Immune protection by immunoglobulins

source of long chain polyunsaturates omega 3 and 6

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

Promote development in the form of growth factors and hormones

Optimum nutrition, ideal source of energy, quickly absorbed

encourage counter-regulation

only indicated if vulnerable and symptomatic

termed a proactive approach

lead to unnecessary intervention

prevent pathological neonatal hypoglycaemia

Small for gestational age (SGA babies)

Moderate to severe perinatal hypoxia ischaemia

Breastfeeding

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

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

Large for gestational age (LGA babies)

Infants whose mothers have taken pethidine

Suspected or early onset sepsis

Hypothermia

Preterm (< 37 weeks gestation)

Infants whose mothers have taken betablockers

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

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

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

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

A continuous supply of glucose is provided via facilitated diffusion

Transient hypoglycemia

Counter-regulation

Counter-current nutrition

Neonatal hypoglycemia

Glyconeogenesis

Glycogenesis

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

ketoacidosis is a normal physiological process

Synthesising glucose from liver substrates (gluconeogenesis)

Inhibiting glucose secretion

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)

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

Inhibiting insulin secretion

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

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

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

unprimed lactocytes begin to deteriorate and ‘shut down’

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

long term milk supply is affected

32 weeks gestation

24 hours of age

2 hours of age

the table

6 hours of age

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

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.

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.

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.

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