Birth and the newborn infant

There is a greater risk of dying on the first day of life than on any other day (except the last).

7.1 The effects of birth on the fetus

7.1.1 Normal physiology (Table 7.1)

The most dramatic events are the switch from placenta to lung as the organ of gas exchange, and the change from fetal to adult circulation (Figure 7.1).

Table 7.1 Normal physiological events at birth

Phenomena	Effects
Stress of labour catecholamine and steroid	↓ Lung liquid and ↑ surfactant release
Compression of thorax in birth canal	Expulsion of lung liquid
Sensory stimuli and clamping of umbilical cord	Initiation of breathing
Air enters lungs ↑ lung tissue oxygen	Pulmonary vascular resistance ↓ ↑ pulmonary blood flow ↑ arterial Po2
Systemic pressure > pulmonary pressure	Foramen ovale closes
Ductus arteriosus fills with oxygen-rich blood	Ductus arteriosus closes

Figure 7.1 Fetal circulation. Follow the circulation in the fetus 1 to 7. Then review the changes which occur at birth, which are listed A to E at the bottom of the figure.

For most fetuses these events occur without problems; a minority suffer potentially damaging asphyxia along the way.

7.2 Perinatal asphyxia and its prevention

In the healthy fetus the Po2 is only about 4 kPa, which is the arterial Po2 at the summit of Mount Everest (normal child 12–15 kPa). The needs of the fetus are fully met thanks to fetal adaptation, but oxygenation around the time of birth is in a state of delicate balance which depends critically on many factors.

Fetal adaptations to hypoxia

High haemoglobin (18 g/dL)
Fetal haemoglobin with left shifted dissociation curve (Chapter 25)
High cardiac output.

It is not surprising that the fetus has good defences against acute hypoxia. These include redistribution of blood flow in favour of vital tissues, and a myocardium and nervous system more resistant to hypoxic damage than those of the adult. Despite this, a small minority of fetuses suffer perinatal brain damage. Fetal hypoxia calls for prompt obstetric action and resuscitation at birth in order to prevent permanent damage.

7.2.1 Resuscitation (Figure 7.2)

Rapid assessment and action is needed for any baby who does not breathe within 30 s of birth, or who exhibits slow or irregular gasping. Bradycardia indicates hypoxia (Tables 7.2 and 7.3).

Figure 7.2 Resuscitation of the newborn. If you are at a delivery, rapidly assess pulse, respiration and colour. All babies are cleaned, dried and wrapped. If assessment is not satisfactory, move down the steps of the triangle, re-assess frequently, and go back up the triangle as the baby improves. External cardiac massage (ECM) and drugs are not used very often. You will need special training when you work with newborns.

Table 7.2 Apgar score, usually recorded at 1, 5 and 10 min after birth

Table 7.3 Pointers to fetal hypoxia

Obstetric	Fetal
Antepartum
Placental disease (pre-eclampsia, diabetes)	Intrauterine growth retardation
Placental abruption	Reduced fetal movements
Severe maternal illness	Abnormal fetal blood flow (Doppler’s)
Intrapartum
Umbilical cord prolapse/compression	Meconium-stained liquor
Obstructed labour/shoulder dystocia	Abnormal fetal heart rate (cardiotocograph)
Placenta praevia/placental abruption	Metabolic acidosis (fetal blood sample)
	Postpartum
	Bradycardia/apnoea Low Apgar score Delayed onset of respiration Metabolic acidosis (cord blood)

Avoid hypothermia by drying, and use the radiant heater (Figure 7.3). If needed, clear secretions from the mouth and then the nose with a soft suction catheter. In the correct position, the neck is extended, allowing for the infant’s large occiput. If hypoxia is not far advanced, breathing can usually be started by stimulation: gentle rubbing with a towel dries and stimulates! Some asphyxiated infants are pale, limp, apnoeic and bradycardic, and intermittent positive pressure ventilation is begun by either bag and mask or tracheal tube.

Figure 7.3 The resuscitaire comprises a heater, source of oxygen and suction, and an equipped platform for neonatal resuscitation.

PRACTICE POINT

In almost all infants, an airway and adequate ventilation is all that is needed for effective resuscitation. Simple actions done well prevent mortality and morbidity.

Infants who recover rapidly should be given to their mothers as soon as possible. Some babies with severe asphyxia need to be admitted to the neonatal unit.

7.2.2 Birth asphyxia

Birth asphyxia is the consequence of intrapartum fetal hypoxia/ischaemia. Most infants will recover rapidly with prompt resuscitation. More severe asphyxia may lead to hypoxic ischaemic encephalopathy (HIE), the acute neurological illness due to the effects of asphyxia on the fetal brain. HIE occurs in 1–2 per 1000 deliveries.

TREATMENT

Perinatal asphyxia induces a sequence of events over the first days, leading to neuronal death by apoptosis. Therapeutic hypothermia (cooling to 34 °C for 3 days), increases the chance of recovery without brain injury, and reduces the risk of cerebral palsy.

HIE is graded by clinical severity in the first days. The grade is important for prognosis (Table 7.4).

Table 7.4 Hypoxic ischaemic encephalopathy (HIE) grading

HIE grade	Prognosis
Mild: irritable with a high-pitched cry and poor feeding	Normal
Moderate: lethargic and hypotonic, poor feeding and occasional fits	40% risk of cerebral palsy
Severe: diminished conscious level, no spontaneous movement, multiple seizures and multi-organ failure	30% mortality90% cerebral palsy

HIE requires intensive care. Some 20% of cerebral palsy is due to intrapartum hypoxic-ischaemic damage.

7.3 Routine care of the normal baby

Labelling. All newborn babies should have name bands attached to wrist and ankle in the delivery room and in the presence of the mother.

Vitamin K. Newborn babies have low levels of vitamin K and its dependent clotting factors. Untreated, in less than 1%, this causes haemorrhagic disease of the newborn with bleeding from the gastrointestinal tract, into the skin or mucous membranes, or rarely into the brain. Haemorrhagic disease is prevented by prophylaxis.