Eating disorders: anorexia nervosa

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Chapter 25 EATING DISORDERS

ANOREXIA NERVOSA

• Anorexia nervosa (AN) is characterised by a refusal to maintain a healthy body weight; resistance to gain weight, an intense fear of gaining weight, disturbance in the way in which shape or weight is experienced and denial of the seriousness of an individual’s current low body weight.

• Assess carefully for protein–calorie restriction.

• Medical complications can include non-alcoholic steatohepatitis.

• Refeeding syndrome may occur if calorie intake is increased too rapidly, leading to sudden death.

• The overall mortality of AN is 5%.

INTRODUCTION

Eating disorders have been the focus of increasing community and professional awareness in recent years. They form a heterogeneous group of illnesses that affect adults, adolescents and, more rarely, children. Anorexia nervosa (AN) is a specific eating disorder and the third most common chronic illness in adolescent females. It affects one in 200 girls between the ages of 15 and 19 years. Males develop AN less commonly, with the male to female ratio between 1:10 and 1:20. The increasing incidence of eating disorders and their impact on the health of a new generation of young people are of particular concern.

Clinicians need to think about eating disorders in patients presenting with weight loss, anorexia or malnutrition.

The key diagnostic features of AN are:

• Refusal to maintain a healthy body weight and resistance to weight gain. There can be a history of weight loss to less than 85% of expected weight for age, sex and height, or a failure to gain expected weight during a period of growth.

• An intense fear of gaining weight or becoming fat even though underweight.

• Disturbance in the way in which body shape or weight is experienced and reported, or denial of the seriousness of the current low body weight.

• Amenorrhoea in post-menarchal patients (i.e. the absence of at least three consecutive menstrual cycles).

The subtypes of AN are:

• Restricting type—during the current episode the patient has not engaged in binge eating or purging behaviour (i.e. self-induced vomiting or the misuse of laxatives, diuretics or enemas)

• Binge-purge type—during the current episode the patient has regularly engaged in binge eating or purging behaviour, on at least three occasions a week, for at least 3 months.

ASSESSMENT

History

After noting the cause for presentation, it is important to take a full history of how the low weight has occurred. This includes the change in weight, particularly noting the maximum and lowest weights, or alternatively change in clothes size. It is important to inquire about dietary intake and eating or purging behaviour. Additionally, the amount and intensity of exercise regimens should also be recorded as a significant minority of patients with AN use strenuous exercising as a major strategy to manipulate their weight.

An inquiry should also be made as to how the patient perceives their body shape, weight and health. Body dissatisfaction—if the patients feels their body is fat or would want to change aspects of their body in which fat is deposited—should also be recorded.

Menstrual history, including the duration of amenorrhoea, and sexual history are important. Bone size and mineralisation are influenced by the duration of amenorrhoea as well the severity of malnutrition.

Family structure and history, as well as history of comorbid psychiatric or medical conditions, are also important information to record at the time of initial assessment.

Physical findings

The protein–calorie malnutrition (PCM) that accompanies AN affects every organ in the body. The clinical presentation may have a number of features in common with hypothyroidism (Table 25.1); mentation and locomotion are slowed, hypothermia, constipation, pretibial oedema may be present, however patients do not have a goitre and thyroid hormones (thyroid stimulating hormone [TSH] and thyroxine [T₄]) remain within normal parameters. Triiodothyronine (T₃; measured by radioimmunoassay) is depressed commensurate with the degree of PCM, and recovers with correction of the malnutrition.

TABLE 25.1 Medical differential diagnosis of anorexia nervosa

• Hypothyroidism

• Inflammatory bowel disease

• Type 1 and 2 diabetes

• Addison’s disease

• Systemic lupus erythematosus

• Brain tumour

On initial inspection, the patient has a wasted appearance with lanugo (fine downy hair) present over the torso and limbs. There is often a generalised pallor with peripheral cyanosis. Capillary refill is delayed (more than 2 seconds). The hands are cool and peripheral pulses are slow and low in volume. Although the circulating volume and red cell mass is decreased, pallor is usually not observed in the palmar creases or conjunctiva. Blood pressure is maintained though there is often a postural drop in excess of 15 mmHg with moderate or severe protein–calorie malnutrition.

Heart sounds tend to be soft. Pericardial effusions are reported in severe PCM, and occur particularly in those patients with very low thyroid hormone (T₃).

The abdomen is scaphoid and skin over the anterior abdominal wall is lax. Muscles of the anterior abdominal wall are typically decreased permitting palpation of abdominal organs easily. An enlarged fatty liver (with a soft, smooth, non-tender lower border) is commonly detected. Stool in the sigmoid colon is also easily palpable in the left lower quadrant.

