Neonatal medicine

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Neonatal medicine

The dramatic reduction in neonatal mortality throughout the developed world has resulted from advances in the management of newborn infants together with improvements in maternal health and obstetric care. Neonatal intensive care became increasingly available in the UK from 1975, and it is since that time that the mortality of very low birthweight (VLBW) infants has fallen (Fig. 10.1).

Figure 10.1 **(a)** The dramatic fall in neonatal mortality rate in England and Wales in the second half of the twentieth century, according to birthweight. In very low birthweight infants (<1500 g), the marked fall in the mortality occurred after the introduction of intensive care. **(b)** Causes of neonatal deaths in England and Wales, 2008. (Adapted from the Audit Commission and ONS 2010).

About 8–10% of babies born in the UK are admitted to a neonatal unit for special medical and nursing care, although whenever possible babies are cared for on postnatal wards to avoid separating mothers from their babies. About 1–3% of babies require intensive care.

In the UK, neonatal units are organised as networks, with units providing either:

• special care (level 1)

• short-term intensive care (level 2)

• long-term intensive care (level 3), usually linked to specialist fetal and obstetric care to form a specialist tertiary perinatal centre.

Modern technology allows even tiny preterm infants to benefit from the full range of intensive care, anaesthesia and surgery. If it is anticipated during pregnancy that the infant is likely to require long-term intensive care or surgery, it is preferable for the transfer to the tertiary centre to be made in utero. When a baby requires transfer postnatally, transport should be by an experienced team of doctors and nurses. Arrangements should also be made for parents to be close to their infant during this stressful time.

Hypoxic-ischaemic encephalopathy

In perinatal asphyxia, gas exchange, either placental or pulmonary, is compromised or ceases altogether, resulting in cardiorespiratory depression. Hypoxia, hypercarbia and metabolic acidosis follow. Compromised cardiac output diminishes tissue perfusion, causing hypoxic-ischaemic injury to the brain and other organs. The neonatal condition is called hypoxic-ischaemic encephalopathy (HIE). It remains an important cause of brain damage, resulting in disability (Fig. 10.2) or death, and its prevention is one of the key aims of modern obstetric care. In developed countries, approximately 0.5–1/1000 liveborn term infants develop HIE and 0.3/1000 have significant neurologic disability. The incidence is higher in developing countries.

Figure 10.2 Brain damage from severe birth asphyxia.

Most cases of hypoxic-ischaemic encephalopathy (HIE) follow a significant hypoxic event immediately before or during labour or delivery. These include:

• Failure of gas exchange across the placenta – excessive or prolonged uterine contractions, placental abruption, ruptured uterus

• Interruption of umbilical blood flow – cord compression including shoulder dystocia, cord prolapse

• Inadequate maternal placental perfusion, maternal hypotension or hypertension – often with intrauterine growth restriction

• Compromised fetus – anemia, intrauterine growth restriction

• Failure of cardiorespiratory adaptation at birth – failure to breathe.

The clinical manifestations start immediately or up to 48 h after asphyxia, and can be graded:

• Mild – the infant is irritable, responds excessively to stimulation, may have staring of the eyes and hyperventilation and has impaired feeding

• Moderate – the infant shows marked abnormalities of tone and movement, cannot feed and may have seizures

• Severe – there are no normal spontaneous movements or response to pain; tone in the limbs may fluctuate between hypotonia and hypertonia; seizures are prolonged and often refractory to treatment; multi-organ failure is present.

The neuronal damage may be immediate from primary neuronal death or may be delayed from reperfusion injury causing secondary neuronal death. This delay offers the opportunity for neuroprotection with mild hypothermia.

Management

Skilled resuscitation and stabilisation of sick infants will minimise neuronal damage. Infants with HIE may need:

• respiratory support

• recording of amplitude-integrated electroencephalogram (aEEG, cerebral function monitor) to detect abnormal background activity to confirm early encephalopathy or identify seizures

• treatment of clinical seizures with anticonvulsants

• fluid restriction because of transient renal impairment

• treatment of hypotension by volume and inotrope support

• monitoring and treatment of hypoglycaemia and electrolyte imbalance, especially hypocalcaemia.

Recent randomised clinical trials have shown that mild hypothermia (cooling to a rectal temperature of 33–34° C for 72 h by wrapping the infant in a cooling blanket) reduces brain damage if started within 6 h of birth.

