Any individual who has had a negligible nutrient intake for many consecutive days and/or is metabolically stressed from a critical illness or major surgery is at risk of<unk> .<unk>  usually occurs within four days of starting to re-feed. Patients can develop fluid and electrolyte imbalance, especially hypophosphatemia, along with neurologic, pulmonary, cardiac, neuromuscular, and hematologic complications. During fasting, the body switches its main fuel source from carbohydrates to fat tissue fatty acids and amino acids as the main energy sources. 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 fasting state, and glucagon secretion is increased. During<unk> , insulin secretion resumes in response to increased blood sugar, resulting in increased glycogen, fat, and protein synthesis.<unk>  increases the basal metabolic rate. The 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. Intracellular movement of electrolytes occurs along with a fall in the serum electrolytes, including phosphate and magnesium. Levels of serum glucose may rise, and B1 vitamin thiamine may fall. Abnormal heart rhythms are the most common cause of death from<unk> , with other significant risks including confusion, coma and convulsions and cardiac failure.
Refeeding syndrome
Dumping syndrome
Diabetic ketoacidosis
Cyclic vomiting syndrome
Milk-alkali syndrome
Idiopathic postprandial syndrome
Alcoholic ketoacidosis
Hyperinsulinism-hyperammonemia syndrome