After reading this chapter you should be able to diagnose and manage:
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birth injury
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short and long-term consequence of preterm birth
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common medical conditions
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common surgical conditions
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congenital anomaly
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common postnatal problems
and
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know the effect of prenatal and perinatal events on neonates
Antenatal assessment of fetal growth
Antenatal assessment of the mother and fetus requires a comprehensive history and examination, investigations for potential congenital infections and chromosomal anomalies and ultrasound monitoring. Ultrasonography will assess the breathing pattern, muscle tone, body movement and amniotic fluid volume. The main aim is to identify early intrauterine growth restriction—IUGR—(also referred to as fetal growth restriction [FGR]).
IUGR is defined as the failure of the fetus to achieve its full growth potential and could be due to maternal, fetal or neonatal causes. It is the biggest risk factor for stillbirth, perinatal and neonatal morbidity and mortality.
Definition and classification
The most common obstetric definition of IUGR is an estimated weight below the 9 th centile for gestational age in the second half of pregnancy. This definition does not distinguish the normal, constitutionally small fetus (small for gestational age [SGA]) from the small fetus whose growth potential is restricted. The latter fetus is at increased risk of perinatal morbidity and mortality whereas the former is not.
IUGR may be:
Symmetrical IUGR (20%–30% of small fetuses) that refers to a growth pattern in which all fetal organs are decreased proportionally and is thought to result from a pathological process manifesting early in gestation.
Asymmetrical IUGR (70%–80 % of small fetuses) where there is a relatively greater decrease in abdominal size (liver volume and subcutaneous fat tissue) than in head circumference and is thought to occur late in gestation.
Screening for intrauterine growth restriction
Fundal height (FH) measurement
Measurement of the distance between the upper edge of the pubic symphysis and the top of the uterine fundus is performed during antenatal care to detect IUGR.
Selective ultrasonography
Indications for a growth scan are:
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first FH measurement below 9th centile at between 26–28 weeks
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no increase in sequential measurements
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sequential measurements do not follow the expected growth
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sequential measurements cross centiles in an upward direction
All women should be assessed at booking for risk factors to identify those who need increased surveillance. Some will be at increased risk of developing fetal growth restriction because of factors in the current pregnancy, in the past medical history or the past obstetric history. Those women with such risk factors will need serial scans at least every 3 weeks from 26–28 weeks until delivery ( Table 2.1 ).
Growth indices
Estimated fetal weight is the most common method of identifying the growth-restricted fetus as it combines multiple biometric measurements including abdominal circumference, biparietal diameter, head circumference and femur length.
Customised growth charts are used to plot both fundal height measurements obtained during clinical examination and estimated fetal weight following an ultrasound examination. They are customised to each individual taking into account the height, weight, ethnicity, and parity of the mother.
Amniotic fluid volume assessment can identify pregnancies with the most severe oligohydramnios as these have high rates of perinatal mortality, congenital anomalies and IUGR.
Doppler velocimetry looks for abnormal doppler wave forms in maternal uterine arteries and fetal vessels (umbilical arteries, middle cerebral arteries, ductus venosus) that will indicate poorer neonatal outcomes.
Abdominal circumference is the most sensitive single biometric indicator of IUGR and is usually performed at approximately 34 weeks of gestation.
Perinatal events and birth injury
Hypoxic-ischaemic encephalopathy
Hypoxic-ischaemic encephalopathy (HIE) is the result of a significant lack of oxygen and reduced blood flow to the fetal brain and other organs during labour and delivery.
Causes include:
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underlying conditions producing circulatory compromise in the mother
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utero-placental problems—umbilical cord prolapse, placental abruption
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fetal conditions—cardiac failure, feto-maternal haemorrhage
Sometimes the insult is more prolonged and chronic in nature, but both acute and chronic asphyxia can lead to HIE.
