Neonatal resuscitation

Most infants do not require resuscitation. Some may not establish effective respiration and require help. Infant resuscitation is covered in Appendix I. The resuscitation routine is altered if the baby is premature or if the amniotic fluid is stained with meconium.

The Apgar score

The Apgar score (named after Virginia Apgar) is calculated at 1 and 5 minutes of life. It gives an indication of the condition of the baby at this time and provides a standard way of documenting the health of the baby in the first few minutes of life. Many parents know about this score. It is sometimes necessary to reassure worried parents that a score of less than 10 at 1 or 5 minutes is not an indicator for a lifetime of under-achievement! (see Table 17.3).

Adaptation to extra-uterine life

The process of delivery, temperature change and the clamping of the umbilical cord results in gasping and the removal of the remaining lung fluid. The pulmonary vascular resistance falls and pulmonary blood flow increases. The increased left atrial filling closes the foramen ovale and oxygenated blood flowing through the ductus arteriosus causes its eventual closure (see also Chapter 9, pp. 91–93).

Examination of the newborn

Every newborn baby is examined soon after birth – usually within the first 24 hours of life. This examination is in part a screening tool but is also an opportunity for parents to raise concerns they might have about their child.

The objectives of the examination are to identify any congenital anomaly not identified by antenatal screening. The most important of these are structural heart lesions (see Chapter 9, pp. 91–95), congenital cataracts and other eye disease detectable through absence of the ‘red reflex’ (see Chapter 14, p. 210), and developmental dysplasia of the hip (see Chapter 6, p. 49) (see Figure 17.1).

Figure 17.1 The post-natal examination.

Birth injuries

Deliveries following an obstructed labour or malpresentation and instrumental deliveries can cause injury. These include nerve palsies, soft-tissue injuries and fractures. The newborn examination will identify these.

Feeding

Vitamin K

Babies have a limited ability to synthesize vitamin K. This persists for the first 3 months of life. In addition, during early infancy when fed entirely on milk, babies have very little supply of vitamin K, especially if exclusively breast-fed. A very small number of babies suffer bleeding due to vitamin K deficiency. This is called ‘haemorrhagic disease of the newborn’.

Haemorrhagic disease of the newborn is prevented when a supplement of vitamin K is given to babies soon after birth. In the 1990s one study suggested a link between vitamin K administration to babies and the future risk of leukaemia.

In 1997 a panel of experts considered all the studies and concluded that, overall, the data do not support an increased risk of cancer caused by vitamin K. The Department of Health recommends that vitamin K supplements should be offered to all newborn babies. Intramuscular injections of vitamin K (phytomenadione, Konakion) prevent haemolytic disease of the newborn in virtually all babies. A single dose is recommended at birth.

Newborn screening

All babies in the UK are offered screening for phenylketonuria (PKU), congenital hypothyroidism, sickle-cell disease, cystic fibrosis (CF) and the rare but treatable fatty acid metabolism disorder medium-chain acyl-CoA dehydrogenase deficiency (MCADD). Blood for testing is taken via a heel prick sample at 5 days of age.

Neonatal encephalopathy

Neonatal encephalopathy is most often caused by perinatal hypoxia (‘birth asphyxia’). This situation arises as a result of a cerebral insult before or during labour or delivery. It occurs in 1–2/1000 deliveries. Prompt and effective resuscitation is an important start to the treatment of this serious condition.

Hypothermia for hypoxic-ischaemic encephalopathy

Previously there was no specific treatment for asphyxia other than stabilization, intensive care and treatment to reduce seizures.

Since 2009, the use of whole-body cooling following perinatal asphyxia has become standard treatment for asphyxiated term infants. It is a safe treatment that improves survival and reduces neurological and neurodevelopmental impairments. Babies who have experienced moderate or severe asphyxia are cooled as soon as possible after birth (cooling should start before 6 hours of age). Cooled babies have their body temperature reduced to 33.5°C for 72 hours, followed by gradual re-warming.

Cooled babies have an increased rate of survival without neurological abnormality (cooling results in reduced risks of cerebral palsy and improved scores on neurodevlopmental assessments).

Jaundice

Most newborn infants become jaundiced. Reasons for this include:

As increased red cell turnover and hepatic immaturity are normal physiological variants in newborn babies, the jaundice arising as a result is termed ‘physiological jaundice’. This term separates it from jaundice that occurs secondary to disease – ‘pathological jaundice’.

Jaundice appearing in the first day of life or persisting beyond 2 weeks of age is, until proven otherwise, assumed to be pathological – a proportion of babies with day 1 jaundice or persisting jaundice will have harmless physiological jaundice but this cannot be assumed until the jaundice is investigated for haemolysis or other causes. (For premature infants, in whom hepatic immaturity is more pronounced, jaundice is not considered abnormal until persisting beyond 3 weeks of age.)

Physiological jaundice starts after day 1 of life, peaks around day 4 or 5, and then gradually resolves over the next week.

Breast milk jaundice is physiological jaundice occurring in a breast-fed baby. Infants who are breast-fed are more likely than formula-fed infants to become jaundiced. Components of the breast milk act as inhibitors of hepatic bilirubin metabolism.

