Refeeding syndrome occurs when electrolyte and fluid shifts happen in malnourished patients undergoing refeeding. It was first described after WWII in prisoners of war who were malnourished in captivity and then cared for by U.S. personnel. Refeeding syndrome is defined as severe electrolyte and fluid shifts associated with metabolic abnormalities in malnourished patients undergoing refeeding. Clinical features include cardiovascular, gastrointestinal, neurological and respiratory symptoms. Risk factors include decreased nutrient intake from conditions like eating disorders, decreased absorption from diseases, and increased catabolism from illnesses. Close monitoring of electrolytes and fluid status is important to prevent complications from refeeding syndrome.
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Refeeding syndrome with Parenteral Nutrition in ESRD
1. Refeeding Syndrome
“Slow and Low”
Vishal Bagchi MBA, RD, LD
Director of Medical and Scientific Affairs
Patient Care America
2. Objectives
After a sustained state of malnutrition or under-nutrition
patients tend to exhibit symptoms of refeeding syndrome
secondary to nutrition support received from oral or
parenteral nutrition.
• Define refeeding syndrome
• Identify causes of refeeding syndrome with subjective
and objective analysis
• Acquire skills to manage refeeding syndrome during
and after oral and/or parenteral nutrition support
3. History
• The syndrome was first described after World
War II in Americans who, held by the Japanese
as prisoners of war, had become malnourished
during captivity and who were then released to
the care of United States personnel in the
Philippines
• A clinical study of malnutrition in Japanese
prisoners of war. -SCHNITKER MA, MATTMAN
PE, BLISS TL. Dec 2nd 1949
5. Definition
• Severe electrolyte and fluid shifts associated with
metabolic abnormalities in malnourished patients
undergoing refeeding, whether orally, enterally,
or parenterally.
– Incidence of RS is unclear due to a lack of strict
definition
– Absence of accepted diagnostic criteria or
internationally agreed guidelines for detecting RS
Crook et al.-2001
6. Starvation and Semi-starvation
• State of Negative Protein-Energy Balance
– Absence of nutrient intake
– Intake below requirements
• Dialysis KDOQI/ASPEN
– Calories 25-35 kcal/kg/day
– Protein 1.2-1.4 gm/kg/day
7. Metabolic Adaptation to Starvation
Post Absorptive state --- Overnight fast after a meal
Fast lasting 12-24 Hours
Fast lasting > 3days
Prolonged Starvation
8. Post-Absorptive State
The Brain Must receive Glucose
Insulin levels fall
Glucose delivery to Tissues 8-10 g/hr
– Increased Glycogenolysis 50%
– Continued Gluconeogensis 50%
Lactate and Pyruvate 50%
Amino acids 50%
Muscle uses mainly fatty acids
– 2/3 fuel oxidation is derived from fatty acids
9. Fasting ~ 2-4 days
Liver glycogen depleted
Insulin levels fall
Glucose production by Gluconeogenesis:
– Lactate and Pyruvate
– Amino acids
Nitrogen loss from amino acid is 10-12 g/day
Branched chain aminoacids released by muscle and
oxidized
Ketone production increases
Brain reduces glucose utilization and increases Ketone
body oxidation
10. Prolonged Starvation 5+days
• Metabolic rate falls
• Nitrogen losses decrease to 4-5 g/day
• Brain now uses ketones as the sole source of
energy
• Muscle uses fatty acid and spares branched-
chain amino acid oxidation
11. Clinical Effects of Starvation
• Resting Energy Expenditure fall by about 25-35%
by 3 weeks
• Serum Albumin Concentrations remain normal
• Serum Prealbumin falls
• Death occurs when body fat is depleted
• Obese persons can withstand prolonged
starvation
15. Pathophysiology
• Marked increase in insulin secretion in response to
nutrient delivery/intake.
• Intracellular shift of glucose
• Uptake of phosphate, magnesium, potassium
• Expansion of extracellular fluid compartment
– Fluid overload
– Pulmonary edema
– Cardiac decompensating
16. Criteria for the determination of refeeding syndrome risk
*National Institute for Health and Clinical Excellence. Nutrition support in adults. CG32, London, England.
