Refeeding syndrome

Refeeding syndrome broadly encompasses clinical complications that can occur as result of potentially fatal fluid and electrolyte shifts in malnourished patients during refeeding by oral, enteral, or parenteral routes and can lead to cardiac arrhythmia, muscle weakness and cramping, seizures, delirium, and death ¹. These shifts result from hormonal and metabolic changes and may cause serious clinical complications. The hallmark biochemical feature of refeeding syndrome is hypophosphatemia [low serum phosphate concentration < 2.5 mg/dL (0.81 mmol/L)]. However, refeeding syndrome is complex and may also feature abnormal sodium and fluid balance; changes in glucose, protein, and fat metabolism; thiamine deficiency; hypokalemia (low blood level of potassium) and hypomagnesemia [low serum magnesium concentration < 1.8 mg/dL (< 0.70 mmol/L)] ². Refeeding syndrome was was first described in Far East prisoners during the Second World War ³.

Estimates of the prevalence of refeeding syndrome vary widely from 0.43% to 34% ⁴. The true incidence of refeeding syndrome is unknown—partly owing to the lack of a universally accepted definition. In a study of 10,197 hospitalised patients the incidence of severe hypophosphatemia was 0.43%, with malnutrition being one of the strongest risk factors ⁵. Studies report a 100% incidence of hypophosphatemia in patients receiving total parenteral nutrition solutions that do not contain phosphorus. When solutions containing phosphate are used, the incidence can decrease to 18% ⁶.

Several prospective and retrospective cohort studies of hyperalimentation in intensive care units have documented the occurrence of refeeding syndrome ⁷. In a well designed prospective cohort study of a heterogeneous group of patients in intensive care units, 34% of patients experienced hypophosphatemia soon after feeding was started (mean (standard deviation) 1.9 (1.1) days) ⁸. Many case reports have highlighted the potentially fatal nature of the condition ⁹. However, it is often not recognized or maybe inappropriately treated, especially on general wards ².

Refeeding syndrome key points

• Refeeding syndrome is a potentially fatal condition, caused by rapid initiation of refeeding after a period of undernutrition
• Refeeding syndrome is characterized by hypophosphatemia, associated with fluid and electrolyte shifts and metabolic and clinical complications
• Awareness of refeeding syndrome and identification of patients at risk is crucial as the condition is preventable and the metabolic complications are avoidable
• Patients at high risk include chronically undernourished patients and those who have had little or no energy intake for more than 10 days
• Refeeding should be started at a low level of energy replacement. Vitamin supplementation should also be started with refeeding and continued for at least 10 days
• Correction of electrolyte and fluid imbalances before feeding is not necessary; it should be done alongside feeding.

Refeeding syndrome causes

The underlying causative factor of refeeding syndrome is the metabolic and hormonal changes caused by rapid refeeding, whether enteral or parenteral. The net result of metabolic and hormonal changes in early starvation is that the body switches from using carbohydrate to using fat and protein as the main source of energy, and the basal metabolic rate decreases by as much as 20-25% ¹⁰.

During prolonged fasting, hormonal and metabolic changes are aimed at preventing protein and muscle breakdown. Muscle and other tissues decrease their use of ketone bodies and use fatty acids as the main energy source. This results in an increase in blood levels of ketone bodies, stimulating the brain to switch from glucose to ketone bodies as its main energy source. The liver decreases its rate of gluconeogenesis, thus preserving muscle protein. During the period of prolonged starvation, several intracellular minerals become severely depleted. However, serum concentrations of these minerals (including phosphate) may remain normal. This is because these minerals are mainly in the intracellular compartment, which contracts during starvation. In addition, there is a reduction in renal excretion ¹¹.

Refeeding

During refeeding, glycaemia leads to increased insulin and decreased secretion of glucagon ¹¹. Insulin stimulates glycogen, fat, and protein synthesis. This process requires minerals such as phosphate and magnesium and cofactors such as thiamine. Insulin stimulates the absorption of potassium into the cells through the sodium-potassium ATPase symporter, which also transports glucose into the cells. Magnesium and phosphate are also taken up into the cells. Water follows by osmosis. These processes result in a decrease in the serum levels of phosphate, potassium, and magnesium, all of which are already depleted. The clinical features of the refeeding syndrome occur as a result of the functional deficits of these electrolytes and the rapid change in basal metabolic rate.

