Introduction

Good-quality neonatal care is extremely important and can have major implications for the rest of a baby’s life. Those born prematurely need skilled intensive support. 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 – precise diagnosis and care can make a difference to the quality of life or even influence whether the baby will survive or die. The aim of this chapter is to highlight some of the more common neonatal problems.

It is essential that the obstetrician, midwife, paediatrician, neonatologist and neonatal nurse collaborate as a team. Effective communication is essential in making the best decisions for baby.

The Transition at Birth

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.

Respiratory system

At term and before birth, the fetal lung contains about 100 mL of liquid. This equals the functional residual capacity. Lung fluid is formed by alveolar cells and is essential for normal lung growth and development.

Transient tachypnea of the newborn (TTN) is respiratory maladaptation and retention of lung fluid, occurring in 1% to 2% of all births. It is self-limiting, rarely lasts longer than 48 hours and is, by definition, transient. It is more common following caesarean sections in which the mother has not been in labour.

Respiratory distress syndrome (RDS) is caused by a deficiency of alveolar surfactant and is more common in pre-term infants (30% at 28 weeks vs 0.1% at term). Surfactant, a complex lipoprotein consisting of phosphatidyl choline, is synthesised by type II pneumocytes within the alveoli and is important in reducing surface tension, allowing the alveoli to expand. Hypoxia, acidosis and hypothermia reduce surfactant production; meconium aspiration and maternal diabetes reduce surfactant efficacy. Antenatal corticosteroids increase surfactant production and thereby reduce the incidence of RDS. Clinically, there is tachypnea, grunting and intercostal recession commencing within the first 4 hours of life; poor oxygenation requiring supplemental oxygen therapy; and chest X-rays demonstrate a generalised reticulogranular appearance referred to as ‘ground glass’ ( Fig. 43.1 ). Some babies spontaneously improve, some babies require continuous positive airway pressure (CPAP), and increasing respiratory distress and oxygen requirements are indications for administration of artificial surfactant.

Fig. 43.1, Respiratory distress syndrome (RDS) following emergency caesarean section. The mother had diabetes, which predisposes to RDS. Note the ground-glass appearance of the lungs.

Meconium staining of amniotic fluid occurs in approximately 1 in 10 births. Inhaled meconium can irritate neonatal lungs and may lead to pneumonitis ( Fig. 43.2 ). This is called meconium aspiration syndrome (MAS) and is a rarer complication with potentially serious effects. Aspiration most commonly occurs in utero and is thought to be associated with fetal distress. Suction of babies on the perineum or routine suction after delivery used to be advised. However, now that we understand that most aspiration occurs in utero and that suctioning the oropharynx may delay aerating the lungs, it is no longer recommended.

Fig. 43.2, Meconium aspiration syndrome. Note the widespread patchy shadowing in both lungs.

Clinical features range from mild neonatal tachypnea to severe respiratory compromise manifested as a large ventilation perfusion mismatch, sepsis complications and persistent pulmonary hypertension of the newborn (PPHN). Treatment includes oxygen, ventilatory support and surfactant therapy (as meconium can displace or inactivate endogenous surfactant). If severe, measures to treat complications such as PPHN also include supporting systemic blood pressure and inhaled nitric oxide. The most severe cases may benefit from extracorporeal membrane oxygenation, in which blood is oxygenated artificially outwith the body and then returned to the systemic circulation (like a lung-bypass machine).

Cardiovascular system

The key event in switching from fetal to neonatal circulation 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. This relaxation allows blood from the right ventricle of the heart to enter the pulmonary circulation, rather than the ductus arteriosus.

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.

Genitourinary system

Routine antenatal ultrasound screening will detect most common renal disorders. In utero, the fetal kidney maintains the amniotic fluid volume. However, the principal organ of excretion of waste metabolites is the placenta. After birth, the kidney must filter the blood for waste metabolites as well as perform fluid homeostasis. Healthy kidneys in a healthy term baby manage this transition with 90% of babies passing urine in the first 24 hours and 98% within 48 hours. There is a very limited reserve of renal function at this point, meaning that dehydration and electrolyte disturbances are common complications of prematurity and any neonatal illness.

Gastrointestinal system

The fetus swallows amniotic fluid at about the same rate as it is produced, maintaining a normal liquor volume in utero. Deficiencies in fetal swallowing result in polyhydramnios. If there has been polyhydramnios during pregnancy, there should be a low threshold for investigating further after the baby is born, including examination for swallowing problems and exclusion of complete oesophageal atresia by the passage of a nasogastric tube.

Haematological system

Haematological problems typically arise from conditions which affect the blood constituents – commonly, red blood cells, haemoglobin and platelets. At birth, babies have a high haematocrit, haemoglobin concentration and white cell count. The initially high haemoglobin concentration, at around 18 g/dL, is a response to the low placental arterial oxygen tension (3–4 kPa). Once the oxygen tension rises after birth, this falls to around 10 g/dL by about 8 weeks of age.

Routine Care at Birth

There are several routine procedures to perform on the newborn soon after birth. However, provided that the baby does not need resuscitation, none of these procedures should prevent the mother from holding and feeding her baby as soon as possible.

Optimal cord clamping

Optimal cord clamping is when placental oxygenation and perfusion of the baby is maintained for at least 60 seconds following birth. Clamping the umbilical cord immediately after birth can deprive the term baby of between 80 to 200 mL of blood.

