Good-quality neonatal care is extremely important, and may have key implications for the rest of a baby’s life. Those born prematurely need skilled intensive support, and those born with presumed hypoxia need resuscitation, prompt assessment and appropriate subsequent care. The early neonatal period is often the time when congenital abnormalities become apparent and precise diagnosis and management can make a difference to the quality of life, or even influence whether the baby will live or die. The aim of this chapter is not to provide a comprehensive guide to neonatal care, but rather to highlight some of the more common neonatal problems which can occur.

It is essential that the obstetrician, midwife, paediatrician, neonatologist and neonatal nurse collaborate closely as a team. High-quality communication is essential if decision-making is to be optimized.

The apparent ease with which most babies make the transition from fetal to neonatal life conceals a host of complex physiological changes in virtually every system. Several relatively common neonatal disorders are related to difficulties with this transition.

The fetal lung at term contains about 100 mL of liquid. This equals the functional residual capacity and in a sense, the fetal lung can be said to form around a liquid cast of the future air spaces. Lung fluid is formed by alveolar cells, and fluid is essential for normal lung growth and development.

The fluid must be cleared at birth to make way for air, and failure to do so leads to breathlessness. This is known as transient tachypnoea of the newborn (TTN). It may last for a day or two, and is commoner after elective caesarean section.

The switch from fetal to neonatal circulation is normally made rapidly after birth. The key event is relaxation of the smooth muscle in the pulmonary blood vessels, which is triggered by the entry of oxygen into the lung with the first breath (note this paradoxical response to oxygen, which is the opposite to that of all other blood vessels).

In some babies, especially when there has been prolonged fetal hypoxia, this circulatory switch does not occur and may itself lead to further hypoxia. This condition is known as persistent fetal circulation and is difficult to distinguish clinically from congenital cyanotic heart disease.

Although the fetal kidney is important in maintaining the amniotic fluid volume, it has a negligible role in the excretion of waste products. After birth, the kidney must excrete all the body’s waste, as well as conserve fluid. In a baby born at term, the kidney is just able to manage this role, although there is always an initial rise in the blood urea and creatinine concentrations. The maximum urine osmolality, which the newborn can attain is about 600 mmol/L (compared with 1800 mmol/L in the adult) and it is therefore not surprising that dehydration and electrolyte disturbances are common complications of neonatal illness.

The fetus swallows amniotic fluid at about the same rate as it is produced, and deficiencies in fetal swallowing result in polyhydramnios. If there has been polyhydramnios, the baby should be examined for swallowing problems and should have an orogastric tube passed in order to exclude complete oesophageal atresia.

The term fetus has a high haemoglobin concentration, at around 18 g/dL. This is a response to the low arterial oxygen tension (3–4 kPa) which characterizes the latter part of intrauterine life. Once the oxygen tension rises after birth, this high haemoglobin is no longer needed, and falls to around 10 g/dL by about 8 weeks of age.

The white cell count at birth is high (12–20 × 10⁹/L) and polymorphs predominate. By 4 days of age, it is usually in the range 7–12 × 10⁹/L and is mainly lymphocytic.

There are several routine observations and procedures to perform on the newborn shortly after birth, but, providing the baby does not need to be resuscitated, none of them should be allowed to prevent the mother from seeing and holding her baby as soon as possible.

Providing all appears well, all that is needed in the labour ward is a brief examination for any obvious external abnormalities. A full routine examination should be deferred until later.

The cord should be checked to see whether it contains the usual two arteries and one vein. A single artery has a 20% association with congenital abnormalities, mainly of the genitourinary system. A plastic cord clamp should be fixed so as to leave about 2 cm of cord proximally. Subsequent care of the cord involves ensuring it is kept clean and dry. If the baby is likely to need intensive care, the cord should be left longer as it provides an accessible route for arterial and central venous cannulation.

Vitamin K does not cross the placenta well and newborn babies have low serum concentrations and poor stores. They do not have gut bacteria to synthesize it for them, and human milk is a relatively poor source of the vitamin. Lack of vitamin K leads to shortage of clotting factors II, VII, IX and X, and about 1 in 1000 breast-fed babies will experience serious bleeding, a condition known as haemorrhagic disease of the newborn. The classical form occurs between days 1–7, although an early form occurs in infants born to mothers taking anticonvulsants and a late (and sometimes more serious form) may also occur, even up to 12 weeks after delivery. Bottle-fed babies are at less risk because formulae are supplemented with vitamins.

Almost complete protection is provided by the administration of vitamin K 1 mg i.m. at the time of birth, and possibly less-complete protection is provided by giving vitamin K 2 mg orally twice in the first week (with a further oral dose at 1 month). Some epidemiological studies have found an association between i.m. vitamin K (as opposed to oral vitamin K) and childhood leukaemias, resulting in a swing away from treatment. Many large subsequent studies have failed to prove the connection.

Evolution has equipped the fetus with a remarkable ability to tolerate asphyxia without adverse consequences, to the extent that sometimes 10 or 15 min of absolute anoxia can be compatible with normal survival. In practice, absolute anoxia only occurs with rare events such as massive placental abruption or cord prolapse. Asphyxia may lead to cerebral palsy, essentially a motor disorder affecting posture and movement which is variably accompanied by mental impairment, epilepsy or sensory defects. Despite popular belief, it is likely that less than 10% of cerebral palsy is caused primarily by perinatal asphyxia.

Neonatologists are wary of making a diagnosis of perinatal asphyxia, unless there is a good antenatal history (e.g. abruption) together with neonatal ‘depression’ (e.g. poor Apgar scores) and evidence of subsequent multi-organ failure. Such multi-organ failure may present with seizures, cerebral oedema, oliguria, haematuria, coagulopathy, jaundice or occasionally pulmonary haemorrhage. The question of predicting the likelihood of neurological injury following a specific birth and the question of whether a subsequent developmental abnormality was caused by a specific intrapartum insult is seldom straightforward.

Current evidence suggests that therapeutic induced hypothermia (‘cooling’) to a rectal temperature of 33–34°C for 72 h improves both survival and neurological outcome at 18 months of age in infants with moderate or severe perinatal asphyxial encephalopathy. Therapeutic hypothermia is considered in infants of > 36 weeks completed gestation, admitted to a neonatal unit with one or more of the following:

 Apgar ≤ 5 at 10 min of age

 continued need for resuscitation, including endotracheal or mask ventilation, at 10 min after birth

 acidosis within 60 min of birth (defined as any occurrence of umbilical cord, arterial or capillary pH < 7.00)

 base deficit ≥ 16 mmol/L in umbilical cord or any blood sample (arterial, venous or capillary) within 60 min of birth.

Infants who fulfil one or more of the above criteria then require close observation for signs of seizures or moderate to severe encephalopathy evidenced by an:

 altered state of consciousness (reduced or absent response to stimulation) and

 abnormal tone (focal or general hypotonia, or flaccid) and

 abnormal primitive reflexes (weak or absent suck or Moro response).