Infants with HIE are often in poor condition at birth and invariably require resuscitation, and the condition is described as mild, moderate or severe encephalopathy (see Sarnat stages in Table 2.1 ).
| Current pregnancy | Past medical history | Past obstetric history |
|---|---|---|
| maternal age over 40 years | chronic hypertension | previous birth weight <9th centile |
| maternal smoking | diabetes | previous stillbirth |
| drug misuse | renal impairment | |
| maternal BMI > 35 | ||
| multiple pregnancy | ||
| hypertension or preeclampsia | ||
| unexplained APH | ||
| concerns related to growth measurements |
| mild – stage 1 | moderate – stage 2 | severe – stage 3 |
|---|---|---|
| hyperalert | lethargic | coma |
| eyes wide open | reduced tone | weak or absent respiratory drive |
| does not sleep | diminished brainstem reflexes (pupil/gag/suck) | no response to stimuli |
| irritable | clinical seizures | floppy |
| seizures absent | diminished brainstem reflexes (pupil/gag/suck) | |
| usually lasts <24 hours | diminished tendon reflexes | |
| EEG severely abnormal |
| Erb’s palsy | Klumpke’s palsy | total palsy | |||
|---|---|---|---|---|---|
| nerve roots | C5, 6 and sometimes T1 | C8, T1 | C5-T1 | ||
| clinical presentation | weakness of arm decreased arm movements arm is adducted and internally rotated with elbow extended, forearm is in pronation and wrist is flexed (‘waiter’s tip’) ( Figure 2.1 ). | weakness of intrinsic muscles of hand leading to ‘claw hand’ | weakness of entire arm | ||
| Moro reflex | absent | present | absent | ||
| biceps reflex | absent | present | absent | ||
| radial reflex | absent | present | absent | ||
| grasp reflex | present | absent | absent | ||
| Severity | |
|---|---|
| grade 1 | germinal matrix haemorrhage with or without IVH (less than 10% of ventricle filled with blood) ( Figure 2.5 ). |
| grade 2 | IVH (10%–50% of ventricle filled with blood), typically without ventricular dilation. |
| grade 3 | IVH (greater than 50% of ventricle filled with blood) typically with ventricular dilation ( Figure 2.6a and 2.6b ). |
| grade 4 | periventricular haemorrhagic infarction. |
Relevant information contributing to the diagnosis of HIE includes:
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evidence of fetal distress
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sentinel events—cord prolapse, antepartum haemorrhage, shoulder dystocia
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low Apgar scores
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placental report indicating dysfunction
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Kleihauer-Betke test—if feto-maternal haemorrhage is suspected
Investigations
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blood gas—identify degree of acidosis
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electrolytes, glucose, calcium if seizures
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amplitude integrated electroencephalography (aEEG)
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infection screen
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cranial ultrasound (oedema or areas of parenchymal or basal ganglia/thalamic damage)
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doppler studies of cerebral flow velocity
Treatment and managment
Supportive treatment is required for those babies with multisystem involvement including ventilation in view of poor respiratory effort. Periods of hypo- and hyperoxia as well as hypo- and hypercapnia may develop and indicate a worse neurological outcome.
Therapeutic hypothermia is the only neuroprotective treatment effective in term infants with moderate or severe HIE. This involves a reduction of core body temperature to 33.5°C for 72 hours followed by a slow rewarming phase (0.5°C/hour increase) over 6 hours. The treatment must be initiated within 6 hours after birth for it to be beneficial.
Infants with HIE may develop overt seizures, whilst others will have seizures on aEEG without a clinical component—’electrical seizure activity’. There is no clear consensus on management, but many would treat seizures with a duration of over 3 min or greater than 3 seizures in 1 hour.
Cardiac dysfunction may require inotropic support and the issue may become evident during cooling when many infants show a hypothermia-induced bradycardia of around 70–90 bpm.
Transient renal impairment is common and careful fluid management is required. Potential hypoglycaemia should be avoided by an adequate glucose infusion rate. Liver dysfunction can cause coagulopathy and severe bleeding, which may require treatment with blood and clotting products. Hepatic and renal drug clearance is often impaired and doses may need adjustment and monitoring.
Important sequelae
Moderate and severe HIE have a high mortality and morbidity rate and many who do survive have significant intellectual disability and poor motor function. Despite therapeutic cooling, the combined outcome of death or disability at 18–24 months is around 50% with 25% mortality and 25% disability.
