According to the Perinatal Society of Australia and New Zealand Perinatal Death Classification, spontaneous preterm birth, alongside congenital abnormalities and unexplained antepartum deaths, accounts for over half of perinatal deaths (AIWH 2006). It has been well documented that preterm births are the primary cause of neonatal morbidity and mortality. Table 41.1 indicates the births by gestational age and birth status for 2006 in Australia.

Table 41.1 Neonatal births and deaths by gestational age, Australia 2006

Gestational age (weeks)	Live births (%)	Fetal deaths (%)
20–27	0.5	58.8
28–31	0.8	9.0
32–36	6.4	14.1

(Data from AIWH 2006)

Birthweight is a key indicator of health status, with low birthweight having a significant effect on a neonate’s wellbeing. Many studies indicate that low-birthweight babies have an increased risk of perinatal mortality, serious conditions during the immediate neonatal period (respiratory distress syndrome, intracranial haemorrhages), bacterial infections, metabolic conditions, feeding problems, lifelong intellectual or physical ability and/or chronic ill-health.

The average birthweight of a preterm is less than 2500 g; however, this varies in relation to the health of the pregnancy, length of gestation at birth and the cause for prematurity. Neonates can be placed into the following World Health Organization (WHO) low-birthweight categories:

• low birthweight (LBW; <2500 g)

• very low birthweight (VLBW; <1500 g)

• extreme low birthweight (ELBW; <1000 g).

These cut-off weights are based on global epidemiological observations whereby two-thirds of preterm babies are classified as low birthweight (Tucker & McQuire 2005). In Australia, approximately 2500 neonates are born each year weighing less than 1500 g, and over 1000 are born in the extreme low birthweight category (Monash Institute of Medical Research 2007). Very-low-birthweight neonates represent 3% of all live births in New Zealand. Of these, more than 37% are born at less than 32 weeks gestation and 32% weigh less than 1500 g (Australian Medical Association 2001).

Preterm neonates represent approximately 75% of neonatal intensive care unit (NICU) level III admissions. In 2004, 5724 Australian babies were admitted to an NICU, with 43.6% being of a gestational age of less than 32 weeks and 39.3% having a birthweight of less than 1500 g (AIWH 2006). Over the past decade, advances in neonatal intensive care have increased the limit of human viability to a much younger gestational age, although the survival rate for neonates born between 22 and 24 weeks is still very low (Pignotti & Donzelli 2008). Overall survival for preterm neonates at more than 28 weeks gestation is between 90% and 98% (Engle et al 2005).

Despite the increased survival of high-risk neonates this has not, however, resulted in decreasing the associated morbidity (American Academy of Pediatrics 2008). The majority of neonates born at less than 25 weeks gestation have an increased risk of death before, during or after

Figure 41.1 Neonate of 23 weeks gestation

birth in the NICU. Those who survive are at risk of death during childhood, and approximately half will suffer from moderate or severe neurodevelopmental disability. At the age of six years, some of those previously considered to be healthy will show some kind of disability (MacDonald 2002; Pignotti & Donzelli 2008). Current evidence indicates that 90% of neonates born at 26–28 weeks gestation will develop into normal, healthy children (Johnston et al 2003).

Characteristics

Preterm neonatal characteristics will depend on the gestational age at birth. Generally, preterm neonates will show the following common characteristics:

• birthweight less than 2500 g

• thin, shiny, pinkish red skin

• prominent surface veins

• little body fat

• little scalp hair, with lots of fine hair (lanugo) on the face and trunk

• weak cry and body tone

• small and underdeveloped genitals.

In addition, the preterm baby will have a head circumference that exceeds that of the chest. The chest tends to be relatively small and narrow, with no breast tissue. The face of the preterm neonate is triangular, with a pointed chin, and the fontanelles and sutures are widely spaced due to poor ossification. Ears on the preterm are easily folded, lacking firmed cartilage. Also, the length of the trunk in proportion to the limbs is greater in the preterm than in the term neonate. The skin in the preterm is pinkish red (plethoric) with prominent surface veins due to the absence of subcutaneous fat and increased level of red blood cells. The protective creamy white substance known as vernix is more plentiful. The limbs are thin, with decreased muscle tone, and the nails are soft. With neonates of less than 34 weeks gestation, the creases in the feet are almost absent. In the preterm female, the labia minora are prominent and gaping, and the male usually has incompletely descended testes. Furthermore the suck-and-swallow reflex is uncoordinated in preterm neonates of less than 34 weeks gestation.

