Prevention and management of refeeding syndrome.

Prevention and management of refeeding syndrome

To ensure adequate prevention, the NICE guidelines recommend a thorough nutritional assessment before refeeding is started.

Recent weight change over time, nutrition, alcohol intake, and social and psychological problems should all be ascertained.

Plasma electrolytes (especially phosphate, sodium, potassium, and magnesium) and glucose should be measured at baseline before feeding and any deficiencies corrected during feeding with close monitoring.

For decades, the key to preventing the syndrome was believed to be lower-calorie refeeding with cautious advancement. preventing the syndrome

The NICE guidelines recommend that refeeding is started at no more than 50% of energy requirements for the 1^st 2 days in " patients who have eaten little or nothing for more than 5 days.” The rate can then be increased if no refeeding problems are detected on clinical and biochemical monitoring.

The prescription for people at high risk of developing refeeding problems should consider:

·      starting nutrition support at a maximum of 10 kcal/kg/day, increasing levels slowly to meet or exceed full needs by 4 to 7 days.

·    using only 5 kcal/kg/day in extreme cases (for example, BMI less than 14 kg/m2 or negligible intake for more than 15 days) and monitoring cardiac rhythm continually in these people and any others who already have or develop any cardiac arrythmias.

·     restoring circulatory volume and monitoring fluid balance and overall clinical status closely.

·     providing immediately before and during the first 10 days of feeding: oral thiamin 200 to 300 mg daily, vitamin B co strong 1 or 2 tablets, 3 times a day (or full dose daily intravenous vitamin B preparation, if necessary) and a balanced multivitamin or trace element supplement once daily.

·   providing oral, enteral or intravenous Maintenance requirement of potassium (likely requirement 2 to 4 mmol/kg/day), phosphate (likely requirement 0.3 to 0.6 mmol/kg/day) and magnesium (likely requirement 0.2 mmol/kg/day intravenous, 0.4 mmol/kg/day oral) unless pre-feeding plasma levels are high; pre-feeding correction of low plasma levels is unnecessary.

The following guidance is a suggestion for possible electrolyte repletion for refeeding syndrome in adolescents with eating disorders:

Pediatric Umbilical Hernia

 Pediatric Umbilical Hernia

Etiology

Umbilical hernia in children results from incomplete closure of the fascia of the umbilical ring, through which intraabdominal contents may protrude.

 After separation of the umbilical cord, usually, the ring undergoes spontaneous closure through the growth of the rectus muscles and fusion of the fascial layers.

A failure or delay in this process leads to the formation of an umbilical hernia.

 The exact etiology is unknown, but usually, occurs through the umbilical vein component of the ring.

Clinical Signs and Symptoms of Refeeding Syndrome.

Clinical Signs and Symptoms of Refeeding Syndrome

References  

1. Fuentebella, J., & Kerner, J. A. (2009). Refeeding Syndrome. Pediatric Clinics of North America, 56(5), 1201–1210. doi:10.1016/j.pcl.2009.06.006.
2. Jason M. Nagata and Andrea K. Garber, refeeding syndrome, Nelson 22th ed 2024, Vol 1, ch 63.

 

 

Pathogenesis of refeeding syndrome.

Pathogenesis of refeeding syndrome

 How does refeeding syndrome develop?

Prolonged fasting:

During prolonged fasting, hormonal and metabolic changes are aimed at preventing protein and muscle breakdown.

Muscle and other tissues decrease their use of ketone bodies and use fatty acids as the main energy source. This results in an increase in blood levels of ketone bodies, stimulating the brain to switch from glucose to ketone bodies as its main energy source.

The liver decreases its rate of gluconeogenesis, thus preserving muscle protein. During the period of prolonged starvation, several intracellular minerals become severely depleted. However, serum concentrations of these minerals (including phosphate) may remain normal. This is because these minerals are mainly in the intracellular compartment, which contracts during starvation. In addition, there is a reduction in renal excretion.

Refeeding:

During refeeding, glycaemia leads to increased insulin and decreased secretion of glucagon. Insulin stimulates glycogen, fat, and protein synthesis. This process requires minerals such as phosphate and magnesium and cofactors such as thiamine. Insulin stimulates the absorption of potassium into the cells through the sodium-potassium ATPase symporter, which also transports glucose into the cells. Magnesium and phosphate are also taken up into the cells. Water follows by osmosis. These processes result in a decrease in the serum levels of phosphate, potassium, and magnesium, all of which are already depleted.

The clinical features of the refeeding syndrome occur as a result of the functional deficits of these electrolytes and the rapid change in basal metabolic rate.