One of the following: Two of the following:
• BMI < 16 (kg/m2 )
• Unintentional weight loss >15% in the
preceding three – six months
• Very little or no nutritional intake for
more than 10 days
• Low levels of serum potassium,
phosphate or magnesium prior to
feed
• BMI < 18.5 (kg/m2 )
• Unintentional weight loss >10% in the
preceding three – six months
• Very little or no nutritional intake for
more than 5 days
• History of alcohol or drug abuse
17. Criteria for confirmation of RS-King’s College
1)Electrolytes Refeeding Syndrome Criteria Dialysis/Normal Reference Range
Potassium < 2.5 mmol/L < 2.5 mEq/L 3.5 to 5.0 mEq/L
Phosphorus < 0.32 mmol/L < 0.99 mg/dL 2.6 – 4.5 mg/dL
Magnesium < 0.5 mmol/L < 1.22 mg/dL 1.7 to 2.2 mg/dL
2)Peripheral edema or acute circulatory fluid overload.
3)Disturbance to organ function including respiratory failure, cardiac failure, pulmonary edema
Adopted from:
Occurrence of refeeding syndrome in adults commenced on artificial nutrition and hydration:
prospective cohort study. Alan Rio, Kevin Whelan, Louise Goff, Dianne Reidlinger, Nigel Smeeton. 01-Oct-2012
18. Monitoring patients at risk of developing RFS
Clinical monitoring
• Early identification of high risk
patients
• Monitor blood pressure and pulse
rate
• Monitor feeding rate
• Meticulously document fluid intake
and output
• Monitor change in body weight
• Monitor for neurologic signs and
symptoms
• Patient education
Biochemical monitoring
• Monitor biochemistry and electrolyte
levels
• Monitor blood glucose levels
• ECG monitoring in severe cases
• Account other sources of energy
(dextrose, propofol, medications)
Gastroenterol Res Pract. 2011; 2011:
410971.
Published online 2010 Aug 25.
19. Study 1
• Rio A et al. BMJ Open 2013;3e002173.
doi:10.1136/bmjopen-2012-002173
• 243 adults prospective cohort study at UK teaching hospital
– BMI < 16 kg/m2
– 15% weight loss 3-6 mos
– No nutritional intake > 10 days
• 2% developed severe electrolyte shifts, acute circulatory
fluid overload, organ failure
• No deaths attributed to RS
20. Study 2
• Zeki S et al. Clin Nutr 2011;30:365-368
• Retrospective 321 patients enterally vs parenterally
• At risk EN patients more likely to develop RH than PN
patients (p = 0.03)
• Death more common in EN group vs PN (p < 0.001)
• No association between development of RH and death
within 7 days
21. Study 3
• Owers EL et al. Clin Nutr. 2015;34:134-139.
• Retrospective 1661 Adults
– 9% documented at risk of refeeding syndrome
– 7% had very low levels of K, Mg, P
– 52% had low levels of K, Mg, P
• Patients at risk of refeeding syndrome had
– 4 days longer hospital LOS
– Weighed 13 kg less
22. IDPN Monitoring Guidelines
• Hypophosphatemia < 2.6 mg/dL
– May add potassium phosphate or sodium phosphate
• Hypokalemia < 2.5 mEq/dL
– Adjust dialysate bath 3k
• Abnormal Intradialytic cramping
– Indicative of hyponatremia or excessive fluid removal
– Administer normal saline
– May add 70-150 mEq to IDPN formula
Renal Care: Resources and Practical Applications By Kerri Lynn Wiggins
26. Risk Factors
• Decreased intake
– eating disorders (especially anorexia nervosa)
– alcoholism
– depression
– fasting
– vomiting
– dysphagia
– chemotherapy
– prolonged NBM
– post-operative
– chronic malnutrition
• Decreased absorption
– inflammatory bowel disease,
– chronic pancreatitis,
– cystic fibrosis,
– short bowel syndrome
• Decreased absorption
– Oncology patients
– Postoperative patients
– Elderly patients (comorbidities, decreased physiological reserve)
– uncontrolled diabetes mellitus (electrolyte depletion, diuresis)
– chronic malnutrition:
– Marasmus
– Prolonged fasting or low energy diet
– -Morbid obesity with profound weight loss
– High stress patient unfed for >7 days
– Long term users of antacids (magnesium and aluminium salts
bind phosphate)
– Long term users of diuretics (loss of electrolytes)
• Increased catabolism
– inflammatory process (infectious and non-infectious)
– cancer
Editor's Notes
Clavical
Glycogenolysis is the biochemical breakdown of glycogen to glucose whereas glycogenesis is the opposite, the formation of glycogen from glucose.Glycogenolysis takes place in the cells of muscle and liver tissues in response to hormonal and neural signals.
Anaerobic glycolysis is the transformation of glucose to lactate when limited amounts of oxygen ...Pyruvate is converted to lactic acid by the enzyme lactate dehydrogenase.