Gestational age assessment

Many scoring systems have been developed over the years in order to estimate the gestational age of the neonate. These scoring systems require a complete and careful examination of the neonate. The scoring system examines developmental characteristics that are primarily related to the neonates’ maturity, thus providing the healthcare professional with an indication of whether the neonate is small for gestational age or preterm. Gestational assessment should be performed within the first 2–42 hours of life, as neuromuscular maturity can be influenced by maternal medications administered during labour. The two most commonly used scoring systems are the Dubowitz and, more recently, the Ballard, an adaptation of the former. The Ballard scoring system evaluates six physical and six neuromuscular characteristics of maturity. Each category is rated from a scale of –1 to 5 (–1 for extreme prematurity through to 5 for postmaturity). At the end of the assessment the physical and neuromuscular scores are added together and matched to the assessment tool (Fig 41.2, overleaf) to give an estimated gestational age.

Figure 41.2 Gestational age assessment tool—the Ballard score

(Ballard et al 1991)

Preterm labour and birth care

In most cases it should be possible to diagnose the onset of preterm labour early enough to ensure that the birth occurs in a maternity unit containing the necessary neonatal services and thus avoid the greater hazard of transfer after birth. During a preterm labour, the midwife should continuously monitor the fetal heart rate to detect any form of fetal compromise. The midwife should also avoid giving narcotics to the woman, in order to prevent respiratory depression in the neonate at birth. All resuscitation equipment must be checked and ready before the birth. It is important that an experienced neonatologist and midwife be present at the birth of the preterm to ensure immediate and expert resuscitation. The degree of resuscitative measures is relatively related to the gestation of the preterm neonate. In general, the approach taken to resuscitate neonates born at greater than 32 weeks gestation is the same as term neonates. Neonates born at less than 32 weeks gestation or less than 1500 g require more active support; while neonates of less than 28 weeks require intubation and assisted ventilation (Fowlie & McGuire 2005).

Cold stress at birth must be prevented, as this increases neonatal oxygen requirements and reduces surfactant production, resulting in hypoglycaemia and acidaemia (Fowlie & McGuire 2005). The neonate, therefore, must be dried quickly and thoroughly with warm towels and placed under a radiant heater immediately after birth.

Specific preterm problems

The preterm neonate is unable to adequately perform many physiological functions, due to anatomical and functional immaturity. The aim of neonatal care is, therefore, to compensate and support these deficiencies until support is no longer needed. The main clinical problems the preterm neonate encounters are:

• Birth asphyxia—can occur if there is any disruption to the oxygen supply prior to or during birth, due to reduced energy reserves of the preterm neonate.

• Respiratory distress—this is the most common problem experienced by preterm neonates, and is exacerbated by younger gestational age. Preterm neonates have weak muscles and immature respiratory control. It is not uncommon for the preterm neonate to breathe well initially but later develop expiratory grunt, apnoeic episodes and cyanosis, requiring respiratory support. Respiratory conditions experienced by preterm neonates are discussed later in this chapter; they include apnoea, respiratory distress syndrome, transient tachypnoea of the newborn, pneumothorax, pneumonia and bronchopulmonary dysplasia.

• Patent ductus arteriosus—the ductus arteriosus fails to close in very preterm neonates due to immaturity and as a consequence of the chemical imbalance that results from hypoxia and ventilation–perfusion mismatching. Closure of the ductus is usually achieved by a course of indomethacin, with surgical ligation sometimes being necessary.

• Metabolic disturbances—these include hypoglycaemia, hypocalcaemia, hypomagnesaemia, hyponatraemia and hypokalaemia.

• Susceptibility to infection—this is increased due to low maternal immunoglobulin G (IgG) levels, a less efficient skin barrier, fewer immune cells, and being subjected to more invasive procedures and multiple caregivers.

• Thermal instability—preterm neonates have little or no brown fat stores to maintain their core temperature. In addition, preterm neonates have a larger surface area relative to their size, with thin skin, which facilitates rapid heat loss. Those born at less than 30 weeks gestation also have porous skin, allowing evaporation of fluids. The aim of care,

therefore, is to maintain body temperature within the thermoneutral range, thus reducing energy and oxygen requirements.

• Jaundice—physiological jaundice in preterm neonates is exacerbated due to an immature liver, resulting in delayed conjugation of bilirubin. This will be discussed in more detail below.

• Neurological problems—these include intracranial haemorrhage, the risk factors for which include poor skull ossification, fragile blood vessels and episodes of hypotension, hypertension or hypoxia.

