Year : 2016 | Volume
: 17 | Issue : 2 | Page : 19--24
Re-feeding syndrome - A case report
Sumathy Jayaraman1, Jasmin Anand2, Vimala Selvaraj3,
1 Reader, College of Nursing, CMC, Vellore, India
2 Professor, College of Nursing, CMC, Vellore, India
3 Charge Nurse, CMC, Vellore, India
Re-feeding syndrome is a metabolic complication that can occur when enteral or parenteral nutritional rehabilitation is initiated for severely malnourished patients.It is fatal if not recognized and treated properly. This article discusses the body’s adaptation to starvation, the pathophysiology, risk factors of re- feeding syndrome, adverse consequences which can occur in the early stages of re-feeding, and its management. It focuses on challenges faced in caring for patient during re-feeding. Starvation causes adaptive reductions in cellular activity and organ function, accompanied by electrolyte and micronutrient depletion. During starvation insulin decreases and glucagon levels rise, resulting in gluconeogenesis and the breakdown of protein and lipid. Free fatty acids and ketone bodies replace glucose as the major energy source. When nutritional rehabilitation is started the re-feeding triggers a shift from fat back to carbohydrate metabolism, with consequent insulin release, and increased shift of potassium, phosphate, magnesium, and water into the cells. In a starved individual, cardiac mass may be significantly depleted, leading to the risk of fluid overload and cardiac failure during re-feeding. Nurses play a significant role in identification and prevention of re-feeding complications.
|How to cite this article:|
Jayaraman S, Anand J, Selvaraj V. Re-feeding syndrome - A case report.Indian J Cont Nsg Edn 2016;17:19-24
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Jayaraman S, Anand J, Selvaraj V. Re-feeding syndrome - A case report. Indian J Cont Nsg Edn [serial online] 2016 [cited 2021 Jun 23 ];17:19-24
Available from: https://www.ijcne.org/text.asp?2016/17/2/19/286294
The re-feeding syndrome is defined as the clinical complications that occur as a result of fluid and electrolyte shifts during nutritional rehabilitation (enteral orparenteral) of malnourished patients. These shifts result from hormonal and metabolic changes and may cause serious clinical complications. The hallmark biochemical feature of re- feeding syndrome is hypophosphataemia. However, the syndrome is complex and may also feature abnormal sodium and fluid balance, changes in glucose, protein, and fat metabolism, hypokalemia, and hypomagnesaemia. Refeeding also causes acute thiamine deficiency resulting in Wernicke’s encephalopathy and Korsakoff’s syndrome (Raoof, George, Saleh, & Sung, 2008).
The National Institute for Health and Care Excellence (NICE) (2006) has delineated the criteria for identifying patients at high risk of re-feeding syndrome. According to NICE a patient is at risk if he/she has one or more of the following:
- Body mass index (kg/m2) <16
- Unintentional weight loss > 15% in the past three to six months
- Little or no nutritional intake for > 10 days
- Low levels of serum potassium, phosphate, oi magnesium levels before feeding is initiated Or the patient has two or more of the following:
- Body mass index < 18.5
- Unintentional weight loss >10% in the past three to six months
- Little or no nutritional intake for > 5 days
- History of alcohol misuse or intake of drugs, such as insulin, chemotherapy, antacids, or diuretics
Effects of starvation
As a result of metabolic and hormonal changes in early starvation the body switches from using carbohydrate to fat and protein as the main source of energy, and the basal metabolic rate decreases by as much as 20-25% (Podolsky et al.,2016).
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 of serum ketone bodies, stimulating the brain to use ketone bodies as its main energy source instead of glucose. 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 (Feldman, Friedman & Brandt, 2016).
Causes of Re-feeding Syndrome
Re-feeding syndrome can develop if food is reintroduced too rapidly after a period of starvation or minimal oral intake. The underlying causative factor of re- feeding syndrome is the metabolic and hormonal changes caused by rapid re-feeding, whether enteral or parenteral. Extreme care should be taken during initiation of nutritional support. Micronutrient deficiencies and fluid and electrolyte shift occur if feed is initiated, given too quickly or unbalanced (Norton, Taylor, & Nunwa, 2008).
