Hypoglycemia is a frequently encountered metabolic problem in neonates. After birth,

neonates lose the continuous supply of transplacental glucose. A high brain-to-body weight

ratio along with developmental immaturity of adaptive mechanisms such as gluconeogenesis

and glycogenolysis further increase the chances of hypoglycemia in neonates. Symptoms of

hypoglycemia are nonspecific and include feeding difficulties, tachypnea, hypotonia, abnormal

cry, jitteriness, apnea, coma, and convulsions. Prolonged and repeated episodes of

hypoglycemia are associated with poor neurologic outcomes.

Exclusive breastfeeding is necessary to meet the metabolic needs of neonates, and any

delay in the early establishment of breastfeeding (eg, supplementing with water, glucose water,

or formula instead of breast milk) predisposes neonates to hypoglycemia. Poor latching to

the breast, decreased frequency of feeding, lack of support from health care workers for the

initiation of early breastfeeding and mother"s perception of having inadequate breast milk are

observed to be the predictors of neonatal hypoglycemia. 

Neonates who are born premature, small for gestational age (SGA), have low birth

weight (LBW), and infant of diabetic mothers are at risk of hypoglycemia. In infants of diabetic

mother, in utero, maternal hyperglycemia increases placental glucose transport and results in

fetal hyperglycemia, which stimulates fetal pancreatic insulin production.  After delivery,

maternal glucose supply ceases even though newborn insulin production continues and results

in hypoglycemia. Preterm infants have low glycogen and fat stores with limited capacity to

generate glucose via the gluconeogenesis pathway or excessive peripheral tissue utilization of

glucose resulting in hypoglycemia.  SGA newborns have low hepatic glycogen storage,

increased glucose consumption due to disease stress, and unstable glucose metabolism

that could result in hypoglycemia. 

These infants should be monitored for their blood glucose level (BGL) routinely, especially, in

the early hours of life.  In addition, attention should be taken to initiate early enteral and or

parenteral nutrition to prevent hypoglycemia in these infants.

It is our unit practice to give exclusive breastfeeding to late preterm and term infants within

first hour of life in case of vaginal delivery and within four hours of life in case of caesarian

birth with plasma glucose level monitoring 4 to 6 hourly. Those infants with plasma glucose <

45mg/dL are initiated add-on feeds using expressed MOM OR formula feeds along with

breastfeeding. These infants may need add-on enteral feeds such as pasteurized donor human

milk or formula due to the deficient milk supply status of the mother in the early days of

postpartum. In addition, obstetric complications and hemodynamic instability also will affect

the milk production in some mothers

Given that the amount of colostrum produced within the first 72 hours postpartum is as low as

30-45 ml and minimal colostrum is being produced in the first day of life, exclusive

breastfeeding in high-risk infants in the first 3 days of life may lead to the need for parenteral

nutrition in many infants. Hence, we decided to study the effect of add-on feeding initiated

within the first hour of life with PDHM/ bovine formula along with breastfeeding on the incidence

of hypoglycemia in these at-risk infants in the first 3 days of life.