Sindrome De Realimentación

R efe e ding Syndrome
Judy Fuentebella, MD*, John A. Kerner, MD
KEYWORDS
 Refeeding syndrome  Pediatric  Hypophosphatemia
 Nutrition support  Malnutrition

Refeeding syndrome (RFS) is a term that describes the metabolic and clinical changes
that occur on aggressive nutritional rehabilitation of a malnourished patient. It is a welldescribed yet often underrecognized entity. Itsrecognition was heightened in the
World War II era when prisoners who had undergone starvation developed cardiac
failure and peripheral edema on nutritional replenishment.1 In Leningrad and The
Netherlands, cases of cardiac insufficiency and edema were reported after refeeding
survivors of the war who were starved because of scant food supplies.2 In 1944, Keys
and colleagues deliberately starved andrefed previously healthy men and observed
cardiac decompensation in some patients who were orally fed.2,3 In the 1960s, the
advent of parenteral nutrition (PN) allowed for a more aggressive means of nutritional
rehabilitation. Reports of hypophosphatemic hyperalimentation syndrome soon followed in the 1970s. In 1980, Silvis and colleagues4 noted paresthesias, seizures, or
coma in conjunctionwith hypophosphatemia in patients receiving PN. In the 1980s,
Weinsier and Krumdieck5 wrote a critical paper that described cardiopulmonary
complications resulting in the death of two chronically undernourished patients who
received PN.
Hypophosphatemia is the hallmark of RFS. Other electrolyte abnormalities are associated with RFS, however, such as hypokalemia and hypomagnesemia. Shifts inglucose, sodium, and fluid balance are also seen in RFS. Consequently, cardiovascular, pulmonary, neuromuscular, hematologic, and gastrointestinal complications
occur. This syndrome can emerge with aggressive oral nutrition, enteral nutrition, or
PN and can be fatal if not recognized and treated in a timely manner.
PATHOPHYSIOLOGY OF STARVATION

During starvation, the body tries to compensatefor the lack of energy by means of
changes in metabolism and hormone regulation. The body goes into a state of

This work was supported in part by the Carl and Patricia Dierkes Endowed Fund for Nutrition
Support and Home Care.
Division of Pediatric Gastroenterology, Hepatology, and Nutrition, Lucile Packard Children’s
Hospital, Stanford University Medical Center, 750 Welch Road, Suite 116,Palo Alto, CA
94304, USA
* Corresponding author.
E-mail address: judyf@stanford.edu (J. Fuentebella).
Pediatr Clin N Am 56 (2009) 1201–1210
doi:10.1016/j.pcl.2009.06.006
pediatric.theclinics.com
0031-3955/09/$ – see front matter ª 2009 Elsevier Inc. All rights reserved.

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Fuentebella & Kerner

catabolism. A shift from carbohydrate metabolism to fat and protein catabolism
occurs,which provides glucose and ketones for energy. This shift to protein catabolism results in a loss of lean body mass, which affects major organs, such as the heart,
lungs, intestines, liver, and kidneys. Atrophy of the myocardium results in poor
contractility and diminished cardiac output. Liver wasting results in decreased protein
synthesis and further alteration in metabolism.Gastrointestinal atrophy causes malabsorption and dysmotility, further exacerbating the malnourished state, and increases
the risk for infection. The kidneys also lose their ability to concentrate urine, resulting
in diuresis.6–8
Cellular mass is also lost, contributing to functional loss of vital organs. Intracellular
loss of electrolytes, including potassium, magnesium, and phosphate, occurs as
aconsequence of this change in metabolism. Insulin secretion decreases and the
basal metabolic rate slows down to 20% to 25% to conserve energy.8 Consequently,
the body becomes bradycardic, hypothermic, and hypotensive. Growth and thyroid
hormones also decrease.6 These changes occur in an effort to conserve protein
and organ function, which aids in survival. It is important to understand the...