source of vitamin E and vitamin B12 to help protect cell structure and making healthy red blood cells

Immune protection by immunoglobulins

source of long chain polyunsaturates omega 3 and 6

Optimum nutrition, ideal source of energy, quickly absorbed

Promote development in the form of growth factors and hormones

prevent pathological neonatal hypoglycaemia

termed a proactive approach

lead to unnecessary intervention

only indicated if vulnerable and symptomatic

encourage counter-regulation

Neonatal hyperinsulinism (congenital disorder)(may have macrosomic or dymorphic appearance)

Breastfeeding

Inborn errors of metabolism (e.g.Family history of MCADD)

Suspected or early onset sepsis

Infants whose mothers have taken pethidine

Preterm (< 37 weeks gestation)

Large for gestational age (LGA babies)

Infants whose mothers have taken betablockers

Hypothermia

Moderate to severe perinatal hypoxia ischaemia

Small for gestational age (SGA babies)

Pituitary or adrenal insufficiency

Fetal glucose uptake is proportional to maternal glucose concentrations

The majority of fetal energy needs are supplied by maternal metabolism via placental circulation

During 3rd trimester of pregnancy glycogen storage decreases in cardiac and skeletal muscle

By 20 to 24 weeks of gestation the fetus begins to store glycogen in the kidneys

A continuous supply of glucose is provided via facilitated diffusion

glucose diffuses across the placental villi by the trophoblast cell lining.

Neonatal hypoglycemia

Glyconeogenesis

Counter-current nutrition

Transient hypoglycemia

Counter-regulation

Glycogenesis

Inhibiting insulin secretion

blood glucose concentration begins to fall and continues to decrease until around 2 to 4 hrs

Generating alternative fuel e.g. ketone bodies released from adipose tissue (fat)

Synthesising glucose from liver substrates (gluconeogenesis)

Breaking down glycogen reserves in the liver and kidney (glycogenolysis)

newborn blood glucose will then begin to rise, regardless of whether or not the baby has been fed

Storing glucose in the form of glycogen (by glycogenesis)

Inhibiting glucose secretion

ketoacidosis is a normal physiological process

The receptor sites on the lactocytes (acini cells) are not ‘primed’

unprimed lactocytes begin to deteriorate and ‘shut down’

The receptor sites on the lactocytes (acini cells) are ‘primed’ as a result of placental expulsion

long term milk supply is affected

is not important as newborns have the ability to counter-regulate

6 hours of age

2 hours of age

24 hours of age

32 weeks gestation

the table

Jess was born at home at 42 weeks gestation. She weighed 4200g at birth. Had skin to skin at birth and rooted but did not feed at the breast. It is now six hours later.

Jennie had a caesarean section at 42 weeks for fetal distress. Her baby required resuscitation at birth but responded well and is now skin to skin.

Josie the mother, is five days postnatal and has just finished a course of antibiotics for UTI

Robbie has just had a normal birth at 35 weeks gestation. His APGAR scores were 9 and 10 and the baby is skin to skin with mother.

Angie gave birth in the water at 39 weeks gestation. Her baby is now skin to skin and suckling at the breast

You have just taken baby Jonnie’s temperature. It is 34.8°C

Mary was born by forceps at 40 weeks gestation, her weight was 2460g. She is skin to skin.

Lizzie gave birth last evening. She is taking labetalol 200mg BD for essential hypertension.