Oedema around the sacrum and pretibial areas may be present, though this usually occurs with refeeding rather than at initial presentation. Inspection of the feet is also important. The decreased peripheral circulation, particularly in patients who exercise excessively, may lead to signs of peripheral vascular insufficiency as well as poor hygiene (and a potential for sepsis).

Clinical findings may vary with patients who have more chronic AN and have adapted to the long standing PCM. These patients are haemodynamically compensated.

Investigations

Baseline investigations are useful in screening for micronutrient deficiencies as well as excluding differential diagnoses, particularly for atypical presentations. A low erythrocyte sedimentation rate (ESR) is typical of anorexia nervosa and distinguishes the eating disorder from malignancies, as well as inflammatory and autoimmune conditions.

Specific evaluation for micronutrient deficiency (e.g. iron, vitamins, trace elements) are unlikely to be clinically useful at initial evaluation.

• Cardiac investigations

– Electrocardiograph

– Dual energy X-ray absorptiometry (DEXA)

– Cerebral computed tomography

Criteria for medical admission

These criteria vary broadly.

• Weight and BMI (body mass index, kg/m²) are important indicators though evidence of medical instability is usually a prerequisite for inpatient admission.

• Alterations in vital signs are key indicators. Lowering of temperature (<35.5°C), heart rate (<40 beats/min) or blood pressure (<70 mmHg systolic, <40 mmHg diastolic) are commonly used cut points. Patients who have lost weight rapidly, but who are not at low weights (i.e. still above the 25th centile BMI) may present with alteration of vital signs, as with very low weight patients (i.e. <5th centile BMI).

• Disturbances in heart rhythm and electrical conduction, as well as heart rate, are criteria for admission. Prolongation of the QT corrected interval above 470 ms should be managed in an inpatient setting, with 450–470 ms being a ‘grey zone’.

• Electrolyte disturbances from manipulation of weight by water loading, restriction or purging should also be managed through inpatient admission. Metabolic disturbance from comorbid illness, such as diabetes, should also be considered as criteria for medical admission.

RESUSCITATION

Medical stabilisation involves replacement of fluid, energy, electrolytes, protein and micronutrients; monitoring of vital signs; and containment of exercising or purging behaviours. Nasogastric feeding provides a practical and efficient means for fluid and nutrient replacement. Intravenous access may be required to manage acute fluid and electrolyte changes, or if there is any gastrointestinal disturbance.

Measures to support the circulation are of the highest priority as invariably neither the airway nor breathing is compromised. Care must be taken not to use fluid replacement routinely, as cardiac failure is relatively easily induced in patients with PCM by volume overload. In particular, for those patients who have been chronically malnourished (i.e. over 6 months) circulatory changes should be induced slowly; and the adaptive physiological changes producing a low volume, low pressure circulation corrected over several days to a week or so depending on the severity of the PCM at presentation.

A continuous infusion of energy is optimal, and periods of ‘fasting’ such as occur during overnight sleep avoided until vital signs can be maintained (see cut points indicated above). For patients with less than 1000 kcal intake prior to admission or those with severe PCM, caloric replacement should commence at ∼1200 kcal per 24 hours. (This is estimated to be about 30% greater than resting energy expenditure.)

Strategies to maintain body temperature above 35.5°C such as space blankets or overhead heating are used.

Vitamin supplements are also commenced. There is great variability here with some units prescribing a multivitamin preparation and other units prescribing individual vitamins such as thiamine on admission. Supplementation of phosphate (e.g. sodium acid phosphate 500 mg) is recommended, particularly if serum levels are decreased on admission. The dose is empirically adjusted from serial measurements of serum phosphate.

Monitoring of vital signs should occur every 6 hours. Serial measurements of electrolytes, blood sugar and phosphate should continue daily until levels are within normal ranges. Mental state should also be assessed daily for mood symptoms as well as the development of delirium, associated with the refeeding syndrome, described below.

REFEEDING

Once medically stable, weaning of nasogastric feeds and increases in regular food can occur. Total daily energy content of regular food or nasogastric feeds should be gradually increased to around 2700 kcal. Increases of 500–1000 kcal per week can be safely made. Sudden death and delirium—the ‘refeeding syndrome’—may occur if the increase in daily caloric intake is too rapid. A weight gain of one kilogram per week can be safely maintained. Patients who have a chronic or relapsing course with AN may be treated less aggressively. Maintaining the serum phosphate level above 1.0 mmol/L is recommended.

In addition to having sufficient energy, the daily intake needs to contain a balance of macronutrients. High-quality proteins are important for rebuilding lost lean tissue mass. It is also important that nutritional rehabilitation be supported by healthy (resistance) exercising. A supervised and graded programme offers potential benefit, though these have not been scientifically investigated to date.

