Refeeding Syndrome 
Epidemiology 
History 
Refeeding was First Observed Following the Refeeding of WWII Prisoners  
 
High-Risk Groups for Refeeding Syndrome 
Anorexia Nervosa  (see Anorexia Nervosa , [[Anorexia Nervosa]])Chemotherapy Patients Homeless/Alcoholic Patients Who Have Not Eaten for Many Days Malnourished Elderly Patients Specific Post-Operative Patients Any Other Patient Who Has Not Received Significant Nutrition for >5 Days  
 
Physiology 
Carbohydrate Load Administered Orally (Oral Intake or Enteral Nutrition)/Intravenously (TPN) Following a Period of Starvation 
During Starvation, Phosphate Stores are Depleted With Refeeding 
Insulin Secretion with Intracellular Shift of Phosphate, Magnesium, and Potassium 
Insulin Secretion Leads to Renal Sodium Reabsorption and Retention, Followed by Fluid Retention  
Enhanced Metabolism of Ketoacids Back to Bicarbonate 
 
 
 
Diagnosis 
Clinical Manifestations 
General Comments 
Most Fatalities are Due to Cardiac Complications  
 
Cardiovascular Manifestations 
Arrhythmias 
Epidemiology : most common cause of death in refeeding syndromeClinical 
Torsade (see Torsade , [[Torsade]]): may occur (due to hypomagnesemia) 
 
 
Congestive Heart Failure (CHF)  (see Congestive Heart Failure , [[Congestive Heart Failure]])
Physiologic Mechanisms 
Impaired Myocardial Contractility: due to starvation-associated myocardial atrophy, hypophosphatemia, and thiamine deficiency 
Sodium and Fluid Retention 
 
 
Hypertension  (see Hypertension , [[Hypertension]])
Hypotension  (see Hypotension , [[Hypotension]])
 
 
Gastrointestinal/Hepatic Manifestations 
Diarrhea  (see Diarrhea , [[Diarrhea]])
Physiology : due to atrophy of intestinal mucosa and pancreatic impairment which occur during starvationTreatment 
May Require Decreasing the Rate of Nutritional Supplementation, Less Complex Carbohydrates, or Elemental Diet 
Generally Resolves within Weeks 
 
 
Elevated Liver Function Tests (LFT’s)  (see xxxx , [[xxxx]])
Epidemiology : may occur during the first few weeks of refeedingPhysiology : due to excessive calories, fat deposition, or cell death-apoptosis from malnutritionClinical : mildly elevated 
Hepatic Steatosis (Fatty Liver)  (see Hepatic Steatosis , [[Hepatic Steatosis]])Nausea/Vomiting  (see Nausea and Vomiting , [[Nausea and Vomiting]])
Treatment : may require decreasing the rate of nutritional supplementation 
 
 
Neurologic Manifestations 
Central Pontine Myelinolysis  (see Central Pontine Myelinolysis , [[Central Pontine Myelinolysis]])
Epidemiology : has been reported in refeeding syndrome associated with anorexia nervosa 
Coma  (see Obtundation-Coma , [[Obtundation-Coma]])Delirium  (see Delirium , [[Delirium]])
Physiology : due to electrolyte abnormalities 
Exacerbation of Thiamine Deficiency  (see Thiamine , [[Thiamine]])
Physiology : thiamine deficiency occurs during starvation, refeeding may exacerbate this deficiencyClinical 
Wernicke’s Encephalopathy (Encephalopathy, Oculomotor Dysfunction, and Ataxia): may occur 
 
 
Parasthesias  (see Parasthesias , [[Parasthesias]])
Physiology : due to electrolyte abnormalities 
Seizures  (see Seizures , [[Seizures]])
Physiology : due to electrolyte abnormalities 
Weakness 
Physiology : impaired muscular contractility (due to hypophosphatemia) 
Tetany  (see Tetany , [[Tetany]])
Physiology : due to hypophosphatemia 
 
 
Pulmonary Manifestations 
Respiratory Failure  (see Respiratory Failure , [[Respiratory Failure]])
Epidemiology : rarePhysiology : impaired diaphragmatic contractility (due to atrophy and/or hypophosphatemia) 
 
 
Renal Manifestations 
Hypokalemia  (see Hypokalemia , [[Hypokalemia]])
Physiology : glucose induces insulin release, resulting in intracellular shift of magnesium, phosphate, and potassium 
Hypomagnesemia  (see Hypomagnesemia , [[Hypomagnesemia]])
Physiology : glucose induces insulin release, resulting in intracellular shift of magnesium, phosphate, and potassium 
Hypophosphatemia  (see Hypophosphatemia , [[Hypophosphatemia]])
Physiology : hallmark and predominant cause of many of the clinical manifestations of the refeeding syndrome
Glucose induces insulin release, resulting in intracellular shift of magnesium, phosphate, and potassium 
 
 
Metabolic Alkalosis  (see Metabolic Alkalosis , [[Metabolic Alkalosis]])
Physiology : due to enhanced metabolism of ketoacids back to bicarbonate 
 
 
Rheumatologic/Orthopedic Manifestations 
Myalgias  (see Myalgias , [[Myalgias]])
Physiology : due to hypophosphatemia 
Peripheral Edema  (see Peripheral Edema , [[Peripheral Edema]])Rhabdomyolysis  (see Rhabdomyolysis , [[Rhabdomyolysis]])
Epidemiology : may occurPhysiology : due to hypophosphatemia 
 
 
Treatment 
Decrease in the Rate of Initial Nutritional Support : as requiredCorrection of Electrolyte Abnormalities : in general, any pre-existing electrolyte abnormalities should be corrected prior to starting feeding
 
References 
Refeeding syndrome: what it is, and how to prevent and treat it.  BMJ. 2008;336(7659):1495 [MEDLINE ] 
Refeeding syndrome.  Pediatr Clin North Am. 2009;56(5):1201 [MEDLINE ] 
Refeeding syndrome: treatment considerations based on collective analysis of literature case reports.  Nutrition. 2010;26(2):156 [MEDLINE ] 
Refeeding hypophosphatemia in adolescents with anorexia nervosa: a systematic review.  Nutr Clin Pract. 2013 Jun;28(3):358-64. Epub 2013 Mar 4 [MEDLINE ] 
 
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