NUTRITION MANAGEMENT IN REFEEDING SYNDROME : Refeeding syndrome is defined as alteration in serum electrolytes (phosphate, potassium, magnesium), deficiency of vitamins as well as fluid and sodium retention. Typically, malnourished patients prone to refeeding syndrome after initiating the parenteral nutrition. 1,2. Even patients whom orally fed after long term starvation can to changes in metabolism futher refeeding syndrome.3,4

Patients specially oncology group who are malnourished are suffering from cachexia often are at higher risk of refeeding syndrome, if remain untreated can be fatal. 


Aggressive nutritional support therapy may be life threatening due to sudden fluid and electrolyte shifts; and patient who have administrated with carb rich diet may manifest with myriad manifestation like neuromuscular, seizures, cardiorespiratory failure or even death.1


Refeeding syndrome reflects changes from catabolic to anabolic metabolism in malnourished or starved patients upon reintroduction of oral, enteral or parentalfedding.6,7,9. Physiogic description of nutritional state requested for understanding refeeding syndrome. The interplay between hormonal and metabolic changes caused by refeeding syndrome and interactions with critical illness metabolic state should be taken in account.

कुटुंबाच्या आहाराचा समतोल आपण कसा राखू शकतो.

There is an increased production of insulin due to glycaemia which leads to decrease in glycogenolysis during refeeding syndrome. Refeeding syndrome often present with salt and water retention, hypokalemia, hypophosphatemia, rapid thiamin depletion and hypomagnesaemia.10. as insulin stimulates glycogen, proteins and fat synthesis requirement of minerals like phosphate and Mg, thiamin increases.

 The nutrition institute for health and clinical excellence (NICE) developed best practice guidelines for the identification, (Table1)

Table I: National Institute for Health and Clinical Excellence criteria for identifying patients at risk of developing refeeding syndrome11.

One or more of the following symptoms:orTwo or more of the following symptoms:
Body mass index < 16 kg/m2Body mass index < 18.5 kg/m2
Unintentional weight loss greater than 15% in the past 3-6 monthsUnintentional weight loss greater than 10% in the past 3-6 months
Little or no nutritional intake for more than 10 daysLittle or no nutritional intake for more than 5 days
Low levels of potassium, phosphate or magnesium before feedingA history of alcohol misuse or drugs, including insulin, chemotherapy, antacids or diuretics

Diet prescription:

There should be initiation with 50% of calories calculated according to BEE. 13 or it is recommended that energy requirements should be calculated at 10 kcal/ kg during starting the feeds. 12, 14.

Malnutrition and critically patients can be feed by more conservative feeds. 12. 15 that is starting from 5 kcal/ kg and can be gradually increase upto 25 to 35 kcals/ kg / day.14 ( Table III)

Table II: Causes of micronutrient inadequacy and the clinical consequences thereof

MicronutrientCauses of micronutrient
System where the inadequacy is presentedClinical consequences of such inadequacy
ThiaminIncreased cellular utilisationNeurologicalWernicke-Korsakoff syndrome (an inflammatory, haemorrhagic degenerative condition of the brain, in coexistence with amnesia)23
Cardiovascular Congestive heart failure, lactic acidosis and beriberi23
SkeletonMuscle weakness23
Phosphate• Cellular phosphate
• Poor phosphate intake24
• Renal tubular phosphate
• Liver disease24
• Septicaemia24
CardiovascularArrhythmia, heart failure, cardiomyopathy and shock23
RenalMetabolic acidosis and acute tubular necrosis23
SkeletonRhabdomyolysis (breakdown of the skeletal muscle fibres), weakness, myalgia and diaphragm weakness23
NeurologicalDelirium, coma, seizures and tetany23
HaematologicalHaemolysis, thrombocytopenia and leukocyte dysfunction23
EndocrineHyperglycaemia, insulin resistance and osteomalacia23
Potassium• Redistribution of potassium
• Gastrointestinal loss of
• Renal potassium loss24
• Renal tubule mechanisms24
CardiovascularHypotension, ventricular arrhythmias, cardiac arrest, bradycardia and tachycardia23
RespiratoryHypoventilation, respiratory distress and respiratory failure23
SkeletonWeakness, fatigue and muscle twitching23
GastrointestinalDiarrhoea, nausea, vomiting, anorexia, paralytic ileus and constipation23
MetabolicMetabolic alkalosis23
Magnesium• Cellular magnesium
• Drug interactions24
• Increased renal loss of
• Poor magnesium intake24
• Alcoholism24
• Diabetes mellitus24
• Hyperaldosteronism24
• Hypercalcaemia24
• Hyperthyroidism24
CardiovascularParoxysmal atrial or ventricular arrhythmias23
RespiratoryHypoventilation, respiratory distress and respiratory failure23
NeuromuscularWeakness, fatigue, muscle cramps, ataxia, vertigo, paraesthaesia, hallucinations, depression and convulsions23
GastrointestinalAbdominal pain, diarrhoea, vomiting, loss of appetite, and constipation23
Other related consequencesAnaemia and hypocalcaemia23
SodiumSerum osmolality changes in the central nervous system25CardiovascularHeart failure and arrhythmia23
RespiratoryRespiratory failure and pulmonary oedema23
RenalRenal failure23
SkeletonMuscle cramps, fatigue, fluid retention and oedema23

Micronutrients and refeeding syndrome:

To prevent refeeding syndrome special consideration should be taken of provision of phosphorus, potassium, vitamin B complex and Mg.

Vitamin B complex:

The recommended thiamin intake range between 200 and 300 mg daily as it acts as a co-enzyme in carbohydrate metabolism. It is important to monitor this vitamin during prevention of refeeding syndrome.