The risk of developing the re-feeding syndrome is directly related to the amount of weight loss during the current episode and the rapidity of the weight restoration process. Patients who weigh less than 70% of ideal body weight or lose weight rapidly are at greatest risk for the syndrome. Thus, patients who weigh less than 70% of their ideal body weight, or have a body mass index 16 or below, require hospitalization for the initial stage of nutritional replenishment. Patients are at the highest risk for the re- feeding syndrome in the first two weeks of nutritional replenishment and weight gain. The risk progressively dissipates over the next few weeks (Podolsky et al., 2016).
Effects of re-feeding on minerals and electrolytes
Phosphorus which is predominantly an intracellular mineral 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 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 (Feldman et al., 2016).
In re-feeding 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 affecting the cellular processes of every physiological system (Feldman et al., 2016).
Potassium, the major intracellular cation, is also depleted in undernutrition. Serum concentration may remain normal during starvation, but with the change to anabolism on re-feeding, potassium is taken up into cells as they increase in volume and as a direct result of insulin secretion. This results in severe hypokalemia. This causes derangements in the electrochemical membrane potential, resulting in arrhythmias and cardiac arrest (Feldman et al., 2016).
Magnesium, predominantly an 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 its deficiency can lead to cardiac dysfunction and neuromuscular complications (Feldman et al., 2016).
Glucose intake after a period of starvation suppresses gluconeogenesis through the release of insulin. Excessive administration may therefore lead to hyperglycaemia, 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 (Mehanna, Moledina, & Travis, 2008).
Although all vitamin deficiencies may occur at variable rates with inadequate nutrition intake, thiamine is of most importance in complications of re-feeding. Thiamine is an essential coenzyme in carbohydrate metabolism. Its deficiency results in Wernicke’s encephalopathy (ocular abnormalities, ataxia, confusional state, hypothermia, coma) or Korsakoff’s syndrome (Podolsky et al., 2016).
Changes in carbohydrate metabolism have a profound effect on sodium and water balance. The introduction of carbohydrate in a diet leads to a rapid decrease in renal excretion of sodium and water. 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 oedema, and cardiac arrhythmia (Feldman etal., 2016).
During re-feeding, glycaemia leads to increased insulin and decreased secretion of glucagon. 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 re-feeding syndrome occur as a result of the functional deficits of these electrolytes and the rapid change in basal metabolic rate (Feldman et al., 2016).
Manifestations of Re-feeding Syndrome
Atrophy of the heart during starvation renders the patient more vulnerable to fluid overload and heart failure when re-feeding is started. Sodium and fluid retention can also increase circulatory volume and lead to volume overload in patients with cardiac atrophy. Thiamine (Vitamin Bl) deficiency may also contribute to heart failure (Mehanna et al., 2008). Most fatalities that occur because of the re-feeding syndrome is due to cardiac complications, including impaired contractility, decreased stroke volume, heart failure, and arrhythmias.
Impaired diaphragmatic contractility due to overall weakness or due to hypophosphatemia may occur, leading to dyspnea and impaired respiratory function (Mehler, 2016). Impaired muscular contractility, weakness, myalgia, and tetany may occur. Hypophosphatemia may also cause rhabdomyolysis, which is manifested by an abnormally high Creatine Kinase (CK) (Mehler, 2016).
Liver function tests including aspartate aminotransferase (AST) and alanine aminotransferase (ALT) may be elevated. Diarrhea may occur, due to atrophy of the intestinal mucosa and pancreatic impairment. The diarrhea generally resolves within the first few weeks of refeeding as the villous surface is reconstituted. Nausea and vomiting may also arise. These symptoms may require decreasing the rate of refeeding or temporarily terminating the re-feeding process (Mehler, 2016). Patients may develop tremors, paresthesias, delirium, and seizures as a result of electrolyte abnormalities during the early stages of re-feeding (Mehler, 2016).
