent patients others unaware outcome fair mortality not raised 12

13 Clinical features AN BN BED Specific psychopathology
strict dieting self-induced vomiting laxative misuse over exercising bulimic episodes ritualistic eating habits anxiety when eating with others over-evaluation of shape & wt

14 Clinical features AN BN BED General psychopathology
depressive symptoms anxiety symptoms obsessional symptoms impaired concentration social withdrawal substance misuse

15 Prognosis 8.7% persistent psychiatric problem requiring hospital care
Outpatient AN – 80% remission after 5 years Keel and Brown, 2010 Inpatient AN – 48% remission after 12 years Fichter et al, 2006 Swedish adolescent females inpatients 9-14-year follow-up study Anorexia nervosa 21.4% dependent on society for income 8.7% persistent psychiatric problem requiring hospital care mortality: 1.2% Hjern et al (2006) B J Psych 189, Prevalence rate refer to age 16 –40 years in women 15

16 How common is ED? AN prevalence 0.3 – 0.9, increasing in young women
BN 1-2 BED 2? Turnbull et al., 1996; Currin et al., 2005

17 An average GP list On an average GP list of 2000 people expect:
1-2 people with full AN 18 people with full BN 40 people with ED-NOS

18 Eating disorders in males
AN % BN 10-15% (0.2%) of young males BED ~20% symptomatology quite similar to females later age of onset (18-26) vs (15-18) higher premorbid weight body image dissatisfaction - lean tissue athletic pursuits / job sexuality osteoporosis more rapid & severe but more exercise, less abuse of laxatives & strict dieting, less concerned with weight, increased co morbidity of substance misuse Age of onset - females 2 yrs ahead in puberty and lower resting metabolic rate Outcome related rto age of onset has yeilded conflicting results and confounded by length of illness Overweight - up to 60% in BN and higher percentage in An than seen in females, more teasing at school Body image - not so much on thinness, diff in cultures USA men vs Austrian Athletics - partic in sports where weight restrictions, eg light weight boxers, athletic training Actors/ models Greater risk if gay ?similar emphasis on body as part of self worth, but ambivalence or avertion to sexual matter ‘asexual’/ sexual anxieties, actively suppressing sexual drive, both in hetero and homosexual Also high feminity scores on personality measures Presence of sexual fantancy and masturbation good predictor of outcome, and absence a poor outcome Personality - 71% BN have axis 2 diagnosis,of cluster B personality, borderline, narcissitic antisocial AN - spread across 3 categories of personality disorder, but high rates of OCD and/or obsessional features 18

19 What causes AN? Complex psychological illness with no single cause
Combination of biological, psychological and sociocultural factors First degree relatives of AN have a ten-fold increased lifetime risk of developing AN (Pinheiro, 2009) Anorexia – specific heritability Bulimia – general heritability

20 Medical complications

21 Etiology Starvation Fluid and electrolyte disturbance
Direct local damage due to eating disorder behaviour Endocrine changes Changes in liver function Refeeding Give examples 21 21

22 Cardiac-related Eliana and Luisel Ramos

23 Multiorgan Failure Christy Henrich Ana Restin

24 Suicide Anna Westin

25 Biochemical abnormalities
Could have any abnormality, hypo >> hyper ↓K ↓ Na ↓Mg ↓glucose

26 Refeeding syndrome Refeeding of severely malnourished AN (esp parenteral) and bingeing Severe intracellular shifts in fluids and electrolytes, esp PO4 (also Mg, K, Thiamine) PO4 nadir in first week Decreased PO4 = decreased ATP Very low PO4 directly cardiotoxic Clinical Muscle weakness Cardiac - arrhythmias, failure, pericardial effusion Neurological – delirium (can occur > 1week and after PO4 has recovered), coma, death Haematological – leukocyte dysfunction, haemolytic anaemia, platelet dysfunction