Major causes include low phosphorus blood levels following intake of foods high in calories or glucose. Phosphorous depletion causes abnormalities in the cardiorespiratory system, which left untreated can be fatal. Symptoms also develop in response to changes in potassium and magnesium levels. Rapid changes in intake can place excessive strain on the impaired heart which is then unable to maintain adequate circulation.

What electrolytes and minerals are involved in refeeding syndrome?

Phosphorus

Phosphorus is predominantly an intracellular mineral. It is essential for all intracellular processes and for the structural integrity of cell membranes. In addition, many enzymes and second messengers are activated by phosphate binding. Importantly it is also required for energy storage in the form of adenosine triphosphate (ATP). It regulates the affinity of haemoglobin for oxygen and thus regulates oxygen delivery to tissues. It is also important in the renal acid-base buffer system.

In refeeding syndrome, chronic whole body depletion of phosphorus occurs. Also, the insulin surge causes a greatly increased uptake and use of phosphate in the cells. These changes lead to a deficit in intracellular as well as extracellular phosphorus. In this environment, even small decreases in serum phosphorus may lead to widespread dysfunction of cellular processes affecting almost every physiological system ¹².

Potassium

Potassium, the major intracellular cation, is also depleted in undernutrition. Again, serum concentration may remain normal. With the change to anabolism on refeeding, potassium is taken up into cells as they increase in volume and number and as a direct result of insulin secretion. This results in severe hypokalaemia. This causes derangements in the electrochemical membrane potential, resulting in, for example, arrhythmias and cardiac arrest.

Magnesium

Magnesium, another predominantly intracellular cation, is an important cofactor in most enzyme systems, including oxidative phosphorylation and ATP production. It is also necessary for the structural integrity of DNA, RNA, and ribosomes. In addition, it affects membrane potential, and deficiency can lead to cardiac dysfunction and neuromuscular complications ¹³.

Glucose

Glucose intake after a period of starvation suppresses gluconeogenesis through the release of insulin. Excessive administration may therefore lead to hyperglycaemia and its sequelae of osmotic diuresis, dehydration, metabolic acidosis, and ketoacidosis. Excess glucose also leads to lipogenesis (again as a result of insulin stimulation), which may cause fatty liver, increased carbon dioxide production, hypercapnoea, and respiratory failure ¹⁴.

Vitamin deficiency

Although all vitamin deficiencies may occur at variable rates with inadequate intake, thiamine is of most importance in complications of refeeding. Thiamine is an essential coenzyme in carbohydrate metabolism. Its deficiency result in Wernicke’s encephalopathy (ocular abnormalities, ataxia, confusional state, hypothermia, coma) or Korsakoff’s syndrome (retrograde and anterograde amnesia, confabulation) ¹⁵.

Sodium, nitrogen, and fluid

Changes in carbohydrate metabolism have a profound effect on sodium and water balance. The introduction of carbohydrate to a diet leads to a rapid decrease in renal excretion of sodium and water ¹⁶. If fluid repletion is then instituted to maintain a normal urine output, patients may rapidly develop fluid overload. This can lead to congestive cardiac failure, pulmonary edema, and cardiac arrhythmia.

Refeeding syndrome prevention

Identification of high risk patients is crucial ¹⁷. Any patient with negligible food intake for more than five days is at risk of developing refeeding problems. Patients may be malnourished as a result of reduced intake (for example, owing to dysphagia, anorexia nervosa, depression, alcoholism); reduced absorption of nutrition (as in, for example, inflammatory bowel disease, celiac disease); or increased metabolic demands (for example, in cancer, surgery). High risk patients include those who have been chronically undernourished, especially those who also have diminished physiological reserve. Patients with dysphagia (for example, as a result of stroke) in particular may be at high risk.

Patients at high risk of refeeding syndrome ¹⁷:

• Patients with anorexia nervosa
• Patients with chronic alcoholism
• Oncology patients
• Postoperative patients
• Elderly patients (comorbidities, decreased physiological reserve)
• Patients with uncontrolled diabetes mellitus (electrolyte depletion, diuresis)
• Patients with chronic malnutrition:
  • Marasmus
  • Prolonged fasting or low energy diet
  • Morbid obesity with profound weight loss
  • High stress patient unfed for >7 days
  • Malabsorptive syndrome (such as inflammatory bowel disease, chronic pancreatitis, cystic fibrosis, short bowel syndrome)
• Long term users of antacids (magnesium and aluminium salts bind phosphate)
• Long term users of diuretics (loss of electrolytes)

Criteria from the guidelines of the National Institute for Health and Clinical Excellence (NICE) for identifying patients at high risk of refeeding problems.