• Gastrointestinal intolerance and necrotising enterocolitis (NEC)—NEC is an inflammatory disease of the bowel usually associated with septicaemia.

• Ophthalmic problems—these include retinopathy of prematurity, with the major risk factor being excessive oxygen exposure or fluctuating quantities; myopia; and strabismus (Henderson & Macdonald 2004; Levene et al 2000).

In addition to the above, preterm neonates also face many another challenges, such as:

• Diminished primitive survival reflexes—these include the suck, swallow and gag reflex.

• Renal immaturity—inability to concentrate urine and excrete an acid load, resulting in late metabolic acidosis.

• Surgical lesions—including the possibility of undescended testes, inguinal and umbilical herniae.

• Haematological problems—this includes haemorrhagic disease of prematurity due to accentuation of the normal neonatal deficiency of vitamin-K-dependent clotting factors; and iron-deficiency anaemia resulting from frequent blood sampling, often requiring a transfusion of packed red blood cells (Henderson & Macdonald 2004; Levene et al 2000).

Clinical point

There is extensive research demonstrating that the use of breastfeeding (Carbajal et al 2003) and sucrose (Gibbins et al 2002; Gradin et al 2002) can safely and effectively provide analgesia to neonates receiving painful procedures (Thomson 2004).

Small for gestational age

A small-for-gestational-age (SGA) neonate can be preterm, term or post-term, as intrauterine growth restriction (IUGR) can commence at any time during pregnancy. This section outlines the definition and causes for an SGA neonate and discusses IUGR, the pathological counterpart for SGA. The main problems encountered by the SGA neonate post-birth are also mentioned.

Definition and cause

‘Small for gestational age’ is a term used to describe a neonate whose birthweight, length and/or head circumference is less than the 10th percentile, or greater than 2 standard deviations below the mean, than for the expected gender-specific gestation. The cut-off birthweight for an SGA term neonate is 2500 g. Consideration to variables such as maternal height, weight, parity, ethnicity and geographical location should be considered when using standardised growth charts, as a birthweight below the 10th percentile in one population may not fall below the 10th percentile growth curve in another (Levene et al 2000).

Some SGA neonates are small because they have reached their appropriate growth potential; these neonates are genetically small, well proportioned and developmentally normal. Other SGA neonates are small as a result of pathological factors affecting the fetal growth process. This pathological condition is known as IUGR and is the most common underlying condition leading to SGA.

The term IUGR suggests a fetus failing to meet its full fetal growth potential due to factors inhibiting the normal growth process (Groom et al 2007). The most common cause for IUGR is uteroplacental dysfunction resulting in the inadequate delivery of oxygen and nutrients necessary for adequate fetal growth and development of organs and tissues. The terms SGA and IUGR are sometimes used interchangeably; however, these terms are not synonymous. A neonate who is born SGA may not necessarily have suffered from IUGR, and neonates who are born after a short period of IUGR are not necessarily SGA (Lee et al 2003).

Generally speaking, IUGR affects approximately 5% of the general obstetric population and carries an increased risk of perinatal mortality and morbidity. Infants who weigh less than 2500 g at term have a perinatal mortality rate that is 5–30 times greater than that of infants whose birthweights are at the 50th percentile. The mortality rate is 70–100 times higher in infants who weigh less than 1000 g (Peleg et al 1998). IUGR fetuses are at greater risk of stillbirth, birth hypoxia, neonatal complications and impaired neurodevelopment, and possibly type 2 diabetes and hypertension in adult life (RCOG 2002; Sheridan 2005). However, the vast majority of term SGA neonates have no appreciable morbidity or mortality (RCOG 2002).

Approximately 80%–85% of neonates with a birthweight below the 10th percentile for gestational age are constitutionally small but healthy; in the remaining 15%–20%, the cause of IUGR is pathological (Peleg et al 1998; Sheridan 2004). Of the 20% of IUGR neonates, only 10%–15% are ‘true’ IUGR cases, and the remaining 5%–10% are affected by chromosomal/structural anomalies or chronic intrauterine infection (Manning 2004). The causes of ‘true’ IUGR are many, including fetal (multiple pregnancy); maternal (medical factors, socioeconomic and nutritional factors, drugs); and placental factors (recurrent abruption, praevia and immunological disorders) (Sheridan 2005).