Prevention and Management
The re-feeding syndrome can have fatal effects on a patient on nutritional rehabilitation. It 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 monitoring the patient clinically and biochemically during the re-feeding process. Complications of the syndrome may be reduced by slowing the rate of nutritional support; proactively correcting electrolyte abnormalities especially phosphorous levels and monitoring for and treating cardiovascular and pulmonary complications (Mehanna et al., 2008).
Mr. S, 47 yr old male was admitted for initiation of enteral feeds under supervision. He had a history of decreased food intake for three years following death of his mother. He was evaluated for organic causes of weight loss and was admitted for feeding under supervision. He weighed 38 kg, height was 180cm, and BMI was 11.7. His serum electrolytes, phosphorus, calcium and magnesium levels were checked and were found to be within normal ranges. He also had normal ECG findings on admission. He was initially started on a low calorie diet via nasogastric tube based on his weight. He was started with 10 kcal/kg/day at 400 kcal with 40 gm protein and a restricted fluid intake of 600 ml/day. He was monitored continuously to identify for re-feeding complications. He was on continous cardiac monitoring. Inj. Thiamine 100 mg was given thrice daily (tds) for 3 days and then was switched to 100 mg tds orally for 7 days. Sodium, potassium, magnesium, calcium, phosphorus and serum creatinine were monitored daily to identify potential imbalances. Liver function test, triglycerides, C reactive protein (CRP), and total blood count was monitored once weekly. He had tachycardia and diarrhea and was complaining of abdominal pain following the initiation of NG feeds. His serum phosphorus dropped to 2.4 mg% initially but after supplementation increased to 4.3 mg%. He gradually started tolerating optimum calories for his weight.
After 18 days of re-feeding he was started on oral feeds with 1200 kcal/day. He was referred to a Psychiatrist to rule out psychological causes for poor feeding and was started on Tab. Amitryptiline. He gradually started tolerating optimum calories for his weight and height. He had complaints of persistent pain in throat and while swallowing which interfered with his feeding for which he was referred to an ENT surgeon. Nasopharyngolaryngoscopy revealed left vocal cord palsy. He was advised to have speech and swallow therapy. He underwent barium swallow which did not reveal any significant abnormality. He also underwent esophageal manometery to rule out cricopharyngeal achalasia and results showed mild oesophageal gastric junction outflow obstruction. As it was very mild no specific treatment was suggested. He was discharged with advice to continue high protein, high calorie diet with vitamin supplements and was asked to come for review after four months.
Caring for Mr. S was challenging. Imbalanced nutrition, electrolyte imbalance and risk for cardiac and aspiration related complications were the main problems that were identified. The nursing care is discussed in detail (Doenges, Moorhouse & Murr, 2014; Gulanick & Myers, 2014)
1. Nursing Diagnosis: Imbalanced nutrition less than body requirement related to unwillingness to eat
Expected outcome: Optimal nutritional status is maintained as evidenced by verbalization and demonstration of interest in selection of food and tolerance of prescribed diet.
Nursing interventions: Mr. S was started on minimum calorie intake to avoid re-feeding complications. He was started on half the normal calorie requirement which is 10-15 kcal/day. As he weighed 38 kg he was started on low calorie diet of 400 kcal/day and 40 gm protein through nasogastric tube. He was continuously monitored for arrhythmias and fluid overload. He was observed for abdominal distension, diarrhoea, and bradycardia which are potential immediate complications of re-feeding. He tolerated feeding but complained of abdominal pain few hours following nasogastric feeding. So continous feeding was stopped and more time gap was given between feeds as per his tolerance. Calories were supplemented by intravenous (IV) 5% Dextrose Normal Saline. Mineral and vitamin supplements were added to the IV fluids. Due to discomfort following enteral feeding he refused feeds.
Continous encouragement and consistent approach of all team members helped him to progress in increasing his tolerance to prescribed calorie intake. After four days of monitoring he was started on small frequent nutritionally intense feeds through nasogastric tube. Oral feeds also were initiated as tolerated. Food items were selected based on his likes. Dietician helped the relative to plan a menu based on his preferences, which he could follow at home. His weight was checked daily. He was encouraged to take small frequent oral feeds to increase his weight. His hemoglobin, serum protein and albumin levels were monitored regularly which remained normal.
