Refeeding syndrome is a symptom complex that develops at the stage of withdrawal from starvation, characterized by life-threatening electrolyte and multiple organ disorders. It is accompanied by dysfunction of the cardiovascular (arrhythmia, edema), respiratory (tachypnea), digestive (vomiting, flatulence), nervous (convulsions, disorders of consciousness) and other systems up to a fatal outcome. Diagnostics includes laboratory tests (blood biochemistry, electrolytes), instrumental studies (ECG monitoring, blood pressure, heart rate, ENMG, indirect calorimetry). Patients are prescribed a hypocaloric diet, infusions of phosphate-containing mixtures, correction of dyselectrolythemia, vitamin therapy.
ICD 10
R63.8 E89.8
General information
Refeeding syndrome (RFS, resumed feeding/nutrition syndrome, overfeeding syndrome) is a potentially fatal condition that occurs during the period of fermentation, characterized by pronounced metabolic, cardiological, gastroenterological, respiratory, neurological, motor disorders. Cases of sudden death of emaciated people after the resumption of feeding are known by the example of concentration camp prisoners. There is no information about the true frequency of refeeding syndrome these days, however, it is known that more than a third of cases of RFS are diagnosed in ICU patients who are in critical condition.
Causes
Refeeding syndrome is provoked by the active resumption of feeding of patients with an extreme degree of exhaustion. As a rule, the condition develops in the first 72 hours after the start of rehabilitation alimony. At the same time, nutrition can be carried out in any way: enteral (independently, through a probe or gastrostomy), parenteral.
Currently, it is believed that the immediate cause of the development of RFS is the use after fasting of foods with a high glycemic index (GI > 80) or the introduction of intravenously highly concentrated glucose solutions. This causes electrolyte and metabolic disorders, leading to multi organ failure and disruption of vital functions. According to the NICE scale, a high risk of RFS exists in the presence of at least one of the following conditions:
- starvation or severe malnutrition during the previous 10 days;
- initial BMI <16 kg/m2;
- loss of more than 15% of body weight in the previous 3-6 months;
- dyselectrolythemia at the time of the beginning of feeding.
Risk factors
Background conditions in which RFS develops most often:
- alimentary dystrophy;
- kwashiorkor;
- anorexia nervosa;
- chronic alcoholism;
- insulin-dependent diabetes mellitus;
- chronic infections (tuberculosis, AIDS);
- anorexia-cachexia syndrome in cancer tumors;
- digestive disorders caused by maldigestion, malabsorption, diarrhea, vomiting;
- abuse of laxatives, diuretics, insulin therapy, chemotherapy.
Pathogenesis
The key points of the pathogenesis of refeeding syndrome are critical disorders of metabolism and water-electrolyte balance, which develop in patients with protein-energy deficiency (PED) against the background of resumption of feeding.
Prolonged malnutrition or starvation is accompanied by an increase in the production of counterinsular hormones (glucagon, cortisol, adrenaline, STH) while reducing insulin production. At the same time, the activation of the catabolic processes of glycogenolysis, lipolysis and proteolysis occurs, the transition of the body from carbohydrate to fat type of metabolism. Against the background of a decrease in intracellular volume, the ionic equilibrium changes (primarily due to the loss of phosphorus, magnesium, potassium by cells), depletion of thiamine and other vitamins.
The restoration of parenteral or enteral nutrition leads to a return to carbohydrate metabolism. The process is accompanied by a sharp increase in the concentration of glucose in the blood plasma and stimulation of insulin secretion, which leads to the activation of the glycolysis process. For the synthesis of ATP, cells need a large amount of magnesium phosphates, glucose, and potassium. The consequence of increased intracellular ion transport is pronounced plasma dyselectrolythemia: hypophosphatemia, hypokalemia, hypomagnesemia.
Hyperglycemia, insulin resistance, ketoacidosis develops. The excretion of sodium in the urine decreases, fluid retention occurs, edema appears. Against the background of vitamin B1 deficiency, aerobic glycolysis is replaced by anaerobic, which results in metabolic acidosis, neurological disorders.
Symptoms
Key pathogenetic mechanisms determine the spectrum of clinical manifestations of refeeding syndrome. Against the background of a deficiency of P, K, Mg in blood plasma, hyperhydration, hyperglycemia, the normal functioning of the cardiovascular, neuromuscular, respiratory systems is disrupted. The RFS clinic develops in the first 2-5 days after the resumption of nutrition. The early signs are peripheral edema caused by the retention of Na and water.
