Refeeding syndrome : physiological background and practical management

Abstract

Refeeding problems have been recognised since the the liberation of starved communities under siege. The main clinical problems may relate to hypophosphataemia, hypomagnesaemia and hypokalaemia with a risk of sudden death; thiamine deficiency with the risk of Wernike’s encephalopathy/Korsakoff psychosis and sodium/water retention. The problems are greatest with oral/enteral feeding and especially with carbohydrate due to it increasing plasma insulin and thus glucose entry into cells. It is difficult to predict patients at risk of refeeding problems so there must be a high clinical suspicion on refeeding any malnourished patient (including any who have had no or very little nutrition for over 5days). Generous vitamin and electrolyte supplementation may be given while monitoring closely and increasing the calorie intake reasonably rapidly from 10 to 20 kcal/kg/24 hours. Often patients in this category are not hungry, but over the course of a few days, the restoration of their appetite is an indication that the risks of refeeding have been managed and it is now safe to increase the feed aiming for repletion. If problems do occur, the feed should be slowed to the previous day’s amount, reduced further or rarely stopped while fluid and electrolyte issues are corrected.

Comparison of a low carbohydrate intake and standard carbohydrate intake on refeeding hypophosphatemia in children and adolescents with anorexia nervosa: a pilot randomised controlled trial

“…The findings of this pilot study support that a caloric equivalent low carbohydrate oral diet (< 40% total energy) commencing at a minimum of 1500 kcal/day has no advantage, compared to a standard carbohydrate oral diet (50–60% total energy) in reducing the incidence of RH and RFS in hospitalised patients with AN. Our study indicates that it is safe to provide higher calorie feeding without needing to initially restrict energy from carbohydrates, or needing to routinely supplement with prophylactic phosphate, which contrasts with previous studies [ 1 , 11 , 12 , 20 ]. The refeeding risks in our study were able to be safely managed with medical monitoring and phosphate supplementation as clinically indicated.…”

“…Rapid introduction of carbohydrates following a period of inadequate food intake is thought to precipitate the electrolyte and fluid shifts that occur during RFS [ 2 , 5 , 20 ]. As the body shifts from a catabolic to an anabolic state, insulin levels increase which in turn increases glucose metabolism.…”

“…As the body shifts from a catabolic to an anabolic state, insulin levels increase which in turn increases glucose metabolism. The demand for phosphate during glucose carbohydrate metabolism is high and serum phosphate levels may fall, thereby increasing the risk of RH and RFS [ 20 , 21 ]. Hence, in aggressive feeding protocols, restricting the amount of carbohydrates during the early stages of nutritional rehabilitation to reduce the demand for phosphate, and/or administering prophylactic phosphate supplementation to attenuate the risk of RH has been trialled, despite limited evidence supporting either practice [ 6 , 7 ].…”

Refeeding Syndrome in Pediatric Age, An Unknown Disease: A Narrative Review

“…When food is eaten again, especially in the form of carbohydrates, insulin levels rise, leading to an increase in glucose uptake and utilization ( 22 ). This chain results in a rapid shift in electrolyte and fluid balance with increased cellular uptake of potassium, magnesium, and phosphate, resulting in serum depletion of these electrolytes ( 23 ). Figure 1 attempts to summarize the pathophysiology of RS in the human body.…”

Refeeding syndrome and psychopharmacological interventions in children and adolescents with Anorexia Nervosa: a focus on olanzapine-related modifications of electrolyte balance

“…These effects could impact the risk of RS by improving appetite and facilitating regular food reintroduction. Numerous studies have investigated the connection between RS and alterations in weight [ 11 , 12 ] and appetite [ 13 ] in individuals with FED. Pathophysiological consequences of olanzapine treatments, moreover, should be acknowledged by clinicians.…”