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Anorexia nervosa in adults and adolescents: The refeeding syndrome

INTRODUCTION AND DEFINITION — Weight gain is the cornerstone of treatment for patients with anorexia nervosa (AN) [1,2]. However, serious and potentially fatal complications can arise when refeeding patients with AN. The refeeding syndrome is defined as the clinical complications that occur as a result of fluid and electrolyte shifts during nutritional rehabilitation of malnourished patients [3]. Patients who weigh less than 70 percent of ideal body weight or lose weight rapidly are at greatest risk for the syndrome. One case series reported an incidence of six percent in adolescents hospitalized for treatment of AN [4].

Patients other than those with AN are at risk for the refeeding syndrome [5]. These include oncology patients undergoing chemotherapy, malnourished elderly patients, certain postoperative patients, and homeless or alcoholic patients who have not eaten for many days.

PATHOGENESIS OF THE REFEEDING SYNDROME — In significantly malnourished patients, the initial stage of oral, enteral, or parenteral nutritional replenishment causes electrolyte and fluid shifts that may precipitate disabling or fatal medical complications [3,6-11]. The refeeding syndrome is marked by:

  • Hypophosphatemia
  • Hypokalemia
  • Hypomagnesemia
  • Vitamin (eg, thiamine) and trace mineral deficiencies
  • Volume overload
  • Edema

The risk of developing the refeeding syndrome is directly related to the amount of weight loss during the current episode and the rapidity of the weight restoration process [7-9,12]. Thus, patients who weigh less than 70 percent of their ideal body weight require hospitalization for the initial stage of nutritional replenishment. Other risk factors for the syndrome include low levels of phosphate, potassium, or magnesium prior to refeeding the patient; and little or no nutritional intake for the previous 5 to 10 days. Patients are at the highest risk for the refeeding syndrome in the first two weeks of nutritional replenishment and weight gain [9]. The risk progressively dissipates over the next few weeks.

MEDICAL COMPLICATIONS — Medical complications that occur as a result of fluid and electrolyte shifts during nutritional rehabilitation of malnourished patients involve multiple organ systems [1,6,7,9,10]. Management of these complications may include reducing the rate of nutritional support and correcting hypophosphatemia, hypokalemia, and hypomagnesemia. (See 'Prevention and management' below.)

Cardiovascular — Most fatalities that occur because of the refeeding syndrome are due to cardiac complications, including impaired contractility, decreased stroke volume, heart failure, and arrhythmias [7,10]. Atrophy of the heart during starvation renders the patient more vulnerable to fluid overload and heart failure. Sodium and fluid retention can also increase circulatory volume and lead to volume overload in patients with cardiac atrophy, and thiamine (vitamin B1) deficiency may also contribute to heart failure [9]. Electrocardiograms, echocardiograms, and consultation with the cardiology service should be obtained as indicated by the patient's clinical status. Heart failure is discussed separately.

Bradycardia is expected with AN [1,13,14]. A normal heart rate may in fact be a harbinger of cardiac compromise in these patients. During the early stages of refeeding, a heart rate > 70 beats per minute may suggest heart failure and the refeeding syndrome.

Hypertension, hypotension, and peripheral edema may also occur during the refeeding syndrome [7,10]. An overview of hypertension, hypotension in the context of shock, and diagnosis and treatment of edema are discussed separately.

Pulmonary — Impaired diaphragmatic contractility due to overall weakness or to hypophosphatemia may occur, leading to dyspnea and impaired respiratory function. Respiratory failure and the need for mechanical ventilation are rare [7,10]. Heart failure may secondarily lead to respiratory symptoms and failure.

Muscular — Impaired contractility, weakness, myalgia, and tetany may occur [7]. Hypophosphatemia may also cause rhabdomyolysis, which is suggested by an abnormally high creatinine phosphokinase (CPK)

Gastrointestinal — Liver function tests may be elevated, and several gastrointestinal symptoms may develop.

Liver function tests, including aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase, and bilirubin, are mildly elevated during the first few weeks of refeeding the patient due to excessive calories and fat deposition [9,15]. These elevations are usually not clinically significant and resolve by reducing the rate of nutritional replenishment. More calories may be reintroduced at a later date once the liver tests have normalized. However, malnutrition and hepatic apoptosis can also elevate liver enzymes, which normalize with nutritional replenishment.

Diarrhea may occur, due to atrophy of the intestinal mucosa and pancreatic impairment [9]. Nausea and vomiting may also arise [7]. These symptoms may require decreasing the rate of refeeding or temporarily terminating the process.

