eating disorder

Fifth stage

Psychiatry
Lec-9
د.الهام

20/11/2016

Eating disorder
Anorexia nervosa

Aetiology

Genetic.
concordance rates MZ:DZ = 65%:32%,
female siblings: 6-10%
Adverse life events
no excess of childhood physical or sexual abuse (compared to psychiatric controls)
Psychodynamic models
Biological

Psychodynamic models:

Family pathology
enmeshment,
rigidity,
overprotectiveness,
lack of conflict resolution,
weak generational boundaries.
Individual pathology
disturbed body image (due to dietary problems in early life,
parents preoccupation with food,
lack of a sense of identity).
Analytical model
regression to childhood,
fixation on the oral stage,
escape from the emotional problems of adolescence.


Biological:
Hypothalamic dysfunction
cause or consequence.
Neuropsychological deficits
reduced vigilance,
attention,
visuospatial abilities,
associative memory (correct with weight gain).
Brain imaging CT:
pseudoatrophy sulcal widening and ventricular enlargement (correct with weight gain).
Functional imaging: unilateral temporal lobe hypoperfusion perhaps related to visuospatial problems/body image distortion.

Differential diagnosis:

Chronic debilitating physical disease
Brain tumours
GI disorders (e.g. Crohn's disease, malabsorption syndromes)
Loss of appetite (may be secondary to drugs e.g. SSRIs, amfetamines)
Depression/OCD (features of which may be associated)

Physical consequences:

Oral
Dental caries.
Cardiovascular
Hypotension;
prolonged QT;
arrhythmias;
cardiomyopathy.
Gastrointestinal
Prolonged GI transit (delayed gastric emptying, altered antral motility, gastric atrophy, decreased intestinal mobility);
constipation.
N.B. Prokinetic agents may accelrrate gastric emptying and relieve gastric bloating, which can accelerate resumption of normal eating habits.
Renal
Renal calculi.
Reproductive
Infertility;
low birth-weight infant.
Dermatological
Dry scaly skin
brittle hair (hair loss);
lanugo (fine downy) body hair.
Neurological
Peripheral neuropathy;
loss of brain volume: ventricular enlargement, sulcal widening, cerebral atrophy, (pseudoatrophy”corrects with weight gain).


Hematologic
Anaemia;
leucopaenia;
thrombocytopaenia.
Endocrine and metabolic
Hypokalemia;
hyponatremia;
hypoglycemia;
hypothermia;
altered thyroid function;
hypercortisolaemia;
amenorrhea;
delay in puberty;
arrested growth;
osteoporosis.

Cardiac complications

The most common cause of death (mortality rate 10%).
Findings may include
Significant bradycardia (30-40bpm)
Hypotension (systolic <70 mmHg)
ECG changes (sinus bradycardia, ST-segment elevation, T wave flattening, low voltage, and right axis deviation) may not be clinically significant unless there are frequent arrhythmias (QT prolongation may indicate increased risk for arrhythmias and sudden death).
Echocardiogram may reveal decreased heart size, decreased left ventricular mass (with associated abnormal systolic function), and mitral valve prolapse (without significant mitral regurgitation). These changes reflect physiological response to malnutrition and will recover on refeeding.


Amenorrhoea
Included in the diagnostic criteria, due to
hypothalamic dysfunction (hypothalamic-pituitary-ovarian axis)
low levels of FSH and LH,
low levels of oestrogen (reversion to the prepubertal state occurs)
LH response to GnRH blunted leading to amenorrhea.
Consequences include
Reduced fertility,
multiple small follicles in the ovaries,
decreased uterine volume, and atrophy.
Note: amenorrhea can persist (in 5-44% of cases) even after recovery and return to normal weight.

Osteopenia:

Both cortical and trabecular bone are affected, and osteopenia persists despite oestrogen therapy. Contributing to bone loss are
low levels of progesterone
decreased IGF-1 levels.
Treatment
No specific treatment exists; however, 1000-1500 mg/d of dietary calcium and 400 IU of vitamin D is recommended to prevent further bone loss and maximize peak bone mass.
Exercise and HRT, although of benefit in adult women, may be harmful for adolescents with anorexia nervosa (causing premature closure of bone epiphysis).