Assessment

The baby’s condition at 1 and 5 minutes of age is assessed by means of the Apgar score (see Table 38.1 and Chapter 38 ). The purpose of this is to have an objective record of how the baby initially responded to the challenge of extrauterine life. It serves as a guide to the need for resuscitation. However, unless the score fails to improve with resuscitation, it has very little predictive value for later disability. A low Apgar score is not synonymous with birth asphyxia. It may reflect, for example, a pre-existing fetal problem or temporary sedation caused by medication administered to the mother prior to birth.

Preventing hypothermia

Newborn babies lose heat faster than they can generate it ( Box 43.1 ). Maintaining normothermia (a temperature between 36.5°C and 37.5°C) is essential to reducing mortality and morbidity, particularly in premature babies. Even brief periods of hypothermia are associated with impaired surfactant production, hypoxia, PPHN and coagulation problems. The birthing room must be warm and draughts kept to a minimum. The baby should be immediately dried, wrapped in dry towels or a blanket and have a hat put on. Any resuscitation should be performed under a radiant heater. Very pre-term babies should be delivered into a polythene bag to minimise evaporative losses as they are particularly at risk due to immature skin, reduced subcutaneous fat and poor vasomotor control.

Box 43.1
Heat balance at birth

Mechanisms of heat loss (in priority order)

  • Evaporation of water (primarily from wet skin but also from wet towels/clothing if not replaced)

  • Convective loss due to air currents

  • Radiation to cold surfaces

  • Conductive loss to cold mattress

Mechanisms of heat gain

  • Skin-to-skin contact with parent

  • Metabolism of brown fat (plentiful in newborn)

  • Muscular activity

  • Radiant heater over cot

  • Warm mattress

Examination

In babies who need no help transitioning at birth, a brief examination for any obvious external abnormalities can be performed initially, and a full routine newborn examination deferred until later.

Weighing and measuring

Weight, length and head circumference measurements provide an assessment of how well the baby had grown in utero and are a baseline against which to judge subsequent growth.

The umbilical cord

The cord should be checked to see whether it contains two arteries and one vein. A single artery may be associated with congenital anomalies. A plastic cord clamp (or other sterile tie) should be placed securely to leave 2 to 3 cm of cord between cord clamp and baby. If the baby is likely to need intensive care, the cord should be left longer (6–8 cm), as it provides an accessible route for arterial and central venous cannulation.

Sterile cutting of the umbilical cord and proper cord care are essential to prevent neonatal infection, especially in populations where mothers are not universally immunised against tetanus (neonatal tetanus has a mortality rate of 70%–100%). Caregivers should be advised against applying any foreign substances to the unhealed cord stump. Keeping the stump clean and dry promotes healing and reduces the risk of omphalitis.

Preventing haemorrhagic disease of the newborn

Vitamin K is essential for clotting but does not cross the placenta well. Thus, newborn babies have low serum concentration and low reserves. A small number of babies who do not receive routine vitamin K prophylaxis will experience significant spontaneous bleeding, a condition known as haemorrhagic disease of the newborn. The classical form occurs between days 1 and 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 birth. Blood may be noticed in babies’ stools, in their urine, or there may be oozing of blood from around the umbilical stump. Babies may suffer spontaneous bruising; in severe cases, they may be sleepy, irritable, or poorly feed because of intracranial bleeding. 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 intramuscularly within 6 hours of birth. Alternatively, 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. With the oral route, there is uncertainty about how much of the intended dose is swallowed and absorbed by the baby.

Perinatal Asphyxia

Evolution has equipped the fetus with a remarkable ability to tolerate asphyxia without adverse consequences, to the extent that sometimes 10 or 15 minutes of absolute anoxia can be compatible with healthy survival. In practice, absolute anoxia occurs only with rare events, such as massive placental abruption or cord prolapse. Perinatal asphyxia can lead to hypoxic ischaemic encephalopathy (HIE). This is a clinically defined syndrome based on neurological dysfunction (difficulty in initiating and maintaining respiration, depression of tone and reflexes, reduced levels of consciousness and seizures) with convincing evidence of antepartum or intrapartum hypoxia. HIE causing moderate or severe encephalopathy occurs in around 2 of 1000 births, and the risk of death or cerebral palsy (CP) in survivors is around 60%. Neonatologists are wary of making a diagnosis of perinatal asphyxia unless there is a clear 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 subsequent neurological impairment following a specific birth and the question of whether this was caused by a specific intrapartum event is seldom straightforward.

Current evidence suggests that therapeutic-induced hypothermia (‘cooling’) to a rectal temperature of 33°C to 34°C within 6 hours of birth for 72 hours improves both survival and neurological outcome at 18 months of age in infants with moderate or severe perinatal asphyxial encephalopathy. Babies who will benefit most from therapeutic hypothermia are those with severe acute compromise, over 36 weeks’ gestation and over 1.8 kg at birth. The lower core body temperature is thought to reduce the amount of inflammation-related harm to the baby’s brain.

If therapeutic hypothermia is being considered, many other factors will have a bearing on the decision, which will almost always be made by a senior neonatologist in conjunction with a specialist cooling centre.

You're Reading a Preview

Become a Clinical Tree membership for Full access and enjoy Unlimited articles

Become membership

If you are a member. Log in here