Pediatric Annals

Special Issue Article 

Refeeding Syndrome

Joseph Runde, DO; Timothy Sentongo, MD

Abstract

Refeeding syndrome describes the metabolic disturbances and clinical sequelae that occur in response to nutritional rehabilitation of patients who are moderate to severely malnourished. When risk factors are not identified and nutrition therapy is not managed appropriately, devastating consequences such as electrolyte depletion and imbalances, fluid overload, arrhythmia, seizure, encephalopathy, and death may occur. As this entity is often unrecognized, especially in pediatrics, becoming familiar with the pathophysiology, clinical manifestations, and management strategies will help clinicians caring for children avoid unnecessary morbidity and mortality. [Pediatr Ann. 2019;48(11):e448–e454.]

Abstract

Refeeding syndrome describes the metabolic disturbances and clinical sequelae that occur in response to nutritional rehabilitation of patients who are moderate to severely malnourished. When risk factors are not identified and nutrition therapy is not managed appropriately, devastating consequences such as electrolyte depletion and imbalances, fluid overload, arrhythmia, seizure, encephalopathy, and death may occur. As this entity is often unrecognized, especially in pediatrics, becoming familiar with the pathophysiology, clinical manifestations, and management strategies will help clinicians caring for children avoid unnecessary morbidity and mortality. [Pediatr Ann. 2019;48(11):e448–e454.]

Our understanding of refeeding syndrome (RFS) began more than 70 years ago with descriptions of starvation and nutritional rehabilitation in prisoners after World War II. One such study observed 24 Japanese soldiers on the island of Luzon in the Philippines after their surrender in September 1945.1 Having subsisted on less than 1,000 calories a day for the final months of the war, the emaciated soldiers were noted to have a “slow” response to nutritional supplementation with many developing unexplained edema and sudden death reported in five of the soldiers.

Although the pathophysiology of RFS has since been elucidated, if risk factors are missed in our pediatric patients then consequences such as electrolyte depletion, fluid overload, arrhythmia, seizure, encephalopathy, and death may ensue. The incidence of RFS can be challenging to pinpoint given variability in studied populations over time with estimated ranges from 0% to 80%.2 One study of vulnerable adolescent patients demonstrated that 28% required supplementation of phosphate as a result of nutritional rehabilitation.3 This article will highlight key features of RFS, including risk factors, so that clinicians taking care of children will be well-equipped to prevent and manage this complicated diagnosis.

Pathophysiology

To understand the cascade of metabolic derangements underlying RFS, it is important to begin by reviewing the mechanisms of starvation. During prolonged calorie restriction or starvation, the body adapts by depleting glycogen stores. Once these are exhausted, catabolism shifts from carbohydrates to fat and protein. Adipose tissue is broken down to fatty acids and glycerol, and muscle tissue to amino acids. Metabolism shifts to utilization of ketones and free fatty acids.4 The net effect is loss of lean body mass and muscle wasting, including of the myocardium.5 Furthermore, intracellular electrolytes and minerals are depleted during starvation resulting in deficiencies of phosphate, potassium, magnesium, and thiamine (Figure 1).

Pathophysiology of starvation. Adapted from references 4–6.

Figure 1.

Pathophysiology of starvation. Adapted from references 4–6.

When a patient who had been previously starved and malnourished is re-fed with a nutrient-dense diet, the resulting sudden surge in plasma glucose and amino acids triggers increased secretion of insulin. This revives the body's metabolism and shifts it from catabolism to anabolism. However, in the setting of low serum and tissue stores of essential electrolytes and micronutrients, there is impaired enzyme activity, further depletion of micronutrients, organ dysfunction, and dramatic fluid shifts with potentially life-threatening consequences (Figure 2).

Pathophysiology of refeeding. Adapted from references 2, 5, and 7.

Figure 2.

Pathophysiology of refeeding. Adapted from references 2, 5, and 7.