The recognition of IUGR involves consideration of risk factors and careful clinical assessment of fetal growth throughout the pregnancy (Manning 2004). If the symphysis fundal height measurement indicates a lag of 4 cm or more, IUGR should be suspected (Bernstein & Gabbe 1996) and further investigations indicated. Fetal growth investigations may include ultrasound, amniotic fluid index (AFI), Doppler studies and biophysical profile (BPP) (Magriples & Copel 2004). Correct postnatal classification of an SGA neonate as being either ‘normal but small’ or ‘IUGR’ requires an accurate assessment of gestational age, correct measurement of birthweight and length at birth, and a precise and comprehensive physical and neurological assessment within 24 hours post-birth. Refer to Chapter 30 for information on physical assessment.

Symmetric and asymmetric SGA neonates

Small for gestational age neonates experiencing IUGR are generally classified as symmetric or asymmetric based on appearance.

Symmetric SGA neonates experience growth restriction either at the time of conception or during the first trimester of pregnancy, when early fetal cellular hyperplasia is impaired; this produces a proportionate decrease in all fetal organs (Sheridan 2005). The causes for this early onset are often related to fetal factors such as chromosomal or structural anomalies, intrauterine infections, severe maternal vascular disease, severe placental insufficiency, or a constitutionally small neonate (Peleg et al 1998). A symmetric IUGR neonate will usually have weight, head circumference and length all below the 10th percentile with, possibly, some limited brain growth. The neonate may appear active on inspection and demonstrate more-developed neurological responses because of a more advanced age in comparison with size. However, the neonate usually appears malnourished with poor skin turgor, sutures in the skull may be separated widely, and the abdomen may be sunken (Klossner & Hatfield 2006).

Asymmetric growth restriction usually occurs at >32 weeks gestation and commonly results from uteroplacental dysfunction. A fetus experiencing asymmetric growth restriction adapts to a hostile intrauterine environment by redistributing blood flow to the vital organs of the brain, heart and placenta (Peleg et al 1998) in an attempt to preserve brain growth. This gives rise to an SGA neonate with normal head size but a small abdominal circumference caused by decreased liver size; scrawny limbs due to

Table 41.2 Causes of IUGR

Fetal	Infection (e.g. cytomegalovirus, herpes, rubella, toxoplasmosis) Multiple gestation Genetic disorders (e.g. trisomy 18, trisomy 21) Congenital malformations (e.g. congenital heart disease, diaphragmatic hernia, tracheo-oesophageal fistula) Inborn errors of metabolism
Maternal	Preeclampsia Chronic kidney disease Advanced diabetes Heart or respiratory disease Malnutrition, anaemia Substance abuse (alcohol, drugs) Cigarette smoking
Placental	Placental abruption Placenta praevia Twin-to-twin transfusion syndrome Small placental size
Environmental	High altitude—low environmental oxygen concentrations Toxins
Constitutional	Familial and racial background

decreased muscle mass; and thinned skin as a result of decreased fat. However, if the insult causing asymmetric growth restriction is sustained long enough or is severe enough, the fetus may lose the ability to compensate and will become symmetrically growth-restricted (Peleg et al 1998). Asymmetrically growth-restricted neonates typically appear thin and pale with loose skin. They have a malnourished, wide-eyed look, with a head that is disproportionately large when compared with the rest of the body. The umbilical cord appears thin and dull-looking, compared with the shiny plump cord of a neonate of average size for gestational age (Klossner & Hatfield 2006).

Labour and birth

Perinatal asphyxia is a risk during labour if IUGR is caused by placental insufficiency, as uterine contractions result in the decrease or cessation of maternal placental perfusion. In addition, perinatal asphyxia may predispose the fetus to meconium aspiration whereby the compromised fetus passes meconium in utero and begins to gasp. (Further information on meconium aspiration can be found later in this chapter in the section on cardiorespiratory conditions.) The fetus should therefore be monitored carefully and continuously during labour. It is also recommended that SGA fetuses are birthed in a maternity unit that has available neonatal expertise and facilities to deal with the associated neonatal morbidities. A healthcare professional skilled in resuscitation should be present at the birth, and where possible a neonatologist should be present if the gestation is extremely preterm or growth restriction is severe (RCOG 2002).

Specific problems

Problems which the SGA neonate may encounter once born include:

• Hypoglycaemia—SGA neonates have decreased tissue glycogen stores, decreased gluconeogenesis and high glucose requirements. Hypoglycaemia may develop any time within the first few days post-birth, particularly when there is a prolonged interval between feeds or nutritional intake is poor. Early enteral and/or intravenous nutrition and glucose monitoring is recommended.