Evaluation: Nutritional intake improved over 18days.He reached optimum calories for his weight which is 30kcal/kg. His intake was 1200 kcal orally on discharge from ward. After initial weight loss of one kg he regained his weight and was 39 kg during discharge from ward.
2.Nursing Diagnosis: Risk for unstable blood glucose level related to excess insulin secretion secondary to excessive calorie intake
Expected outcome: Blood glucose levels are maintained within normal range.
Nursing Interventions: After initiating the feeding Mr. S’ random blood sugar was checked using glucometer thrice daily to monitor for hyperglycemia as a result of gluconeogenesis and lipogenesis which are complications of re-feeding. His calorie intake was increased from 400 kcal to 1200 kcal over a period of 18 days. His total calorie intake was distributed with 50-60% complex sugars, 20-30% protein, and 20-30% fat. Simple carbohydrates like sugar and fruit juices were avoided to prevent increased insulin secretion.
Evaluation: Blood glucose level was maintained within the normal range.
3.Nursing Diagnosis: Risk for electrolyte imbalance related to insulin secretion secondary to re-feeding
Expected outcome: Normal serum electrolyte balance is maintained as evidenced by lab results.
Nursing interventions: Mr. S’ serum potassium, magnesium, calcium, phosphorus, and sodium were monitored daily to identify potential electrolyte imbalances. As insulin secretion in response to re-feeding can cause faster uptake of serum potassium into the cells, potassium correction was given before starting feeds to prevent hypokalemia. In addition, the insulin surge following re-feeding can significantly influence serum phosphorus and magnesium levels. His insulin response therefore, was monitored by checking his random blood sugar thrice daily. A strict intake and output record was maintained to monitor for fluid imbalances which can further lead to imbalance in electrolytes. Continuous cardiac monitoring was done to check for arrhythmias related to altered potassium and magnesium levels in blood. Administered electrolyte replacements when needed based on lab values.
Evaluation: Electrolyte levels were within normal ranges as evidenced by lab values of potassium 4mmol/L, sodium 137mmol/L and phosphorus 4.3mg%.
4.Nursing Diagnosis: Risk for decreased cardiac output related to alteration in heart rate, rhythm, and conduction, cardiac muscle weakness secondary to electrolytes depletion due to re-feeding
Expected outcome: Cardiac output is maintained as evidenced by normal heart rate, rhythm, and conduction, and absence of electrolyte depletion.
Nursing Interventions: Mr. S was on continuous monitoring for heart rate, rhythm and cardiac conduction. His serum sodium, potassium, calcium, magnesium and phosphorus were checked daily. He was on fluid restriction of600 ml /day to avoid heart failure and fluid overload due to cardiac muscle atropy following malnutrition. His fluid intake was increased upto to 30ml/kg (1200ml/day). He was on intravenous fluid administration for calorie replacement as well for electrolyte replacement. As he tolerated oral feeds, intravenous fluid replacement was stopped. He was monitored for arrhythmias and signs of low cardiac output. The fluid intake and the total output was recorded accurately.
Evaluation: Cardiac output was normal as evidenced by absence of arrhythmias, normal serum calcium, magnesium, phosphorus, sodium, and potassium levels.
5.Nursing Diagnosis : Risk for aspiration related to impaired swallowing and tube feeding secondary to vocal cord palsy
Expected outcome: Patent airway is maintained as evidenced by normal breath sounds, absence of coughing, choking, and no aspiration following oral intake of food.
Nursing Interventions: Mr. S was started on nutritional rehabilitation by nasogastric tube feeding. He was not willing to eat food orally as he complained of persistant throat pain and incidents of aspiration with fluids. He was started with 400 kcal initially till he could tolerate 1200 kcal by nasogastric tube feeds. He was assessed for complaints of difficulty in swallowing. He underwent barium swallow and esophageal manometry and results did not reveal any significant abnormality. Hence he was encouraged to drink 50 ml of clear fluids orally every hour along with NG feeds to improve swallowing. The consistency of food was such that he could swallow without any problem. Thereafter he was encouraged to chew and eat slowly under supervision. As he swallowed solid food without any problem, liquids were given under supervision to prevent aspiration. He was given swallow therapy by speech therapist to enhance his confidence. He was encouraged to assume high Fowlers position when feeding and to continue to sit in semi-Fowler’s position for 30 to 45 min after feeding to prevent aspiration.