Several features can help to define the prognosis and those with poor feeding and decreased tone at 2 weeks will have a poor neurodevelopmental outlook. MRI of the brain between day 5–14 can identify abnormal signals in the posterior limb of the internal capsule, which again is indicative of a poor outcome. Epilepsy, vision or hearing difficulties, as well as behaviour and learning difficulties are all recognised consequences of hypoxic ischaemic encephalopathy.
Brachial plexus injury
Brachial plexus palsy is flaccid paralysis of the upper limb seen at birth, due to stretching, rupture or avulsion of some, or all, of the cervical and first thoracic nerve roots ( Table 2.3 ).
Risk factors:
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shoulder dystocia
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birth weight over 4 kg
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maternal diabetes—associated with macrosomia
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breech delivery—difficulty in extracting the trailing arm
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instrumental delivery
Other findings which may be seen are:
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fracture of humerus or clavicle with crepitus or swelling
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Horner’s syndrome—sympathetic nerve damage
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respiratory distress—phrenic nerve injury resulting in diaphragmatic paralysis
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encephalopathy—associated hypoxic ischaemic event
Investigations
Usually limited to chest x-ray to identify a clavicle or humeral fracture or diaphragmatic palsy. Nerve conduction studies or MRI may be required if surgical intervention is indicated.
Treatment and management
Parents are advised of the need for careful handling of infants in the first 1–2 weeks till the inflammation subsides but after this time, a formal exercise programme will be initiated by the physiotherapy team. About 70% to 80% of infants make a full recovery without intervention in 6 weeks to 3 months. The child should be referred to colleagues with expertise in nerve injuries if there is no improvement by 6 weeks.
Antenatal management of preterm labour
Accurate identification of women in true preterm labour allows appropriate application of interventions that can improve neonatal outcome such as the administration of antenatal corticosteroid therapy, prophylaxis against group B streptococcal infection or necessary transfer to a facility with an appropriate level of newborn care.
Risk factors for preterm labour include:
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previous preterm delivery
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multiple pregnancy
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advanced maternal age
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teenage mother
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smoking or drug abuse
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deprivation
Interventions aimed at reducing the risk of preterm birth include:
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education and health promotion programmes including smoking cessation, treatment of drug misuse, maintenance of a normal body mass index and longer intervals between pregnancies
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low-dose aspirin may reduce the risk of spontaneous preterm birth
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cervical cerclage placement may prolong gestation for women with a history of preterm birth
Management of preterm labour
The diagnosis of preterm labour is based on clinical criteria of regular painful uterine contractions accompanied by cervical dilation or effacement. Tocolytics can be used to try and delay preterm labour so that antenatal steroids and magnesium sulphate can be given.
Management of the high-risk pregnancy
Preterm birth can result in significant health consequences in both the short and long term. Pregnancies that are likely to produce infants at high risk of problems include those with:
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intrauterine growth restriction—from maternal, placental or fetal causes
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prolonged preterm rupture of membranes, presenting as infection or risk of infection or related poor lung growth
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congenital malformations from syndromic association
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chronic maternal illness—maternal diabetes and other medical conditions
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acute fetal compromise—placental abruption, cord prolapse
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twin or higher order pregnancy
Initial assessment and intervention in the delivery room:
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pregnancies at risk of difficulties should occur in a hospital with a level 3 NICU. Antenatal steroid administration for lung maturation and magnesium sulphate for neuroprotection should also be administered to the expectant mother.
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delivery room temperature needs to be kept above 25 o C and the use of a plastic covering for the preterm infant will help maintain better thermal control. Each degree below 36.5 o C is associated with increased mortality in preterm babies of about 28%.
Following birth
Most preterm or term infants will not need any intervention. The management outlined in the Resuscitation Council UK algorithm should be followed if intervention is required ( Figure 2.2 ).
Specific aspects of the assessment of the newborn require consideration.