Physical signs

loss of muscle mass
dry skin
brittle hair and nails
callused skin over interphalangeal joints (Russell sign)
anaemia
hypercarotinemia (yellow skin and sclera)
fine, downy, lanugo body hair
eroded tooth enamel
peripheral cyanosis
hypotension
bradycardia
hypothermia
atrophy of the breasts
swelling of the parotid and submandibular glands
swollen tender abdomen (intestinal dilatation due to reduced motility and constipation)
peripheral neuropathy

Assessment

Full psychiatric history
Establish the context in which the problems have arisen (to inform development of a treatment plan).
Confirm the diagnosis of an eating disorder.
Assess risk of self-harm/suicide.
Commonly reported psychiatric symptoms
Concentration/memory/decision-making problems
Irritability
Depression
Low self-esteem
Loss of appetite
Reduced energy
Insomnia
Loss of libido
Social withdrawal
Obsessiveness regarding food
Full medical history
Focus on the medical complications of altered nutrition .
Detail weight changes, dietary patterns, and excessive exercise.
Symptoms commonly elicited on systemic enquiry
General physical health concerns
Amenorrhoea
Cold hands and feet
Weight loss
Constipation
Dry skin
Hair loss
Headaches
Fainting or dizziness
Lethargy


Physical examination
Determine weight and height (calculate BMI).
Assess physical signs of starvation and vomiting .
Routine and focused blood tests.
ECG (and Echocardiogram if indicated).

Blood tests:

FBC
Hb usually normal or elevated (dehydration); if anaemic, investigate further.
Leucopaenia and thrombocytopaenia seen.
ESR
Usually normal or reduced; if elevated, look for other organic cause of weight loss.
U&Es
Raised urea and creatinine (dehydration),
hyponatraemia (excessive water intake or SIADH neurogenic diabetes insipidus, affecting 40%, may be treated with vasopressin, but is reversible following weight gain),
hypokalaemic /hypochloraemic metabolic alkalosis (from vomiting),
metabolic acidosis (laxative abuse).
hypocalcaemia,
hypophosphataemia,
hypomagnesaemia.


Glucose
Hypoglycaemia (prolonged starvation and low glycogen stores).
LFTs
Minimal elevation.
TFTs
Low T3/T4,
increased rT3
(euthyroid sick syndrome, an adaptive mechanism; hormonal replacement not necessary; reverts to normal on re-feeding).
Albumin/total protein
Usually normal.
Cholesterol
May be dramatically elevated (starvation), secondary to decreased T3 levels,
low cholesterol binding globulin,
leakage of intrahepatic cholesterol.
Endocrine
Hypercortisolaemia,
Increase GH levels,
Decrease LHRH,
Decrease LH,
Decrease FSH,
Decrease oestrogens,
Decrease progestogens.


Management
Most patients will be treated as outpatients.
A combined approach is better:
Pharmacological
Fluoxetine (especially if there are clear obsessional ideas regarding food);
previously TCAs or chlorpromazine used for weight gain.
Psychological
Family therapy (more effective in early onset),
individual therapy (behavioural therapy = CBT; may improve long-term outcome).
Education
Nutritional education (to challenge overvalued ideas),
self-help manuals (bibliotherapy).
Hospital admission should only be considered if there are serious medical problems .
Compulsory admission may be required: feeding is regarded as treatment
(Note: Ethical issue regarding patient‘s right to die vs. their ˜right to treatment).

Criteria for admission to hospital

Inpatient management may be necessary for patients with significant medical or psychiatric problems:
Extremely rapid or excessive weight loss that has not responded to outpatient treatment.
Severe electrolyte imbalance (life-threatening risks due to hypokalaemia or hyponatraemia).
Serious physiological complications, e.g. temperature < 36°C; fainting due to bradycardia (PR < 45 bpm) and/or marked postural drop in BP.
Cardiac complications or other acute medical disorders.
Marked change in mental status due to severe malnutrition.
Psychosis or significant risk of suicide.
Failure of outpatient treatment (e.g. inability to break the cycle of disordered eating or engage in effective outpatient psychotherapy).


