Promote development in the form of growth factors and hormones

Optimum nutrition, ideal source of energy, quickly absorbed

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

termed a proactive approach

prevent pathological neonatal hypoglycaemia

lead to unnecessary intervention

only indicated if vulnerable and symptomatic

encourage counter-regulation

Pituitary or adrenal insufficiency

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

Infants whose mothers have taken betablockers

Moderate to severe perinatal hypoxia ischaemia

Hypothermia

Small for gestational age (SGA babies)

Breastfeeding

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

Preterm (< 37 weeks gestation)

Suspected or early onset sepsis

Large for gestational age (LGA babies)

Infants whose mothers have taken pethidine

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

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

A continuous supply of glucose is provided via facilitated diffusion

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

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

Fetal glucose uptake is proportional to maternal glucose concentrations

Neonatal hypoglycemia

Transient hypoglycemia

Glycogenesis

Counter-current nutrition

Glyconeogenesis

Counter-regulation

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

Inhibiting glucose secretion

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

Inhibiting insulin secretion

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

Storing glucose in the form of glycogen (by glycogenesis)

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

Synthesising glucose from liver substrates (gluconeogenesis)

ketoacidosis is a normal physiological process

long term milk supply is affected

unprimed lactocytes begin to deteriorate and ‘shut down’

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

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

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

32 weeks gestation

6 hours of age

24 hours of age

the table

2 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

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.

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

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

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

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

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.