Unit 2: Nutritional Requirements of the Preterm Infant

The monosaccharide glucose is used by the body for energy provision. When glucose is supplied in excess, it can be stored as glycogen. Glycogen, in turn, can be broken down to glucose for use in metabolic processes. If glycogen stores in the body (primarily in liver and muscle) are depleted, glucose can be formed through gluconeogenesis from precursors such as glycerol, pyruvate, lactate, fatty acids and even the glucogenic amino acids.

In the preterm infant (and in the fetus of corresponding gestational age), the brain and heart are major sites of glucose metabolism. Very preterm infants utilize glucose at a rate about double that seen in term infants. This difference is attributable to the high heart and brain weight relative to whole body weight in the preterm infant. Gut, muscle, fat, bone and skin make up proportionally more of the body weight of term infants and these tissues have slower rates of glucose metabolism than the brain and the heart (Hay et al. 2014).

During intrauterine fetal development, glucose and other carbohydrates come from the maternal circulation via the placenta. In the preterm infant, glucose is generally given intravenously at first to cover immediate and high metabolic needs and to avoid hypoglycemia. Hypoglycemia is common in the preterm infant due to the higher glucose need in the first days after birth (higher brain metabolism utilizing large amounts of glucose, decreased fat stores leading to reduced gluconeogenesis, higher energy expenditure due to respiratory distress and hypothermia). 

Preterm infants are quite soon able to produce glucose themselves after birth both by glycogenolysis (though glycogen stores are low in these infants immediately following birth) and by gluconeogenesis. Gluconeogenesis in preterm infants appears to continue even when they are given ample glucose intravenously (Hay et al. 2014).

Glucose supply should exceed the brain glucose needs, allowing enough glucose supply for the heart metabolism. However, glucose oversupplementation should be avoided. Glucose rates over 10 to 11 mg/min/kg may lead to hyperglycemia. Hyperglycemia, particularly in ELBW infants, is normally aggravated by ineffective insulin secretion, elevated catecholamines, higher glycogenolysys stimulated by glucagon and cortisol secretion (or corticosteroids treatment) and absence of enteral nutrition (which stimulates insulin secretion) (Hay et al. 2014). Other adverse effects of excessive glucose supplementation are: increased energy expenditure, increased oxygen consumption, increased carbon dioxide production, tachypnea, fatty infiltration of heart and liver, and fat deposition (which may increase the risk for obesity later in life).

The use of insulin to treat hyperglycemia in the preterm infant is still controversial. A case control study in VLBW preterm infants has shown that although the treatment modestly reduces glycaemia, the risk for hypoglycemia was increased. Additionally, there was evidence of higher mortality in the insulin treated group (Beardsall et al. 2008). A higher parenteral infusion of amino acids (4 g/kg/d) seems to be a better way to prevent hyperglycemia in preterm infants. A higher administration of amino acids consistently shown to be associated with lower serum glycose levels (Burattini et al. 2013).