Clamping of the cord can be delayed for up to 3 minutes in the preterm infant, although there is good evidence that clamping the cord after a good respiratory effort is established is more effective than time based delayed cord clamping. Positive End Expiratory Pressure (PEEP) support has been shown to be beneficial by establishing a functional residual capacity in the lungs. Routine airway suction with or without meconium has no benefit and is therefore not recommended.
Medical conditions in the preterm neonate
Respiratory distress syndrome
Respiratory distress syndrome (RDS) is primarily seen in premature babies and is the result of surfactant deficiency and immature lung development and therefore the incidence decreases with increasing gestational age. Risk factors for RDS include prematurity, maternal diabetes, absence of labour and lack of antenatal steroids. Antenatal steroids, surfactant therapy and noninvasive respiratory support have resulted in reduced mortality from RDS.
The preterm infant with RDS will have tachypnoea, grunting, chest wall retractions, nasal flaring and ‘head bobbing’. As the condition becomes more severe the baby becomes cyanotic and pale and may have apnoeic episodes.
Differential diagnosis
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transient tachypnoea of newborn (TTN)
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aspiration
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pneumonia or sepsis
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cyanotic congenital heart disease
Investigations
The chest x-ray will show the recognised changes of RDS with the reticulogranular pattern (ground glass) in the lung fields, an air bronchogram and low lung volumes ( Figure 2.3 ).
Treatment and management
Antenatal steroids reduce the incidence and severity of RDS and the consequent need for mechanical ventilation. Current recommendation is for them to be offered to all women between 24+0 and 33+6 weeks of pregnancy who are at risk of preterm delivery within 7 days. The ideal therapeutic window for administration is when delivery is expected 1 to 7 days after a complete course of treatment.
Surfactant can be given prophylactically to those infants who are at risk of RDS, even before signs of RDS develops, and is usually given within 10–30 mins of delivery. Rescue surfactant treatment is usually given within 12 hours when specific criteria for RDS severity are met (e.g., receiving noninvasive support and FiO 2 over 30%–40%). Both animal-derived and synthetic surfactants are available, although the former is usually used. New techniques for surfactant administration are minimally invasive surfactant therapy (MIST) and less invasive surfactant administration (LISA). These techniques administer surfactant in spontaneously breathing, nonintubated neonates by using a specialised catheter. These methods are associated with reduced incidence of BPD, duration of invasive ventilation and incidence of pneumothorax.
Mechanical respiratory support
Continuous positive airway pressure (CPAP) is a form of noninvasive respiratory support which delivers constant positive pressure and is delivered through fitted nasal devices. CPAP can be used from birth in a preterm baby to aid respiratory effort or after extubation following a period of ventilation.
Noninvasive positive pressure ventilation (NIPPV) provides support using a face mask or prongs and provides a positive pressure at preset intervals. It is thought to be superior to CPAP in small neonates.
High flow nasal cannulae (HFNC) have a similar efficacy as other forms of noninvasive respiratory support.
Indication for use of invasive mechanical ventilation include deteriorating respiratory function, recurrent apnoea, increasing oxygen requirement and worsening of hemodynamic status. Volume-targeted ventilation results in reduction of broncho-pulmonary dysplasia (BPD), pneumothorax and days of ventilation when compared to pressure limited modes. Early extubation to noninvasive respiratory support should be planned if a ventilated neonate has a good response to surfactant, but if conventional support fails then high frequency ventilation is used as rescue mode.
Ventilatory support aims to maintain oxygen saturations between 91% to 95%, but the high oxygen flows required leads to an increase in the incidence of retinopathy of prematurity and BPD. The use of caffeine citrate in preterm infants under 31 weeks reduces ventilation days, the incidence of BPD and cerebral palsy.
Bronchopulmonary dysplasia
Bronchopulmonary dysplasia (BPD) is defined as the need for respiratory support and supplemental oxygen at 36 weeks postmenstrual age, and its development is inversely proportional to gestational age and birth weight.
The most important risk factors for BPD are prematurity and low birth weight although some antenatal risk factors include maternal smoking and maternal hypertension. Neonates with persistent ductus arteriosus or who need mechanical ventilation with high pressures and volumes are also at risk of developing the condition.
