medical nutrition therapy for refeeding syndrome

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Medical Nutrition Therapy for Refeeding Syndrome. Rachel Hammerling Concordia College, Moorhead MN. Objectives. Be able to describe refeeding syndrome (RFS) Be able to describe the pathophysiology of starvation Identify the main pathophysiologic features of RFS - PowerPoint PPT Presentation

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Medical Nutrition Therapy for Refeeding

Syndrome

Rachel Hammerling

Concordia College, Moorhead MN

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 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

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• 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 patients, incidence of hypophosphatemia = 43 %– Malnutrition one of strongest risk factors

• Parenteral patients = 100% incidence of hypophosphatemia

Pathogenesis

• Electrolytes & minerals involved1) Phosphorus2) Potassium3) Magnesium4) Glucose

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:1) Cardiac

failure2) Dehydration or

fluid overload3) Hypotension4) Pre-renal

failure5) Sudden death

• 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

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:– 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– 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 – Abdominal discomfort– Anorexia– Tremors, seizures, & confusion– Weakness

Hypokalemia

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

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 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

• 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 & 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 & 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– Assuring adequate amounts of vitamins & minerals

5) Organ function, fluid balance, & serum electrolytes– Monitor daily during 1st week & less frequently after

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 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 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

• 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 to correct hyperglycemia levels

– Monitor blood glucose levels during refeeding

Recommendation for Phosphate

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

Magnesium Dose

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)

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

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

• 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

ReferencesCrook, 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, a680. Escott-Stump, S. (2008). Nutrition and diagnosis-related care: sixth ed. (Baltimore, Maryland), 578-580.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).

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