Abdominal pain and constipation may also occur, due to delayed gastric emptying and prolonged colonic transit time [9]. An osmotic laxative such as polyethylene glycol and adequate hydration can alleviate these symptoms.

Neurologic — Patients may develop tremors, paresthesias, delirium, and seizures as a result of electrolyte abnormalities.

The malnourished patient may be thiamine deficient at baseline. With refeeding, intracellular uptake of electrolytes leads to increased utilization of thiamine, and Wernicke's encephalopathy may occur, with signs that include encephalopathy, oculomotor dysfunction, and gait ataxia [9]. Thiamine at a dose of 100 mg should be given at least 30 minutes before starting nutritional replenishment [5]. The clinical manifestations, diagnosis, and treatment of Wernicke's encephalopathy are discussed separately. (See "Wernicke's encephalopathy".)

Central pontine myelinosis has also been reported as a complication of the refeeding syndrome in AN [16].

PREVENTION AND MANAGEMENT — The refeeding syndrome can be avoided by restoring weight with an amount of calories that is close to and above the resting energy expenditure, avoiding rapid increases in the daily caloric intake, and clinically and biochemically monitoring the patient during the refeeding process. Complications of the syndrome may be reduced by slowing the rate of nutritional support, correcting electrolyte abnormalities, and monitoring for and treating cardiovascular and pulmonary complications.

Prevention for inpatients — For inpatients with AN, several steps should be implemented to prevent the refeeding syndrome [7-9,12]:

  • Available dietary and nutritional support staff should be consulted to determine the initial daily calories to be ingested.
  • A standard protocol should be used to feed the patient, including limited intake of sodium and fluids. The amount of daily calories should be raised by 300 to 400 kcal every three to four days. The goal for weight gain should be limited to two to three pounds (one kilogram) per week.
  • Vital signs and weight should be monitored each day.
  • The daily physical examination should focus upon the cardiovascular and pulmonary systems, and upon signs of edema.

Patients with AN are generally bradycardic, and a sudden, sustained increase pulse greater than 70 beats per minute may be a sign of cardiac overload and harbinger of the refeeding syndrome. Clinicians should also check for lower extremity edema during the physical examination.

Once nutritional replenishment has started, clinicians should check serum electrolytes, phosphorous, magnesium, and liver function tests daily or every other day for at least one to two weeks [9]. This can be decreased to twice per week as the patient consistently gains weight, provided serum electrolyte levels remain stable. With continued weight gain and stable electrolyte levels, the frequency of monitoring should be progressively decreased

Treatment — If the refeeding syndrome occurs, clinicians should reduce nutritional support and correct hypophosphatemia, hypokalemia, and hypomagnesemia [7,9]. Moderately to severely ill patients with marked edema or a serum phosphorous < 2 mg/dL should be hospitalized to intravenously correct electrolyte deficiencies. Continuous telemetry may be needed to monitor cardiopulmonary physiology. Management of electrolyte abnormalities is discussed separately:

SUMMARY AND RECOMMENDATIONS

  • The refeeding syndrome is defined as the clinical complications that occur as a result of fluid and electrolyte shifts during nutritional rehabilitation of malnourished patients. (See 'Introduction and definition' above.)
  • The refeeding syndrome is marked by hypophosphatemia, hypokalemia, hypomagnesemia, and volume overload. (See 'Pathogenesis of the refeeding syndrome' above.)
  • Multiple organ systems can be affected as part of the refeeding syndrome. Most fatalities that occur because of the syndrome are due to cardiac complications, including impaired contractility, decreased stroke volume, heart failure, and arrhythmias. (See 'Medical complications' above and 'Cardiovascular' above.)
  • The refeeding syndrome can be avoided by limiting the amount of calories and fluid provided, avoiding rapid increases in the amount of daily calories ingested, and monitoring the patient during the first few weeks of the refeeding process. If the refeeding syndrome occurs, clinicians should immediately slow nutritional replenishment and correct hypophosphatemia, hypokalemia, and hypomagnesemia while evaluating the cardiovascular system. Moderately to severely ill patients with marked edema or a serum phosphorous < 2 mg/dL should be hospitalized to intravenously correct electrolyte deficiencies. (See 'Prevention and management' above.)

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Uppdaterad: 2018-05-25
Åsa Pettersson, Hälsans vårdcentral 2 Jönköping, Vårdcentralerna Bra Liv