Electrolyte Abnormalities in RFS and their Clinical Manifestations

Phosphate

Hypophosphatemia is the most frequently recognized electrolyte abnormality in RFS.8 Rapid re-introduction of glucose after starvation results in a surge of insulin, which causes increased cellular uptake and utilization of phosphate. Serum concentrations of phosphate already low from starvation plummet further and oxidative phosphorylation is impaired.9 This results in inadequate production of adenosine triphosphate (ATP) crucial to glycolysis. Clinical consequences include myopathy and rhabdomyolysis. Children may experience muscle weakness, respiratory compromise, and increased serum creatine kinase. Furthermore, oxygen delivery to tissues is impeded by deficits in 2,3 diphosphoglycerate (2,3 DPG).4 Hematologic abnormalities from depleted ATP and decreased 2,3 DGP include impaired chemotaxis, phagocytosis, and platelet aggregation manifesting as impaired immune function, anemia from hemolysis, and thrombocytopenia. Hypophosphatemia may also result in neuromuscular dysfunction as nervous system conduction is disrupted, resulting in weakness, paresthesia, seizures, and coma.5

Potassium

In the malnourished state, total body potassium stores are depleted. As with phosphate, newly supplied glucose with refeeding results in an insulin surge causing extracellular potassium to shift into cells.10 The resulting hypokalemia leads to cellular membrane hyperpolarization and abnormal muscle contractility.7 Children may experience muscle weakness, rhabdomyolysis, and even respiratory failure. Cardiac tissue will also be affected with electrocardiogram, demonstrating flattened or inverted T waves, ST-segment depression, and prominent U waves. If hypokalemia is severe, ventricular arrhythmias, ectopic beats, bradycardia, tachycardia, and full cardiac arrest are possible. Gastrointestinal sequelae of hypokalemia include nausea, vomiting, constipation, and paralytic ileus whereas the kidneys may have decreased ability to concentrate urine and renal tubule damage.4

Magnesium

As with phosphate and potassium, magnesium is essential for ATP production and needed for enzymatic pathways of carbohydrate metabolism. Magnesium is also essential in the structural integrity of DNA, RNA, and ribosomes.4 Furthermore, magnesium helps sodium and potassium ions cross cell membranes, playing a key role in cell membrane potentials. Therefore, hypomagnesaemia may manifest with arrhythmia or even cardiac arrest.7 Neurological deficits can be grave including altered mental status, weakness, tremors, tetany, seizures, and coma. Gastrointestinal sequelae include nausea, vomiting, and diarrhea. Magnesium is also essential for production of parathyroid hormone; therefore, low levels may result in refractory hypocalcaemia.5,11

Sodium

In RFS, the kidneys respond to the insulin spike by increasing sodium and corresponding water retention.11 For this reason, children are vulnerable to fluid overload and edema as the body moves from a state of starvation to refeeding. Fluid overload is exacerbated if intravenous support is provided in excess or in cases of low albumin levels. Imbalance in intracellular and extracellular fluid may manifest as pulmonary edema, arrhythmia, and congestive heart failure.5

Thiamine

Thiamine is an essential cofactor for enzymes needed in carbohydrate metabolism including pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase, which are both critical in the Krebs cycle.10 Deficiency ultimately causes the metabolism of pyruvate to lactate resulting in severe lactic acidosis. Thiamine deficiency may manifest clinically as beriberi, which is characterized by metabolic acidosis, tachycardia, and high-output heart failure. Other manifestations include Wernicke's encephalopathy and Korsakoff's psychosis. Wernicke's encephalopathy is associated with neurological findings, including altered mental status, ophthalmoplegia, nystagmus, ataxia, memory loss, and brain magnetic resonance imaging changes.12 Korsakoff's syndrome, often considered in alcohol dependence, is characterized by amnesia, confabulation, and chronic malnutrition.13

Glucose

This finding is inconsistently reported in cases of RFS.8 However, glucose intolerance and hyperglycemia may be attributed to the relative insulin resistance that occurs in some patients with severe malnutrition. The underlying mechanism involves increased endogenous production of glucocorticoids as maladaptive response to starvation.14 The hyperglycemia may be responsible for osmotic diuresis, dehydration, hypotension, acidosis, and impaired immune function.5

Differential Diagnosis

As RFS can present with a wide array of electrolyte deficiencies and clinical sequelae, the differential can be broad. In children, it is important to keep an open mind so that other causes of electrolyte abnormality are not overlooked.15 The three main mechanisms leading to most electrolyte deficiencies are (1) shift of the electrolyte from extracellular fluid; (2) decrease in intestinal absorption or parenteral intake; and (3) increased renal losses (Table 1).