MEDICAL COMPLICATIONS

The protein–calorie malnutrition that occurs with anorexia nervosa affects all body organs. Further medical complications arise from purging behaviours, such as vomiting, strenuous exercise and the use of laxatives, as well as other ‘fat burning’ strategies. The resultant effects on pubertal development, growth and bone mineralisation can have a profound effect on survivors.

Fluids and electrolytes

The cardinal feature associated with fluid and electrolyte disturbances in patients with eating disorders is intravascular volume contraction. Vital sign instability with abnormalities in heart rate and blood pressure and skin manifestations are more commonly seen. Serum sodium tends to be in the upper limit of normal range, and blood urea nitrogen (BUN) and creatinine are usually elevated, despite a low muscle mass.

Serum phosphate levels fall in a significant minority of patients during nutritional rehabilitation. Typically this occurs in the first week of refeeding, in over a quarter of patients. Hypophosphataemia is the hallmark of the refeeding syndrome, a well known complication of nutritional rehabilitation in anorexia nervosa.

Endocrine

Delayed puberty is one of the cardinal features of anorexia nervosa during adolescence. It is defined as deviating two standard deviations (SD) below the mean for age and gender.

The presence of amenorrhoea in an adolescent female should prompt the clinician to evaluate other possible causes for this situation. Pregnancy, even though a rare event in a young female with anorexia nervosa, needs to be excluded by obtaining a detailed clinical history including health risk behaviour and, more specifically, sexuality issues.

Amenorrhoea is considered one of the clinical criteria to establish the diagnosis, by DSM-IV criteria. Secondary amenorrhea is hypothalamic in origin, and it is due in part to suppression of the hypothalamic–pituitary–gonadal axis. Other factors include stress, the additive effects of malnutrition, weight loss, starvation and strenuous exercise. A weight of approximately 90% of standard body weight (50th centile for age, sex and height), on average, is required for resumption of menses to occur, and serum oestradiol levels at follow-up best track this process. However, the weight at which an individual patient with anorexia nervosa may resume menses is variable. The use of ancillary methods such as measures of body composition and serum oestradiol may be used to predict this significant landmark in the treatment of patients with eating disorders.

Bone

Up to 50% of bone mass is attained during adolescence in females and 67% for males. The timing of peak bone mineral content velocity and menarche were closely related and followed peak height velocity by approximately a year.

Osteopenia and bone health improves with nutritional rehabilitation, weight restoration and the return to a normal physiology of the endocrine-skeletal homeostasis. To date the gold standard method to evaluate bone mass as it relates to tissue composition is dual energy X-ray absorptiometry (DEXA).

Prevention of osteopenia and optimising bone growth and mineralisation in adolescents with anorexia nervosa may be achieved by a two-track approach. Firstly, with nutritional rehabilitation through weight restoration (promoting development of the muscle-bone unit) and, secondly, by facilitating resumption of normal menstrual physiology. Moderation in weight-bearing exercise should be encouraged, and resistance exercising promoted.

Cardiovascular

Mortality rates associated with eating disorders are noted to be the highest among psychiatric disorders, with sudden death resulting from ventricular dysrhythmias being responsible for up to 50% of deaths. The increase in body weight and basal metabolic rate place a considerable strain on the cardiovascular system. Additional stress is placed on the myocardium as a result of electrolyte abnormalities, hypothermia and autonomic nervous system instability. These changes in association with hypophosphataemia are recognised as the refeeding syndrome, and account for the mortality seen in early nutritional rehabilitation in anorexia nervosa.

Haematological

Bone marrow hypoplasia and its implications in this population have been described. In children and adolescents with anorexia nervosa, the most commonly seen haematological changes include normal or marginally low haemoglobin and haematocrit with abnormal erythrocyte indices, showing increased mean corpuscular volume (MCV), mean corpuscular haemoglobin (MCH), and mean corpuscular haemoglobin concentration (MCHC). These macrocytic changes are rarely associated with folate or vitamin B₁₂ deficiency in this patient population; but need to be considered when present. Other abnormalities include leucopenia and thrombocytopenia. All of these changes are reversible with weight restoration and nutritional rehabilitation.

Microcytic, hypochromic anaemia due to iron deficiency is considered one of the most common nutritional deficiencies for growing adolescents, with a peak prevalence (3.5%–14.2%) between 11 and 19 years of age for both genders. Iron deficiency anaemia is rarely seen in the initial stages of anorexia nervosa in female patients. Low ESR is a common feature of malnourished patients with anorexia nervosa. This parameter may be used to aid in the differential diagnosis of anorexia nervosa from other ominous causes of malnutrition (infectious processes, chronic inflammatory and systemic illnesses).