Treatment and management
Antenatal interventions including the administration of antenatal steroids will make a significant impact of the development of BPD. If the preterm baby needs ventilatory support then noninvasive techniques should be considered, whilst surfactant, caffeine and steroids will all have a protective effect although the potential side effects of each needs to be considered.
The long-term management of BPD will vary depending upon the extent of residual lung dysplasia. Those babies with mild BPD may only require supplemental oxygen for a short period of time and may be discharged with a home oxygen supply. Those with more severe disease may require continued oxygen and home ventilation supported by a dedicated community respiratory team. Further information is presented in Chapter 17 , Respiratory.
The aim of any such treatment will be to ensure maximal growth and development with the intention that developing lung tissue will be sufficient to allow the child to dispense with ventilator support.
Patent ductus arteriosus
The ductus arteriosus in term babies usually closes within 1–3 days after birth but in the preterm neonate about 40% fail to close spontaneously and usually leads to clinical problems. Neonates at risk of developing a clinically significant patent ductus arteriosus (PDA) include those who are small for gestational age, those with late onset sepsis and those who are given excessive fluids during the first days after birth.
A persistent ductus arteriosus is defined as one that is still present one month after the baby should have been born and therefore excludes preterm babies who are still within their due dates. This persistence is associated with BPD, NEC and intraventricular haemorrhage.
Echocardiography is required to assess the presence and impact of a PDA.
The symptomatology of PDA is dependent on ductal size, shunt volume, and the extent of a ‘circulatory steal’ effect. Clinical features of a hemodynamically significant PDA include:
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pan-systolic, pan-diastolic murmur (continuous, machinery murmur)
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active precordium with a wide pulse pressure
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features of cardiac failure
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pulmonary oedema
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high oxygen requirement
Treatment and management
There is limited consensus regarding the treatment of a PDA. Conservative management includes fluid restriction, diuretics and the application of positive end-expiratory ventilatory pressure.
Prophylactic treatment refers to treating all babies within 24 hours, without any screening and prior to any symptoms or signs. Treatment is usually started after 6 hours but before 24 hours of birth with medications such as indomethacin, ibuprofen or paracetamol. However, there is no difference in mortality or composite outcome of death or neuro-disability at 18–36 months with this approach. It is estimated that up to 60% of these infants would close their duct spontaneously.
Though there are advantages of prophylactic treatment in avoiding unnecessary drug exposure, the concern is that the damage could have already been done by the time the PDA becomes symptomatic. Both indomethacin and ibuprofen have been reported to have similar effectiveness for ductal closure (60%–80%), and ibuprofen has been reported to have a better side effect profile. Paracetamol can be used for ductal closure if there is contraindication (NEC, IVH) to use indomethacin or ibuprofen.
Surgical ligation of the PDA is performed in infants with hemodynamically significant PDA where medical treatment has failed or is contraindicated, particularly if the baby remains ventilated and weaning is difficult.
Necrotising enterocolitis (NEC)
Necrotising enterocolitis describes an inflammatory process in the small and large bowel that can affect preterm and, occasionally, term babies. The pathogenesis remains unclear but is multifactorial although there are recognised risk factors that include IUGR, prolonged resuscitation with low APGAR scores and neonatal sepsis. Some factors have been identified that reduce the risk of developing NEC and these include antenatal steroids, breast milk feeding and probiotics.
In preterm neonates, NEC presents around 2–3 weeks of age with features suggestive of sepsis and gastrointestinal obstruction. Abdominal distension, bilious aspirates and blood with mucus in the stool are all characteristic findings. Disease progression leads to peritonitis, hypotension, DIC and shock.
A differential diagnosis would include spontaneous isolated intestinal perforation, congenital bowel anomalies and a food-protein induced enterocolitis.
Investigations
An abdominal x-ray will identify bowel wall oedema and thickening along with intramural and portal venous gas ( Figure 2.4 ). Pneumatosis intestinalis is a pathognomonic finding and indicates that the mucosal surface is damaged and bowel gases have tracked along the tissue planes. Sentinel bowel loops (fixed loops) may indicate bowel necrosis without pneumatosis.