Pathophysiology of Electrolyte Disturbances to Consider in Refeeding Syndrome

Table 1:

Pathophysiology of Electrolyte Disturbances to Consider in Refeeding Syndrome

Management

The most important aspect of management is being aware of patients with risk factors for developing RFS. Imminent RFS can be diagnosed within 72 hours of starting nutrition therapy based on either serum concentration of two electrolytes declining to below normal or serum concentration of one electrolyte falling below normal combined with a typical clinical symptom such as tachycardia, tachypnea, and peripheral edema, or the serum concentration of phosphate declining by >30% or to <0.6 mmol/L.26 The World Health Organization has published helpful guidelines for initiating, advancing, and monitoring outcomes of nutritional intervention in children who are moderate to severely malnourished (Table 2). Management should begin by identifying those children with risk factors. This is accomplished through careful history and nutrition assessment of all patients referred for nutrition support. From there a proactive administration of electrolytes and micronutrients in those with risk factors and close monitoring of patients especially during the early phases of nutrition support are paramount to avoid devastating clinical consequences.

World Health Organization Resting Energy Expenditure Prediction Equationsa

Table 2:

World Health Organization Resting Energy Expenditure Prediction Equations

Identify children at risk. The patients at greatest risk for developing RFS are presented in Figure 3. Both acute and severe malnutrition are important risk factors. In acute cases, weight loss of >10% in a period of less than 3 months and/or undernourishment for 10 to 14 days (eg, children receiving intravenous fluids without supplemental proteins/lipids or appropriately dosed electrolytes) have increased risk factors (Table 3). Severe malnutrition may be environmental or disease related; it is diagnosed based on mid-arm circumference.27

Timeline for management of children who are malnourished with risk factors for refeeding syndrome.

Figure 3.

Timeline for management of children who are malnourished with risk factors for refeeding syndrome.

Risk Factors for Refeeding Syndrome in Children

Table 3:

Risk Factors for Refeeding Syndrome in Children

Calibrate reintroduction of feeds. Nutritional rehabilitation is the goal but in the acute setting, safety is most important. Daily caloric goals should be approximated to 25% to 75% of the estimated basal metabolic rate/resting energy expenditure.5,11,29 If the patient remains stable, a gradual increase of 10% to 25% total calories per day until reaching the goal is appropriate.11,29

Replete electrolytes/micronutrients. If electrolyte deficits or levels downtrend, it is recommended to hold feeds, replace electrolytes, and correct fluid imbalance before resuming nutritional support (Table 4).5,7 Sodium and parenteral fluids should be provided strategically to avoid fluid overload. Protein should not be restricted to promote lean muscle restoration.5,10,11

Electrolyte Repletion and Maintenance Dosing

Table 4:

Electrolyte Repletion and Maintenance Dosing

Monitoring. It is important to consider that electrolyte derangements may not present acutely. As Figure 3 illustrates these abnormalities may occur any time within the first few weeks of rehabilitation. Laboratory monitoring for the first 72 hours and often for 5 to 7 days after the initiation of nutrition therapy may be necessary.5,26,29,32 Furthermore, cardiac dysfunction and neurological symptoms may not present until after the first week of therapy.5 For this reason, children with risk factors should have cardiorespiratory monitoring and regular examinations of neuromuscular and mental status during therapy. Daily weights and strict documentation of intake/output are essential in preventing fluid overload.

Conclusion

Although we have learned much about the pathophysiology and clinical consequences of RFS since the initial descriptions dating back almost 70 years, this entity is still frequently overlooked during clinical care. Therefore, it is essential for all clinicians caring for children to be aware of the risk factors for developing RFS and manage nutrition therapy accordingly to prevent the avoidable metabolic derangements and potentially life-threatening complications.

References

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Pathophysiology of Electrolyte Disturbances to Consider in Refeeding Syndrome