Hypophosphatemia of mild (0.6-0.85 mmol/L) and moderate severity (0.3-0.6 mmol/L) occurs without obvious clinical symptoms and often remains underestimated. With a further decrease in the level of phosphates, dangerous arrhythmias develop, acute left ventricular failure, ODN. Neurological manifestations include paresthesia, convulsions; musculoskeletal disorders – muscle weakness, myalgia, rhabdomyolysis, osteomalacia. Dysfunction of the respiratory muscles causes the patient’s dependence on the ventilator.
Due to hypokalemia, cardiac arrhythmias occur, in severe cases cardiac arrest occurs. Possible respiratory depression, the development of paralysis, paralytic intestinal obstruction. Severe hypomagnesemia causes the occurrence of tetany, tremor, ataxia, arrhythmias. Hypovitaminosis B1 is accompanied by polyneuropathy, dilated cardiomyopathy, acute Wernicke encephalopathy, Korsakov syndrome. Digestive disorders are typical for refeeding syndrome: heaviness after eating, nausea and vomiting, flatulence, diarrhea or constipation.
Complications
Dyselectrolythemia is the main cause of life-threatening disorders: fatal arrhythmias (ventricular fibrillation), conduction disorders, acute respiratory failure, severe neurological complications (central pontine myelinolysis, cerebral edema, coma). Fluid overload can be complicated by congestive heart failure, cardiogenic pulmonary edema. Acute tubular necrosis and renal insufficiency develop on the part of the kidneys. Death occurs as a result of asystole, respiratory arrest, multiple organ dysfunction.
Diagnostics
The diagnosis of refeeding syndrome is established based on a combination of clinical and laboratory data, taking into account the presence of increased risk factors. Patients with this pathology need hospitalization in the ICU, observation by a resuscitator, assessment of the condition by a cardiologist, neurologist, nutritionist. To determine the risk of the RFU, special scales are used: NICE, NRS 2002, MUST. In the hospital is carried out:
- Monitoring of clinical indicators. When the RF occurs, round-the-clock monitoring of blood pressure, BH, heart rate is carried out. The volume of food eaten, liquid drunk and injected solutions, diuresis, the presence of vomiting and stool are recorded.
- Laboratory monitoring. The main biochemical parameters requiring dynamic evaluation are P, K, Na, Mg, glucose, transaminases, urea, creatinine, blood ABB, vitamin B1 levels. Hypophosphatemia is a key marker of refeeding syndrome – it is found in 96% of patients and worsens after the start of feeding.
- Instrumental diagnostics. Indirect calorimetry is carried out to calculate the caloric content of the prescribed food and assess energy consumption. In order to assess concomitant cardiogenic and neurological disorders, an ECG and electroneuromyography are performed.
Treatment
The resumption of feeding of patients with PED is carried out under the guidance of a dietitian. With a high probability of refeeding syndrome, nutrition begins with a hypocaloric diet at the rate of 5-10 kcal / kg / day, gradually increasing the calorie intake. During the first week, electrolyte monitoring is carried out twice a day. The main directions of therapy of refeeding syndrome:
- Correction of hypophosphatemia. It is carried out by prescribing phosphate-containing mixtures of the latest generation for enteral and parenteral nutrition. Independent medicines containing phosphates are not registered in the USA. Food sources of phosphorus are milk, cheese, fish, egg yolk, liver, etc.
- Correction of metabolic and electrolyte disorders. Under the control of laboratory parameters, solutions of magnesia, potassium chloride, sodium chloride, sodium bicarbonate are administered intravenously against the background of renewed nutrition. To replenish vitamin deficiency, thiamine injections are prescribed from the first days, then vitamin complexes of group B. It is necessary to avoid the introduction of concentrated glucose solutions, excessive infusion load.
Prognosis and prevention
Refeeding syndrome can become fatal if it is not recognized in time and properly treated. All patients with chronic PED and/or who have not eaten for more than 10 days should be considered as threatened by the occurrence of the resumed feeding syndrome. Markers of an unfavorable prognosis are a decrease in serum levels of electrolytes, vitamin B1.
To prevent refeeding indroma, it is necessary to conduct a thorough assessment of the patient’s condition before resuming nutrition. Nutritional support should start with low-energy nutrition. During the period of restorative fermentation, plasma electrolytes and cardiac activity indicators should be monitored.