• Temperature instability—SGA neonates have a large surface area and poor subcutaneous fat stores, therefore they should be nursed in a thermoneutral environment.

• Polycythaemia—SGA neonates commonly experience fetal hypoxia which causes increased erythropoietin production. The neonate with polycythaemia at birth appears ruddy and may be tachypnoeic and lethargic.

• Respiratory distress—SGA neonates may experience respiratory distress due to prematurity, meconium aspiration syndrome, or persistent pulmonary hypertension of the newborn.

• Necrotising enterocolitis—SGA neonates, particularly preterms who have had placental insufficiency and abnormal umbilical Doppler studies, are at increased risk.

Outcome

Most infants who are born growth-restricted in utero usually have normal growth rates during infancy and childhood, although studies have demonstrated that at least one-third of SGA IUGR neonates never achieve normal height. A number of studies have also reported an increased risk for low intellectual performance and poor cognitive development among growth-restricted neonates (Bergvall et al 2006; Feldman & Eidelman 2006). Term SGA neonates have no increased risk of severe neurological morbidity compared with the average gestational age (AGA) neonate; however, studies have noted increased hyperactivity, short attention span and learning problems. Preterm SGA neonates, on the other hand, have more minor neurological abnormalities than preterm AGA neonates. The preterm neonates’ neurological development is related to the degree of growth restriction and prematurity. Symmetric SGA neonates are generally smaller and relatively underweight throughout life, whereas asymmetric SGA neonates have an accelerated rate of growth in the first six months followed by normal development.

NUTRITION

Nutrition is vital for adequate neonatal growth, resistance against infection, neurological and cognitive development, and overall long-term health. Nutritional support is paramount to the preterm and sick neonate. Adequate nutrition improves surgical outcome, decreases morbidity and shortens hospital stays (Merenstein & Gardner 2006). The provision of adequate nutrition to a preterm and sick neonate is a challenge to any healthcare professional due to diminished suck–swallow coordination, gastrointestinal immaturity and increased risk of necrotising enterocolitis and acute illnesses; medical interventions, such as umbilical catheters, may also impede the administration of feeds. This section outlines the nutritional requirements, management and risk factors for the preterm and sick neonate.

Clinical point

An NICU neonate’s weight and head circumference are generally measured daily. Results are recorded on a growth chart, indicating adequacy of gestational growth and effectiveness of nutritional support.

Clinical point

Neonates lose 10% of their birthweight in the first week after birth (1–3 days). Following this drop, the expected daily weight gain is 20–30 g/day.

Feeding methods

Nutritional support can be provided either parenterally or enterally or as a combination of the two. Transitional parenteral nutrition (TPN) is used to supplement enteral nutrition in the form of amino acids to the NICU neonate who is unable to tolerate enteral feeds due to gestation or acute illnesses. Parenteral nutrition is administered intravenously via a percutaneous central venous line. Neonates who have experienced significant asphyxia (hypoxia, metabolic acidosis and hypercapnia) or hypotension may have ischaemic injury to the intestine. Therefore it is not uncommon for these infants to receive parenteral fluids before small feeds are introduced, allowing the potentially compromised gastrointestinal mucosa to recover and avoid complications such as necrotising enterocolitis (Hashim & Guillet 2002). Enteral feeding involves the administration of breast milk or breast-milk substitute into the stomach, stimulating gut hormone secretion and motility and thus assisting the functional adaptation of the gastrointestinal tract (Bombell & McGuire 2008).

Intragastric feeding via an orogastric or nasogastric tube, breast, cup or bottle may be tried, depending on the clinical condition, gestational age and the responses of the neonate. Fetal sucking is seen as early as 13 weeks gestation (Hafstrom & Kjellmer 2000); however, the suck–swallow–breathing coordination is not efficient until nearer term. Preterm neonates of less than 34 weeks gestation are therefore usually fed via an orogastric or nasogastric tube (Hashim & Guillet 2002; Levene et al 2000). Illnesses that increase energy expenditure, such as respiratory or cardiac diseases, or neonates with congenital conditions may also prevent the neonate from suckling, resulting in the provision of intragastric feeds. Intermittent gastric feeds benefit the preterm neonate as they have small gastric capacity and assist the sick neonate in the prevention of respiratory compromise from a full stomach (Henderson & Macdonald 2004).

Clinical point

Neonates are obligatory nose-breathers. Nasogastric tubes can cause partial nasal obstruction, increased airway resistance, and increased work of breathing (Daga et al 1999); therefore an orogastric tube is preferred until respiratory compromise is alleviated.