Group B Streptococcus infection

The incidence of Group B Streptococcus infection is estimated to be 0.7/1000 live births, although significant variation in incidence occurs around the world. Group B Streptococcus is a common inhabitant of the maternal genitourinary and gastrointestinal tract. It colonizes about 10–30% of pregnant women. Only 50% of carriers can be detected, and only 50% of these will have a positive culture at the time of labour. Rates of vertical transmission and subsequent colonization of the infant vary from 40% to 75%, but the neonatal infection rate is low. Screening for Group B Streptococcus is therefore too unreliable to be of use. Risk factors which substantially increase the risk of transmission include:

As 66% of Group B Streptococcus-infected infants will present within the first 7 days, any baby showing signs of illness needs to be investigated and treated promptly in order to exclude Group B Streptococcus. The overall mortality is 9.4% (6% for term infants and 18% for preterm infants). Suspected or confirmed Group B Streptococcus is treated with a penicillin or cephalosporin, coupled with an aminoglycoside, e.g. benzylpenicillin and gentamicin.

Respiratory distress syndrome

Respiratory distress syndrome is caused by a deficiency in surfactant and is usually associated with prematurity. Surfactant is a mixture of lipoproteins excreted by type II pneumocytes in the alveolar epithelium, lowering surface tension. Surfactant deficiency leads to a higher surface tension, alveolar collapse and inadequate gas exchange. Other causes of surfactant deficiency include sepsis, hypoxia, acidosis and hypothermia. Exogenous surfactant therapy is given to many premature infants but may also be used in term infants in certain conditions where surfactant deficiency is thought to be a contributing factor in a disease process. One major advance in the prevention of respiratory distress syndrome has been to give mothers antenatal steroids to stimulate fetal surfactant production (see Figure 17.2).

Figure 17.2 X-ray of infant with respiratory distress syndrome. Typical chest X-ray appearance of respiratory distress syndrome with ‘ground glass’ appearance of the lungs and air bronchograms.

Management of respiratory distress is with respiratory support. The majority of babies below 28 weeks’ gestation will require a period of mechanical ventilation. Ventilation is associated with lung injury which may manifest acutely as pneumothorax, and commonly leads to chronic lung disease, with prolonged oxygen dependence.

Chronic lung disease is defined as oxygen dependency (or other respiratory support) at the equivalent of 36 weeks of gestation. The likelihood of chronic lung disease is greatly increased in growth-retarded infants and those with patent ductus arteriosus (see Chapter 9, p. 95). Chronic lung disease renders the infant very susceptible to respiratory infection, particularly with respiratory syncytial virus and right heart failure (cor pulmonale). Steroids – usually dexamethasone – may improve lung function sufficiently to wean a child from respiratory support, but their use is associated with a high incidence of cerebral palsy (>30%) and does not improve long-term survival.

Periventricular haemorrhage

The brain of the premature infant is highly susceptible to haemorrhage. Some degree of periventricular haemorrhage affects 50% of babies weighing less than 1500 g at birth. The floors of the lateral ventricles contain a rich network of vessels. These vessels involute in the 3rd trimester, making haemorrhage rare in infants above 32 weeks gestation. Infants who are unwell with infection, hypoxia, acidosis or hypotension are at particularly high risk.

Haemorrhages are graded according to severity:

Grade I and II haemorrhages are not associated with adverse outcomes, but grade III or IV haemorrhages, particularly if bilateral, are associated with a high risk of cerebral palsy (see Chapter 14, p. 197).

Infection

Defence against infection relies on physical barriers to infection – the skin and respiratory and gut epithelium, as well as the immune system. The skin of the preterm baby is thin and porous and is frequently breached for venepunctures and cannulas.

The immune defences against infection in a term baby include an endowment of transplacentally acquired IgG antibodies received in the third trimester, and IgA antibodies in breast milk. Premature babies are deprived of their inheritance of antibodies and are often too unwell to feed, even if breast milk is available. The immunologically naive immune system is functional but demonstrates impaired responses to antigenic challenge.

Accordingly, premature infants are at extremely high risk of severe and invasive bacterial and fungal infections, and organisms such as coagulase-negative staphylococci, normally considered to be skin commensals, may become pathogenic.

Nutrition

Preterm infants have higher nutritional requirements by weight than term infants. Nutrient accretion occurs predominantly in the third trimester. Therefore, preterm infants have limited reserves of fat, glycogen and micronutrients. In addition, these infants have an accelerated growth phase and may be unable to tolerate large volumes of feed. Specialized breast milk fortifiers and preterm formulas are used for preterm infants to optimize growth and development.

Cleft lip and palate

These embryological abnormalities may be diagnosed antenatally. They are common, affecting 1 in 700 infants. Careful examination is necessary to exclude other abnormalities that might suggest a syndrome such as D George syndrome (see Chapter 18, p. 272) or fetal alcohol syndrome. Most concerning is Pierre Robin syndrome, in which there is cleft palate and an underdeveloped jaw, causing the tongue to obstruct the airway.

Early feeding advice is necessary. Early repair of a cleft lip is possible. A cleft palate repair may be deferred until the baby is several months old. Alongside surgical intervention, speech and language therapy, ENT, audiology and orthodontic support are required.

Congenital gut abnormalities

Obstruction due to atresias and stenosis can occur at any level in the gastrointestinal tract, the more proximal the obstruction is the sooner the child presents.

Neural tube defects

The incidence of neural tube defects has declined over the last 40 years. Antenatal screening (elevated alpha-fetoprotein and/or ultrasound) detects most cases during the early stages of pregnancy, allowing termination. Periconceptual folic acid reduces the risk of recurrence in subsequent pregnancies. The defects are described depending on the site in which the neural tube fails to close (see Table 17.7).

Table 17.7 Neural tube defects

The neurological outcome for these children varies enormously. Early diagnosis, and neurological and neurosurgical assessment are necessary. Walking and continence are the major management issues in the defects compatible with life. Other congenital anomalies are discussed in relevant chapters.