27 Osteoporosis (oestrogen, cortisol, GH, IGF-I)
Early, frequent and serious complication of ED Increased resorption (as result of decreased oestrogen and increased glucocorticoids) and decreased deposition (low IGF-I) No correlation with calcium intake, exercise or HRT 40% of women with AN has osteoporosis (>2.5 SD) 92% of women with AN has osteopenia (>1 SD) (Vestegaard et al, 2002) 7x higher fracture rate than healthy women of same age Treatment Refeeding Weight bearing exercise? HRT? Bisphophanates? Mention positive trial with oestrogen and IGF-I. Few studies on DHEA. 27 27

28 Direct local damage related to binge-eating and purging
Parotid swelling Oesophageal damage GER reflux GI bleed Post-binge pancreatitis Acute gastric dilatation Colonic volvulus prolapse Follow path of food – hand, mouth, parotid, oesophagus – oesophagus tears, rupture, oesophagitis, ulcer, other rare intestinal complications 28 28

29 Gastrointestinal system - chronic
Due to starvation Abnormal oesophageal motility Delayed gastric emptying Increased colonic transit time Laxative abuse -> colonic autonomic nerve degeneration Liver Fatty infiltration (lipogenesis > lipolysis) Increased ALT (less than 4x), benign Rarely can progress to Nonalcoholic steatohepatitis (higher risk in older, dual diagnosis, obesity and AST/ALT>1) Talk about physical discomfort and pain when refeeding and psychological 29 29

30 Cardiovascular System
1/3 of deaths in adults with eating disorders Starvation related Hypotension and bradycardia Mitral valve prolapse Fluid and electrolyte balance related (and severe starvation) Arrhythmias (prolonged QTc) Refeeding Cardiac failure Eating disorder behaviour related Ipecac related cardiomyopathy

31 Endocrine System Reproductive Low FSH, LH, oestrogen, testosterone
Adrenal High cortisol Growth hormone axis High GH, low IGF-I Thyroid Axis Low T3/T4, normal or reduced TSH ‘sick euthyroid’ Appetite Low leptin, high ghrelin and peptide YY Osteoporosis is not only oestrogen related, also mention other hormones. Also IGF1 decreases due to decreased liver production – this leads to increased GH (negative feedback system). Also GH resistance. 31 31

32 Haematology Anaemia Mild leukopenia Thrombocytopaenia Decreased ESR
Talk here about difficulty in identifying infection (no fever, no raised WCC) and other markers (like drop in albumin) that might indicate infection. 32 32

33 Nervous System Starvation related: Pseudoatrophy, enlarged ventricles
Cognitive impairment Peripheral neuropathy

34 Skin and Hair Self-injury Dry skin Skin breakdown, pressure sores
Carotenemia Dry, brittle hair Hair loss Lanugo Carotenemia due to decreased liver clearance. (and relative increased intake). Talk here about how complications that are not medically serious can be the ones that cause most distress to patients. Also talk about anorexia being a great pretender, presenting indifferent forms to various clinicians. 34 34

35 Comorbidity with Diabetes
Type I AN – no increase BN – 3X increase EDNOS – 2X increase Type II BED most prevalent

36 Diabetes Insulin purging women > men Poor glycaemic control
Early diabetic retinopathy Medical complications of ED higher Higher rate of other psychiatric diagnoses Treatment similar

37 How would you recognise the following?
Vomiting Water loading Over exercise Infection in low weight AN Refeeding syndrome

38 Treatment

39 NICE guidelines (2017) recommend Support should include:
NICE OVERVIEW NICE guidelines (2017) recommend Support should include: Psychoeducation Regular physical health monitoring Multidisciplinary Involve family and carers IPT is an alternative, but takes 8-12 months to achieve comparable results 39

40 Evidence based, disorder-specific psychological treatments
Anorexia Nervosa Restricting EDNOS

41 Evidence-based psychological treatments for anorexia
Individual eating-disorder-focused cognitive behavioural therapy (CBT-ED) Maudsley Anorexia Nervosa Treatment for Adults (MANTRA) Specialist supportive clinical management (SSCM) Next step if unsuccessful or unacceptable Eating-disorder-focused focal psychodynamic therapy (FPT) Only 30% of adult cases are recovered at 1 year, 40-50% at 5 yrs Limited evidence of fluoxetine in relapse prevention All better than treatment as usual or dietary counselling alone E.g. CBT-E typically 40+ sessions focussing on food avoidance / anxieties, weight restoration, weight/shape concerns, interpersonal, intrapersonal and systemic maintaining factors