Neurological

Abnormal enlargement of cortical sulci and subarachnoid spaces has been reported in anorexia nervosa. Cerebrospinal fluid volume is increased, and reductions in cerebral grey and white matter volumes have been described. In weight-recovered patients with anorexia nervosa, grey matter volume deficit, but not white matter changes, persist.

Renal

Impairment of renal function occurs in anorexia nervosa from pre-renal and renal factors. In the former, dehydration and low circulating blood pressure and volume contribute to the pre-renal effects. Persistent and severe protein calorie malnutrition results in a diffuse glomerular sclerosis. This is a non-reversible insult to the kidney leading to a progressive decline in glomerular filtration rate and eventually renal failure should nutritional rehabilitation not occur.

Should there be persistent hypokalaemia, as a result of chronic vomiting or diuretic abuse, as in bulimia nervosa and patients who purge in anorexia nervosa, vacuolation of the renal tubules has been observed resulting in impaired tubular function affecting fluid and electrolyte balance.

Liver

Non-alcoholic steatohepatitis (NASH syndrome) occurs in a significant minority of patients with anorexia nervosa. Typically the transaminase levels are in the several hundreds, but not thousands. The raised enzyme levels persist for several weeks at the beginning of nutritional rehabilitation. These changes are usually asymptomatic and uncomplicated. These changes resolve with nutritional rehabilitation.

GOALS FOR THERAPY

The goals for therapy are to achieve nutritional and psychological recovery. Weight goals are linked to reestablishing a healthy body composition such that spontaneous resumption of menses occurs along with increases in lean tissue mass to support increases in bone size and mineralisation. Goal weight can be calculated from weight for age, sex and height centile charts. Endocrine measures can also be used to identify a minimum healthy weight range. Leuteinising hormone, then follicle stimulating hormone and finally oestrogen levels return to adult levels in postmenarchal patients. For premenarchal patients, estimation of fat mass from anthropometry (skinfolds) or DEXA may be used to identify a healthy minimum weight. A body fat percentage of at least 18% is required among adolescent females to sustain pubertal development.

PROGNOSIS

AN has the highest mortality of any psychiatric condition. A crude mortality rate of 5.1% has been consistently reported with a mortality rate of 20%, 20 years after diagnosis.

Most adolescents make a recovery from AN over a three- to five-year period after diagnosis. A significant minority of those who develop AN in adolescence, about one quarter, continue to have a chronic or relapsing course into adulthood.

The morbidity of AN is minimised with early correction of the PCM (kwashiorkor). Ongoing effects to bone health and other organs have been demonstrated. There remains concern that the changes to brain structure and function, particularly in the more malnourished patients, do not fully recover even after nutritional rehabilitation. Protracted PCM certainly can result in organ failure as illustrated by the diffuse glomerular sclerosis and renal failure seen in a small group of chronically malnourished patients.

In addition to this medical morbidity there is a substantial psychological morbidity. Patients have delayed growth and pubertal maturation. They become physically different, and socially isolated from peers around the time of diagnosis and during periods of hospitalisation.

The impact of AN has certainly been moderated with the development of multidisciplinary teams and the clinical collaboration of psychological and medical professionals.

SUMMARY

The overall (crude) mortality of this condition remains high. Despite the greater potential for medical complications because of the impact on growth and pubertal development, AN in children and adolescents carries a better prognosis. Early correction of protein calorie malnutrition increases the potential for recovery before chronic and irreversible organ changes occur. Early intervention and particularly early nutritional rehabilitation minimises the impact of AN on physical health. Weight restoration and nutritional rehabilitation remain the cornerstones of biological treatment with a two-track approach and appropriate psychosocial interventions to achieve recovery from this devastating illness (Figure 25.1).

FIGURE 25.1 Assessment of anorexia nervosa.

FURTHER READING

Berkman ND, Lohr KN, Bulik CM. Outcomes of eating disorders: a systematic review of the literature. Int J Eat Disord. 2007;40:293-309.

Bulik CM, Berkman ND, Brownley KA, et al. Anorexia nervosa treatment: a systematic review of randomized controlled trials. Int J Eat Disord. 2007;40:310-320.

Herzog DB, Greenwood DN, Dorer DJ, et al. Mortality in eating disorders: a descriptive study. Int J Eat Disord. 2000;28:20-26.

Kohn MR, Golden NH, Shenker IR. Cardiac arrest and delirium: presentations of the refeeding syndrome in severely malnourished patients with anorexia nervosa. J Adolesc Health. 1998;22:239-243.

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