Preterm birth is defined by the World Health Organization as birth before 37 completed weeks of pregnancy. This can be subcategorised to late preterm (34–37 weeks), early preterm (<34 weeks), very preterm (28 to <32 weeks) and extremely preterm (<28 weeks).
In Australia, as per the Australian Institute of Health and Welfare in 2016, 8.6 per cent of babies were born preterm, with most of these births occurring at gestational ages between 32 and 36 completed weeks. That’s about 25000 babies every year in Australia. The average gestational age for all preterm births was 33.3 weeks. The common neonatal complications in premature babies are described below.
Respiratory distress syndrome
Respiratory distress syndrome (RDS), or hyaline membrane disease, is almost exclusively a disease of premature infants. It is caused by deficiency of surfactant protein leading to atelectasis, ventilation perfusion mismatch and hypoventilation, with resultant hypoxaemia and hypercarbia. The incidence and severity of RDS are inversely related to the gestational age. Symptoms include tachypnoea, desaturation, respiratory distress and apnoea. Chest radiograph usually shows poor lung expansion, air bronchogram and reticulogranular/ground glass opacity. Advances in treatment, such as antenatal steroids, early use of CPAP, early administration of surfactant and availability of better neonatal care, have improved the survival of extremely premature newborns. Common differential diagnoses are infection, transient tachypnoea of newborn, aspiration syndrome and pulmonary air leaks.
Apnoea of prematurity
Apnoea of prematurity (AOP) is defined as the cessation of breathing for more than 20 seconds, or for less than 20 seconds if it is accompanied by bradycardia or oxygen desaturation. It is rare after 36 weeks of gestation. AOP can be central, obstructive or mixed apnoea. Periodic breathing maybe observed for 2–6 per cent of breathing time in healthy term neonates and as much as 25 per cent of breathing time in preterm neonates. The cause of AOP is the immaturity and/or depression of the central respiratory drive to the respiratory muscles. Younger gestational age at birth is associated with increased incidence of AOP. Extremely premature babies are routinely monitored during neonatal intensive care unit stay and treated prophylactically with caffeine citrate (intravenously or orally) until 34 weeks. Apnoea can be a symptom of infection, RDS, intraventricular haemorrhage (IVH) or hypoglycaemia and should be excluded. The common treatments include tactile stimulation, methylxanthine derivatives, oxygen, nasal CPAP and mechanical ventilation.
Transient tachypnoea of newborn
Transient tachypnoea of newborn (TTN) is a common cause of respiratory distress in neonates and is caused by delayed clearance of a fetal lung fluid. TTN is usually present with other signs of respiratory distress and increased oxygen requirements within the first few hours of life. TTN is more common in late preterm and mature neonates and is a self-resolving disorder with an excellent prognosis, usually over a 24- to 72-hour period. Caesarean delivery is associated with increased risk of TTN. The common differential diagnoses are sepsis, pneumonia, meconium aspiration syndrome, air leak, persistent pulmonary hypertension and cyanotic congenital heart disease. The characteristic x-ray findings include prominent perihilar streaking, which correlates with the engorgement of the lymphatic system with retained lung fluid and fluid in the fissures. The treatment is mainly supportive and includes intravenous fluids, supplemental oxygen, CPAP and escalation of respiratory support if needed.
Bronchopulmonary dysplasia (BPD) is the most common cause of chronic lung disease in infants. It is defined as oxygen requirement at 28 days of age or at 36 weeks gestational age. The incidence is around 48 per cent in gestational age below 27 weeks. The aetiology is multifactorial, including lung immaturity, respiratory distress, oxygen therapy and mechanical ventilation. Gestational age and birth weight are the most important protective factor of BPD. Strategies that avoid excess oxygen and ventilation, better infection control and optimise nutrition are some of the steps to reduce the incidence and severity of BPD. Despite best efforts, BPD remains a problem. Even though lung growth continues to occur in early childhood, studies have showed that survivors have abnormal lung structure and function compared to term equivalents in childhood.
Persistent ductus arteriosus
Persistent ductus arteriosus (PDA) is the persistent communication between descending thoracic aorta and the pulmonary artery. Normally functional closure of the ductus arteriosus occurs in the first few hours of life in infants born at term. The cause of PDA in preterm infants is not fully understood, but contributing factors include the immaturity of the smooth muscle structure and the inability of the immature lungs to clear circulating prostaglandins. The decision to treat PDA is based on its haemodynamic significance. The treatment options are prostaglandin inhibitors (ibuprofen, indomethacin, paracetamol) or surgical ligation.
Feeding intolerance, leading to postnatal growth restriction and failure to thrive, is a major issue in preterm neonates, especially those of extremely low birthweight. Optimisation of feeding without increasing the risk of necrotising enterocolitis is the priority in treatment. Common strategies for this include exclusive use of expressed breastmilk, preferring donor breastmilk over formula where possible, slowing gradation of feeds not more than 20–30 ml per day and carefully monitoring for signs of feeding intolerance.