Hypophosphatemia16–18
Decreased intake or intestinal absorption Inadequate intake in diet (less than 100 mg/day); prolonged diarrhea/steatorrhea, use of intravenous fluid, or total parenteral nutrition without adequate phosphate; use of phosphate binders
Shift from extra to intracellular Insulin; respiratory alkalosis
Increased renal losses Fanconi syndrome; primary or secondary hyperparathyroidism; vitamin D deficiency; use of diuretics
Hypomagnesemia19–21
Decreased intake or intestinal absorption Acute or chronic diarrhea/steatorrhea; less common with vomiting; pancreatitis (saponification of magnesium in necrotic fat, associated with hypocalcemia); prolonged proton pump inhibitor use (with diuretics)
Increased renal losses Hypercalcemia (competition for reabsorption at thick ascending limb of loop of Henle, seen in hyperparathyroid state); medications: diuretics, calcineurin inhibitors, aminoglycosides, amphotericin B, pentamidine, cisplatin
Hypokalemia22,23
Decreased intake or intestinal absorption Prolonged diarrhea/vomiting; malnutrition; prolonged intravenous fluids without potassium
Shift from extra to intracellular Insulin; medications: beta-adrenergics, antipsychotics
Increased renal losses Renal tubular acidosis type 1 due to defective secretion of protons and increased tubular permeability; Fanconi syndrome; glucosuria (diabetic ketoacidosis); medications: diuretics, cisplatin, amphotericin B; genetic disease: Bartter and Gitelman (impaired sodium reabsorption leading to metabolic alkalosis)
Hypernatremia24,25
Increased gastrointestinal water loss Gastroenteritis (number 1 cause); excessive vomiting
Excessive urinary water loss Diabetes insipidus: central vs. nephrogenic (congenital vs acquired);medication: diuretics; hyperglycemia (diabetic ketoacidosis)
Excessive intake Iatrogenic (high sodium concentration in intravenous fluids); inappropriate formula preparation

World Health Organization Resting Energy Expenditure Prediction Equationsa


Female Male
Age (Years) Weight Calculation
0–3 (61 × Wt [kg]) − 51 (60.9 × Wt [kg]) − 54
3–10 (22.5 × Wt [kg]) + 499 (22.7 × Wt [kg]) + 495
10–18 (12.2 × Wt [kg]) + 746 (17.5 × Wt [kg]) + 651

Risk Factors for Refeeding Syndrome in Children

Etiology Specific Considerations
Malnutrition Acute weight loss (>10% in less than 3 months) Undernourishment 10–14 days (patients receiving prolonged intravenous fluids without dextrose, proteins or intravenous lipids) Severe malnutrition (weight for length or body mass index z-score of ≥3) Body weight <80% is ideal Edematous malnutrition (Kwashiorkor)
Gastrointestinal disease Malabsorption   Celiac disease   Cystic fibrosis   Chronic pancreatitis   Inflammatory bowel disease   Intestinal failure   Chronic liver disease Dysphagia/dysmotility (eosinophilic esophagitis) Severe gastroesophageal reflux disease Cyclic vomiting syndrome
Other chronic disease Cancer Cerebral palsy Immunocompromised Chronic lung disease Alcohol or drug use
Congenital disease Prematurity Intrauterine growth restriction, low birth weight Congenital heart disease, chronic lung disease
Eating disorder Anorexia nervosa
Postoperative status Bariatric surgery Prolonged “nothing by mouth” after surgery without adequate nutrition

Electrolyte Repletion and Maintenance Dosing

Electrolyte/Mineral Treatment Dosing Maintenance Dosing
Phosphate
IV dose 0.08–0.64 mmol/kg per dose IV (maximum of 15 mmol/kg per dose) over 6–12 hours; maximum of 1.5 mmol/kg daily dose 0.3–0.6 mmol/kg per day
PO dose 0.3–0.6 mmol/kg per day (mild cases)
Potassium
IV dose 0.3–0.5 mEq/kg per dose IV (maximum of 30 mEq per dose) for more than 1–2 hours 1–2 mmol/kg per day
PO dose Not generally indicated in RFS
Magnesium
IV dose 25–50 mg/kg per dose (0.2–0.4 mEq/kg per dose) with a maximum dose of 2 g IV over 4 hours 0.2–0.4 mmol/kg per day
PO dose 25–50 mg/kg per PO dose (mild cases)
Thiamine
IV dose 15–25 mg per day IV 0.5–1 mg per day
PO dose 10–50 mg per day PO for 2 weeks
Authors

Joseph Runde, DO, is a Fellow, Section of Gastroenterology, Hepatology and Nutrition, The University of Chicago Medical Center. Timothy Sentongo, MD, is an Associate Professor of Pediatric Gastroenterology; the Director, Pediatric Nutrition Support; and the Director, Pediatric Gastrointestinal Endoscopy, Section of Gastroenterology, Hepatology and Nutrition, The University of Chicago Medical Center.

Address correspondence to Joseph Runde, DO, Section of Gastroenterology, Hepatology and Nutrition, The University of Chicago Medical Center, 5841 S. Maryland Avenue, Rm C-474, MC 4065, Chicago, IL 60637; email: Joseph.Runde@uchospitals.edu.

Disclosure: The authors have no relevant financial relationships to disclose.

10.3928/19382359-20191017-02

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