Prognosis

When HIE is mild, complete recovery can be expected. Infants with moderate HIE who have recovered fully on clinical neurological examination and are feeding normally by 2 weeks of age have an excellent long-term prognosis, but if clinical abnormalities persist beyond that time, full recovery is unlikely. Severe HIE has a mortality of 30–40%, and, of the survivors, over 80% have neurodevelopmental disabilities, particularly cerebral palsy. If magnetic resonance imaging (MRI) at 4–14 days in a term infant shows significant abnormalities (bilateral abnormalities in the basal ganglia and thalamus and lack of myelin in the posterior limb of the internal capsule), there is a very high risk of later cerebral palsy (Fig. 10.3).

Figure 10.3 Magnetic resonance image of the brain at term. Left: hypoxic-ischaemic encephalopathy (HIE) showing abnormal (white) signal in the basal ganglia and thalami (arrows) and absence of signal in the internal capsule bilaterally. Right: normal scan showing grey basal ganglia and a white signal from myelin in the posterior limb of the internal capsule.

Although hypoxic-ischaemic injury usually occurs antenatally or during labour or delivery, it may occur postnatally or be caused by a neonatal condition (e.g. inborn error of metabolism or kernicterus). The diagnosis ‘birth asphyxia’ has potentially serious medicolegal implications; it has been recommended that infants who have the clinical features of HIE should only be considered to have birth asphyxia if there is:

• evidence of severe hypoxia antenatally or during labour or at delivery

• resuscitation needed at birth

• features of encephalopathy

• evidence of hypoxic damage to other organs such as liver, kidney, or heart

• no other prenatal or postnatal cause identified

• characteristic findings on MRI neuroimaging.

Summary

Mild hypothermia for moderate and severe HIE reduces death and severe disability and increases the likelihood of survival with normal neurological function.

Birth injuries

Infants may be injured at birth, particularly if they are malpositioned or too large for the pelvic outlet. Injuries may also occur during manual manoeuvres, from forceps blades or at Ventouse deliveries. Fortunately, now that Caesarean section is available in every maternity unit, heroic attempts to achieve a vaginal delivery with resultant severe injuries to the infant have become extremely rare.

Soft tissue injuries

These include:

• Caput succedaneum (Fig. 10.4) – bruising and oedema of the presenting part extending beyond the margins of the skull bones; resolves in a few days

• Cephalhaematoma (Figs 10.4, 10.5) – haematoma from bleeding below the periosteum, confined within the margins of the skull sutures. It usually involves the parietal bone. The centre of the haematoma feels soft. It resolves over several weeks

• Chignon (Fig. 10.6) – oedema and bruising from Ventouse delivery

• Bruising to the face after a face presentation and to the genitalia and buttocks after breech delivery. Preterm infants bruise readily from even mild trauma

• Abrasions to the skin from scalp electrodes applied during labour or from accidental scalpel incision at Caesarean section

• Forceps marks to face from pressure of blades – transient

• Subaponeurotic haemorrhage (Fig. 10.4) (very uncommon) – diffuse, boggy swelling of scalp on examination, blood loss may be severe and lead to hypovolaemic shock and coagulopathy.

Nerve palsies

Brachial nerve palsy results from traction to the brachial plexus nerve roots. They may occur at breech deliveries or with shoulder dystocia. Upper nerve root (C5 and C6) injury results in an Erb palsy (Fig. 10.7). It may be accompanied by phrenic nerve palsy causing an elevated diaphragm. Most palsies resolve completely, but should be referred to an orthopaedic or plastic surgeon if not resolved by 2–3 months. Most recover by 2 years. A facial nerve palsy may result from compression of the facial nerve against the mother’s ischial spine. It is unilateral, and there is facial weakness on crying but the eye remains open. It is usually transient, but methylcellulose drops may be needed for the eye. Rarely, nerve palsies may be from damage to the cervical spine, when there is lack of movement below the level of the lesion.

Fractures

Clavicle

Usually from shoulder dystocia. A snap may be heard at delivery or the infant may have reduced arm movement on the affected side, or a lump from callus formation may be noticed over the clavicle at several days of age. The prognosis is excellent and no specific treatment is required.

Humerus/femur

Usually mid-shaft, occurring at breech deliveries, or fracture of the humerus at shoulder dystocia. There is deformity, reduced movement of the limb and pain on movement. They heal rapidly with immobilisation.

