Updated: Aug 21, 2008
Anorexia nervosa (AN) is a psychiatric disorder with severe physiologic consequences, characterized by the inability or refusal to maintain a minimally normal weight. Patients have a profoundly disturbed body image as well as an intense fear of weight gain despite being moderately to severely underweight.
Diagnostic criteria for anorexia nervosa in the Diagnostic and Statistical Manual of Mental Disorders IV (DSM-IV) include the following:1
The disorder may be further divided into 2 subtypes: (1) restricting, in which severe limitation of food intake is the primary means to weight loss, and (2) binge-eating/purging type, in which there are periods of food intake that are compensated by self-induced vomiting, laxative or diuretic abuse, and/or excessive exercise. Formal recommendations have been made to remove the amenorrhea criteria and the subtype distinctions from the criteria for AN in the upcoming DSM-V.2 In addition, numerous studies have demonstrated subthreshold eating disorders either alone or coexistent with other psychiatric diagnoses suggesting the criteria need to be expanded and a higher prevalence than previously thought.
Other physiologic causes of malnutrition, weight loss, and amenorrhea must be ruled out to make the diagnosis.
Patients with anorexia nervosa often display other personality traits such as a desire for perfection, academic success, lack of age-appropriate sexual activity, and a denial of hunger in the face of starvation. Psychiatric characteristics include excessive dependency needs, developmental immaturity, social isolation, obsessive-compulsive behavior, and constriction of affect. Many patients also have comorbid mood disorders, with depression and dysthymic disorder being most prevalent.
For additional information on eating disorders, see Medscape's Eating Disorders Resource Center.
Anorexia nervosa is the result of a complex interplay between biological, psychological, and social factors, which tend to affect women more than men, and adolescents more than older women. Some evidence suggests a higher rate of the disorder in monozygotic twins than in dizygotic twins, which may indicate a biologic predisposition.
Psychologically, prepubescent patients who subsequently develop anorexia nervosa have a high incidence of premorbid anxiety disorders. The onset of the disorder during puberty has led to the theory that, by exerting control over food intake and body weight, adolescents are attempting to compensate for a lack of autonomy and selfhood. Individuals with anorexia nervosa maintain a lifelong increased incidence of anxiety, depressive disorders, and obsessive-compulsive disorder. Neurobiologists hypothesize that disruption of serotonergic pathways in the brain mediate the development of anorexia nervosa and may account for the frequent coexistence of other psychological disturbances.
The patient's altered body image results in a perception of fatness despite being normal or underweight. Attempts to correct this flaw through food restriction or purging lead to progressive starvation. Modern preoccupation with slenderness and beauty in the Western world may contribute to the mindset of slenderness as a valued quality in adolescents; however, this link has not been proven.
Malnutrition subsequent to self-starvation leads to protein deficiency and disruption of multiple organ systems. In addition to hypoglycemia and vitamin deficiencies, starvation results in release of endogenous opioids, hypercortisolemia, and thyroid function suppression. Neuroendocrine disturbances result in delayed puberty, amenorrhea, anovulation, low estrogen states, increased growth hormone, decreased antidiuretic hormone, hypercarotenemia, and hypothermia. Decreased gonadotropin levels and hypogonadism may occur among males who are affected.
Cardiovascular effects include mitral valve prolapse, supraventricular and ventricular dysrhythmias, long QT syndrome, bradycardia, orthostatic hypotension, and shock due to congestive heart failure.
Renal disturbances include decreased glomerular filtration rate (GFR), elevated BUN, edema, acidosis with dehydration, hypokalemia, hypochloremic alkalosis with vomiting, and hyperaldosteronism.
Gastrointestinal findings include constipation, delayed gastric emptying, and gastric dilation and rupture when binge eating. Patients who induce vomiting develop dental enamel erosion, palatal trauma, enlarged parotids, esophagitis, Mallory-Weiss lesions, and elevated transaminase levels.
The lifetime prevalence of anorexia nervosa in the United States is estimated at 0.3-1%; however, some studies have shown rates as high as 4% among women. The rates among men are estimated at 0.1%. As many as 5% of young women exhibit symptoms of anorexia but do not meet full diagnostic criteria.
Anorexia nervosa is found in all developed countries and in all socioeconomic classes at similar rates (0.3-1% in women, 0.1% in men).
Anorexia nervosa has one of the highest mortality rates of all psychiatric disorders, with rates reported from 5-18%. Patients with restricting subtype tend to have more resistance to recovery.
Approximately 50% of patients will recover with treatment and maintain a normal weight but often not without relapses and with the aid of multiple treatment modalities. Mortality is often due to suicide and less frequently due to complications of starvation.
Anorexia nervosa is significantly more frequent in white populations than in people of other races, but it has been reported among all races.
A link between socioeconomic class and prevalence of eating disorders has not been demonstrated in the literature.
Female-to-male ratio is 10-20:1 in developed countries.
