Refeeding syndrome
Refeeding syndrome | |
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Classification and external resources | |
DiseasesDB | 11205 |
Refeeding syndrome is a syndrome consisting of metabolic disturbances that occur as a result of reinstitution of nutrition to patients who are starved or severely malnourished.[1] The syndrome was first[2] 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.[2]
Syndrome
Any individual who has had negligible nutrient intake for more than 20 consecutive days is at risk of refeeding syndrome. Refeeding syndrome usually occurs within 10 days of starting to feed. Patients can develop fluid and electrolyte disorders, especially hypophosphatemia, along with neurologic, pulmonary, cardiac, neuromuscular, and hematologic complications.
During prolonged fasting the body aims to conserve muscle and protein breakdown by switching to ketone bodies derived from fatty acids as the main energy source. The spleen decreases its rate of red blood cell breakdown thus conserving red blood cells. Many intracellular minerals become severely depleted during this period, although serum levels remain normal. Importantly, insulin secretion is suppressed in this fasted state and glucagon secretion is increased.[1]
During refeeding, insulin secretion resumes in response to increased blood sugar; resulting in increased glycogen, fat and protein synthesis. This process requires phosphates, magnesium and potassium which are already depleted and the stores rapidly become used up. Formation of phosphorylated carbohydrate compounds in the liver and skeletal muscle depletes intracellular ATP and 2,3-diphosphoglycerate in red blood cells, leading to cellular dysfunction and inadequate oxygen delivery to the body's organs. Refeeding increases the basal metabolic rate. Intracellular movement of electrolytes occurs along with a fall in the serum electrolytes, including calcium and magnesium. Levels of serum glucose may rise and the B1 vitamin thiamine may fall. Cardiac arrhythmias are the most common cause of death from refeeding syndrome, with other significant risks including confusion, coma and convulsions and cardiac failure.
This syndrome can occur at the beginning of treatment for anorexia nervosa when patients have an increase in calorie intake and can be lethal.[3] The shifting of electrolytes and fluid balance increases cardiac workload and heart rate. This can lead to acute heart failure. Oxygen consumption is also decreased which strains the respiratory system and can make weaning from ventilation more difficult.
Treatment
Refeeding syndrome can be fatal if not recognized and treated properly. An awareness of the condition and a high index of suspicion are required in order to make the diagnosis.[4] Refeeding syndrome occurs most commonly in those who have lost weight rapidly. The electrolyte disturbances of the refeeding syndrome can occur within the first few days of refeeding. Close monitoring of blood biochemistry is therefore necessary in the early refeeding period. Milk is often the refeeding food of choice in this early period as it is naturally high in phosphate and easily tolerated by those who have been starved. If potassium, phosphate or magnesium are low then this should be corrected via the oral route, or if severe with parenteral treatment. Prescribing thiamine, vitamin B complex (strong) and a multivitamin and mineral is recommended. Biochemistry should be monitored regularly until it is stable. Energy intake should remain only 50-70% that of normally required for the first 3–5 days. Patients who have been starved for some time often experience gastrointestinal disturbance during refeeding, in particular colicky abdominal pain, reflux symptoms, nausea and early satiety.
See also
- Minnesota Starvation Experiment where some effects of refeeding were documented.
References
- 1 2 Mehanna HM, Moledina J, Travis J (June 2008). "Refeeding syndrome: what it is, and how to prevent and treat it". BMJ 336 (7659): 1495–8. doi:10.1136/bmj.a301. PMC: 2440847. PMID 18583681.
- 1 2 Schnitker MA, Mattman PE, Bliss TL (1951). "A clinical study of malnutrition in Japanese prisoners of war". Annals of Internal Medicine 35 (1): 69–96. doi:10.7326/0003-4819-35-1-69. PMID 14847450.
- ↑ Webb GJ, Smith K, Thursby-Pelham F, Smith T, Stroud MA, Da Silva AN (2011). "Complications of emergency refeeding in anorexia nervosa: case series and review". Acute Medicine 10 (2): 69–76. PMID 22041604.
- ↑ Assiotisa A, Elenin, H (2010). "Implications of refeeding syndrome in posteropative total parenteral nutrition". Grand Rounds 10: 63–6.
Bibliography
- Shils, M.E., Shike, M., Ross, A.C., Caballero, B. & Cousins, R.J. (2006). Modern nutrition in health and disease, 10th ed. Lippincott, Williams & Wilkins. Baltimore, MD.
- Mahan, L.K. & Escott-Stump, S.E. (2004) Krause’s Food, Nutrition, & Diet Therapy, 11th ed. Saunders, Philadelphia, PA.
- Hearing S (2004). "Refeeding syndrome: Is underdiagnosed and undertreated, but treatable". BMJ 328 (7445): 908–9. doi:10.1136/bmj.328.7445.908. PMC: 390152. PMID 15087326.
- Crook M, Hally V, Panteli J (2001). "The importance of the refeeding syndrome". Nutrition 17 (7–8): 632–7. doi:10.1016/S0899-9007(01)00542-1. PMID 11448586.
- Lauts N (2005). "Management of the patient with refeeding syndrome". J Infus Nurs 28 (5): 337–42. doi:10.1097/00129804-200509000-00007. PMID 16205500.
- Kraft M, Btaiche I, Sacks G (2005). "Review of the refeeding syndrome". Nutr Clin Pract 20 (6): 625–33. doi:10.1177/0115426505020006625. PMID 16306300.
- National Institute for Clinical Excellence (2008). CG32 Nutrition support in adults: full guideline. http://guidance.nice.org.uk/CG32/Guidance/pdf/English
- Mehanna HM, Moledina J, Travis J. Refeeding syndrome: what it is, and how to prevent and treat it. Bmj 2008;336(7659):1495–1498.
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