Stabilising the preterm or sick infant

Preterm infants of <34 weeks’ gestation and newborn infants who become seriously ill require their condition to be stabilised and monitored (Fig. 10.8). Many of them will need respiratory and circulatory support.

Stabilising preterm or sick infants

Airway, breathing

• Respiratory distress: tachypnoea, laboured breathing with chest wall recession, nasal flaring, expiratory grunting, cyanosis

• Apnoea

Management, as required:

• Clear the airway

• Oxygen

• High-flow humidified oxygen therapy

• CPAP (continuous positive airway pressure)

• Mechanical ventilation

Monitoring

• Oxygen saturation (maintain at 88–95% if preterm)

• Place in plastic bag at birth to keep warm if extremely preterm

• Perform stabilisation under a radiant warmer or in a humidified incubator to avoid hypothermia.

Figure 10.8 Stabilising preterm or sick infants is important to prevent complications. This preterm infant has leads on his limbs for monitoring heart rate and respiratory rate, temperature and oxygen saturation. There are arterial and intravenous cannulae and a nasotracheal tube for artificial ventilation.

Venous and arterial lines

Peripheral intravenous line

Required for intravenous fluids, antibiotics and other drugs.

Umbilical venous catheter

May be used for intravenous access at resuscitation, in extremely preterm infants for the first few days or to administer high osmolality fluids (e.g. high-concentration dextrose) or medications needing central delivery (e.g. inotropes).

Arterial line

• Inserted if frequent blood gas analysis, blood tests and continuous blood pressure monitoring are required. Usually umbilical artery catheter (UAC), sometimes peripheral cannula if for short period or no umbilical artery catheter possible.

• The arterial oxygen tension is maintained at 8–12 kPa (60–90 mmHg) and the CO₂ tension at 4.5–6.5 kPa (35–50 mmHg). Continuous non-invasive transcutaneous arterial blood gas monitoring may also be used.

Central venous line for parenteral nutrition, if indicated

Inserted peripherally when infant is stable.

Chest X-ray with or without abdominal X-ray

Assists in the diagnosis of respiratory disorders and to confirm the position of the tracheal tube and central lines.

Investigations

• Haemoglobin, neutrophil count, platelet count

• Blood urea, creatinine, electrolytes and lactate

• Culture – blood ± CSF ± urine

• Blood glucose

• CRP/acute phase reactant

• Coagulation screen if indicated

Antibiotics

Broad-spectrum antibiotics are given.

Minimal handling

All procedures, especially painful ones, adversely affect oxygenation and the circulation. Handling the infant is kept to a minimum and done as gently, rapidly and efficiently as possible. Analgesia should be provided to prevent pain as necessary.

Parents

Although medical and nursing staff are usually fully occupied stabilising the baby, time must be found for parents and immediate relatives to allow them to see and touch their baby and to be kept fully informed.

The preterm infant

The appearance, the likely clinical course, chances of survival and long-term prognosis depend on the gestational age at birth. The appearance and maturational changes of very preterm infants are described in Table 10.1 and the importance of parental involvement shown in Figures 10.10a and b. The external appearance and neurological findings can be scored to provide an estimate of an infant’s gestational age (see Appendix).

The rate and severity of problems associated with prematurity decline markedly with increasing gestation. Infants born at 23–26 weeks’ gestation encounter many problems (Box 10.1), require many weeks of intensive and special care in hospital and have a high overall mortality. With modern intensive care, the prognosis is excellent after 32 weeks’ gestational age. The severity of an infant’s respiratory disease and of any episodes of infection largely determine the neonatal course and outcome.

Respiratory distress syndrome

In respiratory distress syndrome (RDS), (also called hyaline membrane disease), there is a deficiency of surfactant, which lowers surface tension. Surfactant is a mixture of phospholipids and proteins excreted by the type II pneumocytes of the alveolar epithelium. Surfactant deficiency leads to widespread alveolar collapse and inadequate gas exchange. The more preterm the infant, the higher the incidence of RDS; it is common in infants born before 28 weeks’ gestation and tends to be more severe in boys than girls. Surfactant deficiency is rare at term but may occur in infants of diabetic mothers. The term hyaline membrane disease derives from a proteinaceous exudate seen in the airways on histology. Glucocorticoids, given antenatally to the mother, stimulate fetal surfactant production and are given if preterm delivery is anticipated (see Ch. 9.)