In some professions, the frequency is much higher among men (wrestling, running, modeling) than the general male population.
Anorexia nervosa is primarily a phenomenon of puberty and early adulthood. Eighty-five percent of patients have onset of the disorder between the ages of 13 and 18 years.
Anorexia nervosa has been observed in both the very young and very old. Patients who are older at the time of onset of the disorder have a worse prognosis.
Patients with anorexia nervosa may present to the ED with extreme weight loss, food refusal, dehydration, weakness, or shock. Many present at the urging of family members or friends and are in deep denial of their malnutrition and illness.
Patients with anorexia nervosa may present anywhere along the spectrum of weight loss. They may attempt to hide their weight loss by wearing bulky clothing or many layers.
Anorexia nervosa is a complex combination of biological, psychological, and social factors, which have devastating physical and mental consequences.
| Adrenal Insufficiency and Adrenal Crisis | Inflammatory Bowel Disease |
| Alcohol and Substance Abuse Evaluation | Mitral Valve Prolapse |
| Anxiety | Pediatrics, Dehydration |
| Constipation | Pediatrics, Diabetic Ketoacidosis |
| Depression and Suicide | Shock, Hypovolemic |
| Diabetes Mellitus, Type 1 - A Review | Sinus Bradycardia |
| Diabetes Mellitus, Type 2 - A Review | |
| Hyperthyroidism, Thyroid Storm, and Graves
Disease | |
| Hypokalemia |
Chronic gastrointestinal infections
Malabsorption
Malignancies
Prehospital care of a patient with anorexia nervosa includes stabilization for any life-threatening conditions (eg, shock, cardiac arrhythmias) and basics such as airway, breathing, and circulatory support as needed.
Emergency care of anorexia nervosa should include a basic medical evaluation as well as urgent or timely outpatient psychiatric evaluation.
Most cases of anorexia nervosa encountered in the emergency department will be appropriate for outpatient management if close, planned follow-up is arranged prior to discharge.
Medical therapy in the emergency department consists of electrolyte repletion and stabilization.
Multiple studies have failed to show an overall benefit for pharmacologic treatment of anorexia nervosa with psychiatric medications. However, most patients who recover will be treated with a multidisciplinary approach including medication, psychotherapy, nutritional counseling, and frequent medical evaluations. The most common class studied is SSRIs, which have been shown to be beneficial in patients with bulimia nervosa but not anorexia. However, since many patients with anorexia have concurrent mood disorders, medication may be of benefit.
Necessary in patients with profound malnutrition, dehydration, and purging behaviors.
May be repleted orally or parenterally, depending on the clinical state of the patient.
Essential for transmission of nerve impulses, contraction of cardiac muscle, maintenance of intracellular tonicity, skeletal and smooth muscles, and maintenance of normal renal function. Gradual potassium depletion occurs via renal excretion or GI loss or because of low intake. Depletion usually results from diuretic therapy, primary or secondary hyperaldosteronism, diabetic ketoacidosis, severe diarrhea (if associated with vomiting), or inadequate replacement during prolonged parenteral nutrition. Potassium depletion sufficient to cause 1 mEq/L drop in the serum potassium level requires a loss of approximately 100-200 mEq of potassium from the total body store.
Serum levels >2.5 mEq/L: 10 mEq IV over 1 h, then prn based on frequently obtained lab values; not to exceed 200 mEq/d
Serum levels <2.5 mEq/L: 40 mEq IV over 1 h, then prn based on frequently obtained lab values; not to exceed 400 mEq/d
Must dilute IV prior to administration
Emergent situation:
IV: 0.5-1 mEq/kg over 1-2 h initially; maximum dose not to exceed 40 mEq/dose
May repeat prn based on frequently obtained lab values; must dilute IV prior to administration; administer in ED or ICU with ECG monitoring
PO: 2-5 mEq/kg/d based on primary disease; sometimes requires up to 10 mEq/kg/d
Concurrent use with ACE inhibitors may result in elevated serum potassium concentrations; potassium-sparing diuretics and potassium-containing salt substitutes can produce severe hyperkalemia; inpatients taking digoxin, hypokalemia may result in digoxin toxicity; caution if discontinuing potassium administration in patients maintained on digoxin
Hyperkalemia, renal failure, and conditions in which potassium retention is present and those with oliguria or azotemia, crush injuries, severe hemolytic reactions, anuria, and adrenocortical insufficiency
A - Fetal risk not revealed in controlled studies in humans
Do not infuse rapidly; high plasma concentrations of potassium may cause death due to cardiac depression, arrhythmias, or arrest; plasma levels do not necessarily reflect tissue levels; monitor potassium replacement therapy whenever possible by continuous or serial ECG; when a concentration > 40 mEq/L is infused, local pain and phlebitis may also follow
Moderates nerve and muscle performance and facilitates normal cardiac function. Can be given IV initially, and calcium levels maintained with high calcium diet. Some patients require oral calcium supplementation. The 10% IV solution provides 100 mg/mL of calcium gluconate that equals 9 mg/mL (0.46 mEq/mL) of elemental calcium. One 10 mL ampule contains 93 mg of elemental calcium
100-300 mg elemental calcium IV diluted in 150 mL D5W over 10 min; initial rate of infusion should be 0.3-2 mg of elemental calcium/kg/h
2 mg/kg of elemental calcium IV (about 20 mg/kg of calcium gluconate 10%)
May decrease effects of tetracyclines, atenolol, salicylates, iron salts, and fluoroquinolones; antagonizes effects of verapamil; large intakes of dietary fiber may decrease calcium absorption and levels
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in digitalized patients, respiratory failure, acidosis, or severe hyperphosphatemia
For severe hypophosphatemia (<1 mg/dL), parenteral preparations of phosphate should be used for repletion. IV preparations are available as sodium or potassium phosphate (K2PO4). Response to IV serum phosphorus supplementation is highly variable and is associated with hyperphosphatemia, and hypocalcemia. The rate of infusion and choice of initial dosage should be based on severity of hypophosphatemia and presence of symptoms.