Necrotising enterocolitis (NEC) is the most common acquired disease of gastrointestinal system in premature infants and newborns, causing ulcerative inflammation of the intestinal wall. NEC has high mortality in premature infants of up to 40 per cent. The onset of NEC typically occurs during the first several weeks after birth, with the age of onset inversely related to gestational age at birth. Presenting symptoms may be subtle, nonspecific systemic symptoms or localised abdominally. Management depends on the clinical stage of the disease, measured by Bell’s stages 1–4. Treatment options include nil by mouth, nasogastric decompression and intravenous antibiotics. Advanced-stage NEC needs fluid resuscitation, escalation of respiratory support and surgical intervention.
The incidence of IVH is 15–20 per cent of neonates born before 32 weeks and is uncommon in term newborns. The important predisposing factors include ischemia/reperfusion, fluctuations in cerebral blood flow and increase in the cerebral venous pressures. Risk factors include maternal factors, such as infection/inflammation and haemorrhage; lack of antenatal steroids; and external factors, such as mode of delivery or neonatal transport. IVH is often clinically silent. Diagnosis is invariably made by head ultrasound; a routine practice for all preterm neonates under 32 weeks, in the first two weeks of life. Infants with large IVH may present with rapid clinical deterioration, drop in haemoglobin and neurological signs, such as seizures and altered neurological status. IVH is graded from 1–4 based on the severity. Management mainly consists of supportive care and prevention should be the primary goal. Serial monitoring – by regular head ultrasound and head circumference measurements – is required, with neurosurgical intervention necessary if any progression to post-haemorrhagic hydrocephalus. Several recent studies suggest that even infants with grade 1 and 2 IVH are at increased risk of neurodevelopmental impairment, when compared to those without.
Periventricular leukomalacia (PVL) is a distinctive lesion found in the immature white matter of premature newborns, likely resulting from the interaction of multiple pathogenetic factors. The two key features in the pathogenesis are hypoxia-ischemia affecting the watershed regions of the white matter and the particular vulnerability of periventricular white matter of the premature brain. PVL is a clinically silent lesion, evolving with few or no outward clinical signs until weeks to months later, when a spasticity is first detected, or even at a later age when present with cognitive disabilities in school. The diagnosis is usually made by head ultrasound in the newborn period. The ultrasound can underestimate the incidence of PVL. MRI is more reliable in identifying the abnormal signal intensity, although routine use of MRI to detect white matter injury is not recommended. There is currently no medication available for specific treatment of PVL. Management is limited to identification of cognitive or motor impairments and early intervention therapy.
Extreme preterm and very low birthweight (<1500 g) babies are at risk of late onset sepsis. The mortality rate is higher if there is a gram-negative infection. Nearly half of all late onset sepsis is caused by coagulase-negative staphylococcus.
Preterm infants are more prone to hypothermia, compared to term babies, because of their high ratio of skin surface area to weight, highly permeable skin, decreased subcutaneous fat, less brown fat and reduced glycogen stores. Because of cold stress, they are prone to hypoglycaemia, metabolic acidosis and increased oxygen consumption. Maintaining a thermoneutral environment is very important in management of preterm babies. Extreme preterm babies should be placed in a polyethylene bag soon after delivery to prevent heat loss. Babies are nursed in heated incubators with humidification to reduce evaporative heat loss.
Hypoglycaemia is one of the most common pathologies encountered by preterm infants in the neonatal intensive care unit. Preterm, small for gestational age and intrauterine growth-restricted neonates are especially vulnerable. Nearly 30–60 per cent of these high-risk infants are hypoglycaemic and require immediate intervention. Preterm neonates are uniquely predisposed to developing hypoglycaemia and its associated complications due to their limited glycogen and fat stores, inability to generate new glucose using gluconeogenesis pathways, have higher metabolic demands due to a relatively larger brain size, and are unable to mount a counter-regulatory response to hypoglycaemia. They are usually managed with parenteral fluids in the initial days and feeds are introduced and graded up as per tolerance.
Jaundice is one of the most common conditions requiring medical attention in newborn babies. Approximately 60 per cent of term and 80 per cent of preterm babies develop jaundice in the first week of life. Hyperbilirubinemia occurs when there is an imbalance between bilirubin production, conjugation and elimination. The breakdown of red blood cells and haemoglobin cause unconjugated bilirubin to accumulate in the blood. Unconjugated bilirubin binds to albumin and is transported to the liver where it is converted to conjugated bilirubin. Conjugated bilirubin is water soluble and able to be eliminated via urine and faeces. Unbound unconjugated bilirubin is lipid soluble and can cross the blood-brain barrier. When jaundice has a high peak level, regardless of the cause, treatment is required to prevent brain damage. In addition, some underlying causes of hyperbilirubinemia are serious or even life- threatening illnesses that require urgent treatment. Jaundice is generally managed with phototherapy, optimisation of feeds and fluids, and, in severe cases, exchange transfusion.
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