The development of surfactant therapy has been a major advance. The preparations are natural, derived from extracts of calf or pig lung. They are instilled directly into the lung via a tracheal tube. Multinational placebo-controlled trials show that surfactant treatment reduces mortality from RDS by about 40%, without increasing the morbidity rate (Fig. 10.11).

At delivery or within 4 h of birth, babies with RDS develop clinical signs of:

• tachypnoea >60 breaths/min

• laboured breathing with chest wall recession (particularly sternal and subcostal indrawing) and nasal flaring

• expiratory grunting in order to try to create positive airway pressure during expiration and maintain functional residual capacity

• cyanosis if severe.

The characteristic chest X-ray appearance is shown in Figure 10.12. Treatment with raised ambient oxygen is required, which may need to be supplemented with continuous positive airway pressure (delivered via nasal cannulae) or artificial ventilation via a tracheal tube. The ventilatory requirements need to be adjusted according to the infant’s oxygenation (which is measured continuously), chest wall movements and blood gas analyses. Mechanical ventilation (with intermittent positive pressure ventilation or high-frequency oscillation) may be required. High-flow humidified oxygen therapy, via nasal cannulae, may be used to wean babies from added oxygen therapy.

Surfactant therapy reduces morbidity and mortality of preterm infants with respiratory distress syndrome.

The preterm infant: maturational changes in appearance and development

Figure 10.9 **(a)** Preterm infant. **(b)** Term infant.

Table 10.1

The preterm infant compared with the term infant

Gestation	23–27 weeks	Term (37–42 weeks)
Birthweight (50th centile)	At 24 weeks – male 700 g, female 620 g	At 40 weeks – male 3.55 kg, female 3.4 kg
Skin	Very thin (Fig. 10.9a)	Thick skin (Fig. 10.9b)
	Dark red colour all over body	Pale pink colour
Ears	Pinna soft, no recoil	Pinna firm, cartilage to edge, immediate recoil
Breast tissue	No breast tissue palpable	One or both nodules >1 cm
Genitalia	Male – scrotum smooth, no testes in scrotum	Male – scrotum has rugae, testes in scrotum
	Female – prominent clitoris, labia majora widely separated, labia minora protruding	Female – labia minora and clitoris covered
Breathing	Needs respiratory support. Apnoea common	Rarely needs respiratory support. Apnoea rare
Sucking and swallowing	No coordinated sucking	Coordinated (from 34–35 weeks)
Feeding	Usually needs TPN (total parenteral nutrition), then tube feeding	Cries when hungry. Feeds on demand
Cry	Faint	Loud
Vision, interaction	Eyelids may be fused. Infrequent eye movements. Not available for interaction	Makes eye contact, alert wakefulness
Hearing	Startles to loud noise	Responds to sound
Posture	Limbs extended, jerky movements	Flexed posture, smooth movements

Figure 10.10a Parental involvement in neonatal care. Skin-to-skin contact between infant and parent (Kangaroo care) promotes bonding.

Figure 10.10b Parental involvement in neonatal care. Mother giving her baby expressed breast milk (in syringe) via nasogastric tube, allowing close eye and skin contact between mother and baby.

Respiratory distress syndrome

• Common in very preterm infants

• Caused by surfactant deficiency

• Antenatal corticosteroids and surfactant therapy markedly reduce morbidity and mortality.

Figure 10.11 Meta-analysis of treatment of preterm infants with natural surfactant, showing a dramatic reduction in pneumothoraces and mortality.

Figure 10.12 Chest X-ray in respiratory distress syndrome showing a diffuse granular or ‘ground glass’ appearance of the lungs and an air bronchogram, where the larger airways are outlined. The heart border becomes indistinct or obscured completely with severe disease. A tracheal tube and an umbilical artery catheter are present.

Pneumothorax

In respiratory distress syndrome, air from the overdistended alveoli may track into the interstitium, resulting in pulmonary interstitial emphysema (PIE). In up to 10% of infants ventilated for RDS, air leaks into the pleural cavity and causes a pneumothorax (Fig. 10.13). When this occurs, the infant’s oxygen requirement usually increases, and the breath sounds and chest movement on the affected side are reduced, although this can be difficult to detect clinically. A pneumothorax may be demonstrated by transillumination with a bright fibreoptic light source applied to the chest wall. A tension pneumothorax is treated by inserting a chest drain. In order to try and prevent pneumothoraces, infants are ventilated with the lowest pressures that provide adequate chest movement and satisfactory blood gases.