Admission should not be viewed as punishment by the patient and the goals of inpatient therapy should be fully discussed with the patient (and their family):
Addressing physical and/or psychiatric complications.
Development of a healthy meal plan.
Addressing underlying conflicts (e.g. low self-esteem, planning new coping strategies).
Enhancing communication skills.

Risks of re-feeding

With re-feeding, cardiac decompensation may occur, especially during the first 2 wks (when the myocardium cannot withstand the stress of an increased metabolic demand).
Symptoms include excessive bloating, oedema, and, rarely, congestive cardiac failure (CCF).
To limit these problems:
Measure U&Es and correct abnormalities before re-feeding.
Recheck U&Es every 3 days for the first 7 days and then weekly during re-feeding period.
Attempt to increase daily caloric intake slowly by 200-300 kcal every 3-5 days until sustained weight gain of 1-2 pounds per week is achieved.
Monitor patient regularly for development of tachycardia or oedema.

Prognosis

If untreated, this condition carries one of the highest mortality figures for any psychiatric disorder (10-15%).
If treated, “rule of thirds” (1/3 full recovery, 1/3 partial recovery, 1/3 chronic problems).
Poor prognostic factors include:
chronic illness
late age of onset
bulimic features (vomiting/purging)
anxiety when eating with others
excessive weight loss
poor childhood social adjustment
poor parental relationships
male sex


Bulimia nervosa

Epidemiology

Incidence 1-1.5% of women,
mid-adolescent onset,
presentation in early 20s.

Aetiology

Similar to anorexia nervosa,
also evidence for associated personal/family history of obesity,
family history of affective disorder and/or substance misuse.
Possible dysregulation of eating, related to serotonergic mechanisms (?supersensitivity of 5HT2C secondary to decrease“5HT).

Diagnostic criteria

Persistent preoccupation with eating
Irresistible craving for food
Binges episodes of overeating
Attempts to counter the fattening effects of food (self-induced vomiting, abuse of purgatives, periods of starvation, use of drugse e.g. appetite suppressants, thyroxine, diuretics)
Morbid dread of fatness, with imposed low weight threshold
N.B. In atypical cases, one or more of these features may be absent.


Physical signs
May be similar to anorexia nervosa ; but tend to be less severe.
Specific problems related to “purging “include:
Arrhythmias
Cardiac failure (sudden death)
Electrolyte disturbances (decrease K +, decrease Na+, decrease Cl-, metabolic acidosis [laxatives] or alkalosis [vomiting])
Oesophageal erosions
Oesophageal/gastric perforation
Gastric/duodenal ulcers
Pancreatitis
Constipation/steatorrhea
Dental erosion
Leucopaenia/lymphocytosis.

Differential diagnosis

Upper GI disorders (with associated vomiting)
Brain tumours
Personality disorder
Depressive disorder
OCD
Drug-related increased appetite
Other causes of recurrent overeating (e.g. menstrual-related syndromes, Kleine-Levin syndrome.

Comorbidity

Anxiety/mood disorder
Multiple dyscontrol behaviours e.g.:
Cutting/burning
Overdose
Alcohol/drug misuse
Promiscuity
Other impulse disorders

Treatment

General principles
Full assessment (as for anorexia nervosa).
Usually managed as an outpatient.
Admission only for suicidality, physical problems, extreme refractory cases, or if pregnant (due to increased risk of spontaneous abortion).
Combined approaches improve outcome.
Pharmacological
Most evidence for high-dose SSRIs (fluoxetine 60mg) long-term treatment necessary (>1yr).
Psychotherapy
Best evidence for CBT.
IPT may be as effective long-term, but acts less quickly.
Guided self-help is a useful first step (e.g. bibliotherapy), with education and support often in a group setting.


Prognosis
Generally good, unless there are significant issues of low self-esteem or evidence of severe personality disorder.