Nutrition support should be considered in people who are malnourished, as defined by any of the following ¹⁸:

• Body mass index (BMI) of less than 16 kg/m²
• Unintentional weight loss greater than 15% within the last 3–6 months
• Little or no nutritional intake for more than 10 days
• Low levels of potassium, phosphate or magnesium prior to feeding.

Or patient has two or more of the following ¹⁸:

• Body mass index (BMI) less than 18.5 kg/m²
• Unintentional weight loss greater than 10% within the last 3–6 months
• Little or no nutritional intake for more than 5 days
• A history of alcohol abuse or drugs including insulin, chemotherapy, antacids or diuretics.

People at high risk of developing refeeding problems should be cared for by healthcare professionals who are appropriately skilled and trained and have expert knowledge of nutritional requirements and nutrition support. To ensure adequate prevention, the National Institute for Health and Clinical Excellence (NICE) guidelines recommend a thorough nutritional assessment before refeeding is started ¹⁸. Recent weight change over time, nutrition, alcohol intake, and social and psychological problems should all be ascertained. Plasma electrolytes (especially phosphate, sodium, potassium, and magnesium) and glucose should be measured at baseline before feeding and any deficiencies corrected during feeding with close monitoring ¹⁸.

The prescription for people at high risk of developing refeeding problems should consider ¹⁸:

• Starting nutrition support at a maximum of 10 kcal/kg/day, increasing levels slowly to meet or exceed full needs by 4–7 days
• Using only 5 kcal/kg/day in extreme cases (for example, BMI less than 14 kg/m² or negligible intake for more than 15 days) and monitoring cardiac rhythm continually in these people and any others who already have or develop any cardiac arrythmias
• Restoring circulatory volume and monitoring fluid balance and overall clinical status closely
• Providing immediately before and during the first 10 days of feeding: oral thiamine 200–300 mg daily, vitamin B co strong 1 or 2 tablets, three times a day (or full dose daily intravenous vitamin B preparation, if necessary) and a balanced multivitamin/trace element supplement once daily
• Providing oral, enteral or intravenous supplements of potassium (likely requirement 2–4 mmol/kg/day), phosphate (likely requirement 0.3–0.6 mmol/kg/day) and magnesium (likely requirement 0.2 mmol/kg/day intravenous, 0.4 mmol/kg/day oral) unless pre-feeding plasma levels are high. Pre-feeding correction of low plasma levels is unnecessary.

The National Institute for Health and Clinical Excellence (NICE) guidelines recommend that refeeding is started at no more than 50% of energy requirements in “patients who have eaten little or nothing for more than 5 days.” The rate can then be increased if no refeeding problems are detected on clinical and biochemical monitoring ¹⁸.

For patients at high risk of developing refeeding syndrome, nutritional repletion of energy should be started slowly (maximum 0.042 MJ/kg/24 hours) and should be tailored to each patient. It can then be increased to meet or exceed full needs over four to seven days. In patients who are very malnourished (body mass index ≤14 or a negligible intake for two weeks or more), the National Institute for Health and Clinical Excellence (NICE) guidelines recommend that refeeding should start at a maximum of 0.021 MJ/kg/24 hours, with cardiac monitoring owing to the risk of cardiac arrhythmias ¹⁸. This explicit specification of the rate of refeeding in severely malnourished patients should help avoid complications arising from rapid refeeding and is an improvement on previous guidelines ¹⁹. The NICE guidelines also state that correcting electrolyte and fluid imbalances before feeding is not necessary and that this should be done along with feeding. This is a change from previous guidelines4 and potentially avoids prolongation of malnourishment and its effects on patients.

All guidelines recommend that vitamin supplementation should be started immediately, before and for the first 10 days of refeeding. Circulatory volume should also be restored. Oral, enteral, or intravenous supplements of the potassium, phosphate, calcium, and magnesium should be given unless blood levels are high before refeeding. Good quality studies on the exact levels of supplementation are lacking, however, and so the required levels of these supplements cited by NICE ¹⁸.

Electrolyte levels should be measured once daily for one week, and at least three times in the following week. Urinary electrolytes could also be checked to help assess body losses and to guide replacement.

