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Published byLynette Maxwell Modified over 9 years ago
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Medical Nutrition Therapy for Refeeding Syndrome
Rachel Hammerling Concordia College, Moorhead MN
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Objectives Be able to describe refeeding syndrome (RFS)
Be able to describe the pathophysiology of starvation Identify the main pathophysiologic features of RFS Be able to identify signs & symptoms Identify recommended treatment & standards of care Be able to explain ethical issues involved with treatment & care
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Discovery of RFS Observed & described after WWII
Victims of starvation experienced cardiac and/or neurologic dysfunction After being reintroduced to food Today, rarely see patients who are severely malnourished, as WWII victims were, in the 1st week Neurologic signs & symptoms develop later
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What is RFS? Potentially fatal shifts in fluids & electrolytes
May occur in malnourished patients receiving artificial refeeding Enterally or parenterally Complex syndrome Sodium & fluid imbalance Changes in glucose, protein, fat metabolism Thiamine deficiency Hypokalemia Hypomagnesaemia
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Understanding Starvation
Glucose = main fuel Shifts to protein & fat Insulin ↓ due to ↓ availability of glucose Catabolism of protein → loss of cellular & muscle mass → atrophy of vital organs & internal organs Respiratory & cardiac function ↓ due to muscular wasting & fluid/electrolyte imbalances Body is now surviving by slowly consuming itself
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How common is RFS? True incidence is unknown
Study of 10,197 patients, incidence of hypophosphatemia = 43 % Malnutrition one of strongest risk factors Parenteral patients = 100% incidence of hypophosphatemia
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Pathogenesis Electrolytes & minerals involved Phosphorus Potassium
Magnesium Glucose
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Main Pathophysiologic Features
Disturbances of body-fluid distribution Abnormal glucose & lipid metabolisms Thiamine deficiency Hypophosphatemia Hypomagnesemia Hypokalemia
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Disturbances of Body-Fluid Distribution
CHO refeeding ↓ water & sodium excretion, resulting in weight gain Protein & fat refeeding Result in weight loss & urinary sodium excretion Hypernatremia along with azotemia & metabolic acidosis Can influence body functions: Cardiac failure Dehydration or fluid overload Hypotension Pre-renal failure Sudden death
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Abnormal Glucose & Lipid Metabolisms
Suppress gluconeogenesis → reduced AA usage Less-negative N balance Hyperglycemia Glucose → fat (Lipogenesis) Hypertriglyceridemia, fatty liver, & abnormal liver function tests
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Thiamine Deficiency Can result in Wernicke’s encephalopathy or Korsakov’s syndrome, associated with: Ocular disturbance Confusion Ataxia loss of ability to coordinate muscular movement Coma Short-term memory loss Confabulation Confusion of imagination with memory
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Hypophosphatemia Predominant feature of RFS
Impaired cellular-energy pathways Adenosine triphosphate 2,3-diphosphoglycerate Impaired skeletal-muscle function Including weakness & myopathy Seizures & perturbed mental state Impaired blood clotting processes & hemolysis also can occur
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Hypomagnesemia Most cases not clinically significant Severe cases:
Cardiac arrhythmias Abdominal discomfort Anorexia Tremors, seizures, & confusion Weakness
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Hypokalemia Features are numerous: Cardiac arrhythmias Hypotension
Cardiac arrest Weakness Paralysis Confusion Respiratory Depression
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Signs & Symptoms Electrolyte imbalance
Hypokalemia Hypophosphatemia Hypomagnesemia REMEMBER: Even an overweight or obese patient can be malnourished & a victim for RFS
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Identifying Patients at High Risk of Refeeding Problems
NICE Guidelines (National Institute for Health & Clinical Excellence) Either patient has 1 or more: BMI <16 Unintentional weight loss >15% in past 3-6 mo Little/no nutritional intake for 10 days Low levels of potassium, phosphate, or magnesium before feeding Or patient has 2 or more: BMI <18.5 Unintentional weight loss >10% in past 3-6 mo Little/no nutritional intake for >5 days History of alcohol misuse or drugs
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Patients at high risk: Anorexia nervosa Chronic alcoholism
Oncology patients Postoperative patients Elderly Uncontrolled diabetes mellitus Chronic malnutrition: Marasmus Prolonged fasting or low energy diet Morbid obesity with weight loss Long term antacid users Long term diuretic users
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Gastrointestinal Fistula patients
Usually reveals chronic malnutrition Due to damaged Gl tract & severe abdominal sepsis High risk for RFS Be aware of condition & treat the same Diarrhea commonly occurs & can be treated by enteral nutrition
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Intervention: Objectives
1) Gradually correct starvation Use less than full levels of calorie & fluid requirements 2) Advance calories & volume Monitor cardiac & respiratory side effects 3) Correct vitamin & mineral deficiencies Especially with symptoms
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Intervention: Objectives Cont.