Table III: A summary of the treatment options for micronutrient inadequacy

MicronutrientTreatment options
ThiaminIV 300 mg when the feed is initiated, and 100 mg per day as maintenance12
Mild (2.3-3.0 mg/dl)0.32 mmol/kg*12,26
Increase dietary intake or oral phosphate containing a multivitamin25
Moderate (1.6-0.2 mg/dl)0.64 mmol/kg12,26
Oral supplementation: 2.5-3.5 g/day in divided doses, or 0.32-0.64 mmol/kg IV slowly over 6 hours25
Severe (1.5 mg/dl)1 mmol/kg*12,26
1 mmol/kg IV slowly over 8-12 hours25
Mild (4.0-3.7 mEq/l)40 mEq oral or IV26
Increase dietary intake and/or add salt substitutes25
Oral supplementation: 40-100 mEq daily in divided doses, or 40 mEq IV x 1, or 10 mEq IV over 1 hour x 3-4 doses25
Moderate (3.6-3.4 mEq/l)60 mEq oral or IV26
20 mEq per os every 2 hours x 3 doses, or 10 mEq IV over 1 hour x 4 doses (recheck and repeat, if needed)25
Severe (< 3.3 mEq/l)80 mEq oral or IV26
40 mEq IV over 2-4 hours (recheck and repeat, as needed), or 40 mEq IV over 4 hours, as needed25
MildOral, increase daily intake, or oral supplement
(magnesium lactate)25
Moderate10-15 mmol oral magnesium oxide or citrate12
IV 8-32 mEq (maximum 1.0 mEq/kg) slowly,
with 8 mEq over 1-2 hours daily25
Severe25 mmol/day parenteral magnesium12
IV 32-64 mEq (maximum 1.5 mEq) slowly,
with 8 mEq over 1-2 hours25
Free water restriction25
ModerateConsider free water restriction
Provide half normal saline and/or saline corrected at a rate of 1-2 mEq/l/hour25
Severe3% sodium chloride (correct at a rate of 1-2 mEq/l/hour)25

* Actual body weight (if < 130% of ideal body weight). If > 130% of ideal body weight, then adjust body weight, i.e. [ideal body weight + 0.25 (actual body weight − ideal body weight)]26 IV: intravenous

Consequence of hypophosphatemia during refeeding syndrome:

Since phosphate is mainly found in intracellular compartment, serum concentration do not reflect intracellular concentration accurately. Further more Sr. Phosphate concentration show a diurnal variation. Therefore, the clinical consequences of hypophosphatemia cannot be predicted by the actual serum concentration of phosphates.

observed in the refeeding of malnourished patients.

Phosphorus: the depletion of serum phosphorus is seen in refeeding syndrome which occurs because of the increase in phosphorylation of glucose. 10.

Sr. phosphorous level should be closely monitored to prevent refeeding syndrome as well as neurological symptoms.12

Potassium : to prevent edema and eventually heart failure it is necessary to monitor potassium levels.12 (Table III)


Hypomagnesaemia can lead to cardiac arrhythmia, neuromuscular abnormalities. (Table III).

Therefore, this should be assessed every 8 to 12 hrs. If hypokalemia hypomagnesaemia develop these electrolytes should be supplied accordingly to prevent further complications.

Hyper ammonia: there is increased in plasma concentration of amino acids metabolism reduction in protein degradation in muscles and other tissues is the consequences of adaptive metabolic mechanism during prolonged starvation the concentration of aminoacid in  blood can exceed the capacity of the urea cycle thus hyperammonemia  may occur.


Diarrhea is often found in starving and malnourished patients and can be exaggerated by oral refeeding. Enterocyte dysfunction and atrophy of the intestinal mucosa can originate from starvation and result in a reduction in absorptive capacity to the extent that malab­sorption and osmotic diarrhea may occur during refeeding. Also, an increased mucosal secretion has also been discussed as a cause of diarrhea22.

Treatment of refeeding

syndrome can be assisted by the hospital nutrition team. Patients at-risk for malnutrition or developing refeeding syndrome need to be identiÞ ed. Enteral or parenteral feeding should be started at a reduced caloriÞ c rate (25-50% of daily caloric needs). Carbohydrate intake should be limited. Serum phosphate, magnesium, calcium, potassium, sodium, urea and creatinine levels should be measured and supplementation should be done as needed. Feeding may be stopped and restarted after 24h at a lower rate if symptoms of cardiac failure like tachycardia and tachypnoea develop.

Key points

  • Refeeding syndrome is characterized primarily by neurological, muscular and hematological changes.
  • These changes are associated with profound falls in serum levels of phosphate, potassium magnesium, thiamine etc.
  • Refeeding syndrome can occur when nutrition in the form of carbohydrate (enteral or parenteral) is reintroduced following starvation.
  • Tachypnea and tachycardia may be useful early clinical signs of refeeding syndrome developing in a patient who has been renourished after a period of starvation.
  • Refeeding syndrome is characterized primarily by neurological, muscular and hematological changes. Refeeding syndrome is common during prolonged ICU stay and may be obscured by critical illness, as it resembles multiorgan dysfunction syndrome.
  • Routine phosphate measurements are advised during the first days after introduction of nutritional support as no other factors are helpful to identify patients on ICU admission that will develop refeeding syndrome.
  • Electrolyte (phosphate, potassium, magnesium) and thiamine supplementation is essential for critically ill patients with refeeding syndrome.
  • Hypocaloric feeding for critically ill patients with refeeding hypophosphatemia improves survival rates and caloric restriction for 48 h is warranted.


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