42 Children & adolescents
Family interventions (first line or relapse prevention) produce recovery rates of 60-70% at 1 year, 70-90% at 5 yrs classical family therapy not necessary (Eisler et al. 2003)

43 Evidence based, disorder-specific psychological treatments
Bulimia Nervosa EDNOS Binge Eating Disorder

44 Stepped care approach Explain that treatment limited effect on body weight Bulimia-nervosa-focused guided self-help Individual CBT-ED Regularising eating Reducing compensatory behaviours Introducing emotional regulation skills Problem solving skills Addressing weight and shape concerns – anxieties, perceptual biases, attitudes etc Medication should not be offered as sole treatment

45 Treatment complications

46 Maintaining Factors of AN
Predisposing traits Perpetuating consequences Emotional avoidance Obsessive compulsive traits Interpersonal Relationships Beliefs about The value of AN in the Person’s life

47 The Pros and Cons of anorexia nervosa (Serpell et al., 2002, 2003)
3 most important pro-anorexic beliefs were: Anorexia nervosa keeps me safe helps to communicate distress stifles emotion

48 Iatrogenic Maintaining factors
Overprotection Over zealous use of inpatient treatment. Excluding or disempowering the family. Criticism or confrontation-coercive treatments MHA Use of loss of privilege systems Accommodation Use of treatment without nutritional direction/expectation of change. Engaging in bargaining of treatment goals with the persuasive patient. Enabling Services palliating loneliness and isolation. Providing the opportunity for further striving competing and calibrating against others. Treasure et al., 2011

49 Difficulties Secretiveness – highly functional, denial, difficult to detect Ambivalence – engaging with services, about what recovery or treatment entails Reactions of others (including services) – high expressed emotion, overly controlling, accommodating, dismissing Physical & psychological complications of illness Psychiatric and physical co-morbidity (e.g. PD / Diabetes)

50 Treatment considerations
Collaborative and motivational approach vs MHA Engagement and disengagement Recovery and prognosis Risk management Shared care Medication

51 Recognition and Initial Management of Eating Disorders
Screening The King’s College Risk assessment

52 Screening – The SCOFF questionnaire
Do you make yourself Sick because you feel uncomfortably full? Do you worry you have lost Control over how much you eat? Have you recently lost more than One stone in a 3 month period? Do you believe yourself to be Fat when others say you are too thin? Would you say that Food dominates your life? 2 or more out of 5 predicts an ED with 100% sensitivity and 87.5% specificity Morgan et al (1999)

53 King’s College Medical Risk Assessment
Medical Risk –Psychiatric Risk Psychosocial Risk Insight/Capacity and motivation

54 Surgery: St Stephen’s Gate Medical Practice
NHS Number: XXXXXXXXXXXX Medical monitoring request This box is shared with commissioners and should not contain any identifying information Frequency FBC, u&e, LFT, Ca, PO4, Mg, muscle CK, random glucose X Every two weeks Brief essential examination (weight, pulse, lying/standing blood pressure, core temperature, squat test) Weight only Additional requests: Please do an ECG at baseline u&e only

55 Medical Monitoring Brief Essential Examination – BMI alone is not enough because it is not reliable Special Investigations – Bloods, ECG, Dexa Scan, etc

56 Brief Essential Examination
BMI (single layer of clothing, no shoes/mobiles/wallets/heavy jewelery etc) Sitting/standing blood pressure Pulse rate Peripheral circulation Core temperature A measure of muscle strength – squat test

57 Sit-up/Squat test

58 Investigations FBC, u&e, bicarb, LFT, Ca, PO4, Mg, CK, gluc
Bonescan if >1 year amenorrhoea ECG if BMI<14 or if on drugs that can affect QTc Any other physical investigation pertinent to physical state, eg, TFT


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