Date of Presentation
5-2-2024 12:00 AM
College
Rowan-Virtua School of Osteopathic Medicine
Poster Abstract
Here we briefly review the definition, epidemiology, pathophysiology, clinical risk scenarios, prevention and treatment of the refeeding syndrome. Refeeding syndrome is a condition which arises when a severely malnourished individual has been restarted with increased nutrition in a relatively short period of time. The refeeding process can lead to shifts in a number of fluids and electrolytes. The hallmark feature is hypophosphatemia. The true incidence of refeeding syndrome is unknown. This is said to be partly due to the lack of a universally accepted definition. Populations that are likely to experience this syndrome include patients with maladaptive eating disorders, chronic diseases such as renal failure on hemodialysis and poorly controlled diabetes, chronic alcoholism, and oncological conditions. As the body continues to experience starvation or malnutrition, existing stores of electrolytes and vitamins can be depleted to sustain metabolic activity. Muscle and other tissues decrease their use of ketones and use fatty acid as a major source of energy. This response can be seen as early as 72 hours after complete fasting. During the refeeding process, glucose loads lead to increased levels of insulin. Glucagon is decreased. The process of synthesis of glycogen (as well as the synthesis of protein) leads to the depletion of phosphate, magnesium and thiamine. Along with ATP and DNA synthesis, phosphate plays a role in the activity of the heart’s electrical transduction. Decreased levels of phosphate are associated with decreased cardiac contractility and arrhythmias along with decreased 2,3- DPG production Potassium can also be depleted. The mechanism of hypomagnesemia in the refeeding syndrome is still not entire clear. The introduction of carbohydrate can lead to a decrease in the renal excretion of sodium and water. Thiamine (B1) depletes in patients who undergo starvation or severe malnourishment Overall, hypophosphatemia is a surrogate marker for refeeding syndrome. However, hypophosphatemia has many causes and is not, in itself, diagnostic of the refeeding syndrome. Guidelines exist for the prevention and treatment of refeeding syndrome. Treatment and management vary by guidelines.
Keywords
Refeeding Syndrome, Nutritional Deficiency, Hypophosphatemia
Disciplines
Diagnosis | Emergency Medicine | Medicine and Health Sciences | Nutritional and Metabolic Diseases | Pathological Conditions, Signs and Symptoms | Therapeutics
Document Type
Poster
Included in
Diagnosis Commons, Emergency Medicine Commons, Nutritional and Metabolic Diseases Commons, Pathological Conditions, Signs and Symptoms Commons, Therapeutics Commons
Brief Review: The Refeeding Syndrome
Here we briefly review the definition, epidemiology, pathophysiology, clinical risk scenarios, prevention and treatment of the refeeding syndrome. Refeeding syndrome is a condition which arises when a severely malnourished individual has been restarted with increased nutrition in a relatively short period of time. The refeeding process can lead to shifts in a number of fluids and electrolytes. The hallmark feature is hypophosphatemia. The true incidence of refeeding syndrome is unknown. This is said to be partly due to the lack of a universally accepted definition. Populations that are likely to experience this syndrome include patients with maladaptive eating disorders, chronic diseases such as renal failure on hemodialysis and poorly controlled diabetes, chronic alcoholism, and oncological conditions. As the body continues to experience starvation or malnutrition, existing stores of electrolytes and vitamins can be depleted to sustain metabolic activity. Muscle and other tissues decrease their use of ketones and use fatty acid as a major source of energy. This response can be seen as early as 72 hours after complete fasting. During the refeeding process, glucose loads lead to increased levels of insulin. Glucagon is decreased. The process of synthesis of glycogen (as well as the synthesis of protein) leads to the depletion of phosphate, magnesium and thiamine. Along with ATP and DNA synthesis, phosphate plays a role in the activity of the heart’s electrical transduction. Decreased levels of phosphate are associated with decreased cardiac contractility and arrhythmias along with decreased 2,3- DPG production Potassium can also be depleted. The mechanism of hypomagnesemia in the refeeding syndrome is still not entire clear. The introduction of carbohydrate can lead to a decrease in the renal excretion of sodium and water. Thiamine (B1) depletes in patients who undergo starvation or severe malnourishment Overall, hypophosphatemia is a surrogate marker for refeeding syndrome. However, hypophosphatemia has many causes and is not, in itself, diagnostic of the refeeding syndrome. Guidelines exist for the prevention and treatment of refeeding syndrome. Treatment and management vary by guidelines.