4) Nutrition support in patients at risk should be increased slowly Assuring adequate amounts of vitamins & minerals 5) Organ function, fluid balance, & serum electrolytes Monitor daily during 1st week & less frequently after
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Intervention: Objectives Cont.
6) Monitor for neurological, hematological, & metabolic complications Of hypokalemia, hypophosphatemia, & hyperglycemia 7) Prevent sudden death
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Intervention: Food & Nutrition
Begin 20 kcal/kg for 1st 3 days Progress to 25 kcal/kg Gradually ↑ by 7th day Protein start slow, ↑ gradually To protect & restore lean body mass Restrict CHO to g/day To prevent rapid insulin surge CHO in PN Initiate at 2 mg/kg/min Fat calories should make up the difference
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Intervention: Food & Nutrition
Maintain fluid balance Adjust when edema exists Adjust for sodium & potassium Depending on lab values until normal Supplements Thiamin Other vitamins & minerals as needed
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Common Drugs Used Replacement of phosphorus, potassium, & magnesium
Insulin Used to correct hyperglycemia levels Monitor blood glucose levels during refeeding
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Recommendation for Phosphate
Dose Maintenance requirement mmol/kg/day orally Mild hypophosphatemia ( mmol/l) Moderate hypophosphatemia ( mmol/l) 9 mmol infused into peripheral vein over 12 hours Severe hypophosphatemia (<0.3 mmol/l) 18 mmol infused into peripheral vein over 12 hours
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Recommendation for Magnesium
Dose Maintenance requirement 0.2 mmol/kg/day intravenously (or 0.4 mmol/kg/day orally ) Mild to moderate hypomagnesaemia ( 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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Intervention: Nutrition Education, Counseling, & Care Management
Focus on adequate nutrient intake Consider referral if food insecurity is a concern Offer guidelines according to discharge intervention plan Physician may suggest long-term medication use or therapies
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NICE Guidelines for Management
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Ethical Issues with RFS
Roles between dietitian, counselor, nurse, doctor, and other professionals Working with anorexia patients, oncology patients or older patients Ethnic & religious differences Muslim patients Non-English speaking patients
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Summary Points RFS is caused by rapid refeeding after a period of undernutrition Characterized by hypophosphatemia Patients at high risk: undernourished, little or no energy intake for > 10 days Start refeeding at low levels Correction of electrolyte & fluid imbalances before feeding IS NOT necessary
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References Crook, M. A., Hally, V., & Panteli, J. V. (2001). The importance of the refeeding syndrome. Nutrition (Burbank, Los Angeles County, Calif.), 17(7-8), De Silva, A., Smith, T., & Stroud, M. (2008). Attitudes to NICE guidance on refeeding syndrome. BMJ (Clinical Research Ed.), 337, a680. Escott-Stump, S. (2008). Nutrition and diagnosis-related care: sixth ed. (Baltimore, Maryland), Fan, C., Li, J. (2003). Refeeding syndrome in patients with gastrointestinal fistula. Nutrition (Burbank, Los Angeles County, Calif.), 24(6), Gariballa, S. (2008). Refeeding syndrome: A potentially fatal condition but remains underdiagnosed and undertreated. Nutrition, 24(6), Khardori, R. (2005). Refeeding syndrome and hypophosphatemia. Journal of Intensive Care Medicine, 20(3), Mehanna, H. M., Moledina, J., & Travis, J. (2008). Refeeding syndrome: What it is, and how to prevent and treat it. BMJ (Clinical Research Ed.), 336(7659), Nelms, M., Sucher, K.,& Long, S.(2007). Nutrition therapy and pathophysiology (Belmont, Calif.) , Walker, R. (2006). Alcohol and the liver. Sports Line, 28(6), Yantis, M. A., & Velander, R. (2008). How to recognize and respond to refeeding syndrome. Nursing, 38(5).
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