Medical Nutrition Therapy for Refeeding Syndrome Rachel Hammerling

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Medical Nutrition Therapy for Refeeding Syndrome Rachel Hammerling Concordia College, Moorhead MN

Medical Nutrition Therapy for Refeeding Syndrome Rachel Hammerling Concordia College, Moorhead MN

Objectives • Be able to describe refeeding syndrome (RFS) • Be able to describe

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

Discovery of RFS • Observed & described after WWII • Victims of starvation experienced

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 1 st week – Neurologic signs & symptoms develop later

What is RFS? • Potentially fatal shifts in fluids & electrolytes • May occur

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

Understanding Starvation • Glucose = main fuel – Shifts to protein & fat •

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

How common is RFS? • True incidence is unknown • Study of 10, 197

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

Pathogenesis • Electrolytes & minerals involved 1) 2) 3) 4) Phosphorus Potassium Magnesium Glucose

Pathogenesis • Electrolytes & minerals involved 1) 2) 3) 4) Phosphorus Potassium Magnesium Glucose

Main Pathophysiologic Features • • • Disturbances of body-fluid distribution Abnormal glucose & lipid

Main Pathophysiologic Features • • • Disturbances of body-fluid distribution Abnormal glucose & lipid metabolisms Thiamine deficiency Hypophosphatemia Hypomagnesemia Hypokalemia

Disturbances of Body-Fluid Distribution • Can influence body functions: • CHO refeeding – ↓

Disturbances of Body-Fluid Distribution • Can influence body functions: • CHO refeeding – ↓ water & sodium excretion, resulting in weight gain 1) Cardiac failure 2) Dehydration or • Protein & fat refeeding fluid overload – Result in weight loss & 3) Hypotension urinary sodium excretion 4) Pre-renal failure – Hypernatremia along 5) Sudden death with azotemia & metabolic acidosis

Abnormal Glucose & Lipid Metabolisms • Glucose – Suppress gluconeogenesis → reduced AA usage

Abnormal Glucose & Lipid Metabolisms • Glucose – Suppress gluconeogenesis → reduced AA usage • Less-negative N balance – Hyperglycemia • Glucose → fat (Lipogenesis) – Hypertriglyceridemia, fatty liver, & abnormal liver function tests

Thiamine Deficiency • Can result in Wernicke’s encephalopathy or Korsakov’s syndrome, associated with: –

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

Hypophosphatemia • Predominant feature of RFS • Impaired cellular-energy pathways – Adenosine triphosphate –

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

Hypomagnesemia • Most cases not clinically significant • Severe cases: – Cardiac arrhythmias –

Hypomagnesemia • Most cases not clinically significant • Severe cases: – Cardiac arrhythmias – Abdominal discomfort – Anorexia – Tremors, seizures, & confusion – Weakness

Hypokalemia • Features are numerous: – Cardiac arrhythmias – Hypotension – Cardiac arrest –

Hypokalemia • Features are numerous: – Cardiac arrhythmias – Hypotension – Cardiac arrest – Weakness – Paralysis – Confusion – Respiratory Depression

Signs & Symptoms • Electrolyte imbalance – Hypokalemia – Hypophosphatemia – Hypomagnesemia • REMEMBER:

Signs & Symptoms • Electrolyte imbalance – Hypokalemia – Hypophosphatemia – Hypomagnesemia • REMEMBER: Even an overweight or obese patient can be malnourished & a victim for RFS

Identifying Patients at High Risk of Refeeding Problems • NICE Guidelines (National Institute for

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

Patients at high risk: • • Anorexia nervosa Chronic alcoholism Oncology patients Postoperative patients

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

Gastrointestinal Fistula patients • Usually reveals chronic malnutrition – Due to damaged Gl tract

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

Intervention: Objectives 1) Gradually correct starvation – Use less than full levels of calorie

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

Intervention: Objectives Cont. 4) Nutrition support in patients at risk should be increased slowly

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 1 st week & less frequently after

Intervention: Objectives Cont. 6) Monitor for neurological, hematological, & metabolic complications – Of hypokalemia,

Intervention: Objectives Cont. 6) Monitor for neurological, hematological, & metabolic complications – Of hypokalemia, hypophosphatemia, & hyperglycemia 7) Prevent sudden death

Intervention: Food & Nutrition • • Begin 20 kcal/kg for 1 st 3 days

Intervention: Food & Nutrition • • Begin 20 kcal/kg for 1 st 3 days Progress to 25 kcal/kg Gradually ↑ by 7 th day Protein start slow, ↑ gradually – To protect & restore lean body mass • Restrict CHO to 150 -200 g/day – To prevent rapid insulin surge • CHO in PN – Initiate at 2 mg/kg/min – Fat calories should make up the difference

Intervention: Food & Nutrition • Maintain fluid balance – Adjust when edema exists •

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

Common Drugs Used • Replacement of phosphorus, potassium, & magnesium • Insulin – Used

Common Drugs Used • Replacement of phosphorus, potassium, & magnesium • Insulin – Used to correct hyperglycemia levels – Monitor blood glucose levels during refeeding

Recommendation for Phosphate Dose Maintenance requirement 0. 3 -0. 6 mmol/kg/day orally Mild hypophosphatemia

Recommendation for Phosphate Dose Maintenance requirement 0. 3 -0. 6 mmol/kg/day orally Mild hypophosphatemia (0. 6 -0. 85 mmol/l) 0. 3 -0. 6 mmol/kg/day orally Moderate hypophosphatemia (0. 3 -0. 6 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

Recommendation for Magnesium Dose Maintenance requirement 0. 2 mmol/kg/day intravenously (or 0. 4 mmol/kg/day

Recommendation for Magnesium Dose Maintenance requirement 0. 2 mmol/kg/day intravenously (or 0. 4 mmol/kg/day orally ) Mild to moderate hypomagnesaemia Initially 0. 5 mmol/kg/day over 24 (0. 5 -0. 7 mmol/l) 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)

Intervention: Nutrition Education, Counseling, & Care Management • Focus on adequate nutrient intake •

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

NICE Guidelines for Management

NICE Guidelines for Management

Ethical Issues with RFS • Roles between dietitian, counselor, nurse, doctor, and other professionals

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

Summary Points • RFS is caused by rapid refeeding after a period of undernutrition

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

References Crook, M. A. , Hally, V. , & Panteli, J. V. (2001). The

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), 632 -637. De Silva, A. , Smith, T. , & Stroud, M. (2008). Attitudes to NICE guidance on refeeding syndrome. BMJ (Clinical Research Ed. ), 337, a 680. Escott-Stump, S. (2008). Nutrition and diagnosis-related care: sixth ed. (Baltimore, Maryland), 578580. Fan, C. , Li, J. (2003). Refeeding syndrome in patients with gastrointestinal fistula. Nutrition (Burbank, Los Angeles County, Calif. ), 24(6), 604 -606. Gariballa, S. (2008). Refeeding syndrome: A potentially fatal condition but remains underdiagnosed and undertreated. Nutrition, 24(6), 604 -606. Khardori, R. (2005). Refeeding syndrome and hypophosphatemia. Journal of Intensive Care Medicine, 20(3), 174 -175. 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), 1495 -1498. Nelms, M. , Sucher, K. , & Long, S. (2007). Nutrition therapy and pathophysiology (Belmont, Calif. ). 166 -167, 194 -195. Walker, R. (2006). Alcohol and the liver. Sports Line, 28(6), 21 -22. Yantis, M. A. , & Velander, R. (2008). How to recognize and respond to refeeding syndrome. Nursing, 38(5).