Serum phosphate and calcium should be monitored closely. For less severe hypophosphatemia (1-2 mg/dL), PO phosphate salt preparations can be used. PO preparations are available as sodium or potassium phosphate in capsule or liquid form. Neutra-Phos packets contain 250 mg of phosphorus/packet. Tablets contain either 250, 125.6, or 114 mg each. Liquid preparations available as 250 mg/75 mL.
8 mmol of K2PO4 q6h IV or 0.1 mmol/kg of K2PO4 or Na2PO4 q6h IV (32 mmol/24h) initially
Aggressive IV replacement: 15 mmol of K2PO4 over 6 h or 0.2-0.3 mmol/kg of K2PO4 or Na2PO4 over 6 h
For oral replacement, 250 mg as capsule, liquid, or packet tid/qid is generally adequate; for most patients, once phosphate stores are repleted, PO supplements are no longer required, as the diet has ample phosphate
0.25-0.5 mmol/kg IV over 4-6 h and repeat if symptomatic hypophosphatemia persists
Magnesium and aluminum-containing antacids or sucralfate can act as phosphate binders and decrease serum phosphate levels; potassium-sparing diuretics, ACE inhibitors, and salt substitutes may increase serum phosphate levels
Documented hypersensitivity; hyperphosphatemia, hypocalcemia, hypomagnesemia, hyperkalemia, or renal failure
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in patients with renal insufficiency and metabolic alkalosis; admixture of phosphate and calcium in IV fluids can result in calcium phosphate precipitation
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anorexia, anorexia nervosa, eating disorder, self-starvation, binging, purging, malnutrition, severe weight loss, extreme weight loss, life-threatening weight loss, amenorrhea, intense fear of obesity, primary amenorrhea, secondary amenorrhea, denial of hunger, depression, obsessive-compulsive behavior, binge behavior, purge behavior, anxiety disorder, hypoglycemia, vitamin deficiencies, delayed puberty, anovulation, supraventricular dysrhythmias, ventricular dysrhythmias, long QT syndrome, bradycardia, orthostatic hypotension, shock, congestive heart failure, hypokalemia, hypochloremic alkalosis, hyperaldosteronism, gastric dilation, gastric rupture, dental enamel erosion, palatal trauma, esophagitis, Mallory Weiss lesions, diminished gag reflex, substance abuse
Tracy A Cushing, MD, MPH, Instructor in Medicine, Department of Emergency Medicine, Harvard Medical School; Attending Physician, Department of Emergency Medicine, Mount Auburn Hospital
Tracy A Cushing, MD, MPH is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine, and Wilderness Medical Society
Disclosure: Nothing to disclose.
Ron Waldrop, MD, MS, FAAP, FACEP, CPE, Consulting Staff, Commonwealth Emergency Physicians; Director of Pediatric Quality Care Management, INOVA Loudon Hospital; Adjunct Clinical Professor, Georgetown University School of Medicine
Ron Waldrop, MD, MS, FAAP, FACEP, CPE is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.
Edward Bessman, MD, Chairman, Department of Emergency Medicine, John Hopkins Bayview Medical Center; Assistant Professor, Department of Emergency Medicine, Johns Hopkins University
Edward Bessman, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.
Robert Harwood, MD, MPH, FACEP, FAAEM, Program Director, Department of Emergency Medicine, Advocate Christ Medical Center; Assistant Professor, Department of Emergency Medicine, University of Illinois at Chicago College of Medicine
Robert Harwood, MD, MPH, FACEP, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, Council of Emergency Medicine Residency Directors, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Jonathan Adler, MD, Attending Physician, Department of Emergency Medicine, Massachusetts General Hospital; Division of Emergency Medicine, Harvard Medical School
Jonathan Adler, MD is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine
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