Evaluation: Maintained patent airway as evidenced by absence of aspiration. His swallowing improved considerably with regular small feeds and he was completely on oral feeds at the time of discharge.
6. Nursing Diagnosis: Activity intolerance related to generalized weakness, de-conditioned state secondary to refeeding syndrome
Expected outcome: Tolerance of physical activity as evidenced by performing activities of daily living with heart rate less than 120/minute.
Nursing interventions: Mr. S was thin built with BMI of 11.7. He complained of generalized weakness and calf muscle pain on walking and had been limited in his activities prior to admission. Serum calcium, phosphorus, and potassium were replaced as per requirement. He was encouraged to take adequate rest between activities to prevent energy exhaustion to avoid muscle fatigue due to influx of calcium. Activities of daily living were planned with his input as well as his relative’s assistance. The activities were increased gradually. He was encouraged to do deep breathing exercises to improve lung capacity. He was taught about energy conservation technique to prevent fatigue. During periods of inactivity he was encouraged to do range of motion exercises.
Evaluation: He demonstrated ability to perform his activities of daily living with minimal assistance.
Caring for a patient who is severely malnourished and admitted for ensuring safe re-feeding is highly challenging for nurses and health team members. It is a fearful and traumatic experience for patient and their relatives. The health care team should be aware of re-feeding syndrome and formulate clinical pathways for early identification and treatment. Any patient admitted in the hospital, attending an outpatient clinic, or in community setting should be screened for the risk of malnutrition. Routine nutritional screening should include screening for the risk of re-feeding syndrome also. Screening on patient’s admission to acute care will result in early identification of patients at risk of re-feeding syndrome, enabling the immediate implementation of a re-feeding syndrome protocol, and effective nutritional interventions. An integrated approach to the prevention and treatment of re- feeding syndrome is fundamental to the delivery of high quality care to at-risk individuals. This in turn will improve the effectiveness, safety, and care of people at risk for re- feeding syndrome.
Conflicts of Interest: The authors have declared no conflicts of interest.
|1||Doenges, M. E., Moorhouse, M. E, & Murr, A. C. (2014). Nursing care plans: Guidelines for individualizing client care across the life span. Philadelphia: FA Davis Company.|
|2||Feldman, M., Friedman, L. S., & Brandt, L. J. (2016). Sleisenger and Fordtran’s gastrointestinal and liver disease: Pathophysiology, diagnosis, management, expert consult premium edition-enhanced online features (Vol. 1). Philadelphia: Elsevier Health Sciences.|
|3||Gulanick, M., & Myers, J. L. (2014). Nursing care plans: Diagnoses, interventions, and outcomes. Philadelphia: Elsevier Health Sciences.|
|4||Mehanna, H. M., Moledina, J., & Travis, J. (2008). Refeeding syndrome: What it is, and how to prevent and treat it. British Medical Journal, 335(7659), 1495-1498.|
|5||Mehler, P. (2016) Anorexia nervosa in adults and adolescents, Refeeding syndrome. Retrieved from www.uptodate.com|
|6||National Institute of Health and Care Excellence. (2006). Nutrition support for adults: Oral nutrition support, enteral tube feeding, and parenteral nutrition, retrieved from https://www.nice.org.uk/guidance/cg32|
|7||Norton, C., Taylor, C., & Nunwa, A. (2008). Oxford handbook of gastrointestinal nursing. USA: Oxford University Press.|
|8||Podolsky, K. D., Camilleri, M., Fitz, J.G, Kalloo, N.A., Shanahan, F., & Wang, C. T. (2016). Yamada’s Textbook of gastro enterology (6th ed.). USA: Wiley Blackwell Publishing.|
|9||Raoof, S., George, L., Saleh, A., & Sung, A. (2008). ACP Manual of Critical Care. McGraw-Hill Professional.|