Table 1 Protocol for nutritional, anthropometric and clinical monitoring of nutrition support

Parameter	Frequency	Rationale
Nutritional
Nutrient intake from oral, enteral or parenteral nutrition (including any change in conditions that are affecting food intake)	Daily initially, reducing to twice weekly when stable	To ensure that patient is receiving nutrients to meet requirements and that current method of feeding is still the most appropriate. To allow alteration of intake as indicated
Actual volume of feed delivered*	Daily initially, reducing to twice weekly when stable	To ensure that patient is receiving correct volume of feed. To allow troubleshooting
Fluid balance charts (enteral and parenteral)	Daily initially, reducing to twice weekly when stable	To ensure patient is not becoming over/under hydrated
Anthropometric
Weight*	Daily if concerns regarding fluid balance, otherwise weekly reducing to monthly	To assess ongoing nutritional status, determine whether nutritional goals are being achieved and take into account both body fat and muscle
BMI*	Start of feeding and then monthly
Mid-arm circumference*	Monthly, if weight cannot be obtained or is difficult to interpret
Triceps skinfold thickness	Monthly, if weight cannot be obtained or is difficult to interpret
GI function
Nausea/vomiting*	Daily initially, reducing to twice weekly	To ensure tolerance of feed
Diarrhoea*	Daily initially, reducing to twice weekly	To rule out any other causes of diarrhoea and then assess tolerance of feeds
Constipation*	Daily initially, reducing to twice weekly	To rule out other causes of constipation and then assess tolerance of feeds
Abdominal distension	As necessary	Assess tolerance of feed
Enteral tube – nasally inserted
Gastric tube position (pH less than or equal to 5.5 using pH paper – or noting position of markers on tube once initial position has been confirmed)	Before each feed begins	To ensure tube in correct position
Nasal erosion	Daily	To ensure tolerance of tube
Fixation (is it secure?)	Daily	To help prevent tube becoming dislodged
Is tube in working order (all pieces intact, tube not blocked/kinked)?	Daily	To ensure tube is in working order
Gastrostomy or jejunostomy
Stoma site	Daily	To ensure site not infected/red, no signs of gastric leakage
Tube position (length at external fixation)	Daily	To ensure tube has not migrated from/into stomach and external over granulation
Tube insertion and rotation (gastrostomy without jejunal extension only)	Weekly	Prevent internal overgranulation/prevention of buried bumper syndrome
Balloon water volume (balloon retained gastrostomies only)	Weekly	To prevent tube falling out
Jejunostomy tube position by noting position of external markers	Daily	Confirmation of position
Parenteral nutrition
Catheter entry site*	Daily	Signs of infection/inflammation
Skin over position of catheter tip (peripherally fed people)*	Daily	Signs of thrombophlebitis
Clinical condition
General condition*	Daily	To ensure that patient is tolerating feed and that feeding and route continue to be appropriate
Temperature/blood pressure	Daily initially, then as needed	Sign of infection/fluid balance
Drug therapy*	Daily initially, reducing to monthly when stable	Appropriate preparation of drug (to reduce incidence of tube blockage). To prevent/reduce drug nutrient interactions
Long-/short-term goals
Are goals being met?*	Daily initially, reducing to twice weekly and then progressively to 3–6 monthly, unless clinical condition changes	To ensure that feeding is appropriate to overall care of patient
Are goals still appropriate?*	Daily initially, reducing to twice weekly and then progressively to 3–6 monthly, unless clinical condition changes	To ensure that feeding is appropriate to overall care of patient
People at home having parenteral nutrition should be monitored using observations marked *.

[Source ¹⁸ ]

