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T2-weighted MRI reveals ventriculomegaly (asterisks) and enlargement of cortical sulci (arrow). American Journal of Roentgenology 2013; 200:W328-W335

Introduction

Anorexia nervosa (AN) was first described in 1689 by Richard Morton, who called it nervous consumption. In 1870's Sir William Gull in England coined the terms anorexia nervosa while Charles Lasegue in France described anorexia hysterique.

Epidemiology

  • Prevalence among US female adolescents is 0.5% and 1-2% among adult females.
  • F:M ratio is 10:1.
  • Mortality in patients with AN is 5-7%, and about 5% per decade of life; Death is most often secondary to medical complications of starvation (50%) or suicide (50%).(2)

Diagnosis

General approach

  • All children and adolescents should be screened for eating disorders; this involves history/questionnaires and tracking of height and weight. (1)
  • Those who screen positive, undergo a diagnostic psychiatric and medical evaluation.
  • Severe acute physical signs and medical complications need to be treated immediately.

Diagnostic criteria

Essential features of DSM-5 diagnosis are:

  • (A)Persistent restriction of energy intake
    • This generally means BMI<17 for adults (however, those with BMI>17 may have mild AN, as WHO's cut off is 18.5)
    • In children, BMI below the 10th percentile is consistent with AN diagnosis (1)
  • (B) Fear of become fat or persistent behaviors that prevent weight gain
  • (C) Disturbance of body image

There are two subtypes: restricting AN and binge eating and purging AN. The DSM-IV requirement for amenorrhea was removed in DSM-5.

Differential diagnosis

History and physical exam are essential for ruling out medical causes of anorexia (poor appetite) and weight loss. Some examples include: chronic infection, hyperthyroidism, Addison’s disease, IBD, connective tissue disorders, cystic fibrosis, peptic ulcer disease, disease of the esophagus or small intestine, celiac disease, diarrhea, diabetes, and occult malignancies.(1)

Co-morbidities

Common co-morbid conditions include depression, social anxiety, separation anxiety, OCD, GAD, and substance abuse, and avoidant, dependent, obsessive-compulsive, or passive-aggressive personality disorders.

Treatment principles

  • Outpatient treatment first: "Psychiatric hospitalization, day/partial programs, and residential programs for eating disorders should be considered only when outpatient interventions have been unsuccessful or are unavailable." (1)
    • Treatment should involve a multidisciplinary team, uncommon in outpatient setting.
  • Family-based treatment (FBT), a.k.a. Maudsley Family Therapy is effective and superior to comparison individual therapies for AN.
    • Individual therapies such as adolescent-focused therapy (AFT) and CBT are fairly effective.
  • Medications are used only for co-morbid conditions or refractory cases (1)
    • Use of SSRIs for AN had not been studied in adolescents (mostly negative studies in adults)
    • Atypical antipsychotics have not shown clear benefit in small RCTs of risperdone, quetiapine, and olanzapine.

Nutritional Rehabilitation

Refeeding involves restoring a minimally normal weight and is indicated for all underweight AN patients. Nutritional rehabilitation is most effective alongside multidisciplinary behavioral interventions in AN patients. This involves patient and family engagement, psychoeducation, meal monitoring, and positive reinforcement, nutritional counseling, and psychotherapy.

The weekly target for controlled weight gain generally varies according to the setting:

  • Inpatient – 2 to 3 lbs/week
  • Outpatient – 0.5 to 1 lbs/week

Initial caloric intake goal is typically 30 to 40 kcal/kg/day (1500kcal/day), but may be lower in outpatient setting or in patients with more severe undernourishment. Aggressive refeeding can precipitate potentially fatal refeeding syndrome. (3)

Refeeding Syndrome

Refeeding syndrome is a series of clinical complications of fluid and electrolyte shifts during nutritional rehabilitation of malnourished patients. More undernourished patients are at greater risk Cardinal findings of a refeeding syndrome are

  • Hypophosphatemia
  • Hypokalemia
  • Vitamin (esp. thiamine) deficiencies
  • Volume overload (Congestive heart failure and peripheral edema)

The pathogenesis involves rise in insulin levels when refeeding is initiated.

  • Insulin causes shift of electrolytes intracellularly from the serum, where electrolytes are already depleted.
    • increased cellular metabolism with inadequate stores of phosphate causes tissue hypoxia and resultant myocardial dysfunction and respiratory failure
  • Concurrent anabolic processes use up low stores of vitamins.

The refeeding syndrome can nearly always be avoided by limiting the amount of calories and fluid provided in the early stages of refeeding, treatment with thiamine prior to refeeding, and restoring electrolyte deficiencies.

References

1. Lock, J. et.al. Practice Parameter for the Assessment and Treatment of Children and Adolescents With Eating Disorders. J Am Acad Child Adolesc Psychiatry 2015;54(5):412–425

2. Arcelus J, et. al. Mortality rates in patients with anorexia nervosa and other eating disorders. Arch Gen Psychiatry. 2011; 68:724-731

3. Mehler PS, et. al. Nutritional rehabilitation: practical guidelines for refeeding the anorectic patient. J Nutr Metab 2010; 2010.

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