Table 2 Protocol for laboratory monitoring of nutrition support

Parameter	Frequency	Rationale	Interpretation
Sodium, potassium, urea, creatinine	Baseline Daily until stable Then 1 or 2 times a week	Assessment of renal function, fluid status, and Na and K status	Interpret with knowledge of fluid balance and medication Urinary sodium may be helpful in complex cases with gastrointestinal fluid loss
Glucose	Baseline 1 or 2 times a day (or more if needed) until stable Then weekly	Glucose intolerance is common	Good glycaemic control is necessary
Magnesium, phosphate	Baseline Daily if risk of refeeding syndrome Three times a week until stable Then weekly	Depletion is common and under recognised	Low concentrations indicate poor status
Liver function tests including International Normalised Ratio (INR)	Baseline Twice weekly until stable Then weekly	Abnormalities common during parenteral nutrition	Complex. May be due to sepsis, other disease or nutritional intake
Calcium, albumin	Baseline Then weekly	Hypocalcaemia or hypercalcaemia may occur	Correct measured serum calcium concentration for albumin Hypocalcaemia may be secondary to Mg deficiency Low albumin reflects disease not protein status
C-reactive protein	Baseline Then 2 or 3 times a week until stable	Assists interpretation of protein, trace element and vitamin results	To assess the presence of an acute phase reaction (APR). The trend of results is important
Zinc, copper	Baseline Then every 2–4 weeks, depending on results	Deficiency common, especially when increased losses	People most at risk when anabolic APR causes Zn decrease and Cu increase
Seleniuma	Baseline if risk of depletion Further testing dependent on baseline	Se deficiency likely in severe illness and sepsis, or long-term nutrition support	APR causes Se decrease Long-term status better assessed by glutathione peroxidase
Full blood count and MCV	Baseline 1 or 2 times a week until stable Then weekly	Anaemia due to iron or folate deficiency is common	Effects of sepsis may be important
Iron, ferritin	Baseline Then every 3–6 months	Iron deficiency common in long-term parenteral nutrition	Iron status difficult if APR (Fe decrease, ferritin increase)
Folate, B12	Baseline Then every 2–4 weeks	Iron deficiency is common	Serum folate/B12 sufficient, with full blood count
Manganeseb	Every 3–6 months if on home parenteral nutrition	Excess provision to be avoided, more likely if liver disease	Red blood cell or whole blood better measure of excess than plasma
25-OH Vit Db	6 monthly if on long-term support	Low if housebound	Requires normal kidney function for effect
Bone densitometryb	On starting home parenteral nutrition Then every 2 years	Metabolic bone disease diagnosis	Together with lab tests for metabolic bone disease
a These tests are needed primarily for people having parenteral nutrition in the community. b These tests are rarely needed for people having enteral tube feeding (in hospital or in the community), unless there is cause for concern.

[Source ¹⁸ ]

Refeeding syndrome signs and symptoms

Refeeding syndrome symptoms include:

• development of edema,
• increased liver function tests,
• hypophosphatemia,
• cardiac failure,
• central nervous system depression.

Refeeding syndrome diagnosis

Refeeding syndrome is detected by considering the possibility of its existence and by using the simple biochemical investigations described above. If refeeding syndrome is detected, the rate of feeding should be slowed down and essential electrolytes should be replenished. The hospital specialist dietetics team should be involved.

Refeeding syndrome treatment

The best method for electrolyte repletion has not yet been determined. Hypophosphatemia, hypomagnesemia, and hypokalemia in hospitalized patients are ideally treated with intravenous supplementation (Table​ 3), but this is not without risks. A prospective comparative cohort study of 27 patients with severe hypophosphatemia showed the safety of administering 15-30 mmol phosphate over three hours via a central venous catheter in an intensive care unit ²⁰. However, the researchers reported the need for repeated doses in most patients. Terlevich et al ²¹ reported efficacy of 50 mmol phosphate infused into a peripheral vein over 24 hours in 30 patients with no pre-existing renal dysfunction on general wards. Further infusions may be required and so careful monitoring of blood levels is required. Caution is needed in patients with existing renal impairment, hypocalcemia (which may worsen), or hypercalcemia (which may result in metastatic calcification).

Fluid repletion should be carefully controlled to avoid fluid overload as described earlier. Sodium administration should be limited to the replacement of losses. In patients at high risk of cardiac decompensation, central venous pressure and cardiac rhythm monitoring should be considered.

Table 3. Recommendation for phosphate and magnesium supplementation

Mineral	Dose
Phosphate
Maintenance requirement	0.3-0.6 mmol/kg/day orally
Mild hypophosphataemia (0.6-0.85 mmol/l)	0.3-0.6 mmol/kg/day orally
Moderate hypophosphataemia (0.3-0.6 mmol/l)	9 mmol infused into peripheral vein over 12 hours
Severe hypophosphataemia (<0.3 mmol/l)	18 mmol infused into peripheral vein over 12 hours
Magnesium
Maintenance requirement	0.2 mmol/kg/day intravenously (or 0.4 mmol/kg/day orally )
Mild to moderate hypomagnesaemia (0.5-0.7 mmol/l)	Initially 0.5 mmol/kg/day over 24 hours intravenously, then 0.25 mmol/kg/day for 5 days intravenously
Severe hypomagnesaemia (<0.5 mmol/l)	24 mmol over 6 hours intravenously, then as for